A small study of discussions between clinicians and patients about lung cancer screening with low-dose computed tomography has highlighted a lack of shared decision making and information about potential harms.

“Our findings are consistent with increasingly robust evidence that patients, members of the public, and clinicians tend to overestimate the benefits and underestimate the harms of medical interventions, including treatments, tests, or screening tests,” wrote Alison T. Brenner, PhD, and her colleagues at the University of North Carolina at Chapel Hill, in a presentation of the findings in JAMA Internal Medicine.

The researchers transcribed conversations between 14 patients – who were eligible for lung cancer screening because of their age – and their primary care or pulmonary care physicians. They found that not one physician adequately explained false positives or their consequences, such as the possibility of additional imaging and invasive diagnostic procedures, nor did any discuss the potential for diagnosis and treatment of cancer that would not have affected the individual during his or her lifetime (overdiagnosis).

Researchers used a 12-item scoring system for physician behaviors, with 0-4 points allocated to each item. The items included telling patients there was more than one way to deal with the identified problem, explaining the pros and cons of the available options, exploring patients’ fears and concerns, and offering the patient clear opportunities to ask questions.

Mean scores for each item ranged from 0 to 0.79. Two conversations met the baseline skill criteria – a score of two points – for one item each, two other conversations met the baseline skill criteria for two items. But for 8 of the 12 items, not one conversation achieved even a baseline skill score. The mean total visit length was 13:07 minutes, and the mean time spent discussing LCS was 0:59 minute (range, 0:16-2:19 minutes).

“Although experts disagree on how well the existing evidence suggests an overall net benefit of LCS [lung cancer screening], consensus has emerged on the importance of shared decision making,” wrote the investigators. Current U.S. Preventive Services Task Force recommendations stress that lung cancer screening should not occur without a shared decision-making process, including a thorough discussion of benefits and harms.

The authors said that, while their study was small, it did raise concerns that shared decision making in practice is a long way from what is recommended by the guidelines.

“The fact that the main drivers of harms from LCS (false positives and their sequelae, as well as overdiagnosis) were not adequately explained by physicians is troubling,” they wrote. “However, these findings are consistent with other evidence that discussions between patients and physicians regarding preference-sensitive cancer screening decisions are imbalanced with respect to explaining the pros and cons.”

Based on these findings, the authors called for urgent discussions between clinical leaders, policy makers, and researchers about how to involve patients more meaningfully in discussions about lung cancer screening.

“Until more is known, we believe that guideline and policy makers should not assume that recommending SDM [shared decision-making] for cancer-screening decisions with a ‘tenuous balance of benefits and harms,’ like LCS, will protect patients who would value avoiding screening harms.”

The study was supported by the North Carolina Translational and Clinical Sciences Institute and the National Cancer Institute. No conflicts of interest were declared.

SOURCE: Brenner A et al. JAMA Intern Med. 2018; Aug 13. doi: 10.1001/jamainternmed.2018.3054.

A small study of discussions between clinicians and patients about lung cancer screening with low-dose computed tomography has highlighted a lack of shared decision making and information about potential harms.

“Our findings are consistent with increasingly robust evidence that patients, members of the public, and clinicians tend to overestimate the benefits and underestimate the harms of medical interventions, including treatments, tests, or screening tests,” wrote Alison T. Brenner, PhD, and her colleagues at the University of North Carolina at Chapel Hill, in a presentation of the findings in JAMA Internal Medicine.

The researchers transcribed conversations between 14 patients – who were eligible for lung cancer screening because of their age – and their primary care or pulmonary care physicians. They found that not one physician adequately explained false positives or their consequences, such as the possibility of additional imaging and invasive diagnostic procedures, nor did any discuss the potential for diagnosis and treatment of cancer that would not have affected the individual during his or her lifetime (overdiagnosis).

Researchers used a 12-item scoring system for physician behaviors, with 0-4 points allocated to each item. The items included telling patients there was more than one way to deal with the identified problem, explaining the pros and cons of the available options, exploring patients’ fears and concerns, and offering the patient clear opportunities to ask questions.

Mean scores for each item ranged from 0 to 0.79. Two conversations met the baseline skill criteria – a score of two points – for one item each, two other conversations met the baseline skill criteria for two items. But for 8 of the 12 items, not one conversation achieved even a baseline skill score. The mean total visit length was 13:07 minutes, and the mean time spent discussing LCS was 0:59 minute (range, 0:16-2:19 minutes).

“Although experts disagree on how well the existing evidence suggests an overall net benefit of LCS [lung cancer screening], consensus has emerged on the importance of shared decision making,” wrote the investigators. Current U.S. Preventive Services Task Force recommendations stress that lung cancer screening should not occur without a shared decision-making process, including a thorough discussion of benefits and harms.

The authors said that, while their study was small, it did raise concerns that shared decision making in practice is a long way from what is recommended by the guidelines.

“The fact that the main drivers of harms from LCS (false positives and their sequelae, as well as overdiagnosis) were not adequately explained by physicians is troubling,” they wrote. “However, these findings are consistent with other evidence that discussions between patients and physicians regarding preference-sensitive cancer screening decisions are imbalanced with respect to explaining the pros and cons.”

Based on these findings, the authors called for urgent discussions between clinical leaders, policy makers, and researchers about how to involve patients more meaningfully in discussions about lung cancer screening.

“Until more is known, we believe that guideline and policy makers should not assume that recommending SDM [shared decision-making] for cancer-screening decisions with a ‘tenuous balance of benefits and harms,’ like LCS, will protect patients who would value avoiding screening harms.”

The study was supported by the North Carolina Translational and Clinical Sciences Institute and the National Cancer Institute. No conflicts of interest were declared.

SOURCE: Brenner A et al. JAMA Intern Med. 2018; Aug 13. doi: 10.1001/jamainternmed.2018.3054.

A small study of discussions between clinicians and patients about lung cancer screening with low-dose computed tomography has highlighted a lack of shared decision making and information about potential harms.

“Our findings are consistent with increasingly robust evidence that patients, members of the public, and clinicians tend to overestimate the benefits and underestimate the harms of medical interventions, including treatments, tests, or screening tests,” wrote Alison T. Brenner, PhD, and her colleagues at the University of North Carolina at Chapel Hill, in a presentation of the findings in JAMA Internal Medicine.

The researchers transcribed conversations between 14 patients – who were eligible for lung cancer screening because of their age – and their primary care or pulmonary care physicians. They found that not one physician adequately explained false positives or their consequences, such as the possibility of additional imaging and invasive diagnostic procedures, nor did any discuss the potential for diagnosis and treatment of cancer that would not have affected the individual during his or her lifetime (overdiagnosis).

Researchers used a 12-item scoring system for physician behaviors, with 0-4 points allocated to each item. The items included telling patients there was more than one way to deal with the identified problem, explaining the pros and cons of the available options, exploring patients’ fears and concerns, and offering the patient clear opportunities to ask questions.

Mean scores for each item ranged from 0 to 0.79. Two conversations met the baseline skill criteria – a score of two points – for one item each, two other conversations met the baseline skill criteria for two items. But for 8 of the 12 items, not one conversation achieved even a baseline skill score. The mean total visit length was 13:07 minutes, and the mean time spent discussing LCS was 0:59 minute (range, 0:16-2:19 minutes).

“Although experts disagree on how well the existing evidence suggests an overall net benefit of LCS [lung cancer screening], consensus has emerged on the importance of shared decision making,” wrote the investigators. Current U.S. Preventive Services Task Force recommendations stress that lung cancer screening should not occur without a shared decision-making process, including a thorough discussion of benefits and harms.

The authors said that, while their study was small, it did raise concerns that shared decision making in practice is a long way from what is recommended by the guidelines.

“The fact that the main drivers of harms from LCS (false positives and their sequelae, as well as overdiagnosis) were not adequately explained by physicians is troubling,” they wrote. “However, these findings are consistent with other evidence that discussions between patients and physicians regarding preference-sensitive cancer screening decisions are imbalanced with respect to explaining the pros and cons.”

Based on these findings, the authors called for urgent discussions between clinical leaders, policy makers, and researchers about how to involve patients more meaningfully in discussions about lung cancer screening.

“Until more is known, we believe that guideline and policy makers should not assume that recommending SDM [shared decision-making] for cancer-screening decisions with a ‘tenuous balance of benefits and harms,’ like LCS, will protect patients who would value avoiding screening harms.”

The study was supported by the North Carolina Translational and Clinical Sciences Institute and the National Cancer Institute. No conflicts of interest were declared.

SOURCE: Brenner A et al. JAMA Intern Med. 2018; Aug 13. doi: 10.1001/jamainternmed.2018.3054.

A retrospective cohort study in more than 80,000 children has found no evidence of an increased risk of autism spectrum disorder associated with prenatal tetanus, diphtheria, and acellular pertussis (Tdap) immunization.

Piotr Marcinski/Thinkstock

Of 81,993 children born between 2011 and 2014, 1,341 children (1.6%) were diagnosed with autism spectrum disorder. The incidence of autism spectrum disorder was 3.78 per 1,000 person-years in the Tdap-vaccinated group, and 4.05 per 1,000 person years in the unvaccinated group, representing an unadjusted hazard ratio of 0.98 and an adjusted hazard ratio of 0.85. This was consistent across all the birth cohorts.

Prenatal immunization rates with the prenatal Tdap vaccine ranged from 26% of the 2012 birth cohort to 79% of the 2014 birth cohort, and mean gestational age at vaccination was 28 weeks.

Tracy A. Becerra-Culqui, PhD, MPH, and colleagues of the department of research and evaluation at Kaiser Permanente Southern California, Pasadena, said this was the first study to look at the risk of autism spectrum disorder after maternal exposure to the Tdap vaccine, to their knowledge. “Our results potentially indicate that the maternal Tdap vaccine affects immune trajectories protecting infants against infections that would otherwise lead to neurodevelopmental alterations.”

They highlighted several strengths of their study. One was that maternal Tdap vaccination and information on autism spectrum disorder both were derived from EHRs and therefore not subject to recall bias. The study, published online in Pediatrics, also included children diagnosed with autism spectrum disorder from age 1 year onwards, reflecting the latest evidence on screening and diagnosis of autism.

“Our weighting procedures enabled us to balance the Tdap-exposed and -unexposed groups to compare two populations that were comparable in important measured confounding factors,” Dr. Becerra-Culqui and associates noted.

The investigators found that women who received the Tdap vaccine during pregnancy were more likely to be Asian American or Pacific Islander, to have a bachelor’s degree or higher, be nulliparous, to have also been vaccinated prenatally against influenza, and to deliver at term, compared with unvaccinated women.

However the authors did note that their follow-up was limited to 6.5 years for the earliest birth cohort, and 3.5 years for the latest cohort, so they may not have picked up children who received a later diagnosis of autism spectrum disorder.

The study was supported by Kaiser Permanente Southern California. Five authors declared funding from GlaxoSmithKline, Bayer AG, or the Centers for Disease Control and Prevention for unrelated or separate studies.

SOURCE: Becerra-Culqui T et al. Pediatrics. 2018;142(3):e20180120.

A retrospective cohort study in more than 80,000 children has found no evidence of an increased risk of autism spectrum disorder associated with prenatal tetanus, diphtheria, and acellular pertussis (Tdap) immunization.

Piotr Marcinski/Thinkstock

Of 81,993 children born between 2011 and 2014, 1,341 children (1.6%) were diagnosed with autism spectrum disorder. The incidence of autism spectrum disorder was 3.78 per 1,000 person-years in the Tdap-vaccinated group, and 4.05 per 1,000 person years in the unvaccinated group, representing an unadjusted hazard ratio of 0.98 and an adjusted hazard ratio of 0.85. This was consistent across all the birth cohorts.

Prenatal immunization rates with the prenatal Tdap vaccine ranged from 26% of the 2012 birth cohort to 79% of the 2014 birth cohort, and mean gestational age at vaccination was 28 weeks.

Tracy A. Becerra-Culqui, PhD, MPH, and colleagues of the department of research and evaluation at Kaiser Permanente Southern California, Pasadena, said this was the first study to look at the risk of autism spectrum disorder after maternal exposure to the Tdap vaccine, to their knowledge. “Our results potentially indicate that the maternal Tdap vaccine affects immune trajectories protecting infants against infections that would otherwise lead to neurodevelopmental alterations.”

They highlighted several strengths of their study. One was that maternal Tdap vaccination and information on autism spectrum disorder both were derived from EHRs and therefore not subject to recall bias. The study, published online in Pediatrics, also included children diagnosed with autism spectrum disorder from age 1 year onwards, reflecting the latest evidence on screening and diagnosis of autism.

“Our weighting procedures enabled us to balance the Tdap-exposed and -unexposed groups to compare two populations that were comparable in important measured confounding factors,” Dr. Becerra-Culqui and associates noted.

The investigators found that women who received the Tdap vaccine during pregnancy were more likely to be Asian American or Pacific Islander, to have a bachelor’s degree or higher, be nulliparous, to have also been vaccinated prenatally against influenza, and to deliver at term, compared with unvaccinated women.

However the authors did note that their follow-up was limited to 6.5 years for the earliest birth cohort, and 3.5 years for the latest cohort, so they may not have picked up children who received a later diagnosis of autism spectrum disorder.

The study was supported by Kaiser Permanente Southern California. Five authors declared funding from GlaxoSmithKline, Bayer AG, or the Centers for Disease Control and Prevention for unrelated or separate studies.

SOURCE: Becerra-Culqui T et al. Pediatrics. 2018;142(3):e20180120.

A retrospective cohort study in more than 80,000 children has found no evidence of an increased risk of autism spectrum disorder associated with prenatal tetanus, diphtheria, and acellular pertussis (Tdap) immunization.

Piotr Marcinski/Thinkstock

Of 81,993 children born between 2011 and 2014, 1,341 children (1.6%) were diagnosed with autism spectrum disorder. The incidence of autism spectrum disorder was 3.78 per 1,000 person-years in the Tdap-vaccinated group, and 4.05 per 1,000 person years in the unvaccinated group, representing an unadjusted hazard ratio of 0.98 and an adjusted hazard ratio of 0.85. This was consistent across all the birth cohorts.

Prenatal immunization rates with the prenatal Tdap vaccine ranged from 26% of the 2012 birth cohort to 79% of the 2014 birth cohort, and mean gestational age at vaccination was 28 weeks.

Tracy A. Becerra-Culqui, PhD, MPH, and colleagues of the department of research and evaluation at Kaiser Permanente Southern California, Pasadena, said this was the first study to look at the risk of autism spectrum disorder after maternal exposure to the Tdap vaccine, to their knowledge. “Our results potentially indicate that the maternal Tdap vaccine affects immune trajectories protecting infants against infections that would otherwise lead to neurodevelopmental alterations.”

They highlighted several strengths of their study. One was that maternal Tdap vaccination and information on autism spectrum disorder both were derived from EHRs and therefore not subject to recall bias. The study, published online in Pediatrics, also included children diagnosed with autism spectrum disorder from age 1 year onwards, reflecting the latest evidence on screening and diagnosis of autism.

“Our weighting procedures enabled us to balance the Tdap-exposed and -unexposed groups to compare two populations that were comparable in important measured confounding factors,” Dr. Becerra-Culqui and associates noted.

The investigators found that women who received the Tdap vaccine during pregnancy were more likely to be Asian American or Pacific Islander, to have a bachelor’s degree or higher, be nulliparous, to have also been vaccinated prenatally against influenza, and to deliver at term, compared with unvaccinated women.

However the authors did note that their follow-up was limited to 6.5 years for the earliest birth cohort, and 3.5 years for the latest cohort, so they may not have picked up children who received a later diagnosis of autism spectrum disorder.

The study was supported by Kaiser Permanente Southern California. Five authors declared funding from GlaxoSmithKline, Bayer AG, or the Centers for Disease Control and Prevention for unrelated or separate studies.

SOURCE: Becerra-Culqui T et al. Pediatrics. 2018;142(3):e20180120.

A diverse diet is not necessarily a healthy one, according to an advisory issued by the American Heart Association that has instead emphasized the importance of a healthy eating pattern.

Published in the Aug. 9 online edition of Circulation, the science advisory was prompted by emerging evidence that greater dietary diversity may actually be associated with eating more poor quality foods and higher energy intake, especially among middle-aged adults.

Researchers conducted a literature search across 2000-2017 for studies of dietary diversity – defined as the number of different foods or food groups eaten over a given period of time – and dietary quality.

They found that observational evidence does not support the idea that a more diverse diet is associated with healthy weight or an optimal eating pattern. However, they also noted that many studies had significant limitations that contributed to high levels of inconsistency across all studies.

For example, one study in overweight and obese individuals found increasing dietary diversity was associated with a decrease in body mass index but with respect to intakes of only low–energy dense foods. Another study in Chinese adults saw an increase in diversity in the intake of snacks but not grains, vegetables, fruits, meats, or beverages, and this was associated with a 45% greater odds of being overweight, compared with individuals with a lower diversity of snack consumption.

Similarly, an observational study in 2,505 U.S. adults found individuals in the highest quintile of dietary diversity had a 120% greater gain in waist circumference, compared with those in the lowest quintile.

“Associations with dissimilarity scores are consistent with evidence from feeding studies showing that exposure to foods with different characteristics led to increased energy intake, which may partially explain gain in waist circumference over time,” wrote Marcia C. de Oliveira Otto, PhD, from the University of Texas Health Science Centre at Houston and coauthors.

The same was seen in short-term interventional studies, where most showed that having access to a wider variety of foods actually led to an increase in intake, compared with being served only a single food.

For example, one study showed adults offered a second course of sandwiches with different fillings to the first course actually ate 30% more than those served the same option for both courses.

Another study randomized overweight and obese adults to an unlimited number of snack options consumed less than once a day, or any amount of one favored snack option, with all snacks being within a daily caloric goal. This study found that, over the course of 8 weeks, participants offered a variety of snacks ate 25% more servings than those with the one snack type.

The authors suggested that variety amplifies sensory stimulation and decreases satiety.

“Although calorie restriction goals were achieved in both groups, a significant increase in sensory-specific satiety and monotony ratings over time was observed in participants assigned to the one-snack option but not in participants assigned to a variety of snacks,” they wrote.

The relationship between dietary diversity and dietary quality is also complex. Investigators for a cross-sectional study in China found less-than-optimal consumption of the nine food groups in the Chinese dietary guidelines – in particular, fruits, vegetables, fish, and dairy – in diets with higher diversity scores.

“Overall, limited evidence shows no benefit to diet quality or diet healthfulness associated with increased food count or with a more even distribution of energy across foods, whereas findings from one observational study suggest that greater dissimilarity in foods consumed may be inversely associated with a healthy eating pattern.”

In conclusion, the advisory committee said that it was more appropriate to promote a healthy eating pattern, emphasizing intake of plant foods, protein sources, low-fat dairy, vegetable oils, and nuts.

One author declared research funding from the Hass Avocado Board. No other relevant conflicts of interest were declared.

SOURCE: de Oliveira Otto MC et al. Circulation. 2018 Aug. 9. doi: 10.1161/CIR.0000000000000595.

A diverse diet is not necessarily a healthy one, according to an advisory issued by the American Heart Association that has instead emphasized the importance of a healthy eating pattern.

Published in the Aug. 9 online edition of Circulation, the science advisory was prompted by emerging evidence that greater dietary diversity may actually be associated with eating more poor quality foods and higher energy intake, especially among middle-aged adults.

Researchers conducted a literature search across 2000-2017 for studies of dietary diversity – defined as the number of different foods or food groups eaten over a given period of time – and dietary quality.

They found that observational evidence does not support the idea that a more diverse diet is associated with healthy weight or an optimal eating pattern. However, they also noted that many studies had significant limitations that contributed to high levels of inconsistency across all studies.

For example, one study in overweight and obese individuals found increasing dietary diversity was associated with a decrease in body mass index but with respect to intakes of only low–energy dense foods. Another study in Chinese adults saw an increase in diversity in the intake of snacks but not grains, vegetables, fruits, meats, or beverages, and this was associated with a 45% greater odds of being overweight, compared with individuals with a lower diversity of snack consumption.

Similarly, an observational study in 2,505 U.S. adults found individuals in the highest quintile of dietary diversity had a 120% greater gain in waist circumference, compared with those in the lowest quintile.

“Associations with dissimilarity scores are consistent with evidence from feeding studies showing that exposure to foods with different characteristics led to increased energy intake, which may partially explain gain in waist circumference over time,” wrote Marcia C. de Oliveira Otto, PhD, from the University of Texas Health Science Centre at Houston and coauthors.

The same was seen in short-term interventional studies, where most showed that having access to a wider variety of foods actually led to an increase in intake, compared with being served only a single food.

For example, one study showed adults offered a second course of sandwiches with different fillings to the first course actually ate 30% more than those served the same option for both courses.

Another study randomized overweight and obese adults to an unlimited number of snack options consumed less than once a day, or any amount of one favored snack option, with all snacks being within a daily caloric goal. This study found that, over the course of 8 weeks, participants offered a variety of snacks ate 25% more servings than those with the one snack type.

The authors suggested that variety amplifies sensory stimulation and decreases satiety.

“Although calorie restriction goals were achieved in both groups, a significant increase in sensory-specific satiety and monotony ratings over time was observed in participants assigned to the one-snack option but not in participants assigned to a variety of snacks,” they wrote.

The relationship between dietary diversity and dietary quality is also complex. Investigators for a cross-sectional study in China found less-than-optimal consumption of the nine food groups in the Chinese dietary guidelines – in particular, fruits, vegetables, fish, and dairy – in diets with higher diversity scores.

“Overall, limited evidence shows no benefit to diet quality or diet healthfulness associated with increased food count or with a more even distribution of energy across foods, whereas findings from one observational study suggest that greater dissimilarity in foods consumed may be inversely associated with a healthy eating pattern.”

In conclusion, the advisory committee said that it was more appropriate to promote a healthy eating pattern, emphasizing intake of plant foods, protein sources, low-fat dairy, vegetable oils, and nuts.

One author declared research funding from the Hass Avocado Board. No other relevant conflicts of interest were declared.

SOURCE: de Oliveira Otto MC et al. Circulation. 2018 Aug. 9. doi: 10.1161/CIR.0000000000000595.

A diverse diet is not necessarily a healthy one, according to an advisory issued by the American Heart Association that has instead emphasized the importance of a healthy eating pattern.

Published in the Aug. 9 online edition of Circulation, the science advisory was prompted by emerging evidence that greater dietary diversity may actually be associated with eating more poor quality foods and higher energy intake, especially among middle-aged adults.

Researchers conducted a literature search across 2000-2017 for studies of dietary diversity – defined as the number of different foods or food groups eaten over a given period of time – and dietary quality.

They found that observational evidence does not support the idea that a more diverse diet is associated with healthy weight or an optimal eating pattern. However, they also noted that many studies had significant limitations that contributed to high levels of inconsistency across all studies.

For example, one study in overweight and obese individuals found increasing dietary diversity was associated with a decrease in body mass index but with respect to intakes of only low–energy dense foods. Another study in Chinese adults saw an increase in diversity in the intake of snacks but not grains, vegetables, fruits, meats, or beverages, and this was associated with a 45% greater odds of being overweight, compared with individuals with a lower diversity of snack consumption.

Similarly, an observational study in 2,505 U.S. adults found individuals in the highest quintile of dietary diversity had a 120% greater gain in waist circumference, compared with those in the lowest quintile.

“Associations with dissimilarity scores are consistent with evidence from feeding studies showing that exposure to foods with different characteristics led to increased energy intake, which may partially explain gain in waist circumference over time,” wrote Marcia C. de Oliveira Otto, PhD, from the University of Texas Health Science Centre at Houston and coauthors.

The same was seen in short-term interventional studies, where most showed that having access to a wider variety of foods actually led to an increase in intake, compared with being served only a single food.

For example, one study showed adults offered a second course of sandwiches with different fillings to the first course actually ate 30% more than those served the same option for both courses.

Another study randomized overweight and obese adults to an unlimited number of snack options consumed less than once a day, or any amount of one favored snack option, with all snacks being within a daily caloric goal. This study found that, over the course of 8 weeks, participants offered a variety of snacks ate 25% more servings than those with the one snack type.

The authors suggested that variety amplifies sensory stimulation and decreases satiety.

“Although calorie restriction goals were achieved in both groups, a significant increase in sensory-specific satiety and monotony ratings over time was observed in participants assigned to the one-snack option but not in participants assigned to a variety of snacks,” they wrote.

The relationship between dietary diversity and dietary quality is also complex. Investigators for a cross-sectional study in China found less-than-optimal consumption of the nine food groups in the Chinese dietary guidelines – in particular, fruits, vegetables, fish, and dairy – in diets with higher diversity scores.

“Overall, limited evidence shows no benefit to diet quality or diet healthfulness associated with increased food count or with a more even distribution of energy across foods, whereas findings from one observational study suggest that greater dissimilarity in foods consumed may be inversely associated with a healthy eating pattern.”

In conclusion, the advisory committee said that it was more appropriate to promote a healthy eating pattern, emphasizing intake of plant foods, protein sources, low-fat dairy, vegetable oils, and nuts.

One author declared research funding from the Hass Avocado Board. No other relevant conflicts of interest were declared.

SOURCE: de Oliveira Otto MC et al. Circulation. 2018 Aug. 9. doi: 10.1161/CIR.0000000000000595.

John Lockwood Ochsner, MD, (1927-2018), a world-renowned heart surgeon, will be remembered as a charismatic and skilled surgeon, a dedicated teacher, a loving father, and a role model for the hundreds of surgeons he trained.

Dr. Ochsner was born in 1927 in Madison, Wisc., but was raised in New Orleans. and received his medical degree from Tulane University. He started his surgical residency at the University of Michigan but was drafted into military service during the Korean War. He then completed his residency at Baylor University and received his cardiac training under Michael DeBakey. MD,. Dr. DeBakey was a close family friend who had studied under John’s father at Tulane and had worked in the original Ochsner Clinic. John was very close to Dr. DeBakey, who was also John’s babysitter in early life.

Dr. John, as he was known, grew up in shadow of giants, including his father, Alton, who founded the Ochsner Clinic, and Michael DeBakey who was a protégé of Alton. As John was finishing his training with Dr. DeBakey he was asked to stay on in Houston as a member of Dr. DeBakey’s team. The Ochsner Clinic was expanding rapidly in New Orleans, however, and everyone was desirous of having John return. John initially planned to stay with Dr. DeBakey until the director of the Ochsner Clinic flew to Houston to meet with John to convince him to return to New Orleans. His argument was, “John, you will be a great surgeon wherever you practice, but there is only one hospital that has your name on the front of it!” John returned to the Ochsner Clinic in 1961, where he spent the next 57 years.

John Ochsner was revered as an innovative, energetic and talented surgeon, performing over 12,000 operations, including the first cardiac transplant in the Gulf South. He always said he was happiest in the operating room, and loved teaching young resident surgeons. He believed that “surgery is an art as much as a science. ... You have to improvise almost every case -- no two cases are the same - and that’s where the fun of surgery comes in, making something new that particular moment that you’ve never seen before. ... It’s like opening up a package; it’s always a little different.”

He authored more than 300 peer-reviewed publications and gave innumerable scientific lectures around the world. He served as President of the International Society for Cardiovascular Surgery as well as the American Association for Thoracic Surgery. Over his career, he was elected president of more than 10 medical associations.

John, like his father, was active in many aspects of New Orleans life. He was an avid golfer and tennis player, and was always ready with a joke. He lived life with humor and enthusiasm, and was a member of multiple social clubs, developing lifelong friends from around the world. He was particularly thrilled when he was chosen as Rex, King of Carnival, in 1990, following in the royal footsteps of his father, who was King of Rex in 1948. Both of his granddaughters were presented as Maids of the Rex organization.

John is survived by his wife of over 64 years, Mary Lou Ochsner; a sister, Isabel Mann: two sons, Dr. John Ochsner, Jr., and Frank Ochsner, and two daughters, Joby Ochsner and Dr. Katherine Isabel Ochsner; he has two grandchildren.

 Larry H. Hollier, MD, Professor of Surgery, Chancellor, Louisiana State University Health Science Center at New Orleans

John Lockwood Ochsner, MD, (1927-2018), a world-renowned heart surgeon, will be remembered as a charismatic and skilled surgeon, a dedicated teacher, a loving father, and a role model for the hundreds of surgeons he trained.

Dr. Ochsner was born in 1927 in Madison, Wisc., but was raised in New Orleans. and received his medical degree from Tulane University. He started his surgical residency at the University of Michigan but was drafted into military service during the Korean War. He then completed his residency at Baylor University and received his cardiac training under Michael DeBakey. MD,. Dr. DeBakey was a close family friend who had studied under John’s father at Tulane and had worked in the original Ochsner Clinic. John was very close to Dr. DeBakey, who was also John’s babysitter in early life.

Dr. John, as he was known, grew up in shadow of giants, including his father, Alton, who founded the Ochsner Clinic, and Michael DeBakey who was a protégé of Alton. As John was finishing his training with Dr. DeBakey he was asked to stay on in Houston as a member of Dr. DeBakey’s team. The Ochsner Clinic was expanding rapidly in New Orleans, however, and everyone was desirous of having John return. John initially planned to stay with Dr. DeBakey until the director of the Ochsner Clinic flew to Houston to meet with John to convince him to return to New Orleans. His argument was, “John, you will be a great surgeon wherever you practice, but there is only one hospital that has your name on the front of it!” John returned to the Ochsner Clinic in 1961, where he spent the next 57 years.

John Ochsner was revered as an innovative, energetic and talented surgeon, performing over 12,000 operations, including the first cardiac transplant in the Gulf South. He always said he was happiest in the operating room, and loved teaching young resident surgeons. He believed that “surgery is an art as much as a science. ... You have to improvise almost every case -- no two cases are the same - and that’s where the fun of surgery comes in, making something new that particular moment that you’ve never seen before. ... It’s like opening up a package; it’s always a little different.”

He authored more than 300 peer-reviewed publications and gave innumerable scientific lectures around the world. He served as President of the International Society for Cardiovascular Surgery as well as the American Association for Thoracic Surgery. Over his career, he was elected president of more than 10 medical associations.

John, like his father, was active in many aspects of New Orleans life. He was an avid golfer and tennis player, and was always ready with a joke. He lived life with humor and enthusiasm, and was a member of multiple social clubs, developing lifelong friends from around the world. He was particularly thrilled when he was chosen as Rex, King of Carnival, in 1990, following in the royal footsteps of his father, who was King of Rex in 1948. Both of his granddaughters were presented as Maids of the Rex organization.

John is survived by his wife of over 64 years, Mary Lou Ochsner; a sister, Isabel Mann: two sons, Dr. John Ochsner, Jr., and Frank Ochsner, and two daughters, Joby Ochsner and Dr. Katherine Isabel Ochsner; he has two grandchildren.

 Larry H. Hollier, MD, Professor of Surgery, Chancellor, Louisiana State University Health Science Center at New Orleans

John Lockwood Ochsner, MD, (1927-2018), a world-renowned heart surgeon, will be remembered as a charismatic and skilled surgeon, a dedicated teacher, a loving father, and a role model for the hundreds of surgeons he trained.

Dr. Ochsner was born in 1927 in Madison, Wisc., but was raised in New Orleans. and received his medical degree from Tulane University. He started his surgical residency at the University of Michigan but was drafted into military service during the Korean War. He then completed his residency at Baylor University and received his cardiac training under Michael DeBakey. MD,. Dr. DeBakey was a close family friend who had studied under John’s father at Tulane and had worked in the original Ochsner Clinic. John was very close to Dr. DeBakey, who was also John’s babysitter in early life.

Dr. John, as he was known, grew up in shadow of giants, including his father, Alton, who founded the Ochsner Clinic, and Michael DeBakey who was a protégé of Alton. As John was finishing his training with Dr. DeBakey he was asked to stay on in Houston as a member of Dr. DeBakey’s team. The Ochsner Clinic was expanding rapidly in New Orleans, however, and everyone was desirous of having John return. John initially planned to stay with Dr. DeBakey until the director of the Ochsner Clinic flew to Houston to meet with John to convince him to return to New Orleans. His argument was, “John, you will be a great surgeon wherever you practice, but there is only one hospital that has your name on the front of it!” John returned to the Ochsner Clinic in 1961, where he spent the next 57 years.

John Ochsner was revered as an innovative, energetic and talented surgeon, performing over 12,000 operations, including the first cardiac transplant in the Gulf South. He always said he was happiest in the operating room, and loved teaching young resident surgeons. He believed that “surgery is an art as much as a science. ... You have to improvise almost every case -- no two cases are the same - and that’s where the fun of surgery comes in, making something new that particular moment that you’ve never seen before. ... It’s like opening up a package; it’s always a little different.”

He authored more than 300 peer-reviewed publications and gave innumerable scientific lectures around the world. He served as President of the International Society for Cardiovascular Surgery as well as the American Association for Thoracic Surgery. Over his career, he was elected president of more than 10 medical associations.

John, like his father, was active in many aspects of New Orleans life. He was an avid golfer and tennis player, and was always ready with a joke. He lived life with humor and enthusiasm, and was a member of multiple social clubs, developing lifelong friends from around the world. He was particularly thrilled when he was chosen as Rex, King of Carnival, in 1990, following in the royal footsteps of his father, who was King of Rex in 1948. Both of his granddaughters were presented as Maids of the Rex organization.

John is survived by his wife of over 64 years, Mary Lou Ochsner; a sister, Isabel Mann: two sons, Dr. John Ochsner, Jr., and Frank Ochsner, and two daughters, Joby Ochsner and Dr. Katherine Isabel Ochsner; he has two grandchildren.

 Larry H. Hollier, MD, Professor of Surgery, Chancellor, Louisiana State University Health Science Center at New Orleans

It is never easy to replace a legend. The Vascular Specialist that Russell Samson has left behind does not require saving. There are, however, problems ahead for all vascular surgeons, and my hope is to use this forum to unite us. Vascular surgery is a small specialty in an existential crisis. There are just over 3,000 of us in the United States. Think of Vascular Specialist as your hometown newspaper. Instead of high school sports and bake sales we will cover scientific meetings, clinical trials, and relevant legislation. And maybe the occasional swap meet.

Different points of view are going to be an essential part of this process. Russell Samson represented the posh, privileged world of private practice while I come from the rough and tumble streets of academia (just checking to see if he is still reading). My hope is to bring more. More Tips and Tricks, more Point/Counterpoint, more Letters to the Editor, more input from you.

How can you get involved? If you read something and have a response, send it to me. Volunteer to write up a technical tip or provide a medical debate. Have an idea for a guest editorial? Let me know, preferably before you write it. If it is good I will likely publish it. If not, well we can still be friends. Keep in mind, unlike book publishing, we work on strict deadlines. (To the three people I owe book chapters: Soon, I promise!) We will also be starting a vascular news section for brief committee updates, course registration openings, and relevant policy changes.

Vascular Specialist is now open for submissions. Contact us at [email protected].

It is never easy to replace a legend. The Vascular Specialist that Russell Samson has left behind does not require saving. There are, however, problems ahead for all vascular surgeons, and my hope is to use this forum to unite us. Vascular surgery is a small specialty in an existential crisis. There are just over 3,000 of us in the United States. Think of Vascular Specialist as your hometown newspaper. Instead of high school sports and bake sales we will cover scientific meetings, clinical trials, and relevant legislation. And maybe the occasional swap meet.

Different points of view are going to be an essential part of this process. Russell Samson represented the posh, privileged world of private practice while I come from the rough and tumble streets of academia (just checking to see if he is still reading). My hope is to bring more. More Tips and Tricks, more Point/Counterpoint, more Letters to the Editor, more input from you.

How can you get involved? If you read something and have a response, send it to me. Volunteer to write up a technical tip or provide a medical debate. Have an idea for a guest editorial? Let me know, preferably before you write it. If it is good I will likely publish it. If not, well we can still be friends. Keep in mind, unlike book publishing, we work on strict deadlines. (To the three people I owe book chapters: Soon, I promise!) We will also be starting a vascular news section for brief committee updates, course registration openings, and relevant policy changes.

Vascular Specialist is now open for submissions. Contact us at [email protected].

It is never easy to replace a legend. The Vascular Specialist that Russell Samson has left behind does not require saving. There are, however, problems ahead for all vascular surgeons, and my hope is to use this forum to unite us. Vascular surgery is a small specialty in an existential crisis. There are just over 3,000 of us in the United States. Think of Vascular Specialist as your hometown newspaper. Instead of high school sports and bake sales we will cover scientific meetings, clinical trials, and relevant legislation. And maybe the occasional swap meet.

Different points of view are going to be an essential part of this process. Russell Samson represented the posh, privileged world of private practice while I come from the rough and tumble streets of academia (just checking to see if he is still reading). My hope is to bring more. More Tips and Tricks, more Point/Counterpoint, more Letters to the Editor, more input from you.

How can you get involved? If you read something and have a response, send it to me. Volunteer to write up a technical tip or provide a medical debate. Have an idea for a guest editorial? Let me know, preferably before you write it. If it is good I will likely publish it. If not, well we can still be friends. Keep in mind, unlike book publishing, we work on strict deadlines. (To the three people I owe book chapters: Soon, I promise!) We will also be starting a vascular news section for brief committee updates, course registration openings, and relevant policy changes.

Vascular Specialist is now open for submissions. Contact us at [email protected].

With certification exams coming up, some surgeons may want to brush up.

The Vascular Educational Self-Assessment Program (VESAP), fourth edition, is a great study tool. As with previous editions, VESAP4 contains 10 topic sections, each with dozens of study and test questions, with 550 questions overall. VESAP4 offers both learning and testing modes, plus both Continuing Medical Education and Maintenance of Certification self-assessment credits. This edition also includes a mobile app (Apple products only) for off-line study. The program can be purchased as a comprehensive package or by individual modules. Package cost is $549 for members, $449 for candidates and $649 for non-members. Module pricing is $75, $65 and $85 per module, respectively.

With certification exams coming up, some surgeons may want to brush up.

The Vascular Educational Self-Assessment Program (VESAP), fourth edition, is a great study tool. As with previous editions, VESAP4 contains 10 topic sections, each with dozens of study and test questions, with 550 questions overall. VESAP4 offers both learning and testing modes, plus both Continuing Medical Education and Maintenance of Certification self-assessment credits. This edition also includes a mobile app (Apple products only) for off-line study. The program can be purchased as a comprehensive package or by individual modules. Package cost is $549 for members, $449 for candidates and $649 for non-members. Module pricing is $75, $65 and $85 per module, respectively.

With certification exams coming up, some surgeons may want to brush up.

The Vascular Educational Self-Assessment Program (VESAP), fourth edition, is a great study tool. As with previous editions, VESAP4 contains 10 topic sections, each with dozens of study and test questions, with 550 questions overall. VESAP4 offers both learning and testing modes, plus both Continuing Medical Education and Maintenance of Certification self-assessment credits. This edition also includes a mobile app (Apple products only) for off-line study. The program can be purchased as a comprehensive package or by individual modules. Package cost is $549 for members, $449 for candidates and $649 for non-members. Module pricing is $75, $65 and $85 per module, respectively.

Three generations of women in a family

A large study has revealed “the strongest evidence yet” supporting genetic susceptibility to myeloid malignancies, according to a researcher.

The study showed that first-degree relatives of patients with myeloid malignancies had double the risk of developing a myeloid malignancy themselves, when compared to the general population.

The researchers observed significant risks for developing acute myeloid leukemia (AML), myelodysplastic syndromes (MDS), essential thrombocythemia (ET), and polycythemia vera (PV).

“Our study provides the strongest evidence yet for inherited risk for these diseases—evidence that has proved evasive before, in part, because these cancers are relatively uncommon, and our ability to characterize these diseases has, until recently, been limited,” said Amit Sud, MBChB, PhD, of The Institute of Cancer Research in London, UK.

Dr Sud and his colleagues described their research in a letter to Blood.

The researchers analyzed data from the Swedish Family-Cancer Database, which included 93,199 first-degree relatives of 35,037 patients with myeloid malignancies. The patients had been diagnosed between 1958 and 2015.

First-degree relatives of the patients had an increased risk of all myeloid malignancies, with a standardized incidence ratio (SIR) of 1.99 (95% CI 1.12-2.04).

For individual diseases, there was a significant association between family history and increased risk for:

• AML—SIR=1.53 (95% CI 1.21-2.17)
• ET—SIR=6.30 (95% CI 3.95-9.54)
• MDS—SIR=6.87 (95% CI 4.07-10.86)
• PV—SIR=7.66 (95% CI 5.74-10.02).

Dr Sud and his colleagues noted that the strongest familial relative risks tended to occur for the same disease, but there were significant associations between different myeloid malignancies as well.

Risk by age group

The researchers also looked at familial relative risk for the same disease by patients’ age at diagnosis and observed a significantly increased risk for younger cases for all myeloproliferative neoplasms (MPNs) combined, PV, and MDS.

The SIRs for MPNs were 6.46 (95% CI 5.12-8.04) for patients age 59 or younger and 4.15 (95% CI 3.38-5.04) for patients older than 59.

The SIRs for PV were 10.90 (95% CI 7.12-15.97) for patients age 59 or younger and 5.96 (95% CI 3.93-8.67) for patients older than 59.

The SIRs for MDS were 11.95 (95% CI 6.36-20.43) for patients age 68 or younger and 3.27 (95% CI 1.06-7.63) for patients older than 68.

Risk by number of relatives

Dr Sud and his colleagues also discovered that familial relative risks of all myeloid malignancies and MPNs were significantly associated with the number of first-degree relatives affected by myeloid malignancies or MPNs.

The SIRs for first-degree relatives with 2 or more affected relatives were 4.55 (95% CI 2.08-8.64) for all myeloid malignancies and 17.82 (95% CI 5.79-24.89) for MPNs.

The SIRs for first-degree relatives with 1 affected relative were 1.96 (95% CI 1.79-2.15) for all myeloid malignancies and 4.83 (95% CI 4.14-5.60) for MPNs.

The researchers said these results suggest inherited genetic changes increase the risk of myeloid malignancies, although environmental factors shared in families could also play a role.

“In the future, our findings could help identify people at higher risk than normal because of their family background who could be prioritized for medical help like screening to catch the disease earlier if it arises,” Dr Sud said.

This study was funded by German Cancer Aid, the Swedish Research Council, ALF funding from Region Skåne, DKFZ, and Bloodwise.

Three generations of women in a family

A large study has revealed “the strongest evidence yet” supporting genetic susceptibility to myeloid malignancies, according to a researcher.

The study showed that first-degree relatives of patients with myeloid malignancies had double the risk of developing a myeloid malignancy themselves, when compared to the general population.

The researchers observed significant risks for developing acute myeloid leukemia (AML), myelodysplastic syndromes (MDS), essential thrombocythemia (ET), and polycythemia vera (PV).

“Our study provides the strongest evidence yet for inherited risk for these diseases—evidence that has proved evasive before, in part, because these cancers are relatively uncommon, and our ability to characterize these diseases has, until recently, been limited,” said Amit Sud, MBChB, PhD, of The Institute of Cancer Research in London, UK.

Dr Sud and his colleagues described their research in a letter to Blood.

The researchers analyzed data from the Swedish Family-Cancer Database, which included 93,199 first-degree relatives of 35,037 patients with myeloid malignancies. The patients had been diagnosed between 1958 and 2015.

First-degree relatives of the patients had an increased risk of all myeloid malignancies, with a standardized incidence ratio (SIR) of 1.99 (95% CI 1.12-2.04).

For individual diseases, there was a significant association between family history and increased risk for:

• AML—SIR=1.53 (95% CI 1.21-2.17)
• ET—SIR=6.30 (95% CI 3.95-9.54)
• MDS—SIR=6.87 (95% CI 4.07-10.86)
• PV—SIR=7.66 (95% CI 5.74-10.02).

Dr Sud and his colleagues noted that the strongest familial relative risks tended to occur for the same disease, but there were significant associations between different myeloid malignancies as well.

Risk by age group

The researchers also looked at familial relative risk for the same disease by patients’ age at diagnosis and observed a significantly increased risk for younger cases for all myeloproliferative neoplasms (MPNs) combined, PV, and MDS.

The SIRs for MPNs were 6.46 (95% CI 5.12-8.04) for patients age 59 or younger and 4.15 (95% CI 3.38-5.04) for patients older than 59.

The SIRs for PV were 10.90 (95% CI 7.12-15.97) for patients age 59 or younger and 5.96 (95% CI 3.93-8.67) for patients older than 59.

The SIRs for MDS were 11.95 (95% CI 6.36-20.43) for patients age 68 or younger and 3.27 (95% CI 1.06-7.63) for patients older than 68.

Risk by number of relatives

Dr Sud and his colleagues also discovered that familial relative risks of all myeloid malignancies and MPNs were significantly associated with the number of first-degree relatives affected by myeloid malignancies or MPNs.

The SIRs for first-degree relatives with 2 or more affected relatives were 4.55 (95% CI 2.08-8.64) for all myeloid malignancies and 17.82 (95% CI 5.79-24.89) for MPNs.

The SIRs for first-degree relatives with 1 affected relative were 1.96 (95% CI 1.79-2.15) for all myeloid malignancies and 4.83 (95% CI 4.14-5.60) for MPNs.

The researchers said these results suggest inherited genetic changes increase the risk of myeloid malignancies, although environmental factors shared in families could also play a role.

“In the future, our findings could help identify people at higher risk than normal because of their family background who could be prioritized for medical help like screening to catch the disease earlier if it arises,” Dr Sud said.

This study was funded by German Cancer Aid, the Swedish Research Council, ALF funding from Region Skåne, DKFZ, and Bloodwise.

Three generations of women in a family

A large study has revealed “the strongest evidence yet” supporting genetic susceptibility to myeloid malignancies, according to a researcher.

The study showed that first-degree relatives of patients with myeloid malignancies had double the risk of developing a myeloid malignancy themselves, when compared to the general population.

The researchers observed significant risks for developing acute myeloid leukemia (AML), myelodysplastic syndromes (MDS), essential thrombocythemia (ET), and polycythemia vera (PV).

“Our study provides the strongest evidence yet for inherited risk for these diseases—evidence that has proved evasive before, in part, because these cancers are relatively uncommon, and our ability to characterize these diseases has, until recently, been limited,” said Amit Sud, MBChB, PhD, of The Institute of Cancer Research in London, UK.

Dr Sud and his colleagues described their research in a letter to Blood.

The researchers analyzed data from the Swedish Family-Cancer Database, which included 93,199 first-degree relatives of 35,037 patients with myeloid malignancies. The patients had been diagnosed between 1958 and 2015.

First-degree relatives of the patients had an increased risk of all myeloid malignancies, with a standardized incidence ratio (SIR) of 1.99 (95% CI 1.12-2.04).

For individual diseases, there was a significant association between family history and increased risk for:

• AML—SIR=1.53 (95% CI 1.21-2.17)
• ET—SIR=6.30 (95% CI 3.95-9.54)
• MDS—SIR=6.87 (95% CI 4.07-10.86)
• PV—SIR=7.66 (95% CI 5.74-10.02).

Dr Sud and his colleagues noted that the strongest familial relative risks tended to occur for the same disease, but there were significant associations between different myeloid malignancies as well.

Risk by age group

The researchers also looked at familial relative risk for the same disease by patients’ age at diagnosis and observed a significantly increased risk for younger cases for all myeloproliferative neoplasms (MPNs) combined, PV, and MDS.

The SIRs for MPNs were 6.46 (95% CI 5.12-8.04) for patients age 59 or younger and 4.15 (95% CI 3.38-5.04) for patients older than 59.

The SIRs for PV were 10.90 (95% CI 7.12-15.97) for patients age 59 or younger and 5.96 (95% CI 3.93-8.67) for patients older than 59.

The SIRs for MDS were 11.95 (95% CI 6.36-20.43) for patients age 68 or younger and 3.27 (95% CI 1.06-7.63) for patients older than 68.

Risk by number of relatives

Dr Sud and his colleagues also discovered that familial relative risks of all myeloid malignancies and MPNs were significantly associated with the number of first-degree relatives affected by myeloid malignancies or MPNs.

The SIRs for first-degree relatives with 2 or more affected relatives were 4.55 (95% CI 2.08-8.64) for all myeloid malignancies and 17.82 (95% CI 5.79-24.89) for MPNs.

The SIRs for first-degree relatives with 1 affected relative were 1.96 (95% CI 1.79-2.15) for all myeloid malignancies and 4.83 (95% CI 4.14-5.60) for MPNs.

The researchers said these results suggest inherited genetic changes increase the risk of myeloid malignancies, although environmental factors shared in families could also play a role.

“In the future, our findings could help identify people at higher risk than normal because of their family background who could be prioritized for medical help like screening to catch the disease earlier if it arises,” Dr Sud said.

This study was funded by German Cancer Aid, the Swedish Research Council, ALF funding from Region Skåne, DKFZ, and Bloodwise.

A 25-year-old white man presents to urgent care with a nine-day history of increasing sinus pressure, mild sore throat, dry cough, and low-grade fever. Physical exam of the ears, nose, throat, and chest is unremarkable, but the patient does display mild maxillary sinus tenderness. Sinus pain (and symptom duration) is the primary complaint. The patient was recently exposed to influenza B, but a rapid flu test is negative. A five-day course of amoxicillin-clavulanate is prescribed for a presumed diagnosis of bacterial sinusitis.

One week later, the patient returns with worsening sore throat and a morbilliform rash (see Figures 1 and 2), which covers the trunk, upper arms, and thighs. He has no known allergies to drugs, foods, or other environmental triggers. Examination reveals slightly tender, mobile anterior and posterior cervical lymphadenopathy, as well as bilateral tonsillar erythema and exudates, which were not present at the initial visit.

DISCUSSION

EBV is a pervasive herpesvirus that infects approximately 95% of adults worldwide.¹ More than 90% of adults are seropositive for EBV antibodies by the age of 30.² Although affected individuals are often asymptomatic, some patients develop symptoms of infectious mononucleosis (IM).² An aminopenicillin rash can occur in patients with IM who are treated with amoxicillin or ampicillin, as was the case with this patient.

Incidence and pathophysiology

Infection with EBV most commonly occurs between the ages of 15 and 24.^1,2 Infection before the age of 1 is rarely seen due to circulating maternal antibodies; incidence of IM in those younger than 1 or older than 30 is < 1 per 1,000 cases annually.² The average annual incidence of infection is 0.5% in young adults (ages 15 and 24) but has been reported as high as 4.8%.² About 10% to 20% of people who never knowingly come into contact with the virus will become infected annually; of those, up to 50% will develop IM.² There are no known correlations in incidence based on sex or seasonal changes.²

Like all herpesviridae, EBV causes a latent infection that persists for a lifetime, specifically in replicating B lymphocytes.¹ Saliva is the most common mode of EBV transmission, as viral shedding occurs in the throat and mouth.^1,3 While the viral load in saliva is the highest during the first six months of infection, there are no clear data determining the risk for transmission throughout the course of asymptomatic shedding.⁴ There is a 30-to-50–day incubation period of EBV infection before a patient experiences symptoms of IM.¹ During this period, B lymphocytes and epithelial cells (specifically in the tonsillar crypts) are believed to be the source of viral replication.^1,3

Clinical presentation of IM

Common symptoms of IM include sore throat, fever, and fatigue. Approximately one in 13 patients ages 16 to 20 who pre­sent with a fever and sore throat will be diagnosed with IM.⁶ However, symptomatology alone is more sensitive than specific and is not sufficient to diagnose IM.⁶ Combined fatigue and pharyngitis is sensitive (81%-83%) but not specific, and posterior cervical lymphadenopathy increases the likelihood of IM (specificity, 87%).⁶

Continue to: The classic triad associated with IM includes...

The classic triad associated with IM includes fever, pharyngitis, and cervical lymphadenopathy, with morbilliform rash and palatal petechiae appearing less commonly (3%-15% and 25%, respectively).^1,2,9 In affected patients, a transient truncal rash manifests within the first few days of disease onset.⁷ Tonsillar enlargement is also a common, but not specific, sign of acute IM.² Splenomegaly is found in 15% to 65% of patients, typically developing within three weeks of disease onset.^1,5,9

Hematologic complications occur in 25% to 50% of cases.⁵ Mild thrombocytopenia is common; however, more severe complications—such as hemolytic anemia, hemolytic-uremic syndrome, aplastic anemia, and disseminated intravascular coagulation—have also been associated with IM.⁵ Fulminant and potentially fatal complications are more common in immunocompromised patients.^1,2

Pediatric and geriatric patients (those older than 65) may present with atypical signs and symptoms. For example, children are commonly asymptomatic or may present with a nonspecific viral illness.¹ In addition, pediatric and elderly populations can develop elevated aminotransferase levels, and 26% of elderly patients present with jaundice (compared with 8% of young adults).^2,3,7

Workup/differential diagnosis

Heterophile antibody testing is the most efficient and least expensive diagnostic test to confirm IM (sensitivity, 63%-84%; specificity, 84%-100%).² Within the first week of IM, however, 25% of patients will produce a false-negative antibody test; a complete blood count (CBC) with differential and peripheral smear are appropriate follow-up tests.^1,2,5 Detecting 10% or more atypical lymphocytes on a peripheral smear has a specificity of 95% and sensitivity of 61.3% for detecting IM, and a CBC with a lymphocyte count of less than 4,000 mm has a 99% negative predictive value.² Viral capsid IgM testing can confirm the diagnosis of IM in an unclear clinical situation, such as a negative heterophile antibody test with an absolute lymphocyte count > 4,000 mm or in which 10% or more atypical lymphocytes were detected.²

Pharyngitis is caused by group A streptococci in 15% to 30% of children and 10% of adults worldwide, and 30% of patients with IM have a concomitant infection with group A streptococci.^1,5 Because pharyngitis is a common presenting symptom of IM, rapid antigen strep test is appropriate when working up these patients.² In addition, HIV, cytomegalovirus, human herpesvirus-6, and Toxoplasma gondii should be considered in the differential for patients with pharyngitis, fatigue, malaise, and lymphadenopathy—especially if the group A streptococci/EBV workup is negative.^1,2,5

Continue to: EBV is also a known trigger of...

Treatment/complications

Aminopenicillin rash classically occurs in patients with IM who are treated with amoxicillin or ampicillin. These antibiotics are most commonly prescribed for suspected group A streptococci infection.⁷ Up to 95% of patients with IM who are exposed to these drugs develop this rash within two to 10 days of receiving the first dose of the antibiotic.^9,10 Similar eruptions are often reported following administration of other penicillins, but not with the same frequency seen with ampicillin or amoxicillin (see Table 1).¹¹

The mechanism of the aminopenicillin rash is not completely understood, but one theory is that the activated CD8+ cells react with the drug antigens and deposit in the skin.¹⁰ Another proposed mechanism is that antigens formed against activated polyclonal B cells create immune complexes with the drug, which then deposit in the skin.¹⁰

No known factors increase the incidence of this rash in patients after antibiotic exposure (eg, previous penicillin exposure, antibiotic dose or duration, patient age or ethnicity, atopic history).⁷ The rash generally resolves within a week after antibiotic discontinuation.⁷ Importantly, the development of a rash in a patient with EBV after administration of an aminopenicillin is not associated with an allergy nor is it a sign of an unfavorable reaction to such drugs in the future.¹²

The rash can be described as morbilliform or scarlatiniform and should be distinguished from the rash that acute IM can cause. Five percent of patients with an aminopenicillin rash will have an urticarial presentation, whereas 95% of patients have an exanthematous presentation.^1,9,10 Although it can be quite difficult to distinguish one rash from the other, the aminopenicillin rash is more widespread than that associated with acute IM, covering extensor surfaces and spreading to the face, trunk, neck, mucous membranes, and sometimes the palms and soles.^1,7,9,10 The rash caused by IM begins within the first few days of disease, whereas the aminopenicillin rash will manifest seven to 10 days after antibiotic exposure and is commonly pruritic.¹ Each rash will last about one week.¹

Continue to: CONCLUSION

 

 

CONCLUSION

The diagnosis of EBV can be challenging due to its similarity to group A streptococcal pharyngitis and other viral syndromes. In this case, the development of classic symptoms, along with the morbilliform eruption following administration of an aminopen­icillin, was strongly suggestive of this diagnosis. This pairing of EBV infection and aminopenicillin rash does not indicate a penicillin allergy.

A 25-year-old white man presents to urgent care with a nine-day history of increasing sinus pressure, mild sore throat, dry cough, and low-grade fever. Physical exam of the ears, nose, throat, and chest is unremarkable, but the patient does display mild maxillary sinus tenderness. Sinus pain (and symptom duration) is the primary complaint. The patient was recently exposed to influenza B, but a rapid flu test is negative. A five-day course of amoxicillin-clavulanate is prescribed for a presumed diagnosis of bacterial sinusitis.

One week later, the patient returns with worsening sore throat and a morbilliform rash (see Figures 1 and 2), which covers the trunk, upper arms, and thighs. He has no known allergies to drugs, foods, or other environmental triggers. Examination reveals slightly tender, mobile anterior and posterior cervical lymphadenopathy, as well as bilateral tonsillar erythema and exudates, which were not present at the initial visit.

DISCUSSION

EBV is a pervasive herpesvirus that infects approximately 95% of adults worldwide.¹ More than 90% of adults are seropositive for EBV antibodies by the age of 30.² Although affected individuals are often asymptomatic, some patients develop symptoms of infectious mononucleosis (IM).² An aminopenicillin rash can occur in patients with IM who are treated with amoxicillin or ampicillin, as was the case with this patient.

Incidence and pathophysiology

Infection with EBV most commonly occurs between the ages of 15 and 24.^1,2 Infection before the age of 1 is rarely seen due to circulating maternal antibodies; incidence of IM in those younger than 1 or older than 30 is < 1 per 1,000 cases annually.² The average annual incidence of infection is 0.5% in young adults (ages 15 and 24) but has been reported as high as 4.8%.² About 10% to 20% of people who never knowingly come into contact with the virus will become infected annually; of those, up to 50% will develop IM.² There are no known correlations in incidence based on sex or seasonal changes.²

Like all herpesviridae, EBV causes a latent infection that persists for a lifetime, specifically in replicating B lymphocytes.¹ Saliva is the most common mode of EBV transmission, as viral shedding occurs in the throat and mouth.^1,3 While the viral load in saliva is the highest during the first six months of infection, there are no clear data determining the risk for transmission throughout the course of asymptomatic shedding.⁴ There is a 30-to-50–day incubation period of EBV infection before a patient experiences symptoms of IM.¹ During this period, B lymphocytes and epithelial cells (specifically in the tonsillar crypts) are believed to be the source of viral replication.^1,3

Clinical presentation of IM

Common symptoms of IM include sore throat, fever, and fatigue. Approximately one in 13 patients ages 16 to 20 who pre­sent with a fever and sore throat will be diagnosed with IM.⁶ However, symptomatology alone is more sensitive than specific and is not sufficient to diagnose IM.⁶ Combined fatigue and pharyngitis is sensitive (81%-83%) but not specific, and posterior cervical lymphadenopathy increases the likelihood of IM (specificity, 87%).⁶

Continue to: The classic triad associated with IM includes...

The classic triad associated with IM includes fever, pharyngitis, and cervical lymphadenopathy, with morbilliform rash and palatal petechiae appearing less commonly (3%-15% and 25%, respectively).^1,2,9 In affected patients, a transient truncal rash manifests within the first few days of disease onset.⁷ Tonsillar enlargement is also a common, but not specific, sign of acute IM.² Splenomegaly is found in 15% to 65% of patients, typically developing within three weeks of disease onset.^1,5,9

Hematologic complications occur in 25% to 50% of cases.⁵ Mild thrombocytopenia is common; however, more severe complications—such as hemolytic anemia, hemolytic-uremic syndrome, aplastic anemia, and disseminated intravascular coagulation—have also been associated with IM.⁵ Fulminant and potentially fatal complications are more common in immunocompromised patients.^1,2

Pediatric and geriatric patients (those older than 65) may present with atypical signs and symptoms. For example, children are commonly asymptomatic or may present with a nonspecific viral illness.¹ In addition, pediatric and elderly populations can develop elevated aminotransferase levels, and 26% of elderly patients present with jaundice (compared with 8% of young adults).^2,3,7

Workup/differential diagnosis

Heterophile antibody testing is the most efficient and least expensive diagnostic test to confirm IM (sensitivity, 63%-84%; specificity, 84%-100%).² Within the first week of IM, however, 25% of patients will produce a false-negative antibody test; a complete blood count (CBC) with differential and peripheral smear are appropriate follow-up tests.^1,2,5 Detecting 10% or more atypical lymphocytes on a peripheral smear has a specificity of 95% and sensitivity of 61.3% for detecting IM, and a CBC with a lymphocyte count of less than 4,000 mm has a 99% negative predictive value.² Viral capsid IgM testing can confirm the diagnosis of IM in an unclear clinical situation, such as a negative heterophile antibody test with an absolute lymphocyte count > 4,000 mm or in which 10% or more atypical lymphocytes were detected.²

Pharyngitis is caused by group A streptococci in 15% to 30% of children and 10% of adults worldwide, and 30% of patients with IM have a concomitant infection with group A streptococci.^1,5 Because pharyngitis is a common presenting symptom of IM, rapid antigen strep test is appropriate when working up these patients.² In addition, HIV, cytomegalovirus, human herpesvirus-6, and Toxoplasma gondii should be considered in the differential for patients with pharyngitis, fatigue, malaise, and lymphadenopathy—especially if the group A streptococci/EBV workup is negative.^1,2,5

Continue to: EBV is also a known trigger of...

Treatment/complications

Aminopenicillin rash classically occurs in patients with IM who are treated with amoxicillin or ampicillin. These antibiotics are most commonly prescribed for suspected group A streptococci infection.⁷ Up to 95% of patients with IM who are exposed to these drugs develop this rash within two to 10 days of receiving the first dose of the antibiotic.^9,10 Similar eruptions are often reported following administration of other penicillins, but not with the same frequency seen with ampicillin or amoxicillin (see Table 1).¹¹

The mechanism of the aminopenicillin rash is not completely understood, but one theory is that the activated CD8+ cells react with the drug antigens and deposit in the skin.¹⁰ Another proposed mechanism is that antigens formed against activated polyclonal B cells create immune complexes with the drug, which then deposit in the skin.¹⁰

No known factors increase the incidence of this rash in patients after antibiotic exposure (eg, previous penicillin exposure, antibiotic dose or duration, patient age or ethnicity, atopic history).⁷ The rash generally resolves within a week after antibiotic discontinuation.⁷ Importantly, the development of a rash in a patient with EBV after administration of an aminopenicillin is not associated with an allergy nor is it a sign of an unfavorable reaction to such drugs in the future.¹²

The rash can be described as morbilliform or scarlatiniform and should be distinguished from the rash that acute IM can cause. Five percent of patients with an aminopenicillin rash will have an urticarial presentation, whereas 95% of patients have an exanthematous presentation.^1,9,10 Although it can be quite difficult to distinguish one rash from the other, the aminopenicillin rash is more widespread than that associated with acute IM, covering extensor surfaces and spreading to the face, trunk, neck, mucous membranes, and sometimes the palms and soles.^1,7,9,10 The rash caused by IM begins within the first few days of disease, whereas the aminopenicillin rash will manifest seven to 10 days after antibiotic exposure and is commonly pruritic.¹ Each rash will last about one week.¹

Continue to: CONCLUSION

 

 

CONCLUSION

The diagnosis of EBV can be challenging due to its similarity to group A streptococcal pharyngitis and other viral syndromes. In this case, the development of classic symptoms, along with the morbilliform eruption following administration of an aminopen­icillin, was strongly suggestive of this diagnosis. This pairing of EBV infection and aminopenicillin rash does not indicate a penicillin allergy.

A 25-year-old white man presents to urgent care with a nine-day history of increasing sinus pressure, mild sore throat, dry cough, and low-grade fever. Physical exam of the ears, nose, throat, and chest is unremarkable, but the patient does display mild maxillary sinus tenderness. Sinus pain (and symptom duration) is the primary complaint. The patient was recently exposed to influenza B, but a rapid flu test is negative. A five-day course of amoxicillin-clavulanate is prescribed for a presumed diagnosis of bacterial sinusitis.

One week later, the patient returns with worsening sore throat and a morbilliform rash (see Figures 1 and 2), which covers the trunk, upper arms, and thighs. He has no known allergies to drugs, foods, or other environmental triggers. Examination reveals slightly tender, mobile anterior and posterior cervical lymphadenopathy, as well as bilateral tonsillar erythema and exudates, which were not present at the initial visit.

DISCUSSION

EBV is a pervasive herpesvirus that infects approximately 95% of adults worldwide.¹ More than 90% of adults are seropositive for EBV antibodies by the age of 30.² Although affected individuals are often asymptomatic, some patients develop symptoms of infectious mononucleosis (IM).² An aminopenicillin rash can occur in patients with IM who are treated with amoxicillin or ampicillin, as was the case with this patient.

Incidence and pathophysiology

Infection with EBV most commonly occurs between the ages of 15 and 24.^1,2 Infection before the age of 1 is rarely seen due to circulating maternal antibodies; incidence of IM in those younger than 1 or older than 30 is < 1 per 1,000 cases annually.² The average annual incidence of infection is 0.5% in young adults (ages 15 and 24) but has been reported as high as 4.8%.² About 10% to 20% of people who never knowingly come into contact with the virus will become infected annually; of those, up to 50% will develop IM.² There are no known correlations in incidence based on sex or seasonal changes.²

Like all herpesviridae, EBV causes a latent infection that persists for a lifetime, specifically in replicating B lymphocytes.¹ Saliva is the most common mode of EBV transmission, as viral shedding occurs in the throat and mouth.^1,3 While the viral load in saliva is the highest during the first six months of infection, there are no clear data determining the risk for transmission throughout the course of asymptomatic shedding.⁴ There is a 30-to-50–day incubation period of EBV infection before a patient experiences symptoms of IM.¹ During this period, B lymphocytes and epithelial cells (specifically in the tonsillar crypts) are believed to be the source of viral replication.^1,3

Clinical presentation of IM

Common symptoms of IM include sore throat, fever, and fatigue. Approximately one in 13 patients ages 16 to 20 who pre­sent with a fever and sore throat will be diagnosed with IM.⁶ However, symptomatology alone is more sensitive than specific and is not sufficient to diagnose IM.⁶ Combined fatigue and pharyngitis is sensitive (81%-83%) but not specific, and posterior cervical lymphadenopathy increases the likelihood of IM (specificity, 87%).⁶

Continue to: The classic triad associated with IM includes...

The classic triad associated with IM includes fever, pharyngitis, and cervical lymphadenopathy, with morbilliform rash and palatal petechiae appearing less commonly (3%-15% and 25%, respectively).^1,2,9 In affected patients, a transient truncal rash manifests within the first few days of disease onset.⁷ Tonsillar enlargement is also a common, but not specific, sign of acute IM.² Splenomegaly is found in 15% to 65% of patients, typically developing within three weeks of disease onset.^1,5,9

Hematologic complications occur in 25% to 50% of cases.⁵ Mild thrombocytopenia is common; however, more severe complications—such as hemolytic anemia, hemolytic-uremic syndrome, aplastic anemia, and disseminated intravascular coagulation—have also been associated with IM.⁵ Fulminant and potentially fatal complications are more common in immunocompromised patients.^1,2

Pediatric and geriatric patients (those older than 65) may present with atypical signs and symptoms. For example, children are commonly asymptomatic or may present with a nonspecific viral illness.¹ In addition, pediatric and elderly populations can develop elevated aminotransferase levels, and 26% of elderly patients present with jaundice (compared with 8% of young adults).^2,3,7

Workup/differential diagnosis

Heterophile antibody testing is the most efficient and least expensive diagnostic test to confirm IM (sensitivity, 63%-84%; specificity, 84%-100%).² Within the first week of IM, however, 25% of patients will produce a false-negative antibody test; a complete blood count (CBC) with differential and peripheral smear are appropriate follow-up tests.^1,2,5 Detecting 10% or more atypical lymphocytes on a peripheral smear has a specificity of 95% and sensitivity of 61.3% for detecting IM, and a CBC with a lymphocyte count of less than 4,000 mm has a 99% negative predictive value.² Viral capsid IgM testing can confirm the diagnosis of IM in an unclear clinical situation, such as a negative heterophile antibody test with an absolute lymphocyte count > 4,000 mm or in which 10% or more atypical lymphocytes were detected.²

Pharyngitis is caused by group A streptococci in 15% to 30% of children and 10% of adults worldwide, and 30% of patients with IM have a concomitant infection with group A streptococci.^1,5 Because pharyngitis is a common presenting symptom of IM, rapid antigen strep test is appropriate when working up these patients.² In addition, HIV, cytomegalovirus, human herpesvirus-6, and Toxoplasma gondii should be considered in the differential for patients with pharyngitis, fatigue, malaise, and lymphadenopathy—especially if the group A streptococci/EBV workup is negative.^1,2,5

Continue to: EBV is also a known trigger of...

Treatment/complications

Aminopenicillin rash classically occurs in patients with IM who are treated with amoxicillin or ampicillin. These antibiotics are most commonly prescribed for suspected group A streptococci infection.⁷ Up to 95% of patients with IM who are exposed to these drugs develop this rash within two to 10 days of receiving the first dose of the antibiotic.^9,10 Similar eruptions are often reported following administration of other penicillins, but not with the same frequency seen with ampicillin or amoxicillin (see Table 1).¹¹

The mechanism of the aminopenicillin rash is not completely understood, but one theory is that the activated CD8+ cells react with the drug antigens and deposit in the skin.¹⁰ Another proposed mechanism is that antigens formed against activated polyclonal B cells create immune complexes with the drug, which then deposit in the skin.¹⁰

No known factors increase the incidence of this rash in patients after antibiotic exposure (eg, previous penicillin exposure, antibiotic dose or duration, patient age or ethnicity, atopic history).⁷ The rash generally resolves within a week after antibiotic discontinuation.⁷ Importantly, the development of a rash in a patient with EBV after administration of an aminopenicillin is not associated with an allergy nor is it a sign of an unfavorable reaction to such drugs in the future.¹²

The rash can be described as morbilliform or scarlatiniform and should be distinguished from the rash that acute IM can cause. Five percent of patients with an aminopenicillin rash will have an urticarial presentation, whereas 95% of patients have an exanthematous presentation.^1,9,10 Although it can be quite difficult to distinguish one rash from the other, the aminopenicillin rash is more widespread than that associated with acute IM, covering extensor surfaces and spreading to the face, trunk, neck, mucous membranes, and sometimes the palms and soles.^1,7,9,10 The rash caused by IM begins within the first few days of disease, whereas the aminopenicillin rash will manifest seven to 10 days after antibiotic exposure and is commonly pruritic.¹ Each rash will last about one week.¹

Continue to: CONCLUSION

 

 

CONCLUSION

The diagnosis of EBV can be challenging due to its similarity to group A streptococcal pharyngitis and other viral syndromes. In this case, the development of classic symptoms, along with the morbilliform eruption following administration of an aminopen­icillin, was strongly suggestive of this diagnosis. This pairing of EBV infection and aminopenicillin rash does not indicate a penicillin allergy.

Unless your practice is cash-only, reimbursements from your patients’ health insurance companies are necessary to ensure its survival. Although the reimbursement process appears straightforward (provide a service, submit a claim, and receive a payment), it is actually quite complex, and, if not properly managed, a claim can be denied at any stage of the process.¹ In its 2013 National Health Insurer Report Card, the American Medical Association reported that major payers returned 11% to 29% of claim lines with $0 for payment.^1,2 This often is the case because patients are responsible for the balance, but it also occurs as the result of claim edits (up to 7%) and other denials (up to 5%).^1,2

Claims can be denied for various reasons, including¹:

• missed filing deadlines
• billing for non-covered services
• discrepancies between diagnostic codes, procedures codes, modifiers, and clinician documentation
• missing pre-authorization documentation or a signed Advanced Beneficiary Notice of Non-Coverage.

Strategies for avoiding denials

A psychiatric practice requires a practical system to prevent the occurrence of denials, starting from the point of referral. Working through denials is more costly and time­consuming than preventing them from occurring in the first place. For every 15 denials prevented each month, your practice can save approximately $4,500 per year in costs associated with correcting those claims; by preventing denials, the practice also receives reimbursement sooner.¹ You can be guaranteed to leave significant amounts of money on the table if you are not able to prevent or reduce denials.

The following methods can be used to help reduce the likelihood of having a claim denied.^1,3

Obtain the patient’s health insurance information at first contact and confirm his or her coverage benefits, deductibles, copay requirements, and exclusions before scheduling the first appointment. Verify this information at each of the patient’s subsequent visits to reduce the chances of having a claim denied due to invalid subscriber information. Also, keep in mind that Medicaid eligibility can change daily.

Employ a digital record system, such as electronic medical records, to track authorizations.

Know the filing deadlines for each of your payers. If you miss a deadline, there is no recourse.

Continue to: Check each claim

Check each claim for accurate coding, diagnosis, and payment (eg, copay, co-insurance, and/or deductible, depending on the health insurance plan) taken before the claim is submitted. If your practice size permits, assign a staff member to confirm this information and keep track of deadlines for submissions, resubmissions, and appeals of denied claims. Using a single gatekeeper can help decrease the chances that a denial will “slip through the cracks.”

Confirm that diagnostic codes, procedures codes, and modifiers are justified by the clinician’s documentation. Have a medical coder compare notes with the clinician to determine if any critical information needed to justify the codes used has been omitted.

Implement an electronic system that can automatically identify any changes and updates to the Centers for Medicare and Medicaid Services (CMS) regulations and guidance, International Classification of Diseases (ICD) versions and codes, and Current Procedural Terminology (CPT) codes and guidelines. To help reduce denied claims, educate all staff (schedulers, coders, billers, nursing staff, and other clinicians) frequently about these changes, and provide regular feedback to those involved in correcting denials.

Unless your practice is cash-only, reimbursements from your patients’ health insurance companies are necessary to ensure its survival. Although the reimbursement process appears straightforward (provide a service, submit a claim, and receive a payment), it is actually quite complex, and, if not properly managed, a claim can be denied at any stage of the process.¹ In its 2013 National Health Insurer Report Card, the American Medical Association reported that major payers returned 11% to 29% of claim lines with $0 for payment.^1,2 This often is the case because patients are responsible for the balance, but it also occurs as the result of claim edits (up to 7%) and other denials (up to 5%).^1,2

Claims can be denied for various reasons, including¹:

• missed filing deadlines
• billing for non-covered services
• discrepancies between diagnostic codes, procedures codes, modifiers, and clinician documentation
• missing pre-authorization documentation or a signed Advanced Beneficiary Notice of Non-Coverage.

Strategies for avoiding denials

A psychiatric practice requires a practical system to prevent the occurrence of denials, starting from the point of referral. Working through denials is more costly and time­consuming than preventing them from occurring in the first place. For every 15 denials prevented each month, your practice can save approximately $4,500 per year in costs associated with correcting those claims; by preventing denials, the practice also receives reimbursement sooner.¹ You can be guaranteed to leave significant amounts of money on the table if you are not able to prevent or reduce denials.

The following methods can be used to help reduce the likelihood of having a claim denied.^1,3

Obtain the patient’s health insurance information at first contact and confirm his or her coverage benefits, deductibles, copay requirements, and exclusions before scheduling the first appointment. Verify this information at each of the patient’s subsequent visits to reduce the chances of having a claim denied due to invalid subscriber information. Also, keep in mind that Medicaid eligibility can change daily.

Employ a digital record system, such as electronic medical records, to track authorizations.

Know the filing deadlines for each of your payers. If you miss a deadline, there is no recourse.

Continue to: Check each claim

Check each claim for accurate coding, diagnosis, and payment (eg, copay, co-insurance, and/or deductible, depending on the health insurance plan) taken before the claim is submitted. If your practice size permits, assign a staff member to confirm this information and keep track of deadlines for submissions, resubmissions, and appeals of denied claims. Using a single gatekeeper can help decrease the chances that a denial will “slip through the cracks.”

Confirm that diagnostic codes, procedures codes, and modifiers are justified by the clinician’s documentation. Have a medical coder compare notes with the clinician to determine if any critical information needed to justify the codes used has been omitted.

Implement an electronic system that can automatically identify any changes and updates to the Centers for Medicare and Medicaid Services (CMS) regulations and guidance, International Classification of Diseases (ICD) versions and codes, and Current Procedural Terminology (CPT) codes and guidelines. To help reduce denied claims, educate all staff (schedulers, coders, billers, nursing staff, and other clinicians) frequently about these changes, and provide regular feedback to those involved in correcting denials.

Unless your practice is cash-only, reimbursements from your patients’ health insurance companies are necessary to ensure its survival. Although the reimbursement process appears straightforward (provide a service, submit a claim, and receive a payment), it is actually quite complex, and, if not properly managed, a claim can be denied at any stage of the process.¹ In its 2013 National Health Insurer Report Card, the American Medical Association reported that major payers returned 11% to 29% of claim lines with $0 for payment.^1,2 This often is the case because patients are responsible for the balance, but it also occurs as the result of claim edits (up to 7%) and other denials (up to 5%).^1,2

Claims can be denied for various reasons, including¹:

• missed filing deadlines
• billing for non-covered services
• discrepancies between diagnostic codes, procedures codes, modifiers, and clinician documentation
• missing pre-authorization documentation or a signed Advanced Beneficiary Notice of Non-Coverage.

Strategies for avoiding denials

A psychiatric practice requires a practical system to prevent the occurrence of denials, starting from the point of referral. Working through denials is more costly and time­consuming than preventing them from occurring in the first place. For every 15 denials prevented each month, your practice can save approximately $4,500 per year in costs associated with correcting those claims; by preventing denials, the practice also receives reimbursement sooner.¹ You can be guaranteed to leave significant amounts of money on the table if you are not able to prevent or reduce denials.

The following methods can be used to help reduce the likelihood of having a claim denied.^1,3

Obtain the patient’s health insurance information at first contact and confirm his or her coverage benefits, deductibles, copay requirements, and exclusions before scheduling the first appointment. Verify this information at each of the patient’s subsequent visits to reduce the chances of having a claim denied due to invalid subscriber information. Also, keep in mind that Medicaid eligibility can change daily.

Employ a digital record system, such as electronic medical records, to track authorizations.

Know the filing deadlines for each of your payers. If you miss a deadline, there is no recourse.

Continue to: Check each claim

Check each claim for accurate coding, diagnosis, and payment (eg, copay, co-insurance, and/or deductible, depending on the health insurance plan) taken before the claim is submitted. If your practice size permits, assign a staff member to confirm this information and keep track of deadlines for submissions, resubmissions, and appeals of denied claims. Using a single gatekeeper can help decrease the chances that a denial will “slip through the cracks.”

Confirm that diagnostic codes, procedures codes, and modifiers are justified by the clinician’s documentation. Have a medical coder compare notes with the clinician to determine if any critical information needed to justify the codes used has been omitted.

Implement an electronic system that can automatically identify any changes and updates to the Centers for Medicare and Medicaid Services (CMS) regulations and guidance, International Classification of Diseases (ICD) versions and codes, and Current Procedural Terminology (CPT) codes and guidelines. To help reduce denied claims, educate all staff (schedulers, coders, billers, nursing staff, and other clinicians) frequently about these changes, and provide regular feedback to those involved in correcting denials.

Photo by Bill Branson

Fludarabine, cyclophosphamide, and rituximab are recommended as initial therapy for fit patients with chronic lymphocytic leukemia (CLL) who do not have TP53 disruption, according to new guidelines from the British Society for Haematology.

The guidelines update the 2012 recommendations on CLL to include “significant” developments in treatment.

The new guidelines were published in the British Journal of Haematology.

Anna H. Schuh, MD, of the University of Oxford in the UK, and her coauthors noted that, while these guidelines apply to treatments available outside clinical trials, wherever possible, patients with CLL should be treated within the clinical trial setting.

While recommending fludarabine, cyclophosphamide, and rituximab as first-line therapy, the guideline authors acknowledged that the combination of bendamustine and rituximab is an acceptable alternative for patients who cannot take the triple therapy because of comorbidities such as advanced age, renal impairment, or issues with marrow capacity.

Similarly, less-fit patients can also be considered for chlorambucil-obinutuzumab or chlorambucil-ofatumumab combinations.

All patients diagnosed with CLL should be tested for TP53 deletions and mutations before each line of therapy, the guideline committee recommended.

TP53 disruption makes chemoimmunotherapy ineffective because of either a deletion of chromosome 17p or a mutation in the TP53 gene. However, there is compelling evidence for the efficacy of ibrutinib in these patients, or idelalisib and rituximab for those with cardiac disease or receiving vitamin K antagonists.

With respect to maintenance therapy, the guidelines noted that this was not routinely recommended in CLL as “it is unclear to what extent the progression-free survival benefit is offset by long-term toxicity.”

Patients who are refractory to chemoimmunotherapy, who have relapsed, or who cannot be retreated with chemoimmunotherapy should be treated with idelalisib plus rituximab or ibrutinib monotherapy, the guidelines suggested.

“Deciding whether ibrutinib or idelalisib with rituximab is most appropriate for an individual patient depends on a range of factors, including toxicity profile and convenience of delivery,” the authors wrote.

However, they noted that the value of adding bendamustine to either option was unclear as research had not shown significant, associated gains in median progression-free survival.

Allogeneic stem cell transplant should be considered as an option for patients who have failed chemotherapy, have a TP53 disruption and have not responded to B-cell receptor signaling pathway inhibitors such as ibrutinib, or have Richter’s transformation.

The guidelines also addressed the issue of autoimmune cytopenias, which occur in 5% to 10% of patients with CLL and can actually precede the diagnosis of CLL in about 9% of cases.

In patients where autoimmune cytopenia is the dominant clinical feature, they should be treated with corticosteroids, intravenous immunoglobulin, or rituximab. However, for patients where the cytopenia is triggered by CLL therapy, the guidelines recommended halting treatment and beginning immunosuppression.

The guideline development was supported by the British Society for Haematology. The UK CLL Forum, which was involved in development as well, is a registered charity that receives funding from a number of pharmaceutical companies.

Photo by Bill Branson

Fludarabine, cyclophosphamide, and rituximab are recommended as initial therapy for fit patients with chronic lymphocytic leukemia (CLL) who do not have TP53 disruption, according to new guidelines from the British Society for Haematology.

The guidelines update the 2012 recommendations on CLL to include “significant” developments in treatment.

The new guidelines were published in the British Journal of Haematology.

Anna H. Schuh, MD, of the University of Oxford in the UK, and her coauthors noted that, while these guidelines apply to treatments available outside clinical trials, wherever possible, patients with CLL should be treated within the clinical trial setting.

While recommending fludarabine, cyclophosphamide, and rituximab as first-line therapy, the guideline authors acknowledged that the combination of bendamustine and rituximab is an acceptable alternative for patients who cannot take the triple therapy because of comorbidities such as advanced age, renal impairment, or issues with marrow capacity.

Similarly, less-fit patients can also be considered for chlorambucil-obinutuzumab or chlorambucil-ofatumumab combinations.

All patients diagnosed with CLL should be tested for TP53 deletions and mutations before each line of therapy, the guideline committee recommended.

TP53 disruption makes chemoimmunotherapy ineffective because of either a deletion of chromosome 17p or a mutation in the TP53 gene. However, there is compelling evidence for the efficacy of ibrutinib in these patients, or idelalisib and rituximab for those with cardiac disease or receiving vitamin K antagonists.

With respect to maintenance therapy, the guidelines noted that this was not routinely recommended in CLL as “it is unclear to what extent the progression-free survival benefit is offset by long-term toxicity.”

Patients who are refractory to chemoimmunotherapy, who have relapsed, or who cannot be retreated with chemoimmunotherapy should be treated with idelalisib plus rituximab or ibrutinib monotherapy, the guidelines suggested.

“Deciding whether ibrutinib or idelalisib with rituximab is most appropriate for an individual patient depends on a range of factors, including toxicity profile and convenience of delivery,” the authors wrote.

However, they noted that the value of adding bendamustine to either option was unclear as research had not shown significant, associated gains in median progression-free survival.

Allogeneic stem cell transplant should be considered as an option for patients who have failed chemotherapy, have a TP53 disruption and have not responded to B-cell receptor signaling pathway inhibitors such as ibrutinib, or have Richter’s transformation.

The guidelines also addressed the issue of autoimmune cytopenias, which occur in 5% to 10% of patients with CLL and can actually precede the diagnosis of CLL in about 9% of cases.

In patients where autoimmune cytopenia is the dominant clinical feature, they should be treated with corticosteroids, intravenous immunoglobulin, or rituximab. However, for patients where the cytopenia is triggered by CLL therapy, the guidelines recommended halting treatment and beginning immunosuppression.

The guideline development was supported by the British Society for Haematology. The UK CLL Forum, which was involved in development as well, is a registered charity that receives funding from a number of pharmaceutical companies.

Photo by Bill Branson

Fludarabine, cyclophosphamide, and rituximab are recommended as initial therapy for fit patients with chronic lymphocytic leukemia (CLL) who do not have TP53 disruption, according to new guidelines from the British Society for Haematology.

The guidelines update the 2012 recommendations on CLL to include “significant” developments in treatment.

The new guidelines were published in the British Journal of Haematology.

Anna H. Schuh, MD, of the University of Oxford in the UK, and her coauthors noted that, while these guidelines apply to treatments available outside clinical trials, wherever possible, patients with CLL should be treated within the clinical trial setting.

While recommending fludarabine, cyclophosphamide, and rituximab as first-line therapy, the guideline authors acknowledged that the combination of bendamustine and rituximab is an acceptable alternative for patients who cannot take the triple therapy because of comorbidities such as advanced age, renal impairment, or issues with marrow capacity.

Similarly, less-fit patients can also be considered for chlorambucil-obinutuzumab or chlorambucil-ofatumumab combinations.

All patients diagnosed with CLL should be tested for TP53 deletions and mutations before each line of therapy, the guideline committee recommended.

TP53 disruption makes chemoimmunotherapy ineffective because of either a deletion of chromosome 17p or a mutation in the TP53 gene. However, there is compelling evidence for the efficacy of ibrutinib in these patients, or idelalisib and rituximab for those with cardiac disease or receiving vitamin K antagonists.

With respect to maintenance therapy, the guidelines noted that this was not routinely recommended in CLL as “it is unclear to what extent the progression-free survival benefit is offset by long-term toxicity.”

Patients who are refractory to chemoimmunotherapy, who have relapsed, or who cannot be retreated with chemoimmunotherapy should be treated with idelalisib plus rituximab or ibrutinib monotherapy, the guidelines suggested.

“Deciding whether ibrutinib or idelalisib with rituximab is most appropriate for an individual patient depends on a range of factors, including toxicity profile and convenience of delivery,” the authors wrote.

However, they noted that the value of adding bendamustine to either option was unclear as research had not shown significant, associated gains in median progression-free survival.

Allogeneic stem cell transplant should be considered as an option for patients who have failed chemotherapy, have a TP53 disruption and have not responded to B-cell receptor signaling pathway inhibitors such as ibrutinib, or have Richter’s transformation.

The guidelines also addressed the issue of autoimmune cytopenias, which occur in 5% to 10% of patients with CLL and can actually precede the diagnosis of CLL in about 9% of cases.

In patients where autoimmune cytopenia is the dominant clinical feature, they should be treated with corticosteroids, intravenous immunoglobulin, or rituximab. However, for patients where the cytopenia is triggered by CLL therapy, the guidelines recommended halting treatment and beginning immunosuppression.

The guideline development was supported by the British Society for Haematology. The UK CLL Forum, which was involved in development as well, is a registered charity that receives funding from a number of pharmaceutical companies.