Imaging in the ‘Ivory Tower’: Academic Radiology
Published on the Aug. 25, 2016, Diagnostic Imaging website
By Whitney L. Jackson
Throughout the radiology community, there’s one thing every provider has in common. At one point in time, you all completed a residency as part of your training.
Some radiologists never left academia. Instead of opting for private practice or choosing a career in teleradiology, they’ve chosen to remain in the “Ivory Tower.” They’re providing care to your patients like every other provider, but being a radiologist in an academic setting carries its own habits, benefits, and challenges.
And, according to Vijay Rao, MD, chair of the Board of Directors for the Radiological Society of North American and radiology chair at Jefferson Medical School at Thomas Jefferson University, as well as Tejas Mehta, MD, MPH, chief of breast imaging at Harvard Medical School, it’s a job selection that they are frequently thankful for.
“I love what I do, and if I had to do it all over again, I wouldn’t change a thing,” Mehta said. “You need to be passionate about what you do, and academic radiology provides a great work-life balance at the same time.”
Still, there is much to consider if you’re contemplating an academic radiology career – or much to learn if you’ve never experienced radiology practice from this perspective.
Benefits of Academic Radiology
Alongside being able to, potentially, work side-by-side with some of radiology’s thought leaders, being an academic radiology has some upshots.
1. Subspecialty Reads: The same way your residency gives you the opportunity to concentrate on a subspecialty, opting for an academic career allows you to focus your efforts in one specific area, said Rao, who has spent her career as in head and neck imaging.
“Only academic radiology allows you the luxury of practicing only in your field rather than having to do reads of all types,” she said. “This is very meaningful in contributing to providing the highest levels of care.”
2. Staying Young: Yes, you’ll age in your career, but choosing to remain in an educational institution ensures you’ll be surrounded by the next generation of radiologists at all times. Not only are they likely to be forward-thinking as individuals, but it’s also a requirement that they keep up with the most up-to-date data and technology in providing radiological care. If you’re constantly training aspiring radiologists, your skill set won’t have time to get rusty or dated.
To read the remainder of the article at its original location: http://www.diagnosticimaging.com/practice-management/imaging-ivory-tower-academic-radiology
How Glucocorticoids Can Change Fat Mass and Redistribution
Published on the Aug. 18, 2016, Rheumatology Network website
By Whitney L. J. Howell
For nearly seven decades, glucocorticoid treatment has been a common therapy for rheumatoid arthritis patients. It’s popular for other rheumatic conditions, as well, because it’s cost effective and offers strong anti-inflammatory and immunosuppressive effects. But, awareness of the negative effects is growing.
Glucocorticoids can have detrimental impacts: osteoporosis, hyperglycemia, diabetes, cardiovascular disease and infections. Weight gain, including a red, round face, abdominal obesity with thin limbs, fat pad growth around the neck and back are also common. This weight increase, called the Cushingoid appearance, has been identified for decades and shows how glucocorticoids can impact fat metabolism. But, to date, there’s been little knowledge about how glucocorticoids can change fat mass and redistribution.
Consequently, understanding has also been minimal about the overall combination effect of rheumatoid arthritis and glucocorticoid treatments on body composition. While healthy body compositions have lower proportional body fat and higher proportional fat free mass, obesity increases the risk of high blood pressure, high cholesterol, diabetes, and cardiovascular disease.
To investigate these effects, Nicole P.C. Konijn from the Department of Rheumatology in the Amsterdam Rheumatology and Immunology Center and VU University Medical Center and colleagues conducted a study, published in Rheumatology, on the short-term effects of two high dose, step down prednisolone regimens on body composition in early rheumatoid arthritis patients. In turn, two international glucocorticoid experts from the Department of Rheumatology and Clinical Immunology at Germany’s Carité University Medicine — Frank Buttgereit and Gerd R. Burmester — analyzed the research and published a commentary in Nature Reviews.
Rheumatoid arthritis and the associated chronic inflammation affects between 0.5 percent and 1.0 percent of adults. The joint pain and stiffness associated with the condition is often attributed to a night-time rise of proteins, called cytokines, and hormones in the blood. In particular, these patients see a rise in pro-inflammatory cytokines, such as interleukin-6 and tumor necrosis factor. The same phenomenon is not seen in patients without rheumatoid arthritis.
It’s less widely known, though, that these changes also contribute to the abnormal body composition found in rheumatoid arthritis patients. Understanding this interaction is important, Buttgereit and Burmester wrote, because glucocorticoid treatment is known to facilitate fat accumulation and redistribution between the body’s trunk and limbs.
“Disease exacerbations, decreased physical activity and disuse of muscles can further reduce lean mass, leading to decreased functional capacity and serious consequences for morbidity and mortality,” Buttgereit and Burmester wrote.
Rheumatoid arthritis patients often experience rheumatoid cachexia — the replacement of lean body mass with fat mass. This condition can raise the risk for comorbidities, including diabetes and cardiovascular disease.
According to Buttgereit and Burmester, the data from Konijn’s study is particularly important because it fills in the knowledge gap, affirming there are no major changes in relative body composition that occur with some forms of glucocorticoid treatments. The researchers obtained their results by recording total body mass and using dual energy X-ray absorptiometry, a straight-forward, fast, non-invasive technique for gathering body composition measurements. They measured total fat mass, total lean mass, and trunk:peripheral fat ratio at baseline and after 26 weeks of glucocorticoid treatment.
Overall, Buttgereit and Burmester said, Konijn’s study has two major results. First, in early on-set rheumatoid arthritis patients who had never received glucocorticoid or disease modifying anti-rheumatic drug therapies, total body mass increased by 1.6 kg after 26 weeks of treatment.
The body mass index of glucocorticoid treated patients rose from 25.6 kg to 26.2 kg. That increase makes the presence of overweight and obesity at 26 weeks higher than at baseline. In fact, the 20 patients who were treated with higher cumulative glucocorticoid dose presented a 2.1 kg weight gain – more than the 1.1 kg seen in the 18 patients who received lower cumulative glucocorticoid doses. The 20 patients received a total of 2,275 mg via a combination-therapy regimen called COBRA, and their average daily dose was 12.5 mg. The 18 patients received, 1,750 mg via the same COBRA regimen, and their daily average dose was 9.6 mg.
Based on the second major result, glucocorticoid-treated patients maintained their trunk: peripheral fat ratio and proportional distribution of total body mass and fat mass. In essence, researchers observed no fat redistribution from the body’s limbs to the trunk within the study’s timeframe. The study also didn’t point to a dose-dependent effect of COBRA versus COBRA-light body composition treatment.
These observations were surprising, however, Buttgereit and Burmester said, because it’s known that glucocorticoid treatments alter energy metabolism, induce muscle wasting and fat accumulation, and redistribute fat from body’s limbs to its trunk.
But, Buttgereit and Burmester said, Konijn’s study isn’t without its limitations. Not only was the study short at 26 weeks, but it also included a small number of patients with no control group. In addition, the difference in cumulative glucocorticoid doses between the two groups — only 525 mg after 26 weeks — could be too small to cause a dose-dependent effect.
Researchers also didn’t record any data from the time period prior to rheumatoid arthritis onset, so they can’t determine if the observed total body mass and body mass index changes truly represent a real increase or whether they can be credited to the recovery of body mass previously lost to disease and, then, regained through successful glucocorticoid treatment.
Ultimately, Buttgereit and Burmester wrote, further research should investigate the long-term effects of glucocorticoid treatment in rheumatoid arthritis and other rheumatic diseases. It should also look at how disease processes influence body composition, as well as address whether cytokine-targeting biologic drugs influence body composition.
To read the article at its original location: http://www.rheumatologynetwork.com/rheumatoid-arthritis/how-glucocorticoids-can-change-fat-mass-and-redistribution
Assessing Risk Factors for Disease Outcomes
Published Aug. 19, 2016, Rheumatology Network website
By Whitney L. Jackson
Genetic variations identified in patients with rheumatological diseases could facilitate designing clinical interventions and developing therapeutic treatments, according to a recent existing literature review.
Known as Mendelian randomization, this technique uses genetic variants, called alleles, to test whether specific risk factors are associated with or cause certain disease outcomes. This strategy could help researchers better understand existing, unmeasured confounding factors that can correlate to both dependent and independent variables, particularly environmental exposures, impacting observational studies.
The basic Mendelian randomization principle is if an environmental exposure, such a urate levels, is linked to an outcome, such as cardiovascular disease, a genetic variation will be present. Identifying these genetic variants could be helpful with rheumatological diseases.
To better understand Mendelian randomization and how it touches rheumatological conditions, researchers, led by Philp C. Robinson from the University of Queensland School of Medicine in Australia, published a systematic literature review in Nature, analyzing existing results and how they can be applied to rheumatology.
“Mendelian randomization can shed new light on cause-effect relationships in rheumatology, helping to make the case for investment in confirmatory intervention trials and to generate new hypotheses regarding pathological mechanisms and aetiology,” investigators wrote. “The technique also enables experiments to be performed that would otherwise be unethical, logistically difficult or prohibitively expensive.”
Not only can Mendelian randomization studies potentially direct clinical practice, but it can also help prioritize causal pathway interventions and help avoid unnecessary clinical trials. It can be incorporated into randomized clinical trials that test therapies for common disease risk factors, potentially explaining why targeted-intervention benefits often are lower than expected, researchers said.
Understanding the Mendelian Method
Overall, successful observational studies rely on accurate confounding factor measurements. Without that, research is hampered. However, Mendelian randomization can potentially side-step the limitation by examining single-nucleotide polymorphisms. Single-nucleotide polymorphism generally explains less than 1 percent of any observed variance, so Mendelian randomization studies typically require 10,000+ individual data sets.
Any selected genetic variants shouldn’t be associated with confounders, and they shouldn’t have pleiotropic effects. For Mendelian randomization results to be valid, investigators must satisfy three criteria:
1. Genetic variants used should be associated with – and explain between 0.5 percent to 1.0 percent of – exposure variance to give the study adequate power.
2. Genetic variants shouldn’t be associated with any factors that confound the exposure-outcome relationship.
3. Genetic variants should only influence outcome through exposure and shouldn’t have pleiotropic effects.
Mendelian Randomization & Rheumatology
To date, Mendelian randomization has been applied mainly to the cause-effect relationship between urate levels and cardiometabolic traits, including coronary heart disease, high blood pressure, diabetes, obesity, body mass index, and kidney function. These studies, which also test for reverse causality, have found genetic variants associated with both hyperuricemia and gout have causal relationships with urate levels. Other studies suggest a causal role for vitamin D levels in determining responses to rheumatoid arthritis therapies and disease outcomes, as well as a causal role for high body mass index and osteoarthritis risk.
An existing literature review also revealed causal relationship results based on Mendelian randomization.
N-glycosylation of IgG in Rheumatoid Arthritis: Researchers tested 16 variants associated with IgG-N glycosylation with 14,361 rheumatoid arthritis patients and 43,923 healthy individuals. They didn’t find a causal association of any genetic variants with rheumatoid arthritis, but a lack of data meant the genetic variants weren’t directly associated with the trait. Consequently, via Mendelian randomization, IgG-N glycosylation doesn’t cause rheumatoid arthritis, but it is a disease biomarker.
IL-1 signalling in Rheumatoid Arthritis: Investigators used Mendelian randomization to unearth cardiovascular risks of long-term inhibition of IL-1 signalling. The study used two genetic variants affecting the gene that encodes IL-1 receptor antagonist (IL-1RA) and included 453,411 participants. Results indicated alleles associated with elevated IL-1RA expression were also linked to protection from rheumatoid arthritis and a cardiovascular disease increase.
Phosphate and Bone Mineral Density: According to Mendelian randomization, high phosphate intake affects calcium metabolism. The study, involving fewer than 200 patients, tested the genetic variant FGF23 associated with phosphate levels to identify any causal relationship with bone mineral density in children. The result was null.
Serum urate levels: Although genetic variation in five genes involved with uric acid excretion account for 3 percent to 4 percent of variance in serum urate levels, Mendelian randomization studies don’t point to a causal role for serum urate levels in hyperuricemia phenotypes, including poor kidney function, ischemic heart disease, diabetes, high blood pressure, high cholesterol, high bone mineral density, and high body mass index.
However, researchers said, reverse causality studies identify a causal effect of body fat measurements on urate levels or triglyceride levels. Among 26 serum-urate modifying genetic variants, only four revealed weak associations with blood pressure.
Additionally, a study into five urate-associated variants identified a positive serum urate level-kidney function relationship.
Rheumatoid Arthritis and Cardiovascular Disease: Rheumatoid arthritis is associated with a higher cardiovascular disease risk, and LDL cholesterol-associated genetic variants could help determine which drives the other. Mendelian randomization could also inform the paradoxical relationship between low body mass index and high mortality with rheumatoid arthritis.
Gout and Other Metabolic Diseases: Any causal relationships between gout and comorbidities are unknown. According to researchers, Mendelian randomization studies could be designed to focus on the disease’s inflammatory aspects to reveal existing links.
IL-6 Pathways and Rheumatoid Arthritis: Rheumatoid arthritis is characterized by high interleukin-6 levels with interleukin-6 inhibitors treating established cases. Mendelian randomization cardiovascular studies suggest interleukin-6 receptor inhibition is associated with cardiovascular-disease prevalence. Mendelian randomization can also address whether interleukin-6 or interleukin-6 receptor pathways contribute to cardiovascular disease development in rheumatoid arthritis patients.
Urate Levels and Neurological Disease: Research shows urate levels protect against neurodegenerative condition development, including Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis. Using Mendelian randomization to determine whether this relationship is causal could play into how aggressively providers approach reducing urate in gout.
Alcohol Intake and Rheumatoid Arthritis: Large, existing epidemiological studies suggest moderate alcohol intake reduces rheumatoid arthritis risk. Since alcohol dependence carries a substantial genetic component – approximately 30 percent heritability based on analyzed single-nucleotide polymorphism – Mendelian randomization could further investigate if alcohol intake influences rheumatoid arthritis susceptibility.
Urate Levels and Cancer: The potential urate level and cancer risk link has been well reported and is assumed to be the result of urate’s oxidative intracellular action. However, some studies find those resuls inconclusive. It’s possible the serum urate level effect on cancer risk could be location and malignancy-type dependent.
Overall, researchers said, the urate, gout, and cancer association is complex. Existing studies found higher cancer rates in patients with gout versus those without the condition. Others found no association.
Limitations
Mendelian randomization isn’t a silver bullet for solving all observational-study problems, though. It’s difficult to verify the technique’s underlying assumptions aren’t being violated. And, using genetic risk scores based on multiple variants increases analysis power, but using individual variants provides for easier interpretations of biological function.
Additionally, genetic variants are mostly pulled from genome-wide association studies conducted on middle-aged and older adults. Consequently, any detected effects could arise from years of cumulative environmental exposures. As a result, investigators recommended returning to Mendelian randomization’s origins where any exposure effect on outcomes would be tested with linear or logistic regression only.
“This proposal also contains the suggestion,” researchers wrote, “that Mendelian randomization is particularly valuable in establishing null results in a large, well-powered sample sets with an established association between genetic variant and exposure but no association between genetic variant and outcomes, supporting the conclusion that little or no effect of exposure on outcome exists.”
To read the article at its original location: http://www.rheumatologynetwork.com/rheumatoid-arthritis/assessing-risk-factors-disease-outcomes
Breaking Down Quality Indicators in Post-Op Rehab and PT
Published on the Aug. 15, 2016, Rheumatology Network website
By Whitney L.J. Howell
The Most Common Reasons Driving Readmissions in TJA
Published on the July 27, 2016, Rheumatology Network website
By Whitney L.J. Howell
In today’s healthcare environment, hospital readmission rates are garnering an increasing amount of attention as the industry moves toward bundled payments, making it harder for providers to recoup reimbursement. This could present significant problems for orthopedic surgeons who perform total joint arthroplasties — one of the most commonly performed orthopedic procedures.
But, until now, there’s been no benchmark for what an acceptable rate should be for these procedures. The general belief, though, is lower readmission rates can improve care standards and lower costs. To answer the question about what acceptable readmission rates are for total joint arthroplasties (TJA), Prem N. Ramkumar, M.D., a resident physician of orthopedic surgery at the Cleveland Clinic, led a systemic review and meta-analysis of existing studies, looking for the average 30-day and 90-day readmission rates. The review was published in the September 2015 issue of the American Journal of Orthopedics.
By analyzing 12 total hip arthroplasty and 10 total knee arthroplasty studies, the team reviewed readmission rates for nearly 4 million patients for both time intervals. According to results, the gold standard for hip readmissions was 5.6 percent of the 30-day population and 7.7 percent of the 90-day group. Of the knee readmissions, the benchmark was 3.3 percent of 30-day readmissions and 9.7 percent of 90-day patients.
The cost of these readmissions is already an issue, Dr. Ramkumar said, but the Medicare Access & CHIP Reauthorization Act of 2015 (MACRA) is ramping up and will push more and more providers into merit-based incentive payment systems. To better understand why these readmission rates are important and what you can do to improve your outcomes, Rheumatology Network spoke with Dr. Ramkumar about his study results and what they mean in the MACRA environment.
Rheumatology Network: Why did you decide to look into unplanned readmissions for total joint arthroplasty?
Dr. Ramkumar: Mainly, it was a timeliness issue. With the way reimbursement is being changed for the orthopedic surgeon, I think outcomes were being held against things we usually didn’t measure in the past. Before, how a physician would say whether an outcome was good was essentially based on what the surgeon said. Sometimes, the patient may or may not have agreed, but now there are other eyes on patient care. Now, the doctor-patient relationship isn’t just between those two. For me, it’s really being part of a larger team of players in the hospital and the belief that the readmission rates were timely because it’s one of the few metrics surgeons are being evaluated against.
Why Readmission Rates Matter
RN: Why does it matter?
Dr. Ramkumar: Having this data matters because it’s a benchmark for what our current state is. It’s hard to know how to improve when you don’t have anything to compare yourself to. I felt that our study helped established our benchmark for what we can improve upon. The goal of our study was to establish a benchmark for joint replacement – one of the most heavily utilized surgical procedures.
RN: What are the most important parts of your results? What are their impacts?
Dr. Ramkumar: The most important part was the readmission rate we found for 30 and 90 days, and the impact was establishing this as the gold standard. I think it’s something that our hospital – or even my personal record as a surgeon – should be able to do. That’s the only way of establishing progress. Secondly, it’s important to know what the actual cases behind the readmissions were for someone who had knee or hip replacement surgery. Perhaps the surgeon will pay even more attention to closures because superficial and deep, soft tissue infections are disasters for the patients. But, it’s not hard for the surgeon to re-evaluate and re-assess how they do their own infection protocols and inter-operative handiwork.
RN: What challenges were revealed for orthopedic surgeons?
Dr. Ramkumar: Joint replacement is a tough task. There are increasing pressures to churn out more procedures, and often there’s a temptation to go with what works. Some surgeons try to get everything perfect, but others know the pursuit of perfection may or may not affect the clinical outcomes.
And, the surgeon’s idea of perfection may not be the patient’s idea of it. Surgeons should re-evaluate how patients feel with the joint daily and ensure, mechanically, the joint is stable whether they’re seeing the patient before surgery, doing the procedure or providing post-operative communication. Surgeons aren’t just technicians. They’re involved in every step. It’s a tough burden, but it’s definitely something the study forces us to critically evaluate.
RN: How does this research fit in with MACRA?
Dr. Ramkumar: We have to figure out the exact way to evaluate outcomes. A huge problem is, oftentimes, we expect surgeons to be 100 percent in control of outcomes. So many things go into a patient’s success that are completely left out of the equation from the reimbursement standpoint. A host of factors remain. Patients are different – their anatomy, responses to inter-operative trauma, or abilities with rehabilitation and recovery.
Surgery isn’t a question of whether the surgeon can or should be doing 100 percent of work. A lot depends on the patients’ effort and their intrinsic ability to recover. In terms of MACRA, the program is trying extremely hard, with understandable reasons, to try to control the controllable errors or problems. But, there has to be a level of expectation and understanding that readmission rates can’t reach zero percent because there are patients — who are either sick or otherwise healthy — who don’t handle surgery well. It’s not always the surgeon’s fault, but the surgeon is getting dinged for bad outcomes.
This all leaves the surgeon thinking about consequences and patient selection at the beginning of the cycle. If cutting reimbursement is based on outcomes, well-meaning physicians who put their personal financial resources and labor into becoming a surgeon now have to turn away needy patients. That’s tough for the surgeon and for the patient. From that perspective, I’m sure we’re going to see more patient selectivity from surgeons.
RN: How can your work be used to promote better and improved outcomes?
Dr. Ramkumar: It’s going to end up being a surgeon keeping a score card of their or their department’s readmission rates. That will be compared to the rates we’ve published in the paper. Surgeons looking to control readmission rates can consider patient selection or they can improve post-operative management and instruction for patients. In addition, they can increase their attention toward wound closure — but not that they aren’t paying great attention already because that’s their craft, but they can be on the look-out for the best types of materials and dressings that will allow closures to not ooze or result in possible readmissions.
To read the article at its original location: http://www.rheumatologynetwork.com/news/most-common-reasons-driving-readmissions-tja/page/0/2
Radiology’s Role in Determining Medical Necessity
Published on the July 28, 2016, DiagnosticImaging.com website
By Whitney L.J. Howell
Recently, a New Jersey court handed down a decision that could potential change the role radiologists play when it comes to determining the medical necessity of a study ordered by a referring physician.
Although the current ruling only applies to New Jersey radiologists, industry experts are talking about how it could possibly affect your responsibilities, daily work flow, and liabilities.
The Case
Allstate Insurance brought suit against radiologists who conducted MRIs and X-rays on patients who had submitted personal injury claims. The company argued the providers had not completed their due diligence in checking into whether these studies were warranted, suing to recoup $200,000 of expenditures.
Company lawyers asserted the radiologists were the imaging center’s medical directors and, therefore, bore the responsibility of verifying medical necessity. The radiologists countered that the chiropractors and other referring physicians who send them patients satisfy the state’s requirement of being “verified” providers. But, the judge ultimately ruled the onus of ensuring proper clinical evidence exists to support medical necessity and appropriateness lies with the radiologist.
According to Greg Nicola, MD, treasurer of the Radiological Society of New Jersey, the organization is filing an appeal of the ruling. The American College of Radiology (ACR) also considers the case to be unique – one that will likely only bind New Jersey radiologists, said Tom Hoffman, JD, the ACR’s associate general counsel.
“The lesson remains to realize that the radiologists aren’t in the driver’s seat about medical necessity decisions because they don’t interact daily with the patient,” Hoffman said. “They’re hard pressed to have all the sufficient clinical background on a patient.”
To read the remainder of the article at its original location: http://www.diagnosticimaging.com/practice-management/radiology-role-determining-medical-necessity
Who am I?
I’m a seasoned reporter, writer, freelancer and public relations specialist with a master’s degree in international print journalism from The American University in Washington, D.C.
I launched my journalism career as a stringer for UPI on Sept. 11, 2001, on Capitol Hill. That day led to a two-year stint as a daily political reporter in Montgomery County, Md. As a staff writer for the Association of American Medical Colleges, a public relations specialist for the Duke University Medical Center and the public relations director for the UNC-Chapel Hill School of Nursing, I’ve earned in-depth experience in covering health care, including academic medicine, health care reform, women’s health, pediatrics, radiology, and Medicare.
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