Out-of-state residents appear to be driving the recent increases in marijuana-related emergency department visits in Colorado, Dr. Howard S. Kim and his associates reported online Feb. 24 in the New England Journal of Medicine.

Using statewide data from the Colorado Hospital Association, they found that ED visits related to cannabis by out-of-state residents rose from 78 per 10,000 ED visits in 2012 to 163 per 10,000 in 2014, an increase of 109%. For Colorado residents, cannabis-related ED admissions over that same time period went up 44% – from 70 per 10,000 to 101, said Dr. Kim of Northwestern University, Chicago, and his associates (N Engl J Med. 2016 Feb 24;374[8]:797-8. doi:10.1056/NEJMc1515009).

The investigators also looked at a single urban academic hospital in Aurora, Colo., and found that cannabis-related ED visits there for out-of-state residents went from 85 per 10,000 visits in 2013 to 168 per 10,000 in 2014, compared with respective rates of 106 and 112 for Colorado residents.

“The flattening of the rates of ED visits possibly related to cannabis use among Colorado residents in an urban hospital may represent a learning curve during the period when marijuana was potentially available to Colorado residents for medical use (medical marijuana period) but was largely inaccessible to out-of-state residents,” they suggested.

[email protected]

Out-of-state residents appear to be driving the recent increases in marijuana-related emergency department visits in Colorado, Dr. Howard S. Kim and his associates reported online Feb. 24 in the New England Journal of Medicine.

Using statewide data from the Colorado Hospital Association, they found that ED visits related to cannabis by out-of-state residents rose from 78 per 10,000 ED visits in 2012 to 163 per 10,000 in 2014, an increase of 109%. For Colorado residents, cannabis-related ED admissions over that same time period went up 44% – from 70 per 10,000 to 101, said Dr. Kim of Northwestern University, Chicago, and his associates (N Engl J Med. 2016 Feb 24;374[8]:797-8. doi:10.1056/NEJMc1515009).

The investigators also looked at a single urban academic hospital in Aurora, Colo., and found that cannabis-related ED visits there for out-of-state residents went from 85 per 10,000 visits in 2013 to 168 per 10,000 in 2014, compared with respective rates of 106 and 112 for Colorado residents.

“The flattening of the rates of ED visits possibly related to cannabis use among Colorado residents in an urban hospital may represent a learning curve during the period when marijuana was potentially available to Colorado residents for medical use (medical marijuana period) but was largely inaccessible to out-of-state residents,” they suggested.

[email protected]

Out-of-state residents appear to be driving the recent increases in marijuana-related emergency department visits in Colorado, Dr. Howard S. Kim and his associates reported online Feb. 24 in the New England Journal of Medicine.

Using statewide data from the Colorado Hospital Association, they found that ED visits related to cannabis by out-of-state residents rose from 78 per 10,000 ED visits in 2012 to 163 per 10,000 in 2014, an increase of 109%. For Colorado residents, cannabis-related ED admissions over that same time period went up 44% – from 70 per 10,000 to 101, said Dr. Kim of Northwestern University, Chicago, and his associates (N Engl J Med. 2016 Feb 24;374[8]:797-8. doi:10.1056/NEJMc1515009).

The investigators also looked at a single urban academic hospital in Aurora, Colo., and found that cannabis-related ED visits there for out-of-state residents went from 85 per 10,000 visits in 2013 to 168 per 10,000 in 2014, compared with respective rates of 106 and 112 for Colorado residents.

“The flattening of the rates of ED visits possibly related to cannabis use among Colorado residents in an urban hospital may represent a learning curve during the period when marijuana was potentially available to Colorado residents for medical use (medical marijuana period) but was largely inaccessible to out-of-state residents,” they suggested.

[email protected]

WASHINGTON – Robotic angioplasty may deliver the same advantages when percutaneous coronary intervention is indicated for acute myocardial infarction as currently claimed for an elective PCI, according to results from a proof-of-principle study.

The first robotic PCI system, CorPath 200, was approved by the U.S. Food and Drug Administration in 2012, but the registration trial, called PRECISE (Percutaneous Robotically Enhanced Coronary Intervention), excluded patients with coronary thrombosis, according to a team of investigators at the Frederik Meijer Cardiovascular Institute, Grand Rapids, Mich. The current study focused exclusively on this population.

In “an initial experience” with robotic PCI in 17 acute MI patients led by Dr. Ryan D. Madder, an interventional cardiologist, “technical success” was achieved in 100% of patients with no repeat revascularizations in follow-up so far.

“These preliminary observations support the performance of larger studies to determine the role of robotic PCI in the treatment of acute MI,” said Andrew O’Brien, a medical student at Michigan State University, Ann Arbor, who presented the data at the meeting, sponsored by the Cardiovascular Research Institute at Washington Hospital Center.

The major proven advantage of robotic PCI is that it reduces radiation exposure to the operator, Mr. O’Brien said. While the procedure was performed in this study behind a lead-lined cockpit, it was noted that the operator works solely on the basis of imaging and could be anywhere, including at another facility. In addition, robotic PCI has at least a theoretical advantage of greater precision relative to conventional PCI.

In this study, technical success was defined as less than 30% residual stenosis after PCI in the absence of a PCI-associated death or the need for a repeat revascularization prior to hospital discharge. The median age of the 17 acute MI patients was 59 years with a range of about 10 years younger or older. Most (71%) were male. Radial arterial access was used in all cases.

Only 23% of the patients met criteria for relatively simple lesions (class A or B1). Just over half (53%) had class B2 lesions, which require at least two complicating characteristics, such as moderate tortuosity, irregular contour, or moderate to heavy calcification, and the remainder had class C lesions. In 10 cases (59%), an angiographic filling defect consistent with thrombus was present at the culprit lesion site.

In addition to achieving the goal reduction in residual stenosis without major adverse cardiovascular events in all patients, the investigators reported that procedural time, which averaged 69 minutes from the time of sheath insertion to removal of the guide catheter, was “acceptable.” The longest procedural time was under 100 minutes.

“We used the same criteria for evaluating outcomes as employed in the original PRECISE study,” Mr. O’Brien said. He explained that acute MI patients were excluded in the published PRECISE trial data because there was no protocol at that time for converting to a conventional procedure on an urgent basis in the case of unexpected problems. With more experience, there was greater confidence that urgent complications could be addressed.

In the multicenter PRECISE trial, which led to approval of the robotic system, 164 candidates for elective PCI were enrolled (J Am Coll Cardiol. 2013;61[15]:1596-1600). Technical success was 98.8%. Although there was no control arm, radiation exposure was reported to be 95% lower for operators participating in that study than levels found at the traditional table position.

Data from the current study provide preliminary evidence that robotic PCI is feasible for management of acute MI. While confirmatory studies are needed for this indication, the Michigan investigators also advocated more studies to evaluate whether robotic PCI improves outcome. They cited the potential for more precise placement of stents to reduce the risk of complications.

“Robotic PCI is still not very widely performed,” said coinvestigator Andrew LaCombe, who suggested that its potential advantages deserve broader evaluation.

Dr. Madder disclosed a financial relationship with InfraRedx.

WASHINGTON – Robotic angioplasty may deliver the same advantages when percutaneous coronary intervention is indicated for acute myocardial infarction as currently claimed for an elective PCI, according to results from a proof-of-principle study.

The first robotic PCI system, CorPath 200, was approved by the U.S. Food and Drug Administration in 2012, but the registration trial, called PRECISE (Percutaneous Robotically Enhanced Coronary Intervention), excluded patients with coronary thrombosis, according to a team of investigators at the Frederik Meijer Cardiovascular Institute, Grand Rapids, Mich. The current study focused exclusively on this population.

In “an initial experience” with robotic PCI in 17 acute MI patients led by Dr. Ryan D. Madder, an interventional cardiologist, “technical success” was achieved in 100% of patients with no repeat revascularizations in follow-up so far.

“These preliminary observations support the performance of larger studies to determine the role of robotic PCI in the treatment of acute MI,” said Andrew O’Brien, a medical student at Michigan State University, Ann Arbor, who presented the data at the meeting, sponsored by the Cardiovascular Research Institute at Washington Hospital Center.

The major proven advantage of robotic PCI is that it reduces radiation exposure to the operator, Mr. O’Brien said. While the procedure was performed in this study behind a lead-lined cockpit, it was noted that the operator works solely on the basis of imaging and could be anywhere, including at another facility. In addition, robotic PCI has at least a theoretical advantage of greater precision relative to conventional PCI.

In this study, technical success was defined as less than 30% residual stenosis after PCI in the absence of a PCI-associated death or the need for a repeat revascularization prior to hospital discharge. The median age of the 17 acute MI patients was 59 years with a range of about 10 years younger or older. Most (71%) were male. Radial arterial access was used in all cases.

Only 23% of the patients met criteria for relatively simple lesions (class A or B1). Just over half (53%) had class B2 lesions, which require at least two complicating characteristics, such as moderate tortuosity, irregular contour, or moderate to heavy calcification, and the remainder had class C lesions. In 10 cases (59%), an angiographic filling defect consistent with thrombus was present at the culprit lesion site.

In addition to achieving the goal reduction in residual stenosis without major adverse cardiovascular events in all patients, the investigators reported that procedural time, which averaged 69 minutes from the time of sheath insertion to removal of the guide catheter, was “acceptable.” The longest procedural time was under 100 minutes.

“We used the same criteria for evaluating outcomes as employed in the original PRECISE study,” Mr. O’Brien said. He explained that acute MI patients were excluded in the published PRECISE trial data because there was no protocol at that time for converting to a conventional procedure on an urgent basis in the case of unexpected problems. With more experience, there was greater confidence that urgent complications could be addressed.

In the multicenter PRECISE trial, which led to approval of the robotic system, 164 candidates for elective PCI were enrolled (J Am Coll Cardiol. 2013;61[15]:1596-1600). Technical success was 98.8%. Although there was no control arm, radiation exposure was reported to be 95% lower for operators participating in that study than levels found at the traditional table position.

Data from the current study provide preliminary evidence that robotic PCI is feasible for management of acute MI. While confirmatory studies are needed for this indication, the Michigan investigators also advocated more studies to evaluate whether robotic PCI improves outcome. They cited the potential for more precise placement of stents to reduce the risk of complications.

“Robotic PCI is still not very widely performed,” said coinvestigator Andrew LaCombe, who suggested that its potential advantages deserve broader evaluation.

Dr. Madder disclosed a financial relationship with InfraRedx.

WASHINGTON – Robotic angioplasty may deliver the same advantages when percutaneous coronary intervention is indicated for acute myocardial infarction as currently claimed for an elective PCI, according to results from a proof-of-principle study.

The first robotic PCI system, CorPath 200, was approved by the U.S. Food and Drug Administration in 2012, but the registration trial, called PRECISE (Percutaneous Robotically Enhanced Coronary Intervention), excluded patients with coronary thrombosis, according to a team of investigators at the Frederik Meijer Cardiovascular Institute, Grand Rapids, Mich. The current study focused exclusively on this population.

In “an initial experience” with robotic PCI in 17 acute MI patients led by Dr. Ryan D. Madder, an interventional cardiologist, “technical success” was achieved in 100% of patients with no repeat revascularizations in follow-up so far.

“These preliminary observations support the performance of larger studies to determine the role of robotic PCI in the treatment of acute MI,” said Andrew O’Brien, a medical student at Michigan State University, Ann Arbor, who presented the data at the meeting, sponsored by the Cardiovascular Research Institute at Washington Hospital Center.

The major proven advantage of robotic PCI is that it reduces radiation exposure to the operator, Mr. O’Brien said. While the procedure was performed in this study behind a lead-lined cockpit, it was noted that the operator works solely on the basis of imaging and could be anywhere, including at another facility. In addition, robotic PCI has at least a theoretical advantage of greater precision relative to conventional PCI.

In this study, technical success was defined as less than 30% residual stenosis after PCI in the absence of a PCI-associated death or the need for a repeat revascularization prior to hospital discharge. The median age of the 17 acute MI patients was 59 years with a range of about 10 years younger or older. Most (71%) were male. Radial arterial access was used in all cases.

Only 23% of the patients met criteria for relatively simple lesions (class A or B1). Just over half (53%) had class B2 lesions, which require at least two complicating characteristics, such as moderate tortuosity, irregular contour, or moderate to heavy calcification, and the remainder had class C lesions. In 10 cases (59%), an angiographic filling defect consistent with thrombus was present at the culprit lesion site.

In addition to achieving the goal reduction in residual stenosis without major adverse cardiovascular events in all patients, the investigators reported that procedural time, which averaged 69 minutes from the time of sheath insertion to removal of the guide catheter, was “acceptable.” The longest procedural time was under 100 minutes.

“We used the same criteria for evaluating outcomes as employed in the original PRECISE study,” Mr. O’Brien said. He explained that acute MI patients were excluded in the published PRECISE trial data because there was no protocol at that time for converting to a conventional procedure on an urgent basis in the case of unexpected problems. With more experience, there was greater confidence that urgent complications could be addressed.

In the multicenter PRECISE trial, which led to approval of the robotic system, 164 candidates for elective PCI were enrolled (J Am Coll Cardiol. 2013;61[15]:1596-1600). Technical success was 98.8%. Although there was no control arm, radiation exposure was reported to be 95% lower for operators participating in that study than levels found at the traditional table position.

Data from the current study provide preliminary evidence that robotic PCI is feasible for management of acute MI. While confirmatory studies are needed for this indication, the Michigan investigators also advocated more studies to evaluate whether robotic PCI improves outcome. They cited the potential for more precise placement of stents to reduce the risk of complications.

“Robotic PCI is still not very widely performed,” said coinvestigator Andrew LaCombe, who suggested that its potential advantages deserve broader evaluation.

Dr. Madder disclosed a financial relationship with InfraRedx.

NEW ORLEANS – Three potentially useful blood-based biomarkers of relapse and of the response to glatiramer acetate treatment have been identified in patients with relapsing-remitting multiple sclerosis (RRMS).

The study was small, so much more needs to be done to move the findings to the bedside. Nonetheless, the hope is that the findings will someday help guide treatment decisions and outcomes in MS patients, Adam Kruszewski, a medical student at the University of Maryland, Baltimore, commented in a poster presentation at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

Brian Hoyle/Frontline Medical News

The study had its roots in the researcher’s prior findings that the Response Gene to Complement (RGC)–32 is expressed by CD3+ and CD4+ T cells in peripheral blood mononuclear cells (PBMCs) and in brain tissue from RRMS patients. As well, RGC-32 regulates the expressions of Fas ligand (FasL) and interleukin-21 (IL-21), and the activities of CDC2 and Akt.

In the current study, the investigator explored the potential value of RGC-32, FasL, IL-21, CDC2, and Akt as longitudinal biomarkers of relapse and as a way of gauging the response to the treatment of RRMS patients with glatiramer acetate – one of the most common immunomodulatory approaches used in RRMS therapy.

A cohort of 15 glatiramer acetate–treated RRMS patients was enrolled over a 2-year period. The battery of inclusion criteria included an age of 18-65 years; meeting the McDonald criteria for definite MS; a disease course featuring relapses and remissions; newly diagnosed MS or MS not treated with currently used immunomodulatory drugs for 3 months prior to study entry; no exacerbations in the 4 weeks before the study; no steroid therapy for 4 weeks prior to study enrollment; no treatment with natalizumab (Tysabri), fingolimod (Gilenya), dimethyl fumarate (Tecfidera), mitoxantrone, cyclophosphamide, or investigational drugs during the prior year; and an Extended Disability Status Score (EDSS) of 0-5.5. Exclusion criteria were a history of autoimmune disorders, vascular disease, or active acute or chronic infections; use of antibiotics in the last 30 days; a history of intracranial or intraspinal tumor or metabolic myelopathy; or a history of alcohol or drug abuse.

The 15 patients were clinically monitored and PBMCs were collected at 0, 3, 6, and 12 months. mRNA expression of the five candidate biomarkers in the PBMCs was determined using real-time quantitative polymerase chain reaction testing. Nonresponders to glatiramer acetate treatment were defined as patients who exhibited two or more relapse events following the initiation of the treatment.

Acute relapse was associated with decreased expression of RGC-32 and FasL (both P less than .0001) and increased expression of IL-21 (P = .04). No relapse-associated changes in CDC2 or AKT were evident. Compared with those who did not respond to glatiramer acetate, responders displayed an increased expression of RGC-32 and FasL (both P less than .0001), and a decreased expression of IL-21 (P = .02).

Receiver operating characteristic analysis was done to find the cutoff values that best distinguished treatment responders from nonresponders for each candidate biomarker. The probability of accurately detecting relapse was 90% for RGC-32, 88% for FasL, and 75% for IL-21. The probability of accurately detecting response to glatiramer acetate was 85%, 90%, and 85% in the same respective order.

“Right now, there is no test that can help identify a responder or nonresponder in MS therapy. Often, treatment is started and then a trial and error process with time determines the treatment course,” said Mr. Kruszewski during an interview at the poster.

The aim is to expand these results with RCG-32, FasL, and IL-21 to a randomized, controlled trial with the goal of tailoring treatment at the early stage of MS.

NEW ORLEANS – Three potentially useful blood-based biomarkers of relapse and of the response to glatiramer acetate treatment have been identified in patients with relapsing-remitting multiple sclerosis (RRMS).

The study was small, so much more needs to be done to move the findings to the bedside. Nonetheless, the hope is that the findings will someday help guide treatment decisions and outcomes in MS patients, Adam Kruszewski, a medical student at the University of Maryland, Baltimore, commented in a poster presentation at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

Brian Hoyle/Frontline Medical News

The study had its roots in the researcher’s prior findings that the Response Gene to Complement (RGC)–32 is expressed by CD3+ and CD4+ T cells in peripheral blood mononuclear cells (PBMCs) and in brain tissue from RRMS patients. As well, RGC-32 regulates the expressions of Fas ligand (FasL) and interleukin-21 (IL-21), and the activities of CDC2 and Akt.

In the current study, the investigator explored the potential value of RGC-32, FasL, IL-21, CDC2, and Akt as longitudinal biomarkers of relapse and as a way of gauging the response to the treatment of RRMS patients with glatiramer acetate – one of the most common immunomodulatory approaches used in RRMS therapy.

A cohort of 15 glatiramer acetate–treated RRMS patients was enrolled over a 2-year period. The battery of inclusion criteria included an age of 18-65 years; meeting the McDonald criteria for definite MS; a disease course featuring relapses and remissions; newly diagnosed MS or MS not treated with currently used immunomodulatory drugs for 3 months prior to study entry; no exacerbations in the 4 weeks before the study; no steroid therapy for 4 weeks prior to study enrollment; no treatment with natalizumab (Tysabri), fingolimod (Gilenya), dimethyl fumarate (Tecfidera), mitoxantrone, cyclophosphamide, or investigational drugs during the prior year; and an Extended Disability Status Score (EDSS) of 0-5.5. Exclusion criteria were a history of autoimmune disorders, vascular disease, or active acute or chronic infections; use of antibiotics in the last 30 days; a history of intracranial or intraspinal tumor or metabolic myelopathy; or a history of alcohol or drug abuse.

The 15 patients were clinically monitored and PBMCs were collected at 0, 3, 6, and 12 months. mRNA expression of the five candidate biomarkers in the PBMCs was determined using real-time quantitative polymerase chain reaction testing. Nonresponders to glatiramer acetate treatment were defined as patients who exhibited two or more relapse events following the initiation of the treatment.

Acute relapse was associated with decreased expression of RGC-32 and FasL (both P less than .0001) and increased expression of IL-21 (P = .04). No relapse-associated changes in CDC2 or AKT were evident. Compared with those who did not respond to glatiramer acetate, responders displayed an increased expression of RGC-32 and FasL (both P less than .0001), and a decreased expression of IL-21 (P = .02).

Receiver operating characteristic analysis was done to find the cutoff values that best distinguished treatment responders from nonresponders for each candidate biomarker. The probability of accurately detecting relapse was 90% for RGC-32, 88% for FasL, and 75% for IL-21. The probability of accurately detecting response to glatiramer acetate was 85%, 90%, and 85% in the same respective order.

“Right now, there is no test that can help identify a responder or nonresponder in MS therapy. Often, treatment is started and then a trial and error process with time determines the treatment course,” said Mr. Kruszewski during an interview at the poster.

The aim is to expand these results with RCG-32, FasL, and IL-21 to a randomized, controlled trial with the goal of tailoring treatment at the early stage of MS.

NEW ORLEANS – Three potentially useful blood-based biomarkers of relapse and of the response to glatiramer acetate treatment have been identified in patients with relapsing-remitting multiple sclerosis (RRMS).

The study was small, so much more needs to be done to move the findings to the bedside. Nonetheless, the hope is that the findings will someday help guide treatment decisions and outcomes in MS patients, Adam Kruszewski, a medical student at the University of Maryland, Baltimore, commented in a poster presentation at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

Brian Hoyle/Frontline Medical News

The study had its roots in the researcher’s prior findings that the Response Gene to Complement (RGC)–32 is expressed by CD3+ and CD4+ T cells in peripheral blood mononuclear cells (PBMCs) and in brain tissue from RRMS patients. As well, RGC-32 regulates the expressions of Fas ligand (FasL) and interleukin-21 (IL-21), and the activities of CDC2 and Akt.

In the current study, the investigator explored the potential value of RGC-32, FasL, IL-21, CDC2, and Akt as longitudinal biomarkers of relapse and as a way of gauging the response to the treatment of RRMS patients with glatiramer acetate – one of the most common immunomodulatory approaches used in RRMS therapy.

A cohort of 15 glatiramer acetate–treated RRMS patients was enrolled over a 2-year period. The battery of inclusion criteria included an age of 18-65 years; meeting the McDonald criteria for definite MS; a disease course featuring relapses and remissions; newly diagnosed MS or MS not treated with currently used immunomodulatory drugs for 3 months prior to study entry; no exacerbations in the 4 weeks before the study; no steroid therapy for 4 weeks prior to study enrollment; no treatment with natalizumab (Tysabri), fingolimod (Gilenya), dimethyl fumarate (Tecfidera), mitoxantrone, cyclophosphamide, or investigational drugs during the prior year; and an Extended Disability Status Score (EDSS) of 0-5.5. Exclusion criteria were a history of autoimmune disorders, vascular disease, or active acute or chronic infections; use of antibiotics in the last 30 days; a history of intracranial or intraspinal tumor or metabolic myelopathy; or a history of alcohol or drug abuse.

The 15 patients were clinically monitored and PBMCs were collected at 0, 3, 6, and 12 months. mRNA expression of the five candidate biomarkers in the PBMCs was determined using real-time quantitative polymerase chain reaction testing. Nonresponders to glatiramer acetate treatment were defined as patients who exhibited two or more relapse events following the initiation of the treatment.

Acute relapse was associated with decreased expression of RGC-32 and FasL (both P less than .0001) and increased expression of IL-21 (P = .04). No relapse-associated changes in CDC2 or AKT were evident. Compared with those who did not respond to glatiramer acetate, responders displayed an increased expression of RGC-32 and FasL (both P less than .0001), and a decreased expression of IL-21 (P = .02).

Receiver operating characteristic analysis was done to find the cutoff values that best distinguished treatment responders from nonresponders for each candidate biomarker. The probability of accurately detecting relapse was 90% for RGC-32, 88% for FasL, and 75% for IL-21. The probability of accurately detecting response to glatiramer acetate was 85%, 90%, and 85% in the same respective order.

“Right now, there is no test that can help identify a responder or nonresponder in MS therapy. Often, treatment is started and then a trial and error process with time determines the treatment course,” said Mr. Kruszewski during an interview at the poster.

The aim is to expand these results with RCG-32, FasL, and IL-21 to a randomized, controlled trial with the goal of tailoring treatment at the early stage of MS.

NEW ORLEANS – Research from Australia shows that disability in multiple sclerosis (MS) is independent of past damage, even in people whose disease is moderately advanced, with further disease progression varying widely in severity.

The findings should prompt a rethink of the policy of ceasing treatment when MS-related disability becomes more advanced.

Brian Hoyle/Frontline Medical News

“Our main findings were that moderately advanced multiple sclerosis is indeed independent of previous disease, but still extremely variable. Higher relapse rates later in disease increased the risk of disability worsening. More promisingly, more time spent on therapy later in disease lowered the risk of disability progression to EDSS [Expanded Disability Status Scale] 6 or 6.5,” Nathaniel Lizak said in an interview at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

The study sought to identify factors that modified progression in early and moderately advanced MS. Three prior cohort studies had not shed light on the variability in disease trajectory during moderately advanced MS.

“We wanted to examine how much variability there was later in disease, what determined this variability, and to confirm whether later disease was really independent of previous disease, as was suggested in previous studies,” said Mr. Lizak of Monash University, Clayton, Australia, and the University of Melbourne. The influences of relapse rate and proportion of time treated prior to and during each disability time period, age, and disease duration at baseline on the progression to moderate MS disability (EDSS 6 or 6.5) were assessed. The hypothesis was that, even at a later stage of MS, disease progression varies from patient to patient, and that some patients can benefit from immunomodulatory therapy.

The time between EDSS steps 3-6 (n = 1,560, 71% female, 40.9±9.9 years old at baseline), 4-6 (n = 1,504, 69% female, 43.0±9.6 years old at baseline), and 6-6.5 (n = 1,231, 67% female, 46.5±10.2 years old at baseline) were analyzed for the 32,336 patients included in the MSBase large, international, observational MS cohort study who met the inclusion criteria. Median disease duration at baseline was 9.4, 11.1, and 14.0 years in the same respective order.

Pre- and postbaseline disability trajectories showed large coefficients of variance and did not correlate. The probability of reaching the outcome EDSS was independent of prebaseline variables, but was increased if relapse during any particular EDSS was more frequent (hazard ratios, 1.58-3.07; P less than .001). At each measured stage of MS, higher-efficacy therapies were beneficial and lowered the risk of progression (HR, 0.27-0.68; P less than .02).

Some countries, such as New Zealand, by policy don’t allow patients to receive treatments if they display moderate or significant disability. In other places this can be common practice because of concerns with treatment-related side effects or affordability. The main driver of this practice is that the clinical trials of most MS therapies that have validated these medications specifically recruited patients with low disability scores. So, according to Mr. Lizak, the evidence exists only for therapies at lower disability scores.

“These results are important as they show that there is still hope. Reaching disability landmarks of EDSS 3, 4, and 6 does not guarantee continuous worsening of disability. Doctors still have the ability to reduce their patients’ risk of attaining further disability, even at later stages of disease,” said Mr. Lizak.

The hope is that the data will change clinical practice to encourage more therapy even when substantial disability has accumulated.

“Translating results into everyday practice is difficult, and doctors must always weigh the risks and benefits. We hope that our work will influence the clinical decision to, where in doubt, favor high-efficacy treatments at later disease stages. That’s not to say that patients should be blindly treated, as side effects always merit consideration. But we hope our work will inform neurologists that there is evidence supporting treating patients with more advanced disability. Where, by practice or policy, treatments are not provided to patients who have accumulated significant disability, we hope to change such clinical practice,” said Mr. Lizak.

The study did not require funding. Mr. Lizak had no disclosures.

NEW ORLEANS – Research from Australia shows that disability in multiple sclerosis (MS) is independent of past damage, even in people whose disease is moderately advanced, with further disease progression varying widely in severity.

The findings should prompt a rethink of the policy of ceasing treatment when MS-related disability becomes more advanced.

Brian Hoyle/Frontline Medical News

“Our main findings were that moderately advanced multiple sclerosis is indeed independent of previous disease, but still extremely variable. Higher relapse rates later in disease increased the risk of disability worsening. More promisingly, more time spent on therapy later in disease lowered the risk of disability progression to EDSS [Expanded Disability Status Scale] 6 or 6.5,” Nathaniel Lizak said in an interview at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

The study sought to identify factors that modified progression in early and moderately advanced MS. Three prior cohort studies had not shed light on the variability in disease trajectory during moderately advanced MS.

“We wanted to examine how much variability there was later in disease, what determined this variability, and to confirm whether later disease was really independent of previous disease, as was suggested in previous studies,” said Mr. Lizak of Monash University, Clayton, Australia, and the University of Melbourne. The influences of relapse rate and proportion of time treated prior to and during each disability time period, age, and disease duration at baseline on the progression to moderate MS disability (EDSS 6 or 6.5) were assessed. The hypothesis was that, even at a later stage of MS, disease progression varies from patient to patient, and that some patients can benefit from immunomodulatory therapy.

The time between EDSS steps 3-6 (n = 1,560, 71% female, 40.9±9.9 years old at baseline), 4-6 (n = 1,504, 69% female, 43.0±9.6 years old at baseline), and 6-6.5 (n = 1,231, 67% female, 46.5±10.2 years old at baseline) were analyzed for the 32,336 patients included in the MSBase large, international, observational MS cohort study who met the inclusion criteria. Median disease duration at baseline was 9.4, 11.1, and 14.0 years in the same respective order.

Pre- and postbaseline disability trajectories showed large coefficients of variance and did not correlate. The probability of reaching the outcome EDSS was independent of prebaseline variables, but was increased if relapse during any particular EDSS was more frequent (hazard ratios, 1.58-3.07; P less than .001). At each measured stage of MS, higher-efficacy therapies were beneficial and lowered the risk of progression (HR, 0.27-0.68; P less than .02).

Some countries, such as New Zealand, by policy don’t allow patients to receive treatments if they display moderate or significant disability. In other places this can be common practice because of concerns with treatment-related side effects or affordability. The main driver of this practice is that the clinical trials of most MS therapies that have validated these medications specifically recruited patients with low disability scores. So, according to Mr. Lizak, the evidence exists only for therapies at lower disability scores.

“These results are important as they show that there is still hope. Reaching disability landmarks of EDSS 3, 4, and 6 does not guarantee continuous worsening of disability. Doctors still have the ability to reduce their patients’ risk of attaining further disability, even at later stages of disease,” said Mr. Lizak.

The hope is that the data will change clinical practice to encourage more therapy even when substantial disability has accumulated.

“Translating results into everyday practice is difficult, and doctors must always weigh the risks and benefits. We hope that our work will influence the clinical decision to, where in doubt, favor high-efficacy treatments at later disease stages. That’s not to say that patients should be blindly treated, as side effects always merit consideration. But we hope our work will inform neurologists that there is evidence supporting treating patients with more advanced disability. Where, by practice or policy, treatments are not provided to patients who have accumulated significant disability, we hope to change such clinical practice,” said Mr. Lizak.

The study did not require funding. Mr. Lizak had no disclosures.

NEW ORLEANS – Research from Australia shows that disability in multiple sclerosis (MS) is independent of past damage, even in people whose disease is moderately advanced, with further disease progression varying widely in severity.

The findings should prompt a rethink of the policy of ceasing treatment when MS-related disability becomes more advanced.

Brian Hoyle/Frontline Medical News

“Our main findings were that moderately advanced multiple sclerosis is indeed independent of previous disease, but still extremely variable. Higher relapse rates later in disease increased the risk of disability worsening. More promisingly, more time spent on therapy later in disease lowered the risk of disability progression to EDSS [Expanded Disability Status Scale] 6 or 6.5,” Nathaniel Lizak said in an interview at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

The study sought to identify factors that modified progression in early and moderately advanced MS. Three prior cohort studies had not shed light on the variability in disease trajectory during moderately advanced MS.

“We wanted to examine how much variability there was later in disease, what determined this variability, and to confirm whether later disease was really independent of previous disease, as was suggested in previous studies,” said Mr. Lizak of Monash University, Clayton, Australia, and the University of Melbourne. The influences of relapse rate and proportion of time treated prior to and during each disability time period, age, and disease duration at baseline on the progression to moderate MS disability (EDSS 6 or 6.5) were assessed. The hypothesis was that, even at a later stage of MS, disease progression varies from patient to patient, and that some patients can benefit from immunomodulatory therapy.

The time between EDSS steps 3-6 (n = 1,560, 71% female, 40.9±9.9 years old at baseline), 4-6 (n = 1,504, 69% female, 43.0±9.6 years old at baseline), and 6-6.5 (n = 1,231, 67% female, 46.5±10.2 years old at baseline) were analyzed for the 32,336 patients included in the MSBase large, international, observational MS cohort study who met the inclusion criteria. Median disease duration at baseline was 9.4, 11.1, and 14.0 years in the same respective order.

Pre- and postbaseline disability trajectories showed large coefficients of variance and did not correlate. The probability of reaching the outcome EDSS was independent of prebaseline variables, but was increased if relapse during any particular EDSS was more frequent (hazard ratios, 1.58-3.07; P less than .001). At each measured stage of MS, higher-efficacy therapies were beneficial and lowered the risk of progression (HR, 0.27-0.68; P less than .02).

Some countries, such as New Zealand, by policy don’t allow patients to receive treatments if they display moderate or significant disability. In other places this can be common practice because of concerns with treatment-related side effects or affordability. The main driver of this practice is that the clinical trials of most MS therapies that have validated these medications specifically recruited patients with low disability scores. So, according to Mr. Lizak, the evidence exists only for therapies at lower disability scores.

“These results are important as they show that there is still hope. Reaching disability landmarks of EDSS 3, 4, and 6 does not guarantee continuous worsening of disability. Doctors still have the ability to reduce their patients’ risk of attaining further disability, even at later stages of disease,” said Mr. Lizak.

The hope is that the data will change clinical practice to encourage more therapy even when substantial disability has accumulated.

“Translating results into everyday practice is difficult, and doctors must always weigh the risks and benefits. We hope that our work will influence the clinical decision to, where in doubt, favor high-efficacy treatments at later disease stages. That’s not to say that patients should be blindly treated, as side effects always merit consideration. But we hope our work will inform neurologists that there is evidence supporting treating patients with more advanced disability. Where, by practice or policy, treatments are not provided to patients who have accumulated significant disability, we hope to change such clinical practice,” said Mr. Lizak.

The study did not require funding. Mr. Lizak had no disclosures.

Loss of distensibility of the pulmonary vasculature may be a marker that allows earlier detection of impending pulmonary hypertension, based on hemodynamic data from the medical records of 90 patients across the spectrum of pulmonary vascular disease.

Normal pulmonary circulation is distensible, allowing distension and recruitment of the pulmonary vasculature during exertion that in turn reduces pulmonary vascular resistance. Loss of this distensibility increases resistance and thus pulmonary arterial pressure, and is a characteristic of mild pulmonary vascular disease. Such disease is a precursor of full-blown pulmonary hypertension (PH), which “is a relatively late hemodynamic event in the evolution of pulmonary vascular disease,” said Dr. Edmund M. T. Lau of Université Paris-Sud, and his associates.

The percentage change in vascular diameter per mm Hg increase in distending pressure has been proposed for estimating the distensibility of resistive pulmonary vessels. This “distensibility value” has been assessed in animal studies and in healthy human subjects, but has not yet been assessed as a possible marker of mild pulmonary vascular disease or PH.

The researchers assessed this distensibility value in 31 patients with PH, 33 with mild pulmonary vascular disease but no PH as yet, and 26 control subjects with no pulmonary vascular disease. The data were obtained from the medical records of these patients, who had undergone right-sided heart catheterization, both at rest and during exercise, over a 6-year period.

The percentage change in vascular diameter per mm Hg increase in distending pressure was “strikingly reduced” (0.45%/mm Hg) in the mild pulmonary vascular disease group compared with the control group (1.4%/mm Hg). As expected, the group with PH had the lowest distensibility value, at 0.25%/mm Hg.

Using a cutoff value of 0.76%/mm Hg allowed the researchers to distinguish control subjects from patients with mild disease with a sensitivity of 88% and a specificity of 100%. “To our knowledge, this is the first study to validate the fit of [this] model in subjects with pulmonary vascular disease and to demonstrate that [percentage change in vascular diameter per mm Hg increase in distending pressure] is dramatically reduced in patients who have mild pulmonary vascular disease without manifest PH.

“Taken together, our findings suggest that vascular distensibility is markedly attenuated prior to the development of PH and that [this value] may serve as a useful vascular index in the setting of early disease detection,” Dr. Lau and his associates said (CHEST 2016;149:353-61).

The distensibility value calculated for this study’s control group (1.4%/mm Hg) was slightly lower than that reported in the literature for normal, healthy subjects and in vitro animal vessels (2%/mm Hg). That is likely because the control participants were older than the subjects in previous studies, and vascular distensibility is known to decrease with increasing age, the researchers said.

They added that it might be useful to calculate the distensibility value when patients suspected of having pulmonary vascular disease undergo invasive pulmonary hemodynamic evaluations. “It would be of particular interest to assess [it] in populations at a high risk of developing PH, such as carriers of the BMPR2 mutation and patients with systemic sclerosis.”

Obviously, estimating the distensibility value using noninvasive evaluation would be preferable, the researchers noted. Preliminary studies of healthy control subjects and carriers of the BMPR2 mutation undergoing stress ECG testing have shown that calculating the distensibility value is feasible using Doppler echocardiography data, they added.

This study was supported by Fonds de Dotation Recherche en Santé Respiratoire, Fondation du Souffle, and the INSERM–University of Sydney Exchange Grant. Dr. Lau reported having no relevant financial disclosures; his associates reported ties to Actelion, Aires, Bayer, Bristol-Myers Squibb, GlaxoSmithKline, Novartis, Pfizer, and United Therapeutics Corporation.

Loss of distensibility of the pulmonary vasculature may be a marker that allows earlier detection of impending pulmonary hypertension, based on hemodynamic data from the medical records of 90 patients across the spectrum of pulmonary vascular disease.

Normal pulmonary circulation is distensible, allowing distension and recruitment of the pulmonary vasculature during exertion that in turn reduces pulmonary vascular resistance. Loss of this distensibility increases resistance and thus pulmonary arterial pressure, and is a characteristic of mild pulmonary vascular disease. Such disease is a precursor of full-blown pulmonary hypertension (PH), which “is a relatively late hemodynamic event in the evolution of pulmonary vascular disease,” said Dr. Edmund M. T. Lau of Université Paris-Sud, and his associates.

The percentage change in vascular diameter per mm Hg increase in distending pressure has been proposed for estimating the distensibility of resistive pulmonary vessels. This “distensibility value” has been assessed in animal studies and in healthy human subjects, but has not yet been assessed as a possible marker of mild pulmonary vascular disease or PH.

The researchers assessed this distensibility value in 31 patients with PH, 33 with mild pulmonary vascular disease but no PH as yet, and 26 control subjects with no pulmonary vascular disease. The data were obtained from the medical records of these patients, who had undergone right-sided heart catheterization, both at rest and during exercise, over a 6-year period.

The percentage change in vascular diameter per mm Hg increase in distending pressure was “strikingly reduced” (0.45%/mm Hg) in the mild pulmonary vascular disease group compared with the control group (1.4%/mm Hg). As expected, the group with PH had the lowest distensibility value, at 0.25%/mm Hg.

Using a cutoff value of 0.76%/mm Hg allowed the researchers to distinguish control subjects from patients with mild disease with a sensitivity of 88% and a specificity of 100%. “To our knowledge, this is the first study to validate the fit of [this] model in subjects with pulmonary vascular disease and to demonstrate that [percentage change in vascular diameter per mm Hg increase in distending pressure] is dramatically reduced in patients who have mild pulmonary vascular disease without manifest PH.

“Taken together, our findings suggest that vascular distensibility is markedly attenuated prior to the development of PH and that [this value] may serve as a useful vascular index in the setting of early disease detection,” Dr. Lau and his associates said (CHEST 2016;149:353-61).

The distensibility value calculated for this study’s control group (1.4%/mm Hg) was slightly lower than that reported in the literature for normal, healthy subjects and in vitro animal vessels (2%/mm Hg). That is likely because the control participants were older than the subjects in previous studies, and vascular distensibility is known to decrease with increasing age, the researchers said.

They added that it might be useful to calculate the distensibility value when patients suspected of having pulmonary vascular disease undergo invasive pulmonary hemodynamic evaluations. “It would be of particular interest to assess [it] in populations at a high risk of developing PH, such as carriers of the BMPR2 mutation and patients with systemic sclerosis.”

Obviously, estimating the distensibility value using noninvasive evaluation would be preferable, the researchers noted. Preliminary studies of healthy control subjects and carriers of the BMPR2 mutation undergoing stress ECG testing have shown that calculating the distensibility value is feasible using Doppler echocardiography data, they added.

This study was supported by Fonds de Dotation Recherche en Santé Respiratoire, Fondation du Souffle, and the INSERM–University of Sydney Exchange Grant. Dr. Lau reported having no relevant financial disclosures; his associates reported ties to Actelion, Aires, Bayer, Bristol-Myers Squibb, GlaxoSmithKline, Novartis, Pfizer, and United Therapeutics Corporation.

Loss of distensibility of the pulmonary vasculature may be a marker that allows earlier detection of impending pulmonary hypertension, based on hemodynamic data from the medical records of 90 patients across the spectrum of pulmonary vascular disease.

Normal pulmonary circulation is distensible, allowing distension and recruitment of the pulmonary vasculature during exertion that in turn reduces pulmonary vascular resistance. Loss of this distensibility increases resistance and thus pulmonary arterial pressure, and is a characteristic of mild pulmonary vascular disease. Such disease is a precursor of full-blown pulmonary hypertension (PH), which “is a relatively late hemodynamic event in the evolution of pulmonary vascular disease,” said Dr. Edmund M. T. Lau of Université Paris-Sud, and his associates.

The percentage change in vascular diameter per mm Hg increase in distending pressure has been proposed for estimating the distensibility of resistive pulmonary vessels. This “distensibility value” has been assessed in animal studies and in healthy human subjects, but has not yet been assessed as a possible marker of mild pulmonary vascular disease or PH.

The researchers assessed this distensibility value in 31 patients with PH, 33 with mild pulmonary vascular disease but no PH as yet, and 26 control subjects with no pulmonary vascular disease. The data were obtained from the medical records of these patients, who had undergone right-sided heart catheterization, both at rest and during exercise, over a 6-year period.

The percentage change in vascular diameter per mm Hg increase in distending pressure was “strikingly reduced” (0.45%/mm Hg) in the mild pulmonary vascular disease group compared with the control group (1.4%/mm Hg). As expected, the group with PH had the lowest distensibility value, at 0.25%/mm Hg.

Using a cutoff value of 0.76%/mm Hg allowed the researchers to distinguish control subjects from patients with mild disease with a sensitivity of 88% and a specificity of 100%. “To our knowledge, this is the first study to validate the fit of [this] model in subjects with pulmonary vascular disease and to demonstrate that [percentage change in vascular diameter per mm Hg increase in distending pressure] is dramatically reduced in patients who have mild pulmonary vascular disease without manifest PH.

“Taken together, our findings suggest that vascular distensibility is markedly attenuated prior to the development of PH and that [this value] may serve as a useful vascular index in the setting of early disease detection,” Dr. Lau and his associates said (CHEST 2016;149:353-61).

The distensibility value calculated for this study’s control group (1.4%/mm Hg) was slightly lower than that reported in the literature for normal, healthy subjects and in vitro animal vessels (2%/mm Hg). That is likely because the control participants were older than the subjects in previous studies, and vascular distensibility is known to decrease with increasing age, the researchers said.

They added that it might be useful to calculate the distensibility value when patients suspected of having pulmonary vascular disease undergo invasive pulmonary hemodynamic evaluations. “It would be of particular interest to assess [it] in populations at a high risk of developing PH, such as carriers of the BMPR2 mutation and patients with systemic sclerosis.”

Obviously, estimating the distensibility value using noninvasive evaluation would be preferable, the researchers noted. Preliminary studies of healthy control subjects and carriers of the BMPR2 mutation undergoing stress ECG testing have shown that calculating the distensibility value is feasible using Doppler echocardiography data, they added.

This study was supported by Fonds de Dotation Recherche en Santé Respiratoire, Fondation du Souffle, and the INSERM–University of Sydney Exchange Grant. Dr. Lau reported having no relevant financial disclosures; his associates reported ties to Actelion, Aires, Bayer, Bristol-Myers Squibb, GlaxoSmithKline, Novartis, Pfizer, and United Therapeutics Corporation.

Several older physicians have emphasized to me the importance of choosing an excellent disability insurance policy during residency. However, choosing the right policy can be a difficult task. The policy definitions are complicated, and there is a lot of fine print. To understand this confusing topic, start with answers to these 3 questions: What is my most valuable asset? When is the best point in my career to purchase disability insurance? What would I do if I were no longer able to perform the material and substantial duties of my occupation as a dermatologist?

A Resident’s Assets

In the world of disability insurance, your most valuable assets are your education and your ability to earn an income in the future.^1,2 A resident’s ability to earn an income in the future reflects a massive investment of time, cost of education, and postponed accruement of wealth due to time spent in training. Any negative impact on your health (eg, back injury, vision loss, hand injury) can jeopardize these assets. Purchasing disability insurance while still in dermatology residency will protect this investment; it also will ensure that you obtain a policy while you are still healthy.^1,2

Choosing a Policy

Disability insurance comes in 2 main forms: individual or group. Individual insurance may be slightly more expensive but may offer better coverage than group insurance. Group insurance often is offered through a large medical association such as the American Academy of Dermatology. Group insurance may be less expensive but often has more limits to coverage. A definite must-have in a disability insurance policy is one that has guaranteed renewal and is noncancellable.^1-3

Interestingly, women are considered a higher risk for disability, and many insurance policies will charge a higher monthly rate for women than men because women are slightly more likely than men to develop a disability, and women are more likely to develop a disability that prevents them from being able to work.⁴ Some insurance companies do offer a unisex policy, which does not discriminate.

When choosing a policy, you want to carefully read the vendor’s definition of disability. The best definition of the term disability is going to be one that includes phrases such as “unable to perform the material and substantial duties of your [own] occupation . . . even if you are gainfully employed in another occupation.”^1-3,5,6 This definition of disability is the least restrictive and would allow you to receive full benefits even if you are able to work in another capacity or occupation.^1-3,5,6 The benefit period of the policy also is something to choose carefully. It is recommended to choose a benefit period that extends to at least 65 years of age.^1-3,5 It is important to remember that the devil is in the details; for example, some disability insurance policies with more restrictive definitions will not pay you benefits if you are working in another capacity (eg, a physician who develops an injury that prohibits working with patients and then chooses to work in another capacity).

Some policies will only pay benefits if you become totally disabled. Shy away from these more restrictive policies; instead, look for a policy that has a liberal definition of what constitutes disability and allows you the option to add in a future purchase option rider. It is important that your policy includes a future purchase option rider, which means that as your income increases you have the option to purchase an increase in your disability coverage.^1-3,5 Look for a policy that allows you to be insured without penalizing you for preexisting conditions; during residency is one of the few times some policy vendors will do it, as they assume residents are generally young and healthy.^1-3,5,7

Final Thoughts

When you choose your policy, read the details carefully. Finally, remember that other physicians in the community are available as resources; they can be a wealth of information on different policies. There are many websites available to read more on this topic. Often, your training institution will offer a disability policy for the duration of your residency. Many residents choose to purchase their postresidency policies while in their third or fourth year of training. Take the time to choose a good policy now; you will be glad you did.

Several older physicians have emphasized to me the importance of choosing an excellent disability insurance policy during residency. However, choosing the right policy can be a difficult task. The policy definitions are complicated, and there is a lot of fine print. To understand this confusing topic, start with answers to these 3 questions: What is my most valuable asset? When is the best point in my career to purchase disability insurance? What would I do if I were no longer able to perform the material and substantial duties of my occupation as a dermatologist?

A Resident’s Assets

In the world of disability insurance, your most valuable assets are your education and your ability to earn an income in the future.^1,2 A resident’s ability to earn an income in the future reflects a massive investment of time, cost of education, and postponed accruement of wealth due to time spent in training. Any negative impact on your health (eg, back injury, vision loss, hand injury) can jeopardize these assets. Purchasing disability insurance while still in dermatology residency will protect this investment; it also will ensure that you obtain a policy while you are still healthy.^1,2

Choosing a Policy

Disability insurance comes in 2 main forms: individual or group. Individual insurance may be slightly more expensive but may offer better coverage than group insurance. Group insurance often is offered through a large medical association such as the American Academy of Dermatology. Group insurance may be less expensive but often has more limits to coverage. A definite must-have in a disability insurance policy is one that has guaranteed renewal and is noncancellable.^1-3

Interestingly, women are considered a higher risk for disability, and many insurance policies will charge a higher monthly rate for women than men because women are slightly more likely than men to develop a disability, and women are more likely to develop a disability that prevents them from being able to work.⁴ Some insurance companies do offer a unisex policy, which does not discriminate.

When choosing a policy, you want to carefully read the vendor’s definition of disability. The best definition of the term disability is going to be one that includes phrases such as “unable to perform the material and substantial duties of your [own] occupation . . . even if you are gainfully employed in another occupation.”^1-3,5,6 This definition of disability is the least restrictive and would allow you to receive full benefits even if you are able to work in another capacity or occupation.^1-3,5,6 The benefit period of the policy also is something to choose carefully. It is recommended to choose a benefit period that extends to at least 65 years of age.^1-3,5 It is important to remember that the devil is in the details; for example, some disability insurance policies with more restrictive definitions will not pay you benefits if you are working in another capacity (eg, a physician who develops an injury that prohibits working with patients and then chooses to work in another capacity).

Some policies will only pay benefits if you become totally disabled. Shy away from these more restrictive policies; instead, look for a policy that has a liberal definition of what constitutes disability and allows you the option to add in a future purchase option rider. It is important that your policy includes a future purchase option rider, which means that as your income increases you have the option to purchase an increase in your disability coverage.^1-3,5 Look for a policy that allows you to be insured without penalizing you for preexisting conditions; during residency is one of the few times some policy vendors will do it, as they assume residents are generally young and healthy.^1-3,5,7

Final Thoughts

When you choose your policy, read the details carefully. Finally, remember that other physicians in the community are available as resources; they can be a wealth of information on different policies. There are many websites available to read more on this topic. Often, your training institution will offer a disability policy for the duration of your residency. Many residents choose to purchase their postresidency policies while in their third or fourth year of training. Take the time to choose a good policy now; you will be glad you did.

Several older physicians have emphasized to me the importance of choosing an excellent disability insurance policy during residency. However, choosing the right policy can be a difficult task. The policy definitions are complicated, and there is a lot of fine print. To understand this confusing topic, start with answers to these 3 questions: What is my most valuable asset? When is the best point in my career to purchase disability insurance? What would I do if I were no longer able to perform the material and substantial duties of my occupation as a dermatologist?

A Resident’s Assets

In the world of disability insurance, your most valuable assets are your education and your ability to earn an income in the future.^1,2 A resident’s ability to earn an income in the future reflects a massive investment of time, cost of education, and postponed accruement of wealth due to time spent in training. Any negative impact on your health (eg, back injury, vision loss, hand injury) can jeopardize these assets. Purchasing disability insurance while still in dermatology residency will protect this investment; it also will ensure that you obtain a policy while you are still healthy.^1,2

Choosing a Policy

Disability insurance comes in 2 main forms: individual or group. Individual insurance may be slightly more expensive but may offer better coverage than group insurance. Group insurance often is offered through a large medical association such as the American Academy of Dermatology. Group insurance may be less expensive but often has more limits to coverage. A definite must-have in a disability insurance policy is one that has guaranteed renewal and is noncancellable.^1-3

Interestingly, women are considered a higher risk for disability, and many insurance policies will charge a higher monthly rate for women than men because women are slightly more likely than men to develop a disability, and women are more likely to develop a disability that prevents them from being able to work.⁴ Some insurance companies do offer a unisex policy, which does not discriminate.

When choosing a policy, you want to carefully read the vendor’s definition of disability. The best definition of the term disability is going to be one that includes phrases such as “unable to perform the material and substantial duties of your [own] occupation . . . even if you are gainfully employed in another occupation.”^1-3,5,6 This definition of disability is the least restrictive and would allow you to receive full benefits even if you are able to work in another capacity or occupation.^1-3,5,6 The benefit period of the policy also is something to choose carefully. It is recommended to choose a benefit period that extends to at least 65 years of age.^1-3,5 It is important to remember that the devil is in the details; for example, some disability insurance policies with more restrictive definitions will not pay you benefits if you are working in another capacity (eg, a physician who develops an injury that prohibits working with patients and then chooses to work in another capacity).

Some policies will only pay benefits if you become totally disabled. Shy away from these more restrictive policies; instead, look for a policy that has a liberal definition of what constitutes disability and allows you the option to add in a future purchase option rider. It is important that your policy includes a future purchase option rider, which means that as your income increases you have the option to purchase an increase in your disability coverage.^1-3,5 Look for a policy that allows you to be insured without penalizing you for preexisting conditions; during residency is one of the few times some policy vendors will do it, as they assume residents are generally young and healthy.^1-3,5,7

Final Thoughts

When you choose your policy, read the details carefully. Finally, remember that other physicians in the community are available as resources; they can be a wealth of information on different policies. There are many websites available to read more on this topic. Often, your training institution will offer a disability policy for the duration of your residency. Many residents choose to purchase their postresidency policies while in their third or fourth year of training. Take the time to choose a good policy now; you will be glad you did.

SAN ANTONIO – Prehospital blood transfusions during air medical transport did not improve 24-hour or in-hospital mortality at Vanderbilt University Medical Center, Nashville.

Investigators there reviewed 5,581 patients transported by helicopter to Vanderbilt from the scene of injury from the period of 2007-2013; they excluded patients who died on the helipad or in the ED. Average flight time was 48 minutes; 231 patients (4%) received prehospital blood transfusions (PBT) of up to two units of O negative packed red blood cells, which is all that the helicopters carried. The decision to transfuse was up to helicopter personnel who were advised to transfuse hemodynamically unstable patients and those who had lost more than a half liter of blood.

©Keith Brofsky/Thinkstock

Vanderbilt reviewed its data because although PBT has become widespread in air medical transport, results from military and civilian studies are mixed. “A lot of evidence indicates that early, aggressive resuscitation with blood products improves survival once patients arrive at the hospital. It makes sense that starting the process early would improve outcomes, but relatively little is known about the prehospital environment,” said investigator and general surgery resident Dr. Benjamin Miller.

PBT didn’t seem to help at Vanderbilt. On multivariable regression, in-flight transfusion did not improve 24-hour mortality (OR 1.22; 95% CI 0.61-2.44) or overall in-hospital mortality (OR 1.20; 95% CI 0.55-1.79). It was the same story when 195 transfused patients were matched to 195 who were not transfused, based on mechanism of injury, scene vital signs, injury severity, travel duration, and other measures. Even with matching, PBT did not improve 24-hour mortality (OR 1.04; 95% CI 0.54-1.98) or overall mortality (OR 1.05; 95% CI 0.56-1.96).

There was a trend for improved 24-hour survival with transfusion when injury severity scores were below 20, but it wasn’t statistically significant, perhaps because few of the less injured patients died.

“Our results show no effect of PBT on 24-hour and overall in-hospital mortality. It’s puzzling to us because it’s counterintuitive to the damage control resuscitation strategy,” Dr. Miller said at the annual scientific assembly of the Eastern Association for the Surgery of Trauma.

The findings aren’t robust enough for Vanderbilt to cancel PBT, but they do suggest possible areas for improvement.

Maybe “one or two units of blood are not enough for patients who are severely injured and rapidly exsanguinating, or [maybe] fresh frozen plasma or platelets are needed. Maybe the trigger for transfusion is too low, or too high. It’s time from a prospective study,” Dr. Miller said.

Vanderbilt doesn’t use tranexamic acid to control trauma bleeding. The study didn’t capture volume of crystalloid infused, serum markers of shock, or coagulation study results.

Subjects were in their late 30s, on average, and 70% were men. Transfusions were more likely in younger patients and those with penetrating injuries, poorer at-scene vital signs and Glasgow coma scores, more severe injuries, and lower hematocrits. With the exception of younger age, those factors were also associated with death.

The investigators had no disclosures.

[email protected]

SAN ANTONIO – Prehospital blood transfusions during air medical transport did not improve 24-hour or in-hospital mortality at Vanderbilt University Medical Center, Nashville.

Investigators there reviewed 5,581 patients transported by helicopter to Vanderbilt from the scene of injury from the period of 2007-2013; they excluded patients who died on the helipad or in the ED. Average flight time was 48 minutes; 231 patients (4%) received prehospital blood transfusions (PBT) of up to two units of O negative packed red blood cells, which is all that the helicopters carried. The decision to transfuse was up to helicopter personnel who were advised to transfuse hemodynamically unstable patients and those who had lost more than a half liter of blood.

©Keith Brofsky/Thinkstock

Vanderbilt reviewed its data because although PBT has become widespread in air medical transport, results from military and civilian studies are mixed. “A lot of evidence indicates that early, aggressive resuscitation with blood products improves survival once patients arrive at the hospital. It makes sense that starting the process early would improve outcomes, but relatively little is known about the prehospital environment,” said investigator and general surgery resident Dr. Benjamin Miller.

PBT didn’t seem to help at Vanderbilt. On multivariable regression, in-flight transfusion did not improve 24-hour mortality (OR 1.22; 95% CI 0.61-2.44) or overall in-hospital mortality (OR 1.20; 95% CI 0.55-1.79). It was the same story when 195 transfused patients were matched to 195 who were not transfused, based on mechanism of injury, scene vital signs, injury severity, travel duration, and other measures. Even with matching, PBT did not improve 24-hour mortality (OR 1.04; 95% CI 0.54-1.98) or overall mortality (OR 1.05; 95% CI 0.56-1.96).

There was a trend for improved 24-hour survival with transfusion when injury severity scores were below 20, but it wasn’t statistically significant, perhaps because few of the less injured patients died.

“Our results show no effect of PBT on 24-hour and overall in-hospital mortality. It’s puzzling to us because it’s counterintuitive to the damage control resuscitation strategy,” Dr. Miller said at the annual scientific assembly of the Eastern Association for the Surgery of Trauma.

The findings aren’t robust enough for Vanderbilt to cancel PBT, but they do suggest possible areas for improvement.

Maybe “one or two units of blood are not enough for patients who are severely injured and rapidly exsanguinating, or [maybe] fresh frozen plasma or platelets are needed. Maybe the trigger for transfusion is too low, or too high. It’s time from a prospective study,” Dr. Miller said.

Vanderbilt doesn’t use tranexamic acid to control trauma bleeding. The study didn’t capture volume of crystalloid infused, serum markers of shock, or coagulation study results.

Subjects were in their late 30s, on average, and 70% were men. Transfusions were more likely in younger patients and those with penetrating injuries, poorer at-scene vital signs and Glasgow coma scores, more severe injuries, and lower hematocrits. With the exception of younger age, those factors were also associated with death.

The investigators had no disclosures.

[email protected]

SAN ANTONIO – Prehospital blood transfusions during air medical transport did not improve 24-hour or in-hospital mortality at Vanderbilt University Medical Center, Nashville.

Investigators there reviewed 5,581 patients transported by helicopter to Vanderbilt from the scene of injury from the period of 2007-2013; they excluded patients who died on the helipad or in the ED. Average flight time was 48 minutes; 231 patients (4%) received prehospital blood transfusions (PBT) of up to two units of O negative packed red blood cells, which is all that the helicopters carried. The decision to transfuse was up to helicopter personnel who were advised to transfuse hemodynamically unstable patients and those who had lost more than a half liter of blood.

©Keith Brofsky/Thinkstock

Vanderbilt reviewed its data because although PBT has become widespread in air medical transport, results from military and civilian studies are mixed. “A lot of evidence indicates that early, aggressive resuscitation with blood products improves survival once patients arrive at the hospital. It makes sense that starting the process early would improve outcomes, but relatively little is known about the prehospital environment,” said investigator and general surgery resident Dr. Benjamin Miller.

PBT didn’t seem to help at Vanderbilt. On multivariable regression, in-flight transfusion did not improve 24-hour mortality (OR 1.22; 95% CI 0.61-2.44) or overall in-hospital mortality (OR 1.20; 95% CI 0.55-1.79). It was the same story when 195 transfused patients were matched to 195 who were not transfused, based on mechanism of injury, scene vital signs, injury severity, travel duration, and other measures. Even with matching, PBT did not improve 24-hour mortality (OR 1.04; 95% CI 0.54-1.98) or overall mortality (OR 1.05; 95% CI 0.56-1.96).

There was a trend for improved 24-hour survival with transfusion when injury severity scores were below 20, but it wasn’t statistically significant, perhaps because few of the less injured patients died.

“Our results show no effect of PBT on 24-hour and overall in-hospital mortality. It’s puzzling to us because it’s counterintuitive to the damage control resuscitation strategy,” Dr. Miller said at the annual scientific assembly of the Eastern Association for the Surgery of Trauma.

The findings aren’t robust enough for Vanderbilt to cancel PBT, but they do suggest possible areas for improvement.

Maybe “one or two units of blood are not enough for patients who are severely injured and rapidly exsanguinating, or [maybe] fresh frozen plasma or platelets are needed. Maybe the trigger for transfusion is too low, or too high. It’s time from a prospective study,” Dr. Miller said.

Vanderbilt doesn’t use tranexamic acid to control trauma bleeding. The study didn’t capture volume of crystalloid infused, serum markers of shock, or coagulation study results.

Subjects were in their late 30s, on average, and 70% were men. Transfusions were more likely in younger patients and those with penetrating injuries, poorer at-scene vital signs and Glasgow coma scores, more severe injuries, and lower hematocrits. With the exception of younger age, those factors were also associated with death.

The investigators had no disclosures.

[email protected]

Since early summer, a 51-year-old woman has had an itchy rash on her trunk. It manifested after she intentionally lost more than 200 lb, which resulted in deeper and more pronounced skinfolds. The same skinfolds are repeatedly involved in flares of the rash, which is worse on particularly hot days. She was diagnosed with “yeast infection” but the problem failed to respond to oral fluconazole and topical nystatin.

The patient has multiple health problems, including diabetes, chronic anxiety, and hypertension.

EXAMINATION
There is a deep, linear, concave fold in the skin of the right flank, the long axis of which is transversely oriented. Within this fold, a fiery red rash is seen; its margins exactly match the outline of skin-on-skin contact. The surface of the affected skin is macerated and wet looking. There is neither tenderness nor increased warmth on palpation.

What is the diagnosis?

DISCUSSION
This phenomenon is called intertrigo, and it’s a subject of much confusion. This is especially true in primary care, where almost any intertriginous rash is labeled “yeast infection” and treated with anti-yeast medications that fail as monotherapy. In fact, true yeast infections in or on the skin are quite unusual.

Here is what happens when skin is held on skin: Moisture can accumulate, temperature rises, and skin becomes macerated and starts to break down. Organisms already present on the skin begin to multiply and can contribute to the inflammatory burden. Any pre-existing skin disease (eg, seborrhea, eczema or psoriasis) can flare under these conditions, further breaking down the epidermal barrier. With the right mix of these and other factors (severe obesity, diabetes, immunosuppression, hot weather), yeast can play a bigger role in the problem—but it is usually a minor factor.

Intertrigo is common under the breasts, in the axillae, and in abdominal panniculi. It can also be seen, as in this case, in large folds on the trunk, or even on the legs. Most cases of diaper rash involve at least a component of intertrigo.

The factors that predispose to intertrigo tend to be chronic, making the problem chronic as well. The patient and family (if appropriate) need to understand this, as well as the seasonal effects (the condition will be worse in warm months but improve in winter).

Treatment should be directed at reducing moisture in the area. This can be achieved by opening it up to air as much as possible, using aluminum acetate solution soaks to dry out the skin, placing strips of cotton or linen cloth to separate skinfolds, or applying antiperspirants or talcum-based powder.

For acute treatment, class 4 or 5 steroid creams can be used for short periods. An OTC topical anti-yeast cream, such as clotrimazole or miconazole, can be added.

The onset of such a rash, without obvious predisposing factors, should prompt consideration of other items in the differential. These include cutaneous T-cell lymphoma, Paget’s disease, or zinc deficiency–related conditions. More common lookalikes include contact or irritant dermatitis.

TAKE-HOME LEARNING POINTS
• As its name suggests, intertrigo is a condition affecting the intertriginous areas (eg, skin folds); common locations are under breasts or in the axillae, groin, or panniculi.

• Though yeast organisms can play a role in the development of intertrigo, treatment with anti-yeast products as monotherapy rarely work.

• Instead, management of intertrigo must be directed at the causative factors: heat, sweat, and friction.

• Intertrigo is difficult to treat, in large part because the major causative factors (weight, heat, sweat) are hard to change. 

Since early summer, a 51-year-old woman has had an itchy rash on her trunk. It manifested after she intentionally lost more than 200 lb, which resulted in deeper and more pronounced skinfolds. The same skinfolds are repeatedly involved in flares of the rash, which is worse on particularly hot days. She was diagnosed with “yeast infection” but the problem failed to respond to oral fluconazole and topical nystatin.

The patient has multiple health problems, including diabetes, chronic anxiety, and hypertension.

EXAMINATION
There is a deep, linear, concave fold in the skin of the right flank, the long axis of which is transversely oriented. Within this fold, a fiery red rash is seen; its margins exactly match the outline of skin-on-skin contact. The surface of the affected skin is macerated and wet looking. There is neither tenderness nor increased warmth on palpation.

What is the diagnosis?

DISCUSSION
This phenomenon is called intertrigo, and it’s a subject of much confusion. This is especially true in primary care, where almost any intertriginous rash is labeled “yeast infection” and treated with anti-yeast medications that fail as monotherapy. In fact, true yeast infections in or on the skin are quite unusual.

Here is what happens when skin is held on skin: Moisture can accumulate, temperature rises, and skin becomes macerated and starts to break down. Organisms already present on the skin begin to multiply and can contribute to the inflammatory burden. Any pre-existing skin disease (eg, seborrhea, eczema or psoriasis) can flare under these conditions, further breaking down the epidermal barrier. With the right mix of these and other factors (severe obesity, diabetes, immunosuppression, hot weather), yeast can play a bigger role in the problem—but it is usually a minor factor.

Intertrigo is common under the breasts, in the axillae, and in abdominal panniculi. It can also be seen, as in this case, in large folds on the trunk, or even on the legs. Most cases of diaper rash involve at least a component of intertrigo.

The factors that predispose to intertrigo tend to be chronic, making the problem chronic as well. The patient and family (if appropriate) need to understand this, as well as the seasonal effects (the condition will be worse in warm months but improve in winter).

Treatment should be directed at reducing moisture in the area. This can be achieved by opening it up to air as much as possible, using aluminum acetate solution soaks to dry out the skin, placing strips of cotton or linen cloth to separate skinfolds, or applying antiperspirants or talcum-based powder.

For acute treatment, class 4 or 5 steroid creams can be used for short periods. An OTC topical anti-yeast cream, such as clotrimazole or miconazole, can be added.

The onset of such a rash, without obvious predisposing factors, should prompt consideration of other items in the differential. These include cutaneous T-cell lymphoma, Paget’s disease, or zinc deficiency–related conditions. More common lookalikes include contact or irritant dermatitis.

TAKE-HOME LEARNING POINTS
• As its name suggests, intertrigo is a condition affecting the intertriginous areas (eg, skin folds); common locations are under breasts or in the axillae, groin, or panniculi.

• Though yeast organisms can play a role in the development of intertrigo, treatment with anti-yeast products as monotherapy rarely work.

• Instead, management of intertrigo must be directed at the causative factors: heat, sweat, and friction.

• Intertrigo is difficult to treat, in large part because the major causative factors (weight, heat, sweat) are hard to change. 

Since early summer, a 51-year-old woman has had an itchy rash on her trunk. It manifested after she intentionally lost more than 200 lb, which resulted in deeper and more pronounced skinfolds. The same skinfolds are repeatedly involved in flares of the rash, which is worse on particularly hot days. She was diagnosed with “yeast infection” but the problem failed to respond to oral fluconazole and topical nystatin.

The patient has multiple health problems, including diabetes, chronic anxiety, and hypertension.

EXAMINATION
There is a deep, linear, concave fold in the skin of the right flank, the long axis of which is transversely oriented. Within this fold, a fiery red rash is seen; its margins exactly match the outline of skin-on-skin contact. The surface of the affected skin is macerated and wet looking. There is neither tenderness nor increased warmth on palpation.

What is the diagnosis?

DISCUSSION
This phenomenon is called intertrigo, and it’s a subject of much confusion. This is especially true in primary care, where almost any intertriginous rash is labeled “yeast infection” and treated with anti-yeast medications that fail as monotherapy. In fact, true yeast infections in or on the skin are quite unusual.

Here is what happens when skin is held on skin: Moisture can accumulate, temperature rises, and skin becomes macerated and starts to break down. Organisms already present on the skin begin to multiply and can contribute to the inflammatory burden. Any pre-existing skin disease (eg, seborrhea, eczema or psoriasis) can flare under these conditions, further breaking down the epidermal barrier. With the right mix of these and other factors (severe obesity, diabetes, immunosuppression, hot weather), yeast can play a bigger role in the problem—but it is usually a minor factor.

Intertrigo is common under the breasts, in the axillae, and in abdominal panniculi. It can also be seen, as in this case, in large folds on the trunk, or even on the legs. Most cases of diaper rash involve at least a component of intertrigo.

The factors that predispose to intertrigo tend to be chronic, making the problem chronic as well. The patient and family (if appropriate) need to understand this, as well as the seasonal effects (the condition will be worse in warm months but improve in winter).

Treatment should be directed at reducing moisture in the area. This can be achieved by opening it up to air as much as possible, using aluminum acetate solution soaks to dry out the skin, placing strips of cotton or linen cloth to separate skinfolds, or applying antiperspirants or talcum-based powder.

For acute treatment, class 4 or 5 steroid creams can be used for short periods. An OTC topical anti-yeast cream, such as clotrimazole or miconazole, can be added.

The onset of such a rash, without obvious predisposing factors, should prompt consideration of other items in the differential. These include cutaneous T-cell lymphoma, Paget’s disease, or zinc deficiency–related conditions. More common lookalikes include contact or irritant dermatitis.

TAKE-HOME LEARNING POINTS
• As its name suggests, intertrigo is a condition affecting the intertriginous areas (eg, skin folds); common locations are under breasts or in the axillae, groin, or panniculi.

• Though yeast organisms can play a role in the development of intertrigo, treatment with anti-yeast products as monotherapy rarely work.

• Instead, management of intertrigo must be directed at the causative factors: heat, sweat, and friction.

• Intertrigo is difficult to treat, in large part because the major causative factors (weight, heat, sweat) are hard to change. 

Over the past five years, I have worked as a locum tenens hospitalist with more than 12 different locum tenens companies. I have learned a lot through this process. At one point, I even considered starting my own locum tenens company because of the frustrations I was feeling about the inefficiencies of many of these companies. I would like to help those of you either already practicing as a locum tenens physician or considering practicing through this process to make it as painless as possible.

Here are my tips to be aware of when choosing a locum tenens company to work with.

1. Bigger isn’t necessarily better. There are a few companies that advertise a lot. I’m sure you are all very well aware of them. They send out many emails, call numerous times, and somehow have a banner on every website you visit. These companies tend to have large overhead costs. These costs mean that your hourly rate may be lower. Smaller companies are sometimes less efficient, but as long as you make sure your expectations are heard, they will often give you a rate that the bigger companies cannot afford.
2. State your terms. As physicians, we are often not the most business savvy. Remember that locum tenens companies exist because there is a shortage of hospitalists in some areas. We need to be able to state certain terms; if you don’t like something, then make sure you add that into your contract. For example, patient safety should always come first; make sure you establish a cap for the number of patients you are willing to see per day.
3. Be protective of your CV. Remember that locum tenens companies profit when you work, so they will want to hand out your CV to as many hospitals as possible. While they make it sound like it is in your best interest, it may not be. If a company presents you to a hospital, most of the time the contract you sign with them states that they “own” your presentation for two years. This means that if you do not like the locum tenens company or if another company is offering you more for the same hospital, you have to work with the company that presented you first. Make sure you have a written agreement between you and your locum tenens company with regard to presentations stating which hospitals the locum tenens company can present you to, with a follow-up response from the locum tenens company stating when they presented you.
4. Your recruiter is your best advocate. Make sure you get along. Make sure you have very good communication with your recruiter, who is the one who will be doing all of your scheduling and negotiating. If you do not have a good relationship, move on to a new recruiter or to a new company.
5. Have fun! Working as a locum tenens physician, in my opinion, is the best of everything combined. There are very few jobs where you can decide when you want to work, dictate your terms, and get paid well doing something you love. Locum tenens takes a little bit of getting used to; when you have it figured out, it is empowering and enjoyable. TH

Geeta Arora, MD, is board certified in internal medicine and integrative holistic medicine.

Over the past five years, I have worked as a locum tenens hospitalist with more than 12 different locum tenens companies. I have learned a lot through this process. At one point, I even considered starting my own locum tenens company because of the frustrations I was feeling about the inefficiencies of many of these companies. I would like to help those of you either already practicing as a locum tenens physician or considering practicing through this process to make it as painless as possible.

Here are my tips to be aware of when choosing a locum tenens company to work with.

1. Bigger isn’t necessarily better. There are a few companies that advertise a lot. I’m sure you are all very well aware of them. They send out many emails, call numerous times, and somehow have a banner on every website you visit. These companies tend to have large overhead costs. These costs mean that your hourly rate may be lower. Smaller companies are sometimes less efficient, but as long as you make sure your expectations are heard, they will often give you a rate that the bigger companies cannot afford.
2. State your terms. As physicians, we are often not the most business savvy. Remember that locum tenens companies exist because there is a shortage of hospitalists in some areas. We need to be able to state certain terms; if you don’t like something, then make sure you add that into your contract. For example, patient safety should always come first; make sure you establish a cap for the number of patients you are willing to see per day.
3. Be protective of your CV. Remember that locum tenens companies profit when you work, so they will want to hand out your CV to as many hospitals as possible. While they make it sound like it is in your best interest, it may not be. If a company presents you to a hospital, most of the time the contract you sign with them states that they “own” your presentation for two years. This means that if you do not like the locum tenens company or if another company is offering you more for the same hospital, you have to work with the company that presented you first. Make sure you have a written agreement between you and your locum tenens company with regard to presentations stating which hospitals the locum tenens company can present you to, with a follow-up response from the locum tenens company stating when they presented you.
4. Your recruiter is your best advocate. Make sure you get along. Make sure you have very good communication with your recruiter, who is the one who will be doing all of your scheduling and negotiating. If you do not have a good relationship, move on to a new recruiter or to a new company.
5. Have fun! Working as a locum tenens physician, in my opinion, is the best of everything combined. There are very few jobs where you can decide when you want to work, dictate your terms, and get paid well doing something you love. Locum tenens takes a little bit of getting used to; when you have it figured out, it is empowering and enjoyable. TH

Geeta Arora, MD, is board certified in internal medicine and integrative holistic medicine.

Over the past five years, I have worked as a locum tenens hospitalist with more than 12 different locum tenens companies. I have learned a lot through this process. At one point, I even considered starting my own locum tenens company because of the frustrations I was feeling about the inefficiencies of many of these companies. I would like to help those of you either already practicing as a locum tenens physician or considering practicing through this process to make it as painless as possible.

Here are my tips to be aware of when choosing a locum tenens company to work with.

1. Bigger isn’t necessarily better. There are a few companies that advertise a lot. I’m sure you are all very well aware of them. They send out many emails, call numerous times, and somehow have a banner on every website you visit. These companies tend to have large overhead costs. These costs mean that your hourly rate may be lower. Smaller companies are sometimes less efficient, but as long as you make sure your expectations are heard, they will often give you a rate that the bigger companies cannot afford.
2. State your terms. As physicians, we are often not the most business savvy. Remember that locum tenens companies exist because there is a shortage of hospitalists in some areas. We need to be able to state certain terms; if you don’t like something, then make sure you add that into your contract. For example, patient safety should always come first; make sure you establish a cap for the number of patients you are willing to see per day.
3. Be protective of your CV. Remember that locum tenens companies profit when you work, so they will want to hand out your CV to as many hospitals as possible. While they make it sound like it is in your best interest, it may not be. If a company presents you to a hospital, most of the time the contract you sign with them states that they “own” your presentation for two years. This means that if you do not like the locum tenens company or if another company is offering you more for the same hospital, you have to work with the company that presented you first. Make sure you have a written agreement between you and your locum tenens company with regard to presentations stating which hospitals the locum tenens company can present you to, with a follow-up response from the locum tenens company stating when they presented you.
4. Your recruiter is your best advocate. Make sure you get along. Make sure you have very good communication with your recruiter, who is the one who will be doing all of your scheduling and negotiating. If you do not have a good relationship, move on to a new recruiter or to a new company.
5. Have fun! Working as a locum tenens physician, in my opinion, is the best of everything combined. There are very few jobs where you can decide when you want to work, dictate your terms, and get paid well doing something you love. Locum tenens takes a little bit of getting used to; when you have it figured out, it is empowering and enjoyable. TH

Geeta Arora, MD, is board certified in internal medicine and integrative holistic medicine.

NEW YORK (Reuters Health) - Outcomes of inpatient laparoscopic cholecystectomy in Medicare patients vary widely among hospitals, and most adverse outcomes occur well after patients have been discharged, new findings show.

While the overall adverse outcome rate was 20.7%, risk-adjusted adverse outcomes ranged from 10% in the best-performing decile of hospitals to 32.1% for the worst-performing decile, Dr. Donald E. Fry of MPA Healthcare Solutions in Chicago and colleagues found.

"These differences indicate that a significant number of readmissions and overall adverse outcomes of care after laparoscopic cholecystectomy are potentially preventable," Dr. Fry and his team state in their report, online February 1 in the Annals of Surgery.

Risk-adjusted measurement of care has typically been limited to inpatient events and 30-day mortality rates, they note, but declines in mortality rates, shorter patient stays and a shift toward ambulatory procedures have made this measurement more difficult.

"Surgery for gallbladder disease has experienced one of the most dramatic transitions from extended inpatient care to outpatient or limited inpatient care," they write.

To compare outcomes among hospitals, Dr. Fry and his team looked at Medicare data for 2010-2012 including both inpatient and 90-day post-discharge adverse outcomes for inpatient laparoscopic cholecystectomy.

They created a developmental database including more than 73,000 patients to construct predictive models for adverse outcomes, and a database of more than 83,000 patients treated at 1,570 hospitals, each with 20 or more qualifying cases and 4.5 or more predicted total adverse outcomes, to compare performance.

A total of 509 patients (0.6%) died in the hospital, 5,761 (6.9%) had prolonged length of stay, 1,154 (1.4%) died within 90 days of discharge without being readmitted, and 12,038 (14.5%) were readmitted at least once in the 90 days after discharge.

Gastrointestinal, infectious and cardiovascular events were the most common readmission causes.

"Strategies for improvement begin with hospitals and surgeons knowing what the results of their care happen to be," Dr. Fry told Reuters Health by email. "Since many readmissions and Emergency Department visits of post-discharge surgical cases occur at hospitals other than the facility of the index

hospitalization, the actual results of care may not be appreciated by the providers."

He added: "Improvement strategies need to focus on the reasons patients were readmitted. Better pain management will reduce readmissions for constipation, abdominal distention, nausea and vomiting. Increased contact by clinicians with their patients after discharge can identify early evidence of

pulmonary problems or potential urinary tract infection. Earlier recognition of evolving issues can provide interventions that avoid readmissions. Better overall strategies to avoid cardiac events and hypovolemia that may play in central nervous system events and renal failure should be of benefit."

Dr. Fry and his colleagues are now investigating whether similar differences in outcomes occur with other types of surgical procedures, as well as the frequency of and reasons for post-discharge emergency room visits.

"A final message for surgeons in this research is that Medicare has begun an initiative into bundled payments," Dr. Fry said. "Surgeons and hospitals need to establish better trackingmethods for post-discharge patients so that they know the results of care and so that they can develop focused strategies for better outcomes. There will be a substantial financial penalty for those who cannot adapt to the new payment model that CMS is implementing."

NEW YORK (Reuters Health) - Outcomes of inpatient laparoscopic cholecystectomy in Medicare patients vary widely among hospitals, and most adverse outcomes occur well after patients have been discharged, new findings show.

While the overall adverse outcome rate was 20.7%, risk-adjusted adverse outcomes ranged from 10% in the best-performing decile of hospitals to 32.1% for the worst-performing decile, Dr. Donald E. Fry of MPA Healthcare Solutions in Chicago and colleagues found.

"These differences indicate that a significant number of readmissions and overall adverse outcomes of care after laparoscopic cholecystectomy are potentially preventable," Dr. Fry and his team state in their report, online February 1 in the Annals of Surgery.

Risk-adjusted measurement of care has typically been limited to inpatient events and 30-day mortality rates, they note, but declines in mortality rates, shorter patient stays and a shift toward ambulatory procedures have made this measurement more difficult.

"Surgery for gallbladder disease has experienced one of the most dramatic transitions from extended inpatient care to outpatient or limited inpatient care," they write.

To compare outcomes among hospitals, Dr. Fry and his team looked at Medicare data for 2010-2012 including both inpatient and 90-day post-discharge adverse outcomes for inpatient laparoscopic cholecystectomy.

They created a developmental database including more than 73,000 patients to construct predictive models for adverse outcomes, and a database of more than 83,000 patients treated at 1,570 hospitals, each with 20 or more qualifying cases and 4.5 or more predicted total adverse outcomes, to compare performance.

A total of 509 patients (0.6%) died in the hospital, 5,761 (6.9%) had prolonged length of stay, 1,154 (1.4%) died within 90 days of discharge without being readmitted, and 12,038 (14.5%) were readmitted at least once in the 90 days after discharge.

Gastrointestinal, infectious and cardiovascular events were the most common readmission causes.

"Strategies for improvement begin with hospitals and surgeons knowing what the results of their care happen to be," Dr. Fry told Reuters Health by email. "Since many readmissions and Emergency Department visits of post-discharge surgical cases occur at hospitals other than the facility of the index

hospitalization, the actual results of care may not be appreciated by the providers."

He added: "Improvement strategies need to focus on the reasons patients were readmitted. Better pain management will reduce readmissions for constipation, abdominal distention, nausea and vomiting. Increased contact by clinicians with their patients after discharge can identify early evidence of

pulmonary problems or potential urinary tract infection. Earlier recognition of evolving issues can provide interventions that avoid readmissions. Better overall strategies to avoid cardiac events and hypovolemia that may play in central nervous system events and renal failure should be of benefit."

Dr. Fry and his colleagues are now investigating whether similar differences in outcomes occur with other types of surgical procedures, as well as the frequency of and reasons for post-discharge emergency room visits.

"A final message for surgeons in this research is that Medicare has begun an initiative into bundled payments," Dr. Fry said. "Surgeons and hospitals need to establish better trackingmethods for post-discharge patients so that they know the results of care and so that they can develop focused strategies for better outcomes. There will be a substantial financial penalty for those who cannot adapt to the new payment model that CMS is implementing."

NEW YORK (Reuters Health) - Outcomes of inpatient laparoscopic cholecystectomy in Medicare patients vary widely among hospitals, and most adverse outcomes occur well after patients have been discharged, new findings show.

While the overall adverse outcome rate was 20.7%, risk-adjusted adverse outcomes ranged from 10% in the best-performing decile of hospitals to 32.1% for the worst-performing decile, Dr. Donald E. Fry of MPA Healthcare Solutions in Chicago and colleagues found.

"These differences indicate that a significant number of readmissions and overall adverse outcomes of care after laparoscopic cholecystectomy are potentially preventable," Dr. Fry and his team state in their report, online February 1 in the Annals of Surgery.

Risk-adjusted measurement of care has typically been limited to inpatient events and 30-day mortality rates, they note, but declines in mortality rates, shorter patient stays and a shift toward ambulatory procedures have made this measurement more difficult.

"Surgery for gallbladder disease has experienced one of the most dramatic transitions from extended inpatient care to outpatient or limited inpatient care," they write.

To compare outcomes among hospitals, Dr. Fry and his team looked at Medicare data for 2010-2012 including both inpatient and 90-day post-discharge adverse outcomes for inpatient laparoscopic cholecystectomy.

They created a developmental database including more than 73,000 patients to construct predictive models for adverse outcomes, and a database of more than 83,000 patients treated at 1,570 hospitals, each with 20 or more qualifying cases and 4.5 or more predicted total adverse outcomes, to compare performance.

A total of 509 patients (0.6%) died in the hospital, 5,761 (6.9%) had prolonged length of stay, 1,154 (1.4%) died within 90 days of discharge without being readmitted, and 12,038 (14.5%) were readmitted at least once in the 90 days after discharge.

Gastrointestinal, infectious and cardiovascular events were the most common readmission causes.

"Strategies for improvement begin with hospitals and surgeons knowing what the results of their care happen to be," Dr. Fry told Reuters Health by email. "Since many readmissions and Emergency Department visits of post-discharge surgical cases occur at hospitals other than the facility of the index

hospitalization, the actual results of care may not be appreciated by the providers."

He added: "Improvement strategies need to focus on the reasons patients were readmitted. Better pain management will reduce readmissions for constipation, abdominal distention, nausea and vomiting. Increased contact by clinicians with their patients after discharge can identify early evidence of

pulmonary problems or potential urinary tract infection. Earlier recognition of evolving issues can provide interventions that avoid readmissions. Better overall strategies to avoid cardiac events and hypovolemia that may play in central nervous system events and renal failure should be of benefit."

Dr. Fry and his colleagues are now investigating whether similar differences in outcomes occur with other types of surgical procedures, as well as the frequency of and reasons for post-discharge emergency room visits.

"A final message for surgeons in this research is that Medicare has begun an initiative into bundled payments," Dr. Fry said. "Surgeons and hospitals need to establish better trackingmethods for post-discharge patients so that they know the results of care and so that they can develop focused strategies for better outcomes. There will be a substantial financial penalty for those who cannot adapt to the new payment model that CMS is implementing."