Hospitalists and ED physicians belong to two of the largest U.S. medical specialties and increasingly they are the only physicians seen by some hospitalized patients. Comanagement between the specialties is increasing in some hospitals, and in others, they might be the only physicians in the building after hours. They share similar workspaces, schedules, and responsibility for decisions about the most expensive care in medicine.

And yet there is not enough collaboration between the two specialties beyond brief phone encounters at handoff, says hospitalist Alpesh Amin, MD, MPA, MACP, SFHM, executive director of the hospitalist program at the University of California at Irvine. Dr. Amin coauthored a recent review highlighting opportunities for closer HM-ED collaboration with Charles Pollack Jr., MD, MA, FACEP, FAAEM, FAHA, who chairs the emergency department at Pennsylvania Hospital in Philadelphia.

A good place to start is for the two groups to simply sit down together regularly to discuss matters of common interest, perhaps monthly or quarterly, Dr. Amin says.

"Talk about clinical pathway development for common hospital diagnoses and how to improve admission processes," he adds. "There may be a role for the hospitalist in the emergency department when the patient gets handed off for hospital admission."

Collaboration also can improve patient flow and reduce ED diversion, shorten boarding times in the ED, and enhance quality and patient safety, Dr. Amin adds. "It's about how to optimize patient care for the benefit of the patient and the hospital," he says.

Visit our website for more information on hospitalists in the ED.

Hospitalists and ED physicians belong to two of the largest U.S. medical specialties and increasingly they are the only physicians seen by some hospitalized patients. Comanagement between the specialties is increasing in some hospitals, and in others, they might be the only physicians in the building after hours. They share similar workspaces, schedules, and responsibility for decisions about the most expensive care in medicine.

And yet there is not enough collaboration between the two specialties beyond brief phone encounters at handoff, says hospitalist Alpesh Amin, MD, MPA, MACP, SFHM, executive director of the hospitalist program at the University of California at Irvine. Dr. Amin coauthored a recent review highlighting opportunities for closer HM-ED collaboration with Charles Pollack Jr., MD, MA, FACEP, FAAEM, FAHA, who chairs the emergency department at Pennsylvania Hospital in Philadelphia.

A good place to start is for the two groups to simply sit down together regularly to discuss matters of common interest, perhaps monthly or quarterly, Dr. Amin says.

"Talk about clinical pathway development for common hospital diagnoses and how to improve admission processes," he adds. "There may be a role for the hospitalist in the emergency department when the patient gets handed off for hospital admission."

Collaboration also can improve patient flow and reduce ED diversion, shorten boarding times in the ED, and enhance quality and patient safety, Dr. Amin adds. "It's about how to optimize patient care for the benefit of the patient and the hospital," he says.

Visit our website for more information on hospitalists in the ED.

Hospitalists and ED physicians belong to two of the largest U.S. medical specialties and increasingly they are the only physicians seen by some hospitalized patients. Comanagement between the specialties is increasing in some hospitals, and in others, they might be the only physicians in the building after hours. They share similar workspaces, schedules, and responsibility for decisions about the most expensive care in medicine.

And yet there is not enough collaboration between the two specialties beyond brief phone encounters at handoff, says hospitalist Alpesh Amin, MD, MPA, MACP, SFHM, executive director of the hospitalist program at the University of California at Irvine. Dr. Amin coauthored a recent review highlighting opportunities for closer HM-ED collaboration with Charles Pollack Jr., MD, MA, FACEP, FAAEM, FAHA, who chairs the emergency department at Pennsylvania Hospital in Philadelphia.

A good place to start is for the two groups to simply sit down together regularly to discuss matters of common interest, perhaps monthly or quarterly, Dr. Amin says.

"Talk about clinical pathway development for common hospital diagnoses and how to improve admission processes," he adds. "There may be a role for the hospitalist in the emergency department when the patient gets handed off for hospital admission."

Collaboration also can improve patient flow and reduce ED diversion, shorten boarding times in the ED, and enhance quality and patient safety, Dr. Amin adds. "It's about how to optimize patient care for the benefit of the patient and the hospital," he says.

Visit our website for more information on hospitalists in the ED.

The Centers for Disease Control and Prevention is urging hepatitis C testing for all Americans born between 1945 and 1965, as new data indicate that the baby boomers account for the largest proportion of cases yet are largely ignorant of their status.

"The take-home message from today’s report is that you may not remember everything that happened in the ’60s and ’70s, but your liver does," said CDC Director Thomas Frieden in a briefing with reporters.

"The bottom line here is, if you were born between those years, get tested," he said. "And if you’re positive, get follow-up testing."

Besides targeting consumers, the CDC also issued updated testing recommendations for physicians.

The guidelines, published May 7 in Morbidity and Mortality Weekly Report (MMWR), update the CDC’s 2003 testing recommendations.

The agency issued the update "because of changes in the availability of certain commercial HCV [hepatitis C virus] antibody tests, evidence that many persons who are identified as reactive by an HCV antibody test might not subsequently be evaluated to determine if they have current HCV infection, and significant advances in the development of antiviral agents with improved efficacy against HCV," according to the report.

The CDC first proposed such broad testing a year ago. New surveillance data published in MMWR give credence to the idea that baby boomers seem to be at particular risk.

Researchers from the CDC and the New York City Department of Health and Mental Hygiene analyzed hepatitis C testing data from 2005 to 2011 from eight U.S. sites: Colorado, Connecticut, Minnesota, New Mexico, New York City, New York State, Oregon, and San Francisco. Health officials at all of the sites received CDC funding for conducting enhanced surveillance.

The analysis found that 63% of the 217,755 people with newly reported positive HCV were born in the years 1945-1965. Of the total who tested positive, 107,209 (49%) had a positive antibody test, and 110,546 (51%) had a positive follow-up RNA test. That means about half of those who have an initial positive test are not following up with a confirmatory RNA test.

That is discouraging, said Dr. Frieden. "Right now, there are better hepatitis C treatments available than ever, and there are more treatments coming in the coming year," he said. "So, confirming that someone is infected is more important than ever."

The CDC estimates 100,000-120,000 deaths could be prevented with proper testing and follow-up care.

About 3 million people are currently infected; half will end up with cirrhosis, and at least a third will die from complications. Eighty percent of people with hepatitis C are chronically infected.

The CDC is updating its 2003 guidance for physicians on hepatitis C testing by urging that a positive HCV antibody test be followed up with RNA testing.

The findings in the MMWR study "give us an idea of the gap between those who are and are not receiving the test, and show us that we have a substantial challenge in front of us," said Dr. John Ward, director of the division of viral hepatitis in the CDC’s National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention.

Baby boomers are likely to have been infected in their teens or 20s through transfusions or risky behaviors such as injection drug use. The CDC says risk factors for hepatitis C infection also include:

• Receiving clotting factor concentrates made before 1987, when more advanced methods for manufacturing those products were developed.

• Having a solid organ transplant before July 1992, when better testing became available.

• Chronic hemodialysis.

• Known exposure to HCV, such as needlesticks involving HCV-positive blood.

• HIV infection.

• Being born to an HCV-positive mother.

The CDC is exploring ways to make testing more available and to reach out to patients, Dr. Ward said. The agency has funded 25-30 demonstration projects, he added. Among the projects being tested: routine screening in the emergency department, and built-in reminders for physicians to test patients born in the target years.

Dr. Frieden urged immediate adoption of those reminders. "For health care providers, it’s very important to put in automatic systems to make sure that if someone has a positive antibody test, they go on to have follow-up testing and then get into care," he said.

The CDC issued its testing recommendations to coincide with Hepatitis Awareness Month and Hepatitis Testing Day, which is May 19.

aault@frontlinemedcom.com

On Twitter @aliciaault

The Centers for Disease Control and Prevention is urging hepatitis C testing for all Americans born between 1945 and 1965, as new data indicate that the baby boomers account for the largest proportion of cases yet are largely ignorant of their status.

"The take-home message from today’s report is that you may not remember everything that happened in the ’60s and ’70s, but your liver does," said CDC Director Thomas Frieden in a briefing with reporters.

"The bottom line here is, if you were born between those years, get tested," he said. "And if you’re positive, get follow-up testing."

Besides targeting consumers, the CDC also issued updated testing recommendations for physicians.

The guidelines, published May 7 in Morbidity and Mortality Weekly Report (MMWR), update the CDC’s 2003 testing recommendations.

The agency issued the update "because of changes in the availability of certain commercial HCV [hepatitis C virus] antibody tests, evidence that many persons who are identified as reactive by an HCV antibody test might not subsequently be evaluated to determine if they have current HCV infection, and significant advances in the development of antiviral agents with improved efficacy against HCV," according to the report.

The CDC first proposed such broad testing a year ago. New surveillance data published in MMWR give credence to the idea that baby boomers seem to be at particular risk.

Researchers from the CDC and the New York City Department of Health and Mental Hygiene analyzed hepatitis C testing data from 2005 to 2011 from eight U.S. sites: Colorado, Connecticut, Minnesota, New Mexico, New York City, New York State, Oregon, and San Francisco. Health officials at all of the sites received CDC funding for conducting enhanced surveillance.

The analysis found that 63% of the 217,755 people with newly reported positive HCV were born in the years 1945-1965. Of the total who tested positive, 107,209 (49%) had a positive antibody test, and 110,546 (51%) had a positive follow-up RNA test. That means about half of those who have an initial positive test are not following up with a confirmatory RNA test.

That is discouraging, said Dr. Frieden. "Right now, there are better hepatitis C treatments available than ever, and there are more treatments coming in the coming year," he said. "So, confirming that someone is infected is more important than ever."

The CDC estimates 100,000-120,000 deaths could be prevented with proper testing and follow-up care.

About 3 million people are currently infected; half will end up with cirrhosis, and at least a third will die from complications. Eighty percent of people with hepatitis C are chronically infected.

The CDC is updating its 2003 guidance for physicians on hepatitis C testing by urging that a positive HCV antibody test be followed up with RNA testing.

The findings in the MMWR study "give us an idea of the gap between those who are and are not receiving the test, and show us that we have a substantial challenge in front of us," said Dr. John Ward, director of the division of viral hepatitis in the CDC’s National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention.

Baby boomers are likely to have been infected in their teens or 20s through transfusions or risky behaviors such as injection drug use. The CDC says risk factors for hepatitis C infection also include:

• Receiving clotting factor concentrates made before 1987, when more advanced methods for manufacturing those products were developed.

• Having a solid organ transplant before July 1992, when better testing became available.

• Chronic hemodialysis.

• Known exposure to HCV, such as needlesticks involving HCV-positive blood.

• HIV infection.

• Being born to an HCV-positive mother.

The CDC is exploring ways to make testing more available and to reach out to patients, Dr. Ward said. The agency has funded 25-30 demonstration projects, he added. Among the projects being tested: routine screening in the emergency department, and built-in reminders for physicians to test patients born in the target years.

Dr. Frieden urged immediate adoption of those reminders. "For health care providers, it’s very important to put in automatic systems to make sure that if someone has a positive antibody test, they go on to have follow-up testing and then get into care," he said.

The CDC issued its testing recommendations to coincide with Hepatitis Awareness Month and Hepatitis Testing Day, which is May 19.

aault@frontlinemedcom.com

On Twitter @aliciaault

The Centers for Disease Control and Prevention is urging hepatitis C testing for all Americans born between 1945 and 1965, as new data indicate that the baby boomers account for the largest proportion of cases yet are largely ignorant of their status.

"The take-home message from today’s report is that you may not remember everything that happened in the ’60s and ’70s, but your liver does," said CDC Director Thomas Frieden in a briefing with reporters.

"The bottom line here is, if you were born between those years, get tested," he said. "And if you’re positive, get follow-up testing."

Besides targeting consumers, the CDC also issued updated testing recommendations for physicians.

The guidelines, published May 7 in Morbidity and Mortality Weekly Report (MMWR), update the CDC’s 2003 testing recommendations.

The agency issued the update "because of changes in the availability of certain commercial HCV [hepatitis C virus] antibody tests, evidence that many persons who are identified as reactive by an HCV antibody test might not subsequently be evaluated to determine if they have current HCV infection, and significant advances in the development of antiviral agents with improved efficacy against HCV," according to the report.

The CDC first proposed such broad testing a year ago. New surveillance data published in MMWR give credence to the idea that baby boomers seem to be at particular risk.

Researchers from the CDC and the New York City Department of Health and Mental Hygiene analyzed hepatitis C testing data from 2005 to 2011 from eight U.S. sites: Colorado, Connecticut, Minnesota, New Mexico, New York City, New York State, Oregon, and San Francisco. Health officials at all of the sites received CDC funding for conducting enhanced surveillance.

The analysis found that 63% of the 217,755 people with newly reported positive HCV were born in the years 1945-1965. Of the total who tested positive, 107,209 (49%) had a positive antibody test, and 110,546 (51%) had a positive follow-up RNA test. That means about half of those who have an initial positive test are not following up with a confirmatory RNA test.

That is discouraging, said Dr. Frieden. "Right now, there are better hepatitis C treatments available than ever, and there are more treatments coming in the coming year," he said. "So, confirming that someone is infected is more important than ever."

The CDC estimates 100,000-120,000 deaths could be prevented with proper testing and follow-up care.

About 3 million people are currently infected; half will end up with cirrhosis, and at least a third will die from complications. Eighty percent of people with hepatitis C are chronically infected.

The CDC is updating its 2003 guidance for physicians on hepatitis C testing by urging that a positive HCV antibody test be followed up with RNA testing.

The findings in the MMWR study "give us an idea of the gap between those who are and are not receiving the test, and show us that we have a substantial challenge in front of us," said Dr. John Ward, director of the division of viral hepatitis in the CDC’s National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention.

Baby boomers are likely to have been infected in their teens or 20s through transfusions or risky behaviors such as injection drug use. The CDC says risk factors for hepatitis C infection also include:

• Receiving clotting factor concentrates made before 1987, when more advanced methods for manufacturing those products were developed.

• Having a solid organ transplant before July 1992, when better testing became available.

• Chronic hemodialysis.

• Known exposure to HCV, such as needlesticks involving HCV-positive blood.

• HIV infection.

• Being born to an HCV-positive mother.

The CDC is exploring ways to make testing more available and to reach out to patients, Dr. Ward said. The agency has funded 25-30 demonstration projects, he added. Among the projects being tested: routine screening in the emergency department, and built-in reminders for physicians to test patients born in the target years.

Dr. Frieden urged immediate adoption of those reminders. "For health care providers, it’s very important to put in automatic systems to make sure that if someone has a positive antibody test, they go on to have follow-up testing and then get into care," he said.

The CDC issued its testing recommendations to coincide with Hepatitis Awareness Month and Hepatitis Testing Day, which is May 19.

aault@frontlinemedcom.com

On Twitter @aliciaault

SAN DIEGO -- Percutaneous transluminal venous angioplasty – also known as "liberation therapy" -- doesn't help people with multiple sclerosis and may increase MS brain activity in the short term, according to a small, randomized, sham-controlled trial from the State University of New York at Buffalo, the first randomized trial to investigate the procedure.

The technique "was ineffective in correcting" chronic cerebrospinal venous insufficiency (CCSVI), the recently described condition it targets. "The results ... caution against widespread adoption of venous angioplasty in the management of patients with MS outside of rigorous clinical trials," the investigators concluded.

The findings follow a recent Food and Drug Administration warning that PTVA (percutaneous transluminal venous angioplasty) can cause deaths and injuries, including strokes, damage to the treated vein, blood clots, cranial nerve damage, abdominal bleeding, and detachment and migration of stents.

The idea is to use balloon angioplasty and stents to widen veins in the chest and neck that appear to be narrowed in some MS patients. Proponents of the procedure say that those narrowed veins impair blood flow and lead to disease progression. The researchers who discovered the problem dubbed it CCSVI. A cottage industry has since sprung up to offer PTVA to MS patients.

The FDA noted in its warning that there have been no "controlled ... rigorously conducted, properly targeted" studies of the issue; that may have changed when Dr. Robert Zivadinov, a professor in the department of neurology at SUNY-Buffalo, presented his team’s findings at the annual meeting of the American Academy of Neurology.

"When you reopened those veins in the neck, I think something happened in reperfusing the brain and re-exacerbating disease activity. The message of this is clear. The majority of patients who are relapsing-remitting should not undergo this treatment," he said in an interview.

Ten patients got PTVA in the first phase of the study. The second phase randomized 9 to PTVA and 10 to a sham intervention. Most had relapsing-remitting MS.

There were no MS relapses in the first phase, but PTVA patients had more relapses (4 vs. 1; P = .389) and more MRI disease activity (cumulative number of new contrast-enhancing lesions (19 vs. 3; P = .062) and new T2 lesions (17 vs. 3; P = .066) in the 6 months following treatment in phase II.

PTVA patients also didn’t fare any better on Expanded Disability Status Scale (EDSS) scores, Multiple Sclerosis Functional Composite scores, 6-minute walk tests, or measures of cognition and quality of life.

"We chose very active patients who had one relapse in the previous year or [gadolinium-] enhancing lesions in the 3 months before. The sample size is small, but [more than half] of patients in the treatment group showed increased activity," Dr. Zivadinov said.

The majority of the subjects were women. On average, they were about 45 years old, had been diagnosed with MS for 11 years, and were mildly to moderately disabled (mean EDSS score about 4). Most were on interferon, glatiramer acetate, or both.

Venous angioplasty didn’t cause any serious complications, and it restored venous outflow to at least 50% of normal in most patients. Phase I patients had a better than 75% improvement overall. Phase II patients had less benefit; there were no differences in venous hemodynamic insufficiency scores between treated and sham patients.

The treatment "failed to provide any sustained improvement in venous outflow as measured through duplex and/or clinical and MRI outcomes," and "more sizable changes in venous outflow [were] associated with increased disease activity primarily noted on MRI," Dr. Zivadinov and his colleagues concluded.

The work was funded primarily by SUNY-Buffalo’s Neuroimaging Analysis Center and Baird MS Research Center. Dr. Zivadinov receives personal compensation from Teva Pharmaceuticals, Biogen Idec, EMD Serono, Bayer, Genzyme-Sanofi, Novartis, Bracco Imaging, and Questcor Pharmaceuticals.

aotto@frontlinemedcom.com

SAN DIEGO -- Percutaneous transluminal venous angioplasty – also known as "liberation therapy" -- doesn't help people with multiple sclerosis and may increase MS brain activity in the short term, according to a small, randomized, sham-controlled trial from the State University of New York at Buffalo, the first randomized trial to investigate the procedure.

The technique "was ineffective in correcting" chronic cerebrospinal venous insufficiency (CCSVI), the recently described condition it targets. "The results ... caution against widespread adoption of venous angioplasty in the management of patients with MS outside of rigorous clinical trials," the investigators concluded.

The findings follow a recent Food and Drug Administration warning that PTVA (percutaneous transluminal venous angioplasty) can cause deaths and injuries, including strokes, damage to the treated vein, blood clots, cranial nerve damage, abdominal bleeding, and detachment and migration of stents.

The idea is to use balloon angioplasty and stents to widen veins in the chest and neck that appear to be narrowed in some MS patients. Proponents of the procedure say that those narrowed veins impair blood flow and lead to disease progression. The researchers who discovered the problem dubbed it CCSVI. A cottage industry has since sprung up to offer PTVA to MS patients.

The FDA noted in its warning that there have been no "controlled ... rigorously conducted, properly targeted" studies of the issue; that may have changed when Dr. Robert Zivadinov, a professor in the department of neurology at SUNY-Buffalo, presented his team’s findings at the annual meeting of the American Academy of Neurology.

"When you reopened those veins in the neck, I think something happened in reperfusing the brain and re-exacerbating disease activity. The message of this is clear. The majority of patients who are relapsing-remitting should not undergo this treatment," he said in an interview.

Ten patients got PTVA in the first phase of the study. The second phase randomized 9 to PTVA and 10 to a sham intervention. Most had relapsing-remitting MS.

There were no MS relapses in the first phase, but PTVA patients had more relapses (4 vs. 1; P = .389) and more MRI disease activity (cumulative number of new contrast-enhancing lesions (19 vs. 3; P = .062) and new T2 lesions (17 vs. 3; P = .066) in the 6 months following treatment in phase II.

PTVA patients also didn’t fare any better on Expanded Disability Status Scale (EDSS) scores, Multiple Sclerosis Functional Composite scores, 6-minute walk tests, or measures of cognition and quality of life.

"We chose very active patients who had one relapse in the previous year or [gadolinium-] enhancing lesions in the 3 months before. The sample size is small, but [more than half] of patients in the treatment group showed increased activity," Dr. Zivadinov said.

The majority of the subjects were women. On average, they were about 45 years old, had been diagnosed with MS for 11 years, and were mildly to moderately disabled (mean EDSS score about 4). Most were on interferon, glatiramer acetate, or both.

Venous angioplasty didn’t cause any serious complications, and it restored venous outflow to at least 50% of normal in most patients. Phase I patients had a better than 75% improvement overall. Phase II patients had less benefit; there were no differences in venous hemodynamic insufficiency scores between treated and sham patients.

The treatment "failed to provide any sustained improvement in venous outflow as measured through duplex and/or clinical and MRI outcomes," and "more sizable changes in venous outflow [were] associated with increased disease activity primarily noted on MRI," Dr. Zivadinov and his colleagues concluded.

The work was funded primarily by SUNY-Buffalo’s Neuroimaging Analysis Center and Baird MS Research Center. Dr. Zivadinov receives personal compensation from Teva Pharmaceuticals, Biogen Idec, EMD Serono, Bayer, Genzyme-Sanofi, Novartis, Bracco Imaging, and Questcor Pharmaceuticals.

aotto@frontlinemedcom.com

SAN DIEGO -- Percutaneous transluminal venous angioplasty – also known as "liberation therapy" -- doesn't help people with multiple sclerosis and may increase MS brain activity in the short term, according to a small, randomized, sham-controlled trial from the State University of New York at Buffalo, the first randomized trial to investigate the procedure.

The technique "was ineffective in correcting" chronic cerebrospinal venous insufficiency (CCSVI), the recently described condition it targets. "The results ... caution against widespread adoption of venous angioplasty in the management of patients with MS outside of rigorous clinical trials," the investigators concluded.

The findings follow a recent Food and Drug Administration warning that PTVA (percutaneous transluminal venous angioplasty) can cause deaths and injuries, including strokes, damage to the treated vein, blood clots, cranial nerve damage, abdominal bleeding, and detachment and migration of stents.

The idea is to use balloon angioplasty and stents to widen veins in the chest and neck that appear to be narrowed in some MS patients. Proponents of the procedure say that those narrowed veins impair blood flow and lead to disease progression. The researchers who discovered the problem dubbed it CCSVI. A cottage industry has since sprung up to offer PTVA to MS patients.

The FDA noted in its warning that there have been no "controlled ... rigorously conducted, properly targeted" studies of the issue; that may have changed when Dr. Robert Zivadinov, a professor in the department of neurology at SUNY-Buffalo, presented his team’s findings at the annual meeting of the American Academy of Neurology.

"When you reopened those veins in the neck, I think something happened in reperfusing the brain and re-exacerbating disease activity. The message of this is clear. The majority of patients who are relapsing-remitting should not undergo this treatment," he said in an interview.

Ten patients got PTVA in the first phase of the study. The second phase randomized 9 to PTVA and 10 to a sham intervention. Most had relapsing-remitting MS.

There were no MS relapses in the first phase, but PTVA patients had more relapses (4 vs. 1; P = .389) and more MRI disease activity (cumulative number of new contrast-enhancing lesions (19 vs. 3; P = .062) and new T2 lesions (17 vs. 3; P = .066) in the 6 months following treatment in phase II.

PTVA patients also didn’t fare any better on Expanded Disability Status Scale (EDSS) scores, Multiple Sclerosis Functional Composite scores, 6-minute walk tests, or measures of cognition and quality of life.

"We chose very active patients who had one relapse in the previous year or [gadolinium-] enhancing lesions in the 3 months before. The sample size is small, but [more than half] of patients in the treatment group showed increased activity," Dr. Zivadinov said.

The majority of the subjects were women. On average, they were about 45 years old, had been diagnosed with MS for 11 years, and were mildly to moderately disabled (mean EDSS score about 4). Most were on interferon, glatiramer acetate, or both.

Venous angioplasty didn’t cause any serious complications, and it restored venous outflow to at least 50% of normal in most patients. Phase I patients had a better than 75% improvement overall. Phase II patients had less benefit; there were no differences in venous hemodynamic insufficiency scores between treated and sham patients.

The treatment "failed to provide any sustained improvement in venous outflow as measured through duplex and/or clinical and MRI outcomes," and "more sizable changes in venous outflow [were] associated with increased disease activity primarily noted on MRI," Dr. Zivadinov and his colleagues concluded.

The work was funded primarily by SUNY-Buffalo’s Neuroimaging Analysis Center and Baird MS Research Center. Dr. Zivadinov receives personal compensation from Teva Pharmaceuticals, Biogen Idec, EMD Serono, Bayer, Genzyme-Sanofi, Novartis, Bracco Imaging, and Questcor Pharmaceuticals.

aotto@frontlinemedcom.com

LAKE BUENA VISTA, FLA. – Ultrasound expedites clinical decision making and often dictates the next step to pursue when managing children in the emergency department.

"It makes sense to use ultrasound for pediatric patients, but there’s been a delay in picking up this idea. Only now is (the use of bedside ultrasonography) becoming more prevalent in pediatric emergency medicine, Dr. Stephanie J. Doniger said at a meeting sponsored by the American College of Emergency Physicians and the American Academy of Pediatrics.

"Among the advantages is that we really never have to perform sedation, and the absolutely most important thing, we don’t need to use ionizing radiation," said Dr. Doniger, director of emergency ultrasound at Children’s Hospital and Research Center, Oakland, Calif.

Still, she said, there are no clear guidelines for ultrasonography’s use in pediatric emergencies. No one body oversees the quality in training or in outcomes. In 2009, ACEP updated its guidelines on bedside ultrasound in the emergency department. The group gave a nod to pediatric use, calling ultrasonography "an ideal diagnostic tool for children ... As in adult patients, emergency ultrasound in children can be life saving, time saving, [can] increase procedural efficiency, and [can] maximize patient safety."

The document says ultrasound is particularly useful in performing the FAST exam, and for bladder evaluations prior to instilling a catheter in infants. Dr. Doniger noted a number of other applications as well.

Ultrasonography is valuable for assessing dehydration by providing a look at the inferior vena cava. "We’re looking here for collapsibility during inspiration. Collapsibility of more than 50% correlates with dehydration."

Appendicitis is tough to image, radiographs are unreliable, and "CTs aren’t great, but we do them if we have to." But ultrasound provides a very good look into what lies beneath, and is one more way to reduce a child’s cumulative radiation dose.

A 2008 study found that a 5-minute bedside ultrasound had a sensitivity of 65% and a specificity of 90% for appendicitis. The positive predictive value was 84%, and the negative predictive value, 76%.

"That might not sound great, but it is a good result to rule in disease. If you have a high suspicion of appendicitis, then use it; if a low suspicion, then don’t."

When looking for an infected appendix, start at the point of maximal tenderness and move to the right while the child is in an oblique position. "It helps if you prop up the hip with some towels," Dr. Doniger said. "The bowel will move away and you’ll have a better view when you compress."

Look for a noncompressible tubular structure with a diameter greater than 6 mm.

The probe can also help find intussusception – a condition that x-rays identify 40%-90% of the time. The ultrasound image of intussusception is target- or doughnut-shaped – a figure formed when the bowel retracts back into itself. A study found that even beginning sonographers can identify this classic sign. Their exams had a sensitivity of 85%, a specificity of 97%, a positive predictive value of 85%, and a negative predictive value of 97%.

Even something that seems innocuous on the surface – like a splinter – will give up its secrets under the ultrasound probe. Foreign bodies may or may not show up on an x-ray, but they are obviously hypoechoic on ultrasound, she said.

Dr. Doniger presented the case of a 13-year-old who thought he got a splinter under his fingernail, but wasn’t sure. He came to the emergency department after his finger became stiff and a little painful. Ultrasound identified the culprit as splinter of wood that was more than 1 inch long.

Guiding the needle during an evaluation for painful hips for effusion is another great use for ultrasound, she said. A 2009 study determined that, compared with ultrasound alone; sonography-guided arthrocentesis for symptomatic hips had 90% sensitivity and 100% specificity, with a 100% positive predictive value and a 92% negative predictive value.

Ultrasound also provides valuable assistance in identifying the landmarks for successful needle placement when performing a spinal tap. A 2007 study equally randomized 46 children to finding the landmarks by palpation or with ultrasound. There were six failed attempts in the palpation group and one in the ultrasound group. Ultrasound was particularly helpful in obese children; four of seven palpation placements failed, compared with no failures in the ultrasound group.

None of the authors declared any financial relationships. The study was funded by the Lynn Sage Cancer Research Foundation, the Avon Foundation, and a private contribution.

msullivan@frontlinemedcom.com

LAKE BUENA VISTA, FLA. – Ultrasound expedites clinical decision making and often dictates the next step to pursue when managing children in the emergency department.

"It makes sense to use ultrasound for pediatric patients, but there’s been a delay in picking up this idea. Only now is (the use of bedside ultrasonography) becoming more prevalent in pediatric emergency medicine, Dr. Stephanie J. Doniger said at a meeting sponsored by the American College of Emergency Physicians and the American Academy of Pediatrics.

"Among the advantages is that we really never have to perform sedation, and the absolutely most important thing, we don’t need to use ionizing radiation," said Dr. Doniger, director of emergency ultrasound at Children’s Hospital and Research Center, Oakland, Calif.

Still, she said, there are no clear guidelines for ultrasonography’s use in pediatric emergencies. No one body oversees the quality in training or in outcomes. In 2009, ACEP updated its guidelines on bedside ultrasound in the emergency department. The group gave a nod to pediatric use, calling ultrasonography "an ideal diagnostic tool for children ... As in adult patients, emergency ultrasound in children can be life saving, time saving, [can] increase procedural efficiency, and [can] maximize patient safety."

The document says ultrasound is particularly useful in performing the FAST exam, and for bladder evaluations prior to instilling a catheter in infants. Dr. Doniger noted a number of other applications as well.

Ultrasonography is valuable for assessing dehydration by providing a look at the inferior vena cava. "We’re looking here for collapsibility during inspiration. Collapsibility of more than 50% correlates with dehydration."

Appendicitis is tough to image, radiographs are unreliable, and "CTs aren’t great, but we do them if we have to." But ultrasound provides a very good look into what lies beneath, and is one more way to reduce a child’s cumulative radiation dose.

A 2008 study found that a 5-minute bedside ultrasound had a sensitivity of 65% and a specificity of 90% for appendicitis. The positive predictive value was 84%, and the negative predictive value, 76%.

"That might not sound great, but it is a good result to rule in disease. If you have a high suspicion of appendicitis, then use it; if a low suspicion, then don’t."

When looking for an infected appendix, start at the point of maximal tenderness and move to the right while the child is in an oblique position. "It helps if you prop up the hip with some towels," Dr. Doniger said. "The bowel will move away and you’ll have a better view when you compress."

Look for a noncompressible tubular structure with a diameter greater than 6 mm.

The probe can also help find intussusception – a condition that x-rays identify 40%-90% of the time. The ultrasound image of intussusception is target- or doughnut-shaped – a figure formed when the bowel retracts back into itself. A study found that even beginning sonographers can identify this classic sign. Their exams had a sensitivity of 85%, a specificity of 97%, a positive predictive value of 85%, and a negative predictive value of 97%.

Even something that seems innocuous on the surface – like a splinter – will give up its secrets under the ultrasound probe. Foreign bodies may or may not show up on an x-ray, but they are obviously hypoechoic on ultrasound, she said.

Dr. Doniger presented the case of a 13-year-old who thought he got a splinter under his fingernail, but wasn’t sure. He came to the emergency department after his finger became stiff and a little painful. Ultrasound identified the culprit as splinter of wood that was more than 1 inch long.

Guiding the needle during an evaluation for painful hips for effusion is another great use for ultrasound, she said. A 2009 study determined that, compared with ultrasound alone; sonography-guided arthrocentesis for symptomatic hips had 90% sensitivity and 100% specificity, with a 100% positive predictive value and a 92% negative predictive value.

Ultrasound also provides valuable assistance in identifying the landmarks for successful needle placement when performing a spinal tap. A 2007 study equally randomized 46 children to finding the landmarks by palpation or with ultrasound. There were six failed attempts in the palpation group and one in the ultrasound group. Ultrasound was particularly helpful in obese children; four of seven palpation placements failed, compared with no failures in the ultrasound group.

None of the authors declared any financial relationships. The study was funded by the Lynn Sage Cancer Research Foundation, the Avon Foundation, and a private contribution.

msullivan@frontlinemedcom.com

LAKE BUENA VISTA, FLA. – Ultrasound expedites clinical decision making and often dictates the next step to pursue when managing children in the emergency department.

"It makes sense to use ultrasound for pediatric patients, but there’s been a delay in picking up this idea. Only now is (the use of bedside ultrasonography) becoming more prevalent in pediatric emergency medicine, Dr. Stephanie J. Doniger said at a meeting sponsored by the American College of Emergency Physicians and the American Academy of Pediatrics.

"Among the advantages is that we really never have to perform sedation, and the absolutely most important thing, we don’t need to use ionizing radiation," said Dr. Doniger, director of emergency ultrasound at Children’s Hospital and Research Center, Oakland, Calif.

Still, she said, there are no clear guidelines for ultrasonography’s use in pediatric emergencies. No one body oversees the quality in training or in outcomes. In 2009, ACEP updated its guidelines on bedside ultrasound in the emergency department. The group gave a nod to pediatric use, calling ultrasonography "an ideal diagnostic tool for children ... As in adult patients, emergency ultrasound in children can be life saving, time saving, [can] increase procedural efficiency, and [can] maximize patient safety."

The document says ultrasound is particularly useful in performing the FAST exam, and for bladder evaluations prior to instilling a catheter in infants. Dr. Doniger noted a number of other applications as well.

Ultrasonography is valuable for assessing dehydration by providing a look at the inferior vena cava. "We’re looking here for collapsibility during inspiration. Collapsibility of more than 50% correlates with dehydration."

Appendicitis is tough to image, radiographs are unreliable, and "CTs aren’t great, but we do them if we have to." But ultrasound provides a very good look into what lies beneath, and is one more way to reduce a child’s cumulative radiation dose.

A 2008 study found that a 5-minute bedside ultrasound had a sensitivity of 65% and a specificity of 90% for appendicitis. The positive predictive value was 84%, and the negative predictive value, 76%.

"That might not sound great, but it is a good result to rule in disease. If you have a high suspicion of appendicitis, then use it; if a low suspicion, then don’t."

When looking for an infected appendix, start at the point of maximal tenderness and move to the right while the child is in an oblique position. "It helps if you prop up the hip with some towels," Dr. Doniger said. "The bowel will move away and you’ll have a better view when you compress."

Look for a noncompressible tubular structure with a diameter greater than 6 mm.

The probe can also help find intussusception – a condition that x-rays identify 40%-90% of the time. The ultrasound image of intussusception is target- or doughnut-shaped – a figure formed when the bowel retracts back into itself. A study found that even beginning sonographers can identify this classic sign. Their exams had a sensitivity of 85%, a specificity of 97%, a positive predictive value of 85%, and a negative predictive value of 97%.

Even something that seems innocuous on the surface – like a splinter – will give up its secrets under the ultrasound probe. Foreign bodies may or may not show up on an x-ray, but they are obviously hypoechoic on ultrasound, she said.

Dr. Doniger presented the case of a 13-year-old who thought he got a splinter under his fingernail, but wasn’t sure. He came to the emergency department after his finger became stiff and a little painful. Ultrasound identified the culprit as splinter of wood that was more than 1 inch long.

Guiding the needle during an evaluation for painful hips for effusion is another great use for ultrasound, she said. A 2009 study determined that, compared with ultrasound alone; sonography-guided arthrocentesis for symptomatic hips had 90% sensitivity and 100% specificity, with a 100% positive predictive value and a 92% negative predictive value.

Ultrasound also provides valuable assistance in identifying the landmarks for successful needle placement when performing a spinal tap. A 2007 study equally randomized 46 children to finding the landmarks by palpation or with ultrasound. There were six failed attempts in the palpation group and one in the ultrasound group. Ultrasound was particularly helpful in obese children; four of seven palpation placements failed, compared with no failures in the ultrasound group.

None of the authors declared any financial relationships. The study was funded by the Lynn Sage Cancer Research Foundation, the Avon Foundation, and a private contribution.

msullivan@frontlinemedcom.com

"How have you been treating this?" I asked Ivan. He had a rash on his shin.

"Plantain leaves," he explained.

Plantains, of course. Fry ’em or apply ’em.

Home remedies have always intrigued me. Take Preparation H ointment. Good for bags under the eyes, they say. Also good for hemorrhoids. Really good for people who have trouble telling the difference.

Or tea tree oil. I’ve heard about that for years, but never took the time to find out what a tea tree is. A tree shaped like a "T"? A tree that grows tea? A tree made out of tea?

Turns out it is Melaleuca alternifolia, a source of traditional remedies among the indigenous Bundjalung people of Eastern Australia. (Thank you, Wikipedia.) It may kill viruses, bacteria, and fungi. And it makes a dandy shampoo.

Got poison ivy? Try jewelweed (if you can find it). Or rat vein tea (not sure I want to find that). Or boiled sweet fern. Or (of course) tea tree oil.

Do home remedies work? Truth be told, I don’t claim to know one way or the other. Anyhow, I find a different question more interesting – not whether home remedies work, but why people think they do.

The answer to that seems straightforward. People think home remedies work because other people say so. Vicks VapoRub ointment for toenail fungus? Hank says it cleared him right up! His buddy, Frankie, on the other hand, swears by apple cider vinegar for his own toenails. He’s also sure it got rid of Frankie Jr.’s head lice, although back at school, other kids complained that Frankie Jr. smelled like a salad. And his wife Franchette uses it to help reverse the signs of aging.

Which points to something about the popularity of home remedies: There is a big difference between the way patients think and the way doctors do. Many of these cures – most nowadays are either traditional, natural, or both – are supposed to be good for ... well, just about anything. The list of uses for plantains, for instance, includes rashes, wounds, ulcerations, cuts, swelling, sprains, bruises, burns, eczema, cracked lips, poison ivy, mosquito bites, diaper rash, boils, hemorrhoids, blisters, snake bites, spider bites, splinters, and thorns.

Or take another popular item, jojoba oil (that’s ho-HO-ba to you). Named by the Tohono O’odham people of the Sonoran desert (repositories of ancient wisdom, presumably), jojoba is recommended for the treatment of wrinkles; hair loss; joint pain; hemorrhoids (take note, Preparation H nonresponders!); smoker’s cough; and constipation. It also lubricates locks and engines, and it is good for covering homemade cucumbers. Look it up.

Lists like these might make a physician skeptical, prone to wonder which mechanism of action could possibly explain such disparate effects and what studies could be designed to support or refute them. Considerations like these do not generally trouble patients. If something is good, well, it’s just good, for one thing or for many. Doctors split. Patients lump.

I thought I’d heard every folk remedy there is, earnest or whimsical, until Tibor came by last month. A well-spoken gent with a thick, Hungarian accent, Tibor pulled up his shirt and showed me a lot of eczema.

"Two things make it better," he explained. "The first thing, I swim every day in a chlorinated pool to cool it off."

That was a surprise, considering how many eczema patients are convinced that chlorine makes them worse.

And the second?

"Yogurt," he said. "I put on nonfat yogurt." But not just any nonfat yogurt.

"I tried all different kinds," Tibor went on. "I tried flavored yogurt, I tried Greek yogurt. But the best is plain nonfat yogurt."

A controlled experiment!

I asked Tibor where he got the idea for applying yogurt to his rash.

"My mother suggested some kind of peasant remedy when I was a kid," he said. "It may have been sour cream."

So it was some kind of rash, treated with something dairy. I tried to picture little Tibor covered with sour cream. I couldn’t.

"I put the yogurt on last night," said Tibor, proudly rolling up his sleeve to show me an almost eczema-free arm. "See how well it works!"

Anecdotal, perhaps, but still impressive. It cures eczema! It lowers cholesterol! It’s on sale!

Take that, tea tree oil.

Dr. Rockoff practices dermatology in Brookline, Mass.

"How have you been treating this?" I asked Ivan. He had a rash on his shin.

"Plantain leaves," he explained.

Plantains, of course. Fry ’em or apply ’em.

Home remedies have always intrigued me. Take Preparation H ointment. Good for bags under the eyes, they say. Also good for hemorrhoids. Really good for people who have trouble telling the difference.

Or tea tree oil. I’ve heard about that for years, but never took the time to find out what a tea tree is. A tree shaped like a "T"? A tree that grows tea? A tree made out of tea?

Turns out it is Melaleuca alternifolia, a source of traditional remedies among the indigenous Bundjalung people of Eastern Australia. (Thank you, Wikipedia.) It may kill viruses, bacteria, and fungi. And it makes a dandy shampoo.

Got poison ivy? Try jewelweed (if you can find it). Or rat vein tea (not sure I want to find that). Or boiled sweet fern. Or (of course) tea tree oil.

Do home remedies work? Truth be told, I don’t claim to know one way or the other. Anyhow, I find a different question more interesting – not whether home remedies work, but why people think they do.

The answer to that seems straightforward. People think home remedies work because other people say so. Vicks VapoRub ointment for toenail fungus? Hank says it cleared him right up! His buddy, Frankie, on the other hand, swears by apple cider vinegar for his own toenails. He’s also sure it got rid of Frankie Jr.’s head lice, although back at school, other kids complained that Frankie Jr. smelled like a salad. And his wife Franchette uses it to help reverse the signs of aging.

Which points to something about the popularity of home remedies: There is a big difference between the way patients think and the way doctors do. Many of these cures – most nowadays are either traditional, natural, or both – are supposed to be good for ... well, just about anything. The list of uses for plantains, for instance, includes rashes, wounds, ulcerations, cuts, swelling, sprains, bruises, burns, eczema, cracked lips, poison ivy, mosquito bites, diaper rash, boils, hemorrhoids, blisters, snake bites, spider bites, splinters, and thorns.

Or take another popular item, jojoba oil (that’s ho-HO-ba to you). Named by the Tohono O’odham people of the Sonoran desert (repositories of ancient wisdom, presumably), jojoba is recommended for the treatment of wrinkles; hair loss; joint pain; hemorrhoids (take note, Preparation H nonresponders!); smoker’s cough; and constipation. It also lubricates locks and engines, and it is good for covering homemade cucumbers. Look it up.

Lists like these might make a physician skeptical, prone to wonder which mechanism of action could possibly explain such disparate effects and what studies could be designed to support or refute them. Considerations like these do not generally trouble patients. If something is good, well, it’s just good, for one thing or for many. Doctors split. Patients lump.

I thought I’d heard every folk remedy there is, earnest or whimsical, until Tibor came by last month. A well-spoken gent with a thick, Hungarian accent, Tibor pulled up his shirt and showed me a lot of eczema.

"Two things make it better," he explained. "The first thing, I swim every day in a chlorinated pool to cool it off."

That was a surprise, considering how many eczema patients are convinced that chlorine makes them worse.

And the second?

"Yogurt," he said. "I put on nonfat yogurt." But not just any nonfat yogurt.

"I tried all different kinds," Tibor went on. "I tried flavored yogurt, I tried Greek yogurt. But the best is plain nonfat yogurt."

A controlled experiment!

I asked Tibor where he got the idea for applying yogurt to his rash.

"My mother suggested some kind of peasant remedy when I was a kid," he said. "It may have been sour cream."

So it was some kind of rash, treated with something dairy. I tried to picture little Tibor covered with sour cream. I couldn’t.

"I put the yogurt on last night," said Tibor, proudly rolling up his sleeve to show me an almost eczema-free arm. "See how well it works!"

Anecdotal, perhaps, but still impressive. It cures eczema! It lowers cholesterol! It’s on sale!

Take that, tea tree oil.

Dr. Rockoff practices dermatology in Brookline, Mass.

"How have you been treating this?" I asked Ivan. He had a rash on his shin.

"Plantain leaves," he explained.

Plantains, of course. Fry ’em or apply ’em.

Home remedies have always intrigued me. Take Preparation H ointment. Good for bags under the eyes, they say. Also good for hemorrhoids. Really good for people who have trouble telling the difference.

Or tea tree oil. I’ve heard about that for years, but never took the time to find out what a tea tree is. A tree shaped like a "T"? A tree that grows tea? A tree made out of tea?

Turns out it is Melaleuca alternifolia, a source of traditional remedies among the indigenous Bundjalung people of Eastern Australia. (Thank you, Wikipedia.) It may kill viruses, bacteria, and fungi. And it makes a dandy shampoo.

Got poison ivy? Try jewelweed (if you can find it). Or rat vein tea (not sure I want to find that). Or boiled sweet fern. Or (of course) tea tree oil.

Do home remedies work? Truth be told, I don’t claim to know one way or the other. Anyhow, I find a different question more interesting – not whether home remedies work, but why people think they do.

The answer to that seems straightforward. People think home remedies work because other people say so. Vicks VapoRub ointment for toenail fungus? Hank says it cleared him right up! His buddy, Frankie, on the other hand, swears by apple cider vinegar for his own toenails. He’s also sure it got rid of Frankie Jr.’s head lice, although back at school, other kids complained that Frankie Jr. smelled like a salad. And his wife Franchette uses it to help reverse the signs of aging.

Which points to something about the popularity of home remedies: There is a big difference between the way patients think and the way doctors do. Many of these cures – most nowadays are either traditional, natural, or both – are supposed to be good for ... well, just about anything. The list of uses for plantains, for instance, includes rashes, wounds, ulcerations, cuts, swelling, sprains, bruises, burns, eczema, cracked lips, poison ivy, mosquito bites, diaper rash, boils, hemorrhoids, blisters, snake bites, spider bites, splinters, and thorns.

Or take another popular item, jojoba oil (that’s ho-HO-ba to you). Named by the Tohono O’odham people of the Sonoran desert (repositories of ancient wisdom, presumably), jojoba is recommended for the treatment of wrinkles; hair loss; joint pain; hemorrhoids (take note, Preparation H nonresponders!); smoker’s cough; and constipation. It also lubricates locks and engines, and it is good for covering homemade cucumbers. Look it up.

Lists like these might make a physician skeptical, prone to wonder which mechanism of action could possibly explain such disparate effects and what studies could be designed to support or refute them. Considerations like these do not generally trouble patients. If something is good, well, it’s just good, for one thing or for many. Doctors split. Patients lump.

I thought I’d heard every folk remedy there is, earnest or whimsical, until Tibor came by last month. A well-spoken gent with a thick, Hungarian accent, Tibor pulled up his shirt and showed me a lot of eczema.

"Two things make it better," he explained. "The first thing, I swim every day in a chlorinated pool to cool it off."

That was a surprise, considering how many eczema patients are convinced that chlorine makes them worse.

And the second?

"Yogurt," he said. "I put on nonfat yogurt." But not just any nonfat yogurt.

"I tried all different kinds," Tibor went on. "I tried flavored yogurt, I tried Greek yogurt. But the best is plain nonfat yogurt."

A controlled experiment!

I asked Tibor where he got the idea for applying yogurt to his rash.

"My mother suggested some kind of peasant remedy when I was a kid," he said. "It may have been sour cream."

So it was some kind of rash, treated with something dairy. I tried to picture little Tibor covered with sour cream. I couldn’t.

"I put the yogurt on last night," said Tibor, proudly rolling up his sleeve to show me an almost eczema-free arm. "See how well it works!"

Anecdotal, perhaps, but still impressive. It cures eczema! It lowers cholesterol! It’s on sale!

Take that, tea tree oil.

Dr. Rockoff practices dermatology in Brookline, Mass.

When I first started with this practice, our local imaging facilities took care of obtaining authorizations for the CT scans and MRI studies that I ordered. It is easy for them; they know just what to say to get insurance providers to pay for these costly tests.

But of course, this is exactly the kind of conflict of interest that we try to avoid in medicine, so about 2 years ago the largest private insurer in Rhode Island changed the rules. This is an entirely reasonable change. But it is also quite inconvenient and time consuming, and, ultimately, it is not clear that it is saving the health care industry all that much money.

Today, if I want an imaging procedure done, I need to get approval for it myself. This usually means my secretary fills out the initial paperwork, the request gets denied, and then, after a series of faxes and phone tag that can take days to weeks, I get on the phone with a physician somewhere else in the world who is purportedly helping me make better patient-care decisions.

Some months ago I was trying to get an approval for a CT scan of the chest for a patient whom I suspected of having sarcoidosis. After an initial denial by the insurance company, I finally got hold of a physician for a "peer-to-peer" evaluation. The person on the other end of the line was a radiologist. He denied my request for a CT scan because the chest x-ray had not shown any evidence of sarcoidosis. Of course, I argued, that was precisely the reason I needed the CT scan. I also respectfully suggested that, being a radiologist, he ought to know.

If it were truly a peer-to-peer evaluation, the person on the other end of the line would have the ability to understand my reasoning, and would have sound counterarguments. If the idea is to reduce the cost of health care, then it is the job of the person on the other end of the line to educate me about why I might be wrong or let me know of alternatives that are cheaper, but no less valuable, that I may have overlooked. It’s either that or recognize that there aren’t any alternatives, and that I have exercised careful decision making.

Instead, all they do is pose questions to me, and then, after having made the patient, my staff, and myself go through all the trouble, finally approve my request. The goal ought to be thoughtful collaboration that ultimately drives health care costs down. Instead, it feels like the goal is to actively discourage me from making more requests by making the process too onerous.

My so-called peers would understand that my elderly patient on Coumadin might be better off with a Lidoderm patch than with some other systemic alternatives. If they were truly my peers, they would understand why it is royally unreasonable to withhold infliximab from a patient who has been doing well on it for years. More recently, because Blue Cross & Blue Shield of Rhode Island started using a new pharmacy benefits manager, we’ve even had to fill out prior authorization requests for methotrexate and prednisone. Do they really think we’re cavalier about writing prescriptions for such toxic medications?

Also, how much money are they saving, exactly? They probably spend a lot more money employing people to do this work than they are saving by denying these prescriptions, some of which are generic. In addition, there’s the cost to my patients’ productivity when they take time out of work. Certainly, it would be cheaper for the insurance company to pay for the cost of Voltaren gel rather than pay for a GI bleed requiring hospitalization, blood transfusions, and possible invasive interventions.

The rising cost of health care in the United States has not led to improved patient outcomes. It begs the question: How much of the increased cost is because of the increasing administrative hurdles?

Dr. Chan practices rheumatology in Pawtucket, R.I.

When I first started with this practice, our local imaging facilities took care of obtaining authorizations for the CT scans and MRI studies that I ordered. It is easy for them; they know just what to say to get insurance providers to pay for these costly tests.

But of course, this is exactly the kind of conflict of interest that we try to avoid in medicine, so about 2 years ago the largest private insurer in Rhode Island changed the rules. This is an entirely reasonable change. But it is also quite inconvenient and time consuming, and, ultimately, it is not clear that it is saving the health care industry all that much money.

Today, if I want an imaging procedure done, I need to get approval for it myself. This usually means my secretary fills out the initial paperwork, the request gets denied, and then, after a series of faxes and phone tag that can take days to weeks, I get on the phone with a physician somewhere else in the world who is purportedly helping me make better patient-care decisions.

Some months ago I was trying to get an approval for a CT scan of the chest for a patient whom I suspected of having sarcoidosis. After an initial denial by the insurance company, I finally got hold of a physician for a "peer-to-peer" evaluation. The person on the other end of the line was a radiologist. He denied my request for a CT scan because the chest x-ray had not shown any evidence of sarcoidosis. Of course, I argued, that was precisely the reason I needed the CT scan. I also respectfully suggested that, being a radiologist, he ought to know.

If it were truly a peer-to-peer evaluation, the person on the other end of the line would have the ability to understand my reasoning, and would have sound counterarguments. If the idea is to reduce the cost of health care, then it is the job of the person on the other end of the line to educate me about why I might be wrong or let me know of alternatives that are cheaper, but no less valuable, that I may have overlooked. It’s either that or recognize that there aren’t any alternatives, and that I have exercised careful decision making.

Instead, all they do is pose questions to me, and then, after having made the patient, my staff, and myself go through all the trouble, finally approve my request. The goal ought to be thoughtful collaboration that ultimately drives health care costs down. Instead, it feels like the goal is to actively discourage me from making more requests by making the process too onerous.

My so-called peers would understand that my elderly patient on Coumadin might be better off with a Lidoderm patch than with some other systemic alternatives. If they were truly my peers, they would understand why it is royally unreasonable to withhold infliximab from a patient who has been doing well on it for years. More recently, because Blue Cross & Blue Shield of Rhode Island started using a new pharmacy benefits manager, we’ve even had to fill out prior authorization requests for methotrexate and prednisone. Do they really think we’re cavalier about writing prescriptions for such toxic medications?

Also, how much money are they saving, exactly? They probably spend a lot more money employing people to do this work than they are saving by denying these prescriptions, some of which are generic. In addition, there’s the cost to my patients’ productivity when they take time out of work. Certainly, it would be cheaper for the insurance company to pay for the cost of Voltaren gel rather than pay for a GI bleed requiring hospitalization, blood transfusions, and possible invasive interventions.

The rising cost of health care in the United States has not led to improved patient outcomes. It begs the question: How much of the increased cost is because of the increasing administrative hurdles?

Dr. Chan practices rheumatology in Pawtucket, R.I.

When I first started with this practice, our local imaging facilities took care of obtaining authorizations for the CT scans and MRI studies that I ordered. It is easy for them; they know just what to say to get insurance providers to pay for these costly tests.

But of course, this is exactly the kind of conflict of interest that we try to avoid in medicine, so about 2 years ago the largest private insurer in Rhode Island changed the rules. This is an entirely reasonable change. But it is also quite inconvenient and time consuming, and, ultimately, it is not clear that it is saving the health care industry all that much money.

Today, if I want an imaging procedure done, I need to get approval for it myself. This usually means my secretary fills out the initial paperwork, the request gets denied, and then, after a series of faxes and phone tag that can take days to weeks, I get on the phone with a physician somewhere else in the world who is purportedly helping me make better patient-care decisions.

Some months ago I was trying to get an approval for a CT scan of the chest for a patient whom I suspected of having sarcoidosis. After an initial denial by the insurance company, I finally got hold of a physician for a "peer-to-peer" evaluation. The person on the other end of the line was a radiologist. He denied my request for a CT scan because the chest x-ray had not shown any evidence of sarcoidosis. Of course, I argued, that was precisely the reason I needed the CT scan. I also respectfully suggested that, being a radiologist, he ought to know.

If it were truly a peer-to-peer evaluation, the person on the other end of the line would have the ability to understand my reasoning, and would have sound counterarguments. If the idea is to reduce the cost of health care, then it is the job of the person on the other end of the line to educate me about why I might be wrong or let me know of alternatives that are cheaper, but no less valuable, that I may have overlooked. It’s either that or recognize that there aren’t any alternatives, and that I have exercised careful decision making.

Instead, all they do is pose questions to me, and then, after having made the patient, my staff, and myself go through all the trouble, finally approve my request. The goal ought to be thoughtful collaboration that ultimately drives health care costs down. Instead, it feels like the goal is to actively discourage me from making more requests by making the process too onerous.

My so-called peers would understand that my elderly patient on Coumadin might be better off with a Lidoderm patch than with some other systemic alternatives. If they were truly my peers, they would understand why it is royally unreasonable to withhold infliximab from a patient who has been doing well on it for years. More recently, because Blue Cross & Blue Shield of Rhode Island started using a new pharmacy benefits manager, we’ve even had to fill out prior authorization requests for methotrexate and prednisone. Do they really think we’re cavalier about writing prescriptions for such toxic medications?

Also, how much money are they saving, exactly? They probably spend a lot more money employing people to do this work than they are saving by denying these prescriptions, some of which are generic. In addition, there’s the cost to my patients’ productivity when they take time out of work. Certainly, it would be cheaper for the insurance company to pay for the cost of Voltaren gel rather than pay for a GI bleed requiring hospitalization, blood transfusions, and possible invasive interventions.

The rising cost of health care in the United States has not led to improved patient outcomes. It begs the question: How much of the increased cost is because of the increasing administrative hurdles?

Dr. Chan practices rheumatology in Pawtucket, R.I.

MAUI, HAWAII – "Slow Mohs" has gained near-universal acceptance among skin cancer specialists as a definitive surgical technique for complete removal of lentigo maligna melanoma while simultaneously sparing normal tissue, according to Dr. Ellen Marmur of Mount Sinai School of Medicine, New York.

The big advantage that slow Mohs has over standard wide local excision with 0.5- to 1-cm margins is a 5-year cure rate approaching 100%. In contrast, standard excision has a recurrence rate of up to 20%, she said at the Hawaii Dermatology Seminar, sponsored by Global Academy for Medical Education/Skin Disease Education Foundation.

Bruce C. Jancin/IMNG Medical Media

Slow Mohs is a modified form of Mohs micrographic surgery. The surgery compares with conventional Mohs: It is staged, margin-controlled excision. But in slow Mohs, rush permanent sections are sent off to the pathologist rather than the frozen sections integral to conventional Mohs.

Dr. Marmur relies upon slow Mohs, with "bread-loafing" of the central tumor by the pathologist, because the permanent sections better preserve the tumor’s microscopic features. Interpreting atypical melanocytes in frozen sections can be quite a challenge. However, she added, some Mohs surgeons have found that using rapid immunostains also markedly improves the sensitivity and specificity of frozen sections in lentigo maligna surgery.

Slow Mohs takes place over the course of days, she said. "Basically, you do your Wood’s lamp to define the lesion diameter, you measure out your margins, you excise the tumor, pack the area with a bandage, and send the patient home. You rush your pathology, and you don’t do any reconstruction until you get the margins clear."

A pathology report that comes back stating narrow margins are present is "a heart stopper," she added.

"You have the option of observing the area if the margin is clear but the tumor was close to the margin. That’s a good approach for an elderly patient or when the lentigo maligna was in a cosmetically important area."

Lentigo maligna melanoma accounts for 4% of all cases of melanoma. It typically arises on sun-damaged skin in individuals in their 70s or older. Common sites include the malar area, forehead, nose, and temple. The differential diagnosis includes seborrheic keratosis, pigmented actinic keratosis, and pigmented nevus.

Lentigo maligna becomes lentigo maligna melanoma when malignant melanoma cells invade the dermis and deeper appendages. Roughly 5% of lentigo malignas eventually progress to invasive melanoma, according to Dr. Marmur. Typically, a lentigo maligna undergoes extended gradual horizontal growth before beginning a vertical growth phase.

"It spreads like an oil slick for many years," Dr. Marmur said at the seminar.

Established treatment modalities for patients who aren’t surgical candidates include cryotherapy, radiotherapy, and topical imiquimod 5%. All have disadvantages, including high 5-year recurrence rates.

Dr. Marmur noted that a newer nonsurgical therapy drawing considerable interest involves off-label use of topical combination therapy with imiquimod and tazarotene gel. The concept is to use the topical retinoid to disrupt the stratum corneum in order to enhance imiquimod penetration, thereby achieving a greater inflammatory response than possible with imiquimod alone.

Initial data have been published by researchers at the University of Utah, Salt Lake City. They randomized 90 patients with 91 lentigo malignas to imiquimod 5% cream applied 5 days per week for 3 months or to the imiquimod regimen plus tazarotene 0.1% gel on the other 2 days per week. After 3 months of topical therapy, patients underwent conservative staged excision with frozen section analysis with Melan A immunostaining to confirm negative margins.

Of those treated with dual topical therapy for 3 months, 29 of 37 lesions (78%) had complete responses with no residual lentigo maligna at the time of staged excision. So did 27 of 42 (64%) treated with imiquimod alone (Arch. Dermatol. 2012;148:592-6).

The modest difference in outcome was not significant (P = .17). Nevertheless, the Utah investigators wrote that topical pretreatment appears to reduce surgical defect sizes, an important consideration in lentigo maligna because the lesions are often large and located on cosmetically sensitive facial sites. At the patient’s first visit, the researchers saucerize the entire tumor to remove all visible evidence of lentigo maligna and nip in the bud any invasive element that might be present. One month later, after the wound has healed by secondary intention, the patient begins topical imiquimod therapy 5 days per week. If no inflammation is observed, tazarotene gel is added on the other 2 days per week. After 3 months of topical therapy, the patient goes off treatment for 2 months so the inflammatory response can subside. Then a staged excision is performed with 2-mm margins around the perimeter of the original tumor outline.

"This is an interesting thought, but it’s still not considered standard of care," Dr. Marmur commented in describing the Utah research.

Bruce C. Jancin/IMNG Medical Media

Session chair Dr. Allan C. Halpern, chief of the dermatology service at Memorial Sloan-Kettering Cancer Center in New York, said he and his colleagues, like the Utah group, are using a lot of topical imiquimod as adjunctive therapy for lentigo maligna.

"Because we’re a referral center, we see all those patients whose melanomas unfortunately do recur at the edge of large surgeries. We see a lot of patients whose local surgeons have chased around their faces for a certain amount of time. So I think the general concept of the cure rates of surgery is a bit overstated. I’m not trying to sell an off-label use of a drug, but I think sometimes imiquimod can be very helpful," Dr. Halpern said.

He offered a clinical pearl in diagnosing lentigo maligna: Consider a broad shave biopsy of a suspicious lesion rather than a deeper, smaller-diameter biopsy.

"Sampling errors are a real problem with lentigo maligna. We learned early on that if you take a large lentigo maligna and do multiple biopsies of the same lesion and send them to what we think are our very expert pathologists, on average, we get two or three back that were melanoma and two or three back that were pigmented actinic keratoses. The sampling error tends to be more in the horizontal than in the depth for these very early lesions," according to Dr. Halpern.

Dr. Marmur and Dr. Halpern reported having no relevant financial interests. SDEF and this news organization are owned by the same parent company.

bjancin@frontlinemedcom.com

MAUI, HAWAII – "Slow Mohs" has gained near-universal acceptance among skin cancer specialists as a definitive surgical technique for complete removal of lentigo maligna melanoma while simultaneously sparing normal tissue, according to Dr. Ellen Marmur of Mount Sinai School of Medicine, New York.

The big advantage that slow Mohs has over standard wide local excision with 0.5- to 1-cm margins is a 5-year cure rate approaching 100%. In contrast, standard excision has a recurrence rate of up to 20%, she said at the Hawaii Dermatology Seminar, sponsored by Global Academy for Medical Education/Skin Disease Education Foundation.

Bruce C. Jancin/IMNG Medical Media

Slow Mohs is a modified form of Mohs micrographic surgery. The surgery compares with conventional Mohs: It is staged, margin-controlled excision. But in slow Mohs, rush permanent sections are sent off to the pathologist rather than the frozen sections integral to conventional Mohs.

Dr. Marmur relies upon slow Mohs, with "bread-loafing" of the central tumor by the pathologist, because the permanent sections better preserve the tumor’s microscopic features. Interpreting atypical melanocytes in frozen sections can be quite a challenge. However, she added, some Mohs surgeons have found that using rapid immunostains also markedly improves the sensitivity and specificity of frozen sections in lentigo maligna surgery.

Slow Mohs takes place over the course of days, she said. "Basically, you do your Wood’s lamp to define the lesion diameter, you measure out your margins, you excise the tumor, pack the area with a bandage, and send the patient home. You rush your pathology, and you don’t do any reconstruction until you get the margins clear."

A pathology report that comes back stating narrow margins are present is "a heart stopper," she added.

"You have the option of observing the area if the margin is clear but the tumor was close to the margin. That’s a good approach for an elderly patient or when the lentigo maligna was in a cosmetically important area."

Lentigo maligna melanoma accounts for 4% of all cases of melanoma. It typically arises on sun-damaged skin in individuals in their 70s or older. Common sites include the malar area, forehead, nose, and temple. The differential diagnosis includes seborrheic keratosis, pigmented actinic keratosis, and pigmented nevus.

Lentigo maligna becomes lentigo maligna melanoma when malignant melanoma cells invade the dermis and deeper appendages. Roughly 5% of lentigo malignas eventually progress to invasive melanoma, according to Dr. Marmur. Typically, a lentigo maligna undergoes extended gradual horizontal growth before beginning a vertical growth phase.

"It spreads like an oil slick for many years," Dr. Marmur said at the seminar.

Established treatment modalities for patients who aren’t surgical candidates include cryotherapy, radiotherapy, and topical imiquimod 5%. All have disadvantages, including high 5-year recurrence rates.

Dr. Marmur noted that a newer nonsurgical therapy drawing considerable interest involves off-label use of topical combination therapy with imiquimod and tazarotene gel. The concept is to use the topical retinoid to disrupt the stratum corneum in order to enhance imiquimod penetration, thereby achieving a greater inflammatory response than possible with imiquimod alone.

Initial data have been published by researchers at the University of Utah, Salt Lake City. They randomized 90 patients with 91 lentigo malignas to imiquimod 5% cream applied 5 days per week for 3 months or to the imiquimod regimen plus tazarotene 0.1% gel on the other 2 days per week. After 3 months of topical therapy, patients underwent conservative staged excision with frozen section analysis with Melan A immunostaining to confirm negative margins.

Of those treated with dual topical therapy for 3 months, 29 of 37 lesions (78%) had complete responses with no residual lentigo maligna at the time of staged excision. So did 27 of 42 (64%) treated with imiquimod alone (Arch. Dermatol. 2012;148:592-6).

The modest difference in outcome was not significant (P = .17). Nevertheless, the Utah investigators wrote that topical pretreatment appears to reduce surgical defect sizes, an important consideration in lentigo maligna because the lesions are often large and located on cosmetically sensitive facial sites. At the patient’s first visit, the researchers saucerize the entire tumor to remove all visible evidence of lentigo maligna and nip in the bud any invasive element that might be present. One month later, after the wound has healed by secondary intention, the patient begins topical imiquimod therapy 5 days per week. If no inflammation is observed, tazarotene gel is added on the other 2 days per week. After 3 months of topical therapy, the patient goes off treatment for 2 months so the inflammatory response can subside. Then a staged excision is performed with 2-mm margins around the perimeter of the original tumor outline.

"This is an interesting thought, but it’s still not considered standard of care," Dr. Marmur commented in describing the Utah research.

Bruce C. Jancin/IMNG Medical Media

Session chair Dr. Allan C. Halpern, chief of the dermatology service at Memorial Sloan-Kettering Cancer Center in New York, said he and his colleagues, like the Utah group, are using a lot of topical imiquimod as adjunctive therapy for lentigo maligna.

"Because we’re a referral center, we see all those patients whose melanomas unfortunately do recur at the edge of large surgeries. We see a lot of patients whose local surgeons have chased around their faces for a certain amount of time. So I think the general concept of the cure rates of surgery is a bit overstated. I’m not trying to sell an off-label use of a drug, but I think sometimes imiquimod can be very helpful," Dr. Halpern said.

He offered a clinical pearl in diagnosing lentigo maligna: Consider a broad shave biopsy of a suspicious lesion rather than a deeper, smaller-diameter biopsy.

"Sampling errors are a real problem with lentigo maligna. We learned early on that if you take a large lentigo maligna and do multiple biopsies of the same lesion and send them to what we think are our very expert pathologists, on average, we get two or three back that were melanoma and two or three back that were pigmented actinic keratoses. The sampling error tends to be more in the horizontal than in the depth for these very early lesions," according to Dr. Halpern.

Dr. Marmur and Dr. Halpern reported having no relevant financial interests. SDEF and this news organization are owned by the same parent company.

bjancin@frontlinemedcom.com

MAUI, HAWAII – "Slow Mohs" has gained near-universal acceptance among skin cancer specialists as a definitive surgical technique for complete removal of lentigo maligna melanoma while simultaneously sparing normal tissue, according to Dr. Ellen Marmur of Mount Sinai School of Medicine, New York.

The big advantage that slow Mohs has over standard wide local excision with 0.5- to 1-cm margins is a 5-year cure rate approaching 100%. In contrast, standard excision has a recurrence rate of up to 20%, she said at the Hawaii Dermatology Seminar, sponsored by Global Academy for Medical Education/Skin Disease Education Foundation.

Bruce C. Jancin/IMNG Medical Media

Slow Mohs is a modified form of Mohs micrographic surgery. The surgery compares with conventional Mohs: It is staged, margin-controlled excision. But in slow Mohs, rush permanent sections are sent off to the pathologist rather than the frozen sections integral to conventional Mohs.

Dr. Marmur relies upon slow Mohs, with "bread-loafing" of the central tumor by the pathologist, because the permanent sections better preserve the tumor’s microscopic features. Interpreting atypical melanocytes in frozen sections can be quite a challenge. However, she added, some Mohs surgeons have found that using rapid immunostains also markedly improves the sensitivity and specificity of frozen sections in lentigo maligna surgery.

Slow Mohs takes place over the course of days, she said. "Basically, you do your Wood’s lamp to define the lesion diameter, you measure out your margins, you excise the tumor, pack the area with a bandage, and send the patient home. You rush your pathology, and you don’t do any reconstruction until you get the margins clear."

A pathology report that comes back stating narrow margins are present is "a heart stopper," she added.

"You have the option of observing the area if the margin is clear but the tumor was close to the margin. That’s a good approach for an elderly patient or when the lentigo maligna was in a cosmetically important area."

Lentigo maligna melanoma accounts for 4% of all cases of melanoma. It typically arises on sun-damaged skin in individuals in their 70s or older. Common sites include the malar area, forehead, nose, and temple. The differential diagnosis includes seborrheic keratosis, pigmented actinic keratosis, and pigmented nevus.

Lentigo maligna becomes lentigo maligna melanoma when malignant melanoma cells invade the dermis and deeper appendages. Roughly 5% of lentigo malignas eventually progress to invasive melanoma, according to Dr. Marmur. Typically, a lentigo maligna undergoes extended gradual horizontal growth before beginning a vertical growth phase.

"It spreads like an oil slick for many years," Dr. Marmur said at the seminar.

Established treatment modalities for patients who aren’t surgical candidates include cryotherapy, radiotherapy, and topical imiquimod 5%. All have disadvantages, including high 5-year recurrence rates.

Dr. Marmur noted that a newer nonsurgical therapy drawing considerable interest involves off-label use of topical combination therapy with imiquimod and tazarotene gel. The concept is to use the topical retinoid to disrupt the stratum corneum in order to enhance imiquimod penetration, thereby achieving a greater inflammatory response than possible with imiquimod alone.

Initial data have been published by researchers at the University of Utah, Salt Lake City. They randomized 90 patients with 91 lentigo malignas to imiquimod 5% cream applied 5 days per week for 3 months or to the imiquimod regimen plus tazarotene 0.1% gel on the other 2 days per week. After 3 months of topical therapy, patients underwent conservative staged excision with frozen section analysis with Melan A immunostaining to confirm negative margins.

Of those treated with dual topical therapy for 3 months, 29 of 37 lesions (78%) had complete responses with no residual lentigo maligna at the time of staged excision. So did 27 of 42 (64%) treated with imiquimod alone (Arch. Dermatol. 2012;148:592-6).

The modest difference in outcome was not significant (P = .17). Nevertheless, the Utah investigators wrote that topical pretreatment appears to reduce surgical defect sizes, an important consideration in lentigo maligna because the lesions are often large and located on cosmetically sensitive facial sites. At the patient’s first visit, the researchers saucerize the entire tumor to remove all visible evidence of lentigo maligna and nip in the bud any invasive element that might be present. One month later, after the wound has healed by secondary intention, the patient begins topical imiquimod therapy 5 days per week. If no inflammation is observed, tazarotene gel is added on the other 2 days per week. After 3 months of topical therapy, the patient goes off treatment for 2 months so the inflammatory response can subside. Then a staged excision is performed with 2-mm margins around the perimeter of the original tumor outline.

"This is an interesting thought, but it’s still not considered standard of care," Dr. Marmur commented in describing the Utah research.

Bruce C. Jancin/IMNG Medical Media

Session chair Dr. Allan C. Halpern, chief of the dermatology service at Memorial Sloan-Kettering Cancer Center in New York, said he and his colleagues, like the Utah group, are using a lot of topical imiquimod as adjunctive therapy for lentigo maligna.

"Because we’re a referral center, we see all those patients whose melanomas unfortunately do recur at the edge of large surgeries. We see a lot of patients whose local surgeons have chased around their faces for a certain amount of time. So I think the general concept of the cure rates of surgery is a bit overstated. I’m not trying to sell an off-label use of a drug, but I think sometimes imiquimod can be very helpful," Dr. Halpern said.

He offered a clinical pearl in diagnosing lentigo maligna: Consider a broad shave biopsy of a suspicious lesion rather than a deeper, smaller-diameter biopsy.

"Sampling errors are a real problem with lentigo maligna. We learned early on that if you take a large lentigo maligna and do multiple biopsies of the same lesion and send them to what we think are our very expert pathologists, on average, we get two or three back that were melanoma and two or three back that were pigmented actinic keratoses. The sampling error tends to be more in the horizontal than in the depth for these very early lesions," according to Dr. Halpern.

Dr. Marmur and Dr. Halpern reported having no relevant financial interests. SDEF and this news organization are owned by the same parent company.

bjancin@frontlinemedcom.com

Nonsteroidal anti-inflammatory drugs (NSAIDs) have therapeutic applications that "have spanned several centuries," according to Rao and Knaus (J. Pharm. Pharm. Sci. 2008;11:81s-110s). NSAIDs are among the increasing number of anti-inflammatory agents used to target bioactive lipids produced from arachidonic acid. Although this drug class is one of the most often used in practice and has been well studied by investigators, the role of NSAIDs for cutaneous purposes has been relatively limited (J. Cutan. Med. Surg. 2002;6:241-56). Indeed, only three topical NSAIDs are approved for use in the United States, for a narrow range of conditions.

Diclofenac sodium 1.5% topical solution (containing dimethyl sulfoxide to enhance penetration) and diclofenac sodium gel 1% are currently approved in the United States for hand and knee osteoarthritis (Postgrad. Med. 2010;122:98-106). The diclofenac hydroxyethylpyrrolidine (epolamine) 1.3% patch was approved by the U.S. Food and Drug Administration for soft-tissue injuries in January 2007, although it has long been available in more than 40 countries (Int. J. Clin. Pract. 2010;64:1546-53; Clin. Ther. 2010;32:1001-14).

A winning adverse event profile

Significantly, topical NSAIDs have not been associated with the adverse events resulting from oral NSAIDs, which engender various dose-related side effects (Semin. Arthritis. Rheum. 2009;39:203-12). Mild and self-limiting local skin reactions are the most common adverse side effects from topical NSAID products. The diclofenac products are approved in the European Union, as are ibuprofen creams and gels, ketoprofen gel, felbinac gel and cutaneous foam, and piroxicam gel.

The efficacy and safety of these products have been established through meta-analyses. In a recent study, researchers cautioned that the patient, the drug, and the drug delivery mechanism should be considered in topical NSAID selection, because the pharmacokinetic absorption from topical preparations can vary with different formulations of the same drug, depending on the agent, the underlying disorder, and the application site (Am. J. Ther. 2012 Feb 22 [Epub ahead of print]).

Easing osteoarthritis

Although oral NSAIDs have been the mainstays of hand and knee osteoarthritis treatment regimens, their dose- and age-related side effect profiles (including adverse effects on the cardiovascular, renal, and gastrointestinal systems) have prompted the use of topical NSAIDs, which yield comparable efficacy with far less systemic risk. Results of a Jan. 1, 2005, to March 31, 2010, literature review showed that topical products exhibited superior efficacy compared with placebo, with similar adverse event profiles. Topicals also showed efficacy comparable to that of oral diclofenac, with side effects seen primarily at the application site and no ulcers, perforations, or bleeding (Postgrad. Med. 2010;122(6):98-106).

In 2009, Barthel et al. evaluated the efficacy and safety of topical diclofenac sodium gel (DSG) 1% in a randomized, double-blind, vehicle-controlled trial of 492 adults (aged 35 years and older) with mild to moderate symptomatic knee osteoarthritis lasting at least 6 months. Patients received 4 g of topical treatment of DSG or vehicle four times daily for 12 weeks. The investigators noted significant reductions in the DSG group compared with the vehicle group according to the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain and physical function subscales, as well as global rating of disease. They also observed significantly better efficacy results with DSG as early as week 1 of treatment. Gastrointestinal reactions occurred in 5.9% of the DSG group and 5.0% of the vehicle group, and application site reactions emerged in 5.1% of the DSG group and 2.5% of the vehicle group (Semin. Arthritis Rheum. 2009;39:203-12).

In 2010, Baraf et al. also conducted a 12-week efficacy and safety study of topical DSG 1% for symptomatic knee osteoarthritis. This randomized, double-blind, parallel-group, multicenter trial of patients at least 35 years of age with symptomatic Kellgren-Lawrence grade (KLG) 1 to 3 osteoarthritis in one or both knees for at least 6 months assigned 208 subjects to DSG treatment and 212 to vehicle. The investigators found significant improvement according to WOMAC metrics in the DSG patients compared with placebo patients. Unlike the Barthel report, no gastrointestinal upset was noted in this study. Application site reactions were the most common side effect, occurring in 4.8% of the DSG group and 0% of the vehicle group (Phys. Sportsmed. 2010;38:19-28).

In 2012, Baraf et al. extended their previous work and assessed the safety of topical DSG 1% for the treatment of knee and hand osteoarthritis in older and younger patients. They also compared the treatment in those with or without comorbid hypertension, type 2 diabetes, or cerebrovascular or cardiovascular disease. This post hoc analysis of pooled data from five randomized, double-blind, placebo-controlled trials included 1,426 patients 35 years of age and older with mild to moderate osteoarthritis of the knee and 783 patients 40 years of age and older with mild to moderate osteoarthritis of the hand. Participants applied 4 g of DSG or vehicle to affected knees q.i.d. for 12 weeks or 2 g of DSG or vehicle to affected hands q.i.d. for 8 weeks. The investigators found that the adverse event profile was similar across comparisons of patients with knee osteoarthritis. Among patients with hand osteoarthritis, the only differences were that the adverse event profile was lower in patients with type 2 diabetes than in patients without the condition, and higher in patients with cerebrovascular or cardiovascular disease than in patients without those conditions. The authors concluded that the rates of adverse side effects were similar and low between the two groups (Am. J. Geriatr. Pharmacother. 2012;10:47-60).

To further examine the efficacy and tolerability of the diclofenac epolamine topical patch (DETP), investigators reviewed data from eight studies from 1984 to 2009, including data on patients with acute pain from soft-tissue injuries or localized periarticular disorders. Significant reductions in spontaneous pain from baseline due to DETP were seen (range, 26%-88% on day 7 and 56%-61% on day 14). In addition, significant decreases in pain scores were linked to DETP use compared with a placebo patch in two studies and compared with diclofenac diethylammonium topical gel in one study. Adverse events were low across studies; reactions at the application site and nausea were the most common events (Clin. Ther. 2010;32:1001-14).

Oral ibuprofen and combination therapy

Notably, ibuprofen has demonstrated effectiveness in the treatment of acne, as inflammatory acne lesions are infiltrated with neutrophils and ibuprofen suppresses leukocyte chemotaxis (Dermatology. 2003;206:68-73). Ibuprofen is generally considered safe, with low potential for causing gastrointestinal, cardiovascular, or renal risks compared with other NSAIDs and selective cyclooxygenase-2 inhibitors (coxibs), which have been removed from the market (Inflammopharmacology 2009;17:275-342; J. Pharm. Pharm. Sci. 2008;11:81s-110s).

In a double-blind study of 60 patients aged 15-35 years with acne vulgaris, patients were randomly assigned to one of four groups: oral ibuprofen (600 mg) plus tetracycline (250 mg) four times daily; ibuprofen (600 mg) plus placebo four times daily; tetracycline (250 mg) plus placebo four times daily; and two placebos four times daily. Interestingly, the combination therapy was the only approach that yielded an effect statistically superior to that of placebo in reducing total lesion counts. The use of ibuprofen alone netted improvements comparable to those afforded by tetracycline but with fewer side effects (J. Am. Acad. Dermatol. 1984;11:1076-81).

NSAIDs are also used for the treatment of sunburn. In 1992, Hughes et al. investigated ameliorating UVB-induced skin injury by nonsteroidal drugs (oral ibuprofen or indomethacin) plus topical betamethasone dipropionate in 24 subjects. Measurements of erythema and increased skin blood flow, performed serially, revealed a synergistic effect of oral NSAIDs combined with topical corticosteroids to repair UVB-induced skin damage (Dermatology 1992;184:54-8).

Conclusion

An ideal anti-inflammatory agent has not yet been developed, but topical NSAIDs appear to fit the bill in terms of reducing or eliminating the adverse side effects associated with oral NSAID regimens. However, topical NSAIDs are approved for only a narrow range of indications, and more research is necessary to determine whether they are appropriate for a wider array of dermatologic conditions.

Dr. Baumann is in private practice in Miami Beach. She did not disclose any conflicts of interest. 

Nonsteroidal anti-inflammatory drugs (NSAIDs) have therapeutic applications that "have spanned several centuries," according to Rao and Knaus (J. Pharm. Pharm. Sci. 2008;11:81s-110s). NSAIDs are among the increasing number of anti-inflammatory agents used to target bioactive lipids produced from arachidonic acid. Although this drug class is one of the most often used in practice and has been well studied by investigators, the role of NSAIDs for cutaneous purposes has been relatively limited (J. Cutan. Med. Surg. 2002;6:241-56). Indeed, only three topical NSAIDs are approved for use in the United States, for a narrow range of conditions.

Diclofenac sodium 1.5% topical solution (containing dimethyl sulfoxide to enhance penetration) and diclofenac sodium gel 1% are currently approved in the United States for hand and knee osteoarthritis (Postgrad. Med. 2010;122:98-106). The diclofenac hydroxyethylpyrrolidine (epolamine) 1.3% patch was approved by the U.S. Food and Drug Administration for soft-tissue injuries in January 2007, although it has long been available in more than 40 countries (Int. J. Clin. Pract. 2010;64:1546-53; Clin. Ther. 2010;32:1001-14).

A winning adverse event profile

Significantly, topical NSAIDs have not been associated with the adverse events resulting from oral NSAIDs, which engender various dose-related side effects (Semin. Arthritis. Rheum. 2009;39:203-12). Mild and self-limiting local skin reactions are the most common adverse side effects from topical NSAID products. The diclofenac products are approved in the European Union, as are ibuprofen creams and gels, ketoprofen gel, felbinac gel and cutaneous foam, and piroxicam gel.

The efficacy and safety of these products have been established through meta-analyses. In a recent study, researchers cautioned that the patient, the drug, and the drug delivery mechanism should be considered in topical NSAID selection, because the pharmacokinetic absorption from topical preparations can vary with different formulations of the same drug, depending on the agent, the underlying disorder, and the application site (Am. J. Ther. 2012 Feb 22 [Epub ahead of print]).

Easing osteoarthritis

Although oral NSAIDs have been the mainstays of hand and knee osteoarthritis treatment regimens, their dose- and age-related side effect profiles (including adverse effects on the cardiovascular, renal, and gastrointestinal systems) have prompted the use of topical NSAIDs, which yield comparable efficacy with far less systemic risk. Results of a Jan. 1, 2005, to March 31, 2010, literature review showed that topical products exhibited superior efficacy compared with placebo, with similar adverse event profiles. Topicals also showed efficacy comparable to that of oral diclofenac, with side effects seen primarily at the application site and no ulcers, perforations, or bleeding (Postgrad. Med. 2010;122(6):98-106).

In 2009, Barthel et al. evaluated the efficacy and safety of topical diclofenac sodium gel (DSG) 1% in a randomized, double-blind, vehicle-controlled trial of 492 adults (aged 35 years and older) with mild to moderate symptomatic knee osteoarthritis lasting at least 6 months. Patients received 4 g of topical treatment of DSG or vehicle four times daily for 12 weeks. The investigators noted significant reductions in the DSG group compared with the vehicle group according to the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain and physical function subscales, as well as global rating of disease. They also observed significantly better efficacy results with DSG as early as week 1 of treatment. Gastrointestinal reactions occurred in 5.9% of the DSG group and 5.0% of the vehicle group, and application site reactions emerged in 5.1% of the DSG group and 2.5% of the vehicle group (Semin. Arthritis Rheum. 2009;39:203-12).

In 2010, Baraf et al. also conducted a 12-week efficacy and safety study of topical DSG 1% for symptomatic knee osteoarthritis. This randomized, double-blind, parallel-group, multicenter trial of patients at least 35 years of age with symptomatic Kellgren-Lawrence grade (KLG) 1 to 3 osteoarthritis in one or both knees for at least 6 months assigned 208 subjects to DSG treatment and 212 to vehicle. The investigators found significant improvement according to WOMAC metrics in the DSG patients compared with placebo patients. Unlike the Barthel report, no gastrointestinal upset was noted in this study. Application site reactions were the most common side effect, occurring in 4.8% of the DSG group and 0% of the vehicle group (Phys. Sportsmed. 2010;38:19-28).

In 2012, Baraf et al. extended their previous work and assessed the safety of topical DSG 1% for the treatment of knee and hand osteoarthritis in older and younger patients. They also compared the treatment in those with or without comorbid hypertension, type 2 diabetes, or cerebrovascular or cardiovascular disease. This post hoc analysis of pooled data from five randomized, double-blind, placebo-controlled trials included 1,426 patients 35 years of age and older with mild to moderate osteoarthritis of the knee and 783 patients 40 years of age and older with mild to moderate osteoarthritis of the hand. Participants applied 4 g of DSG or vehicle to affected knees q.i.d. for 12 weeks or 2 g of DSG or vehicle to affected hands q.i.d. for 8 weeks. The investigators found that the adverse event profile was similar across comparisons of patients with knee osteoarthritis. Among patients with hand osteoarthritis, the only differences were that the adverse event profile was lower in patients with type 2 diabetes than in patients without the condition, and higher in patients with cerebrovascular or cardiovascular disease than in patients without those conditions. The authors concluded that the rates of adverse side effects were similar and low between the two groups (Am. J. Geriatr. Pharmacother. 2012;10:47-60).

To further examine the efficacy and tolerability of the diclofenac epolamine topical patch (DETP), investigators reviewed data from eight studies from 1984 to 2009, including data on patients with acute pain from soft-tissue injuries or localized periarticular disorders. Significant reductions in spontaneous pain from baseline due to DETP were seen (range, 26%-88% on day 7 and 56%-61% on day 14). In addition, significant decreases in pain scores were linked to DETP use compared with a placebo patch in two studies and compared with diclofenac diethylammonium topical gel in one study. Adverse events were low across studies; reactions at the application site and nausea were the most common events (Clin. Ther. 2010;32:1001-14).

Oral ibuprofen and combination therapy

Notably, ibuprofen has demonstrated effectiveness in the treatment of acne, as inflammatory acne lesions are infiltrated with neutrophils and ibuprofen suppresses leukocyte chemotaxis (Dermatology. 2003;206:68-73). Ibuprofen is generally considered safe, with low potential for causing gastrointestinal, cardiovascular, or renal risks compared with other NSAIDs and selective cyclooxygenase-2 inhibitors (coxibs), which have been removed from the market (Inflammopharmacology 2009;17:275-342; J. Pharm. Pharm. Sci. 2008;11:81s-110s).

In a double-blind study of 60 patients aged 15-35 years with acne vulgaris, patients were randomly assigned to one of four groups: oral ibuprofen (600 mg) plus tetracycline (250 mg) four times daily; ibuprofen (600 mg) plus placebo four times daily; tetracycline (250 mg) plus placebo four times daily; and two placebos four times daily. Interestingly, the combination therapy was the only approach that yielded an effect statistically superior to that of placebo in reducing total lesion counts. The use of ibuprofen alone netted improvements comparable to those afforded by tetracycline but with fewer side effects (J. Am. Acad. Dermatol. 1984;11:1076-81).

NSAIDs are also used for the treatment of sunburn. In 1992, Hughes et al. investigated ameliorating UVB-induced skin injury by nonsteroidal drugs (oral ibuprofen or indomethacin) plus topical betamethasone dipropionate in 24 subjects. Measurements of erythema and increased skin blood flow, performed serially, revealed a synergistic effect of oral NSAIDs combined with topical corticosteroids to repair UVB-induced skin damage (Dermatology 1992;184:54-8).

Conclusion

An ideal anti-inflammatory agent has not yet been developed, but topical NSAIDs appear to fit the bill in terms of reducing or eliminating the adverse side effects associated with oral NSAID regimens. However, topical NSAIDs are approved for only a narrow range of indications, and more research is necessary to determine whether they are appropriate for a wider array of dermatologic conditions.

Dr. Baumann is in private practice in Miami Beach. She did not disclose any conflicts of interest. 

Nonsteroidal anti-inflammatory drugs (NSAIDs) have therapeutic applications that "have spanned several centuries," according to Rao and Knaus (J. Pharm. Pharm. Sci. 2008;11:81s-110s). NSAIDs are among the increasing number of anti-inflammatory agents used to target bioactive lipids produced from arachidonic acid. Although this drug class is one of the most often used in practice and has been well studied by investigators, the role of NSAIDs for cutaneous purposes has been relatively limited (J. Cutan. Med. Surg. 2002;6:241-56). Indeed, only three topical NSAIDs are approved for use in the United States, for a narrow range of conditions.

Diclofenac sodium 1.5% topical solution (containing dimethyl sulfoxide to enhance penetration) and diclofenac sodium gel 1% are currently approved in the United States for hand and knee osteoarthritis (Postgrad. Med. 2010;122:98-106). The diclofenac hydroxyethylpyrrolidine (epolamine) 1.3% patch was approved by the U.S. Food and Drug Administration for soft-tissue injuries in January 2007, although it has long been available in more than 40 countries (Int. J. Clin. Pract. 2010;64:1546-53; Clin. Ther. 2010;32:1001-14).

A winning adverse event profile

Significantly, topical NSAIDs have not been associated with the adverse events resulting from oral NSAIDs, which engender various dose-related side effects (Semin. Arthritis. Rheum. 2009;39:203-12). Mild and self-limiting local skin reactions are the most common adverse side effects from topical NSAID products. The diclofenac products are approved in the European Union, as are ibuprofen creams and gels, ketoprofen gel, felbinac gel and cutaneous foam, and piroxicam gel.

The efficacy and safety of these products have been established through meta-analyses. In a recent study, researchers cautioned that the patient, the drug, and the drug delivery mechanism should be considered in topical NSAID selection, because the pharmacokinetic absorption from topical preparations can vary with different formulations of the same drug, depending on the agent, the underlying disorder, and the application site (Am. J. Ther. 2012 Feb 22 [Epub ahead of print]).

Easing osteoarthritis

Although oral NSAIDs have been the mainstays of hand and knee osteoarthritis treatment regimens, their dose- and age-related side effect profiles (including adverse effects on the cardiovascular, renal, and gastrointestinal systems) have prompted the use of topical NSAIDs, which yield comparable efficacy with far less systemic risk. Results of a Jan. 1, 2005, to March 31, 2010, literature review showed that topical products exhibited superior efficacy compared with placebo, with similar adverse event profiles. Topicals also showed efficacy comparable to that of oral diclofenac, with side effects seen primarily at the application site and no ulcers, perforations, or bleeding (Postgrad. Med. 2010;122(6):98-106).

In 2009, Barthel et al. evaluated the efficacy and safety of topical diclofenac sodium gel (DSG) 1% in a randomized, double-blind, vehicle-controlled trial of 492 adults (aged 35 years and older) with mild to moderate symptomatic knee osteoarthritis lasting at least 6 months. Patients received 4 g of topical treatment of DSG or vehicle four times daily for 12 weeks. The investigators noted significant reductions in the DSG group compared with the vehicle group according to the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain and physical function subscales, as well as global rating of disease. They also observed significantly better efficacy results with DSG as early as week 1 of treatment. Gastrointestinal reactions occurred in 5.9% of the DSG group and 5.0% of the vehicle group, and application site reactions emerged in 5.1% of the DSG group and 2.5% of the vehicle group (Semin. Arthritis Rheum. 2009;39:203-12).

In 2010, Baraf et al. also conducted a 12-week efficacy and safety study of topical DSG 1% for symptomatic knee osteoarthritis. This randomized, double-blind, parallel-group, multicenter trial of patients at least 35 years of age with symptomatic Kellgren-Lawrence grade (KLG) 1 to 3 osteoarthritis in one or both knees for at least 6 months assigned 208 subjects to DSG treatment and 212 to vehicle. The investigators found significant improvement according to WOMAC metrics in the DSG patients compared with placebo patients. Unlike the Barthel report, no gastrointestinal upset was noted in this study. Application site reactions were the most common side effect, occurring in 4.8% of the DSG group and 0% of the vehicle group (Phys. Sportsmed. 2010;38:19-28).

In 2012, Baraf et al. extended their previous work and assessed the safety of topical DSG 1% for the treatment of knee and hand osteoarthritis in older and younger patients. They also compared the treatment in those with or without comorbid hypertension, type 2 diabetes, or cerebrovascular or cardiovascular disease. This post hoc analysis of pooled data from five randomized, double-blind, placebo-controlled trials included 1,426 patients 35 years of age and older with mild to moderate osteoarthritis of the knee and 783 patients 40 years of age and older with mild to moderate osteoarthritis of the hand. Participants applied 4 g of DSG or vehicle to affected knees q.i.d. for 12 weeks or 2 g of DSG or vehicle to affected hands q.i.d. for 8 weeks. The investigators found that the adverse event profile was similar across comparisons of patients with knee osteoarthritis. Among patients with hand osteoarthritis, the only differences were that the adverse event profile was lower in patients with type 2 diabetes than in patients without the condition, and higher in patients with cerebrovascular or cardiovascular disease than in patients without those conditions. The authors concluded that the rates of adverse side effects were similar and low between the two groups (Am. J. Geriatr. Pharmacother. 2012;10:47-60).

To further examine the efficacy and tolerability of the diclofenac epolamine topical patch (DETP), investigators reviewed data from eight studies from 1984 to 2009, including data on patients with acute pain from soft-tissue injuries or localized periarticular disorders. Significant reductions in spontaneous pain from baseline due to DETP were seen (range, 26%-88% on day 7 and 56%-61% on day 14). In addition, significant decreases in pain scores were linked to DETP use compared with a placebo patch in two studies and compared with diclofenac diethylammonium topical gel in one study. Adverse events were low across studies; reactions at the application site and nausea were the most common events (Clin. Ther. 2010;32:1001-14).

Oral ibuprofen and combination therapy

Notably, ibuprofen has demonstrated effectiveness in the treatment of acne, as inflammatory acne lesions are infiltrated with neutrophils and ibuprofen suppresses leukocyte chemotaxis (Dermatology. 2003;206:68-73). Ibuprofen is generally considered safe, with low potential for causing gastrointestinal, cardiovascular, or renal risks compared with other NSAIDs and selective cyclooxygenase-2 inhibitors (coxibs), which have been removed from the market (Inflammopharmacology 2009;17:275-342; J. Pharm. Pharm. Sci. 2008;11:81s-110s).

In a double-blind study of 60 patients aged 15-35 years with acne vulgaris, patients were randomly assigned to one of four groups: oral ibuprofen (600 mg) plus tetracycline (250 mg) four times daily; ibuprofen (600 mg) plus placebo four times daily; tetracycline (250 mg) plus placebo four times daily; and two placebos four times daily. Interestingly, the combination therapy was the only approach that yielded an effect statistically superior to that of placebo in reducing total lesion counts. The use of ibuprofen alone netted improvements comparable to those afforded by tetracycline but with fewer side effects (J. Am. Acad. Dermatol. 1984;11:1076-81).

NSAIDs are also used for the treatment of sunburn. In 1992, Hughes et al. investigated ameliorating UVB-induced skin injury by nonsteroidal drugs (oral ibuprofen or indomethacin) plus topical betamethasone dipropionate in 24 subjects. Measurements of erythema and increased skin blood flow, performed serially, revealed a synergistic effect of oral NSAIDs combined with topical corticosteroids to repair UVB-induced skin damage (Dermatology 1992;184:54-8).

Conclusion

An ideal anti-inflammatory agent has not yet been developed, but topical NSAIDs appear to fit the bill in terms of reducing or eliminating the adverse side effects associated with oral NSAID regimens. However, topical NSAIDs are approved for only a narrow range of indications, and more research is necessary to determine whether they are appropriate for a wider array of dermatologic conditions.

Dr. Baumann is in private practice in Miami Beach. She did not disclose any conflicts of interest. 

A recent Agency for Healthcare Research and Quality (AHRQ) report, “Making Health Care Safer II: An Updated Critical Analysis of the Evidence for Patient Safety Practices,” holds nearly 1,000 pages of practice-management tips for improving outcomes. But where does a hospitalist begin when reviewing such a massive playbook for progress?

Jim Battles, PhD, an AHRQ social science analyst for patient safety who worked on the report, says the best place to start is by asking yourself: “What keeps you up at night? … What scares the heck out of you?”

The report, a follow-up to the influential and controversial 2001 report “Making Health Care Safer: A Critical Analysis of Patient Safety Practices,” is viewed by its authors as the next step in the continuum of improving patient outcomes. The latest research culled a list of more than 100 patient-safety practices (PSPs) down to 10 that should be “strongly encouraged” and another dozen that are “encouraged.” Battles looks at the 2001 report as more about pushing physicians to think about PSPs, with the updated version as a guidebook on how to think about it.

Listen to AHRQ analyst Jim Battles, PhD, talk about how hospitalists and others should view the new report

Paul Shekelle, MD, PhD, director of the Southern California Evidence-Based Practice Center site of RAND Corp., which AHRQ commissioned to produce the report, says that some might look at safety initiatives since the landmark Institute of Medicine report “To Err is Human” in 1999 and question whether enough progress has been made. But all progress is meaningful to individual patients, and the improvements of the past decade and a half have been important, he adds.

“What I believe is that we’ve made a lot of progress in certain areas,” Dr. Shekelle says, “but this can't be seen when we look at aggregate data, because the improvements we have seen don't account for a sufficiently large proportion in aggregate of the overall patient safety problem.”

Dr. Shekelle—one of three co-principal investigators on the report, along with Peter Pronovost, MD, PhD, FCCM, of Johns Hopkins School of Medicine in Baltimore and HM pioneer Robert Wachter, MD, MHM, chief of the division of hospital medicine at the University of California at San Francisco—says he hopes physicians realize that while the report’s recommendations are evidence-based, they’re not a magic bullet.

“One of the main messages of our report is this is not like writing a prescription for a statin,” Dr. Shekelle says. “This is going to take work. It’s going to take local adaptation, and it’s going to take talking to your front-line clinicians to try and find out how to make this thing work.”

Dr. Wachter, who helped craft both the 2001 and 2013 reports, says patient safety “can be one of those things that is so compelling and so dramatic that you develop a little bit of Nike syndrome—let’s just do it, let’s just computerize, let’s just do teamwork training, let’s do simulation.” However, the healthcare system has a much better, deeper understanding of patient safety and “the role of context, the role of the setting, the role of collateral interventions. It’s generally not going to be one thing that’s the magic bullet, but it’s going to be one thing embedded in a series of other activities that are designed to make sure that you have the right design and the right culture.”

Drs. Wachter and Shekelle and Battles agree that much of the difficulty with patient safety practices is rooted in healthcare system cultures. Each uses different terms to describe the roadblock, as Dr. Wachter discusses implementation science and Battles highlights the difference between the technical work of PSPs and their “social adoption.” But all concur that unless PSPs are committed for the long haul, implementation might be little more than lip service.

“It’s a responsibility of the CEO, the CMO, the CNO, and environmental services, all the way down,” Battles says. “You have to develop around these practices the shared ownership of the risk you’re trying to mitigate. Otherwise, this list of practices, OK, it’s a nice list. But you’ve got to say, ‘What are the risks and hazards to my organization, and how can I apply these evidence practices to the problem?’” TH

Richard Quinn is a freelance writer in New Jersey.

A recent Agency for Healthcare Research and Quality (AHRQ) report, “Making Health Care Safer II: An Updated Critical Analysis of the Evidence for Patient Safety Practices,” holds nearly 1,000 pages of practice-management tips for improving outcomes. But where does a hospitalist begin when reviewing such a massive playbook for progress?

Jim Battles, PhD, an AHRQ social science analyst for patient safety who worked on the report, says the best place to start is by asking yourself: “What keeps you up at night? … What scares the heck out of you?”

The report, a follow-up to the influential and controversial 2001 report “Making Health Care Safer: A Critical Analysis of Patient Safety Practices,” is viewed by its authors as the next step in the continuum of improving patient outcomes. The latest research culled a list of more than 100 patient-safety practices (PSPs) down to 10 that should be “strongly encouraged” and another dozen that are “encouraged.” Battles looks at the 2001 report as more about pushing physicians to think about PSPs, with the updated version as a guidebook on how to think about it.

Listen to AHRQ analyst Jim Battles, PhD, talk about how hospitalists and others should view the new report

Paul Shekelle, MD, PhD, director of the Southern California Evidence-Based Practice Center site of RAND Corp., which AHRQ commissioned to produce the report, says that some might look at safety initiatives since the landmark Institute of Medicine report “To Err is Human” in 1999 and question whether enough progress has been made. But all progress is meaningful to individual patients, and the improvements of the past decade and a half have been important, he adds.

“What I believe is that we’ve made a lot of progress in certain areas,” Dr. Shekelle says, “but this can't be seen when we look at aggregate data, because the improvements we have seen don't account for a sufficiently large proportion in aggregate of the overall patient safety problem.”

Dr. Shekelle—one of three co-principal investigators on the report, along with Peter Pronovost, MD, PhD, FCCM, of Johns Hopkins School of Medicine in Baltimore and HM pioneer Robert Wachter, MD, MHM, chief of the division of hospital medicine at the University of California at San Francisco—says he hopes physicians realize that while the report’s recommendations are evidence-based, they’re not a magic bullet.

“One of the main messages of our report is this is not like writing a prescription for a statin,” Dr. Shekelle says. “This is going to take work. It’s going to take local adaptation, and it’s going to take talking to your front-line clinicians to try and find out how to make this thing work.”

Dr. Wachter, who helped craft both the 2001 and 2013 reports, says patient safety “can be one of those things that is so compelling and so dramatic that you develop a little bit of Nike syndrome—let’s just do it, let’s just computerize, let’s just do teamwork training, let’s do simulation.” However, the healthcare system has a much better, deeper understanding of patient safety and “the role of context, the role of the setting, the role of collateral interventions. It’s generally not going to be one thing that’s the magic bullet, but it’s going to be one thing embedded in a series of other activities that are designed to make sure that you have the right design and the right culture.”

Drs. Wachter and Shekelle and Battles agree that much of the difficulty with patient safety practices is rooted in healthcare system cultures. Each uses different terms to describe the roadblock, as Dr. Wachter discusses implementation science and Battles highlights the difference between the technical work of PSPs and their “social adoption.” But all concur that unless PSPs are committed for the long haul, implementation might be little more than lip service.

“It’s a responsibility of the CEO, the CMO, the CNO, and environmental services, all the way down,” Battles says. “You have to develop around these practices the shared ownership of the risk you’re trying to mitigate. Otherwise, this list of practices, OK, it’s a nice list. But you’ve got to say, ‘What are the risks and hazards to my organization, and how can I apply these evidence practices to the problem?’” TH

Richard Quinn is a freelance writer in New Jersey.

A recent Agency for Healthcare Research and Quality (AHRQ) report, “Making Health Care Safer II: An Updated Critical Analysis of the Evidence for Patient Safety Practices,” holds nearly 1,000 pages of practice-management tips for improving outcomes. But where does a hospitalist begin when reviewing such a massive playbook for progress?

Jim Battles, PhD, an AHRQ social science analyst for patient safety who worked on the report, says the best place to start is by asking yourself: “What keeps you up at night? … What scares the heck out of you?”

The report, a follow-up to the influential and controversial 2001 report “Making Health Care Safer: A Critical Analysis of Patient Safety Practices,” is viewed by its authors as the next step in the continuum of improving patient outcomes. The latest research culled a list of more than 100 patient-safety practices (PSPs) down to 10 that should be “strongly encouraged” and another dozen that are “encouraged.” Battles looks at the 2001 report as more about pushing physicians to think about PSPs, with the updated version as a guidebook on how to think about it.

Listen to AHRQ analyst Jim Battles, PhD, talk about how hospitalists and others should view the new report

Paul Shekelle, MD, PhD, director of the Southern California Evidence-Based Practice Center site of RAND Corp., which AHRQ commissioned to produce the report, says that some might look at safety initiatives since the landmark Institute of Medicine report “To Err is Human” in 1999 and question whether enough progress has been made. But all progress is meaningful to individual patients, and the improvements of the past decade and a half have been important, he adds.

“What I believe is that we’ve made a lot of progress in certain areas,” Dr. Shekelle says, “but this can't be seen when we look at aggregate data, because the improvements we have seen don't account for a sufficiently large proportion in aggregate of the overall patient safety problem.”

Dr. Shekelle—one of three co-principal investigators on the report, along with Peter Pronovost, MD, PhD, FCCM, of Johns Hopkins School of Medicine in Baltimore and HM pioneer Robert Wachter, MD, MHM, chief of the division of hospital medicine at the University of California at San Francisco—says he hopes physicians realize that while the report’s recommendations are evidence-based, they’re not a magic bullet.

“One of the main messages of our report is this is not like writing a prescription for a statin,” Dr. Shekelle says. “This is going to take work. It’s going to take local adaptation, and it’s going to take talking to your front-line clinicians to try and find out how to make this thing work.”

Dr. Wachter, who helped craft both the 2001 and 2013 reports, says patient safety “can be one of those things that is so compelling and so dramatic that you develop a little bit of Nike syndrome—let’s just do it, let’s just computerize, let’s just do teamwork training, let’s do simulation.” However, the healthcare system has a much better, deeper understanding of patient safety and “the role of context, the role of the setting, the role of collateral interventions. It’s generally not going to be one thing that’s the magic bullet, but it’s going to be one thing embedded in a series of other activities that are designed to make sure that you have the right design and the right culture.”

Drs. Wachter and Shekelle and Battles agree that much of the difficulty with patient safety practices is rooted in healthcare system cultures. Each uses different terms to describe the roadblock, as Dr. Wachter discusses implementation science and Battles highlights the difference between the technical work of PSPs and their “social adoption.” But all concur that unless PSPs are committed for the long haul, implementation might be little more than lip service.

“It’s a responsibility of the CEO, the CMO, the CNO, and environmental services, all the way down,” Battles says. “You have to develop around these practices the shared ownership of the risk you’re trying to mitigate. Otherwise, this list of practices, OK, it’s a nice list. But you’ve got to say, ‘What are the risks and hazards to my organization, and how can I apply these evidence practices to the problem?’” TH

Richard Quinn is a freelance writer in New Jersey.

Click here to listen to Dr. Agarwal-Antal

Click here to listen to Dr. Agarwal-Antal

Click here to listen to Dr. Agarwal-Antal