Mixed Topics

Sexual harassment is known to be more pervasive in male-dominated workplaces and flourishes in a climate of tolerance and culture of silence, according to Bernadette Aulivola, MD, of Loyola University Medical Center, Maywood, Ill.

“We sought to examine the prevalence of sexual harassment in academic vascular surgery practices, identify factors associated with occurrence, determine reporting barriers, and identify any gender bias that exists,” said Dr. Aulivola.

In Wednesday’s VESS session, Dr. Aulivola will present the results of an anonymous survey that she and Matthew R. Smeds, MD, of Saint Louis University, conducted to examine the issue. The survey was emailed to 346 vascular surgery faculty members at 52 training sites in the United States.

“This research stemmed from a similar project done in vascular surgery trainees (residents and trainees) that identified a significant amount of harassment occurring at this level with a concomitant fear of reporting and lack of knowledge of institutional reporting mechanisms. We thought an analysis of harassment at the attending physician level may be relevant. There is significant gender bias in medicine in general and a not insignificant rate of harassment that occurs,” Dr. Smeds said in an interview.

Of the invitations sent, 149 (43%) completed the survey. Among these, 48/149 (32%) thought harassment occurred more commonly in surgical specialties with historical male dominance. In addition, ignoring the behavior, and hierarchy/power dynamics were the most common reasons given for its occurrence. Overall, 61/149 (41%) reported experiencing workplace harassment. Being told unwanted sexually explicit comments/questions/jokes, being called a sexist slur/nickname, or being paid unwanted flirtation were the most commonly described behaviors.

Those harassed were significantly more likely to be female (37% vs. 13%), and on average had experienced 2.6 (of 10) types of harassment. Despite 84% of respondents acknowledging institutional reporting mechanisms, only 7.2% of the harassing behaviors were reported.

The most common reasons for not reporting including feeling the behavior was “harmless” (67%) or “nothing positive would come of it” (28%), although 30% of respondents feared repercussions or felt uncomfortable identifying as a target of sexual harassment and only 59% of respondents reported that they would feel comfortable discussing the issue with departmental/divisional leadership.

“A significant number of vascular surgeons in academic practice have experienced workplace sexual harassment,” Dr. Aulivola said. “While most are aware of institutional reporting mechanisms, very few events are reported and less than 60% of respondents feel comfortable reporting to departmental/divisional leadership. Female vascular surgeons believe gender influences hiring, promotion, compensation, and attainment of life goals. Further work is necessary to identify methods of reducing workplace sexual harassment and optimize gender disparity in academic vascular surgery practice,” she concluded. 

Wednesday, June 12
12:30-4:15 p.m.
Gaylord National, Maryland D
V2: VESS Paper Session 2: VESS18

Sexual harassment is known to be more pervasive in male-dominated workplaces and flourishes in a climate of tolerance and culture of silence, according to Bernadette Aulivola, MD, of Loyola University Medical Center, Maywood, Ill.

“We sought to examine the prevalence of sexual harassment in academic vascular surgery practices, identify factors associated with occurrence, determine reporting barriers, and identify any gender bias that exists,” said Dr. Aulivola.

In Wednesday’s VESS session, Dr. Aulivola will present the results of an anonymous survey that she and Matthew R. Smeds, MD, of Saint Louis University, conducted to examine the issue. The survey was emailed to 346 vascular surgery faculty members at 52 training sites in the United States.

“This research stemmed from a similar project done in vascular surgery trainees (residents and trainees) that identified a significant amount of harassment occurring at this level with a concomitant fear of reporting and lack of knowledge of institutional reporting mechanisms. We thought an analysis of harassment at the attending physician level may be relevant. There is significant gender bias in medicine in general and a not insignificant rate of harassment that occurs,” Dr. Smeds said in an interview.

Of the invitations sent, 149 (43%) completed the survey. Among these, 48/149 (32%) thought harassment occurred more commonly in surgical specialties with historical male dominance. In addition, ignoring the behavior, and hierarchy/power dynamics were the most common reasons given for its occurrence. Overall, 61/149 (41%) reported experiencing workplace harassment. Being told unwanted sexually explicit comments/questions/jokes, being called a sexist slur/nickname, or being paid unwanted flirtation were the most commonly described behaviors.

Those harassed were significantly more likely to be female (37% vs. 13%), and on average had experienced 2.6 (of 10) types of harassment. Despite 84% of respondents acknowledging institutional reporting mechanisms, only 7.2% of the harassing behaviors were reported.

The most common reasons for not reporting including feeling the behavior was “harmless” (67%) or “nothing positive would come of it” (28%), although 30% of respondents feared repercussions or felt uncomfortable identifying as a target of sexual harassment and only 59% of respondents reported that they would feel comfortable discussing the issue with departmental/divisional leadership.

“A significant number of vascular surgeons in academic practice have experienced workplace sexual harassment,” Dr. Aulivola said. “While most are aware of institutional reporting mechanisms, very few events are reported and less than 60% of respondents feel comfortable reporting to departmental/divisional leadership. Female vascular surgeons believe gender influences hiring, promotion, compensation, and attainment of life goals. Further work is necessary to identify methods of reducing workplace sexual harassment and optimize gender disparity in academic vascular surgery practice,” she concluded. 

Wednesday, June 12
12:30-4:15 p.m.
Gaylord National, Maryland D
V2: VESS Paper Session 2: VESS18

Sexual harassment is known to be more pervasive in male-dominated workplaces and flourishes in a climate of tolerance and culture of silence, according to Bernadette Aulivola, MD, of Loyola University Medical Center, Maywood, Ill.

“We sought to examine the prevalence of sexual harassment in academic vascular surgery practices, identify factors associated with occurrence, determine reporting barriers, and identify any gender bias that exists,” said Dr. Aulivola.

In Wednesday’s VESS session, Dr. Aulivola will present the results of an anonymous survey that she and Matthew R. Smeds, MD, of Saint Louis University, conducted to examine the issue. The survey was emailed to 346 vascular surgery faculty members at 52 training sites in the United States.

“This research stemmed from a similar project done in vascular surgery trainees (residents and trainees) that identified a significant amount of harassment occurring at this level with a concomitant fear of reporting and lack of knowledge of institutional reporting mechanisms. We thought an analysis of harassment at the attending physician level may be relevant. There is significant gender bias in medicine in general and a not insignificant rate of harassment that occurs,” Dr. Smeds said in an interview.

Of the invitations sent, 149 (43%) completed the survey. Among these, 48/149 (32%) thought harassment occurred more commonly in surgical specialties with historical male dominance. In addition, ignoring the behavior, and hierarchy/power dynamics were the most common reasons given for its occurrence. Overall, 61/149 (41%) reported experiencing workplace harassment. Being told unwanted sexually explicit comments/questions/jokes, being called a sexist slur/nickname, or being paid unwanted flirtation were the most commonly described behaviors.

Those harassed were significantly more likely to be female (37% vs. 13%), and on average had experienced 2.6 (of 10) types of harassment. Despite 84% of respondents acknowledging institutional reporting mechanisms, only 7.2% of the harassing behaviors were reported.

The most common reasons for not reporting including feeling the behavior was “harmless” (67%) or “nothing positive would come of it” (28%), although 30% of respondents feared repercussions or felt uncomfortable identifying as a target of sexual harassment and only 59% of respondents reported that they would feel comfortable discussing the issue with departmental/divisional leadership.

“A significant number of vascular surgeons in academic practice have experienced workplace sexual harassment,” Dr. Aulivola said. “While most are aware of institutional reporting mechanisms, very few events are reported and less than 60% of respondents feel comfortable reporting to departmental/divisional leadership. Female vascular surgeons believe gender influences hiring, promotion, compensation, and attainment of life goals. Further work is necessary to identify methods of reducing workplace sexual harassment and optimize gender disparity in academic vascular surgery practice,” she concluded. 

Wednesday, June 12
12:30-4:15 p.m.
Gaylord National, Maryland D
V2: VESS Paper Session 2: VESS18

Come see exhibitors present new ideas, showcase new technologies, and discuss the latest trends in vascular surgery. All Vascular Live events will take place at the Vascular Live stage in the Auditorium, on the lower level of the convention center.

Thursday, June 13

12:15 – 12:45 p.m.
Sponsored by Gore
Case Examples from the EU of the New GORE^® TAG^® Conformable Thoracic Stent Graft with ACTIVE CONTROL^® System
Speaker: Prof. Dittmar Böckler

12:45 – 1:15 p.m.
Sponsored by Gore
Lower Limb Stent Grafting: Complex Cases and Techniques in SFA and Aortoiliac Disease
Speaker: Krishna Mannava, MD

3 – 3:30 p.m.
Sponsored by Silk Road Medical
Latest (Breaking) Clinical Evidence Strongly Supports Developing a TCAR Program – Why and How from a Vascular Surgery Perspective
Speakers: Sumaira Macdonald, MD; Jeffrey Jim, MD; Marc L. Schermerhorn, MD; and Michael C. Stoner, MD
 

5:30 – 6 p.m.
Sponsored by Thompson Surgical
Technological Advances and the Evolution of the ‘Mini-Open’ Anterior Spine Exposure Technique
Speaker: Jonathan E. Schoeff, MD

6 – 6:30 p.m.
Sponsored by Amgen
Criticality of LDC-C Lowering in Patients with PAD
Speaker: Marc P. Bonaca, MD
 

Friday, June 14

9:30 – 10 a.m.
Sponsored by Abbott
Access & Closure Techniques for Complex Aortic Cases
Speaker: Jason T. Lee, MD

12:30 – 1 p.m.
Sponsored by Abbott
A Clinical Review of the WavelineQ 4F EndoAVF System
Speakers: Todd Berland, MD; Paul B. Kreienberg, MD; and Eric K. Peden, MD

1 – 1:30 p.m.
Sponsored by Abbott
EPDs in the Lower Limb: Why and When to Use Them
Speaker: April Estelle Nedeau, MD

3 – 3:30 p.m.
Sponsored by Medtronic
Clinical Significance of Sac Regression with Case Examples
Speaker: TBD
 

Vascular Live presentations are not eligible for CME credit. 

Come see exhibitors present new ideas, showcase new technologies, and discuss the latest trends in vascular surgery. All Vascular Live events will take place at the Vascular Live stage in the Auditorium, on the lower level of the convention center.

Thursday, June 13

12:15 – 12:45 p.m.
Sponsored by Gore
Case Examples from the EU of the New GORE^® TAG^® Conformable Thoracic Stent Graft with ACTIVE CONTROL^® System
Speaker: Prof. Dittmar Böckler

12:45 – 1:15 p.m.
Sponsored by Gore
Lower Limb Stent Grafting: Complex Cases and Techniques in SFA and Aortoiliac Disease
Speaker: Krishna Mannava, MD

3 – 3:30 p.m.
Sponsored by Silk Road Medical
Latest (Breaking) Clinical Evidence Strongly Supports Developing a TCAR Program – Why and How from a Vascular Surgery Perspective
Speakers: Sumaira Macdonald, MD; Jeffrey Jim, MD; Marc L. Schermerhorn, MD; and Michael C. Stoner, MD
 

5:30 – 6 p.m.
Sponsored by Thompson Surgical
Technological Advances and the Evolution of the ‘Mini-Open’ Anterior Spine Exposure Technique
Speaker: Jonathan E. Schoeff, MD

6 – 6:30 p.m.
Sponsored by Amgen
Criticality of LDC-C Lowering in Patients with PAD
Speaker: Marc P. Bonaca, MD
 

Friday, June 14

9:30 – 10 a.m.
Sponsored by Abbott
Access & Closure Techniques for Complex Aortic Cases
Speaker: Jason T. Lee, MD

12:30 – 1 p.m.
Sponsored by Abbott
A Clinical Review of the WavelineQ 4F EndoAVF System
Speakers: Todd Berland, MD; Paul B. Kreienberg, MD; and Eric K. Peden, MD

1 – 1:30 p.m.
Sponsored by Abbott
EPDs in the Lower Limb: Why and When to Use Them
Speaker: April Estelle Nedeau, MD

3 – 3:30 p.m.
Sponsored by Medtronic
Clinical Significance of Sac Regression with Case Examples
Speaker: TBD
 

Vascular Live presentations are not eligible for CME credit. 

Come see exhibitors present new ideas, showcase new technologies, and discuss the latest trends in vascular surgery. All Vascular Live events will take place at the Vascular Live stage in the Auditorium, on the lower level of the convention center.

Thursday, June 13

12:15 – 12:45 p.m.
Sponsored by Gore
Case Examples from the EU of the New GORE^® TAG^® Conformable Thoracic Stent Graft with ACTIVE CONTROL^® System
Speaker: Prof. Dittmar Böckler

12:45 – 1:15 p.m.
Sponsored by Gore
Lower Limb Stent Grafting: Complex Cases and Techniques in SFA and Aortoiliac Disease
Speaker: Krishna Mannava, MD

3 – 3:30 p.m.
Sponsored by Silk Road Medical
Latest (Breaking) Clinical Evidence Strongly Supports Developing a TCAR Program – Why and How from a Vascular Surgery Perspective
Speakers: Sumaira Macdonald, MD; Jeffrey Jim, MD; Marc L. Schermerhorn, MD; and Michael C. Stoner, MD
 

5:30 – 6 p.m.
Sponsored by Thompson Surgical
Technological Advances and the Evolution of the ‘Mini-Open’ Anterior Spine Exposure Technique
Speaker: Jonathan E. Schoeff, MD

6 – 6:30 p.m.
Sponsored by Amgen
Criticality of LDC-C Lowering in Patients with PAD
Speaker: Marc P. Bonaca, MD
 

Friday, June 14

9:30 – 10 a.m.
Sponsored by Abbott
Access & Closure Techniques for Complex Aortic Cases
Speaker: Jason T. Lee, MD

12:30 – 1 p.m.
Sponsored by Abbott
A Clinical Review of the WavelineQ 4F EndoAVF System
Speakers: Todd Berland, MD; Paul B. Kreienberg, MD; and Eric K. Peden, MD

1 – 1:30 p.m.
Sponsored by Abbott
EPDs in the Lower Limb: Why and When to Use Them
Speaker: April Estelle Nedeau, MD

3 – 3:30 p.m.
Sponsored by Medtronic
Clinical Significance of Sac Regression with Case Examples
Speaker: TBD
 

Vascular Live presentations are not eligible for CME credit. 

The Exhibit Hall is an integral part of the Vascular Annual Meeting. All members of the vascular team, as well as other attendees, will be able to see a wide-ranging array of products of interest to vascular surgeons and their teams from dozens of vendors.

The VAM website (vsweb.org/VAM19) and mobile app offer a listing of exhibitors. A real-time floor plan (vsweb.org/FloorMap) helps attendees navigate the Exhibit Hall to find the products they most want to see.

Martin Allred

This year’s Exhibit Hall also will include the Office Vascular Care Pavilion, of interest particularly for those clinicians who perform procedures in outpatient and office-based settings. Five vendors currently plan to exhibit at the pavilion, and four presentations for office-based providers are scheduled. 

The Exhibit Hall on the lower level also hosts fun and games – literally. It’s the site for the Opening and Closing receptions, on Thursday and Friday evenings, respectively and the Scavenger Hunt. And attendees can also take advantage of non-CME learning opportunities, giveaways, training opportunities and networking potential.

The Opening Reception takes place from 5 to 6:30 p.m., coinciding with the Interactive Poster Session. The Closing Reception is from 4:30 to 5:30 p.m. Friday. It’s a great time to browse the exhibits, talk with vendors, meet up with friends and colleagues, sip on a beverage, and enjoy the food.

Participate in Scavenger Hunt

Games? That would be the Vascular Annual Meeting Scavenger Hunt, sure to be a hit with those with even a bit of a competitive streak. It’s simple and it’s fun. Just download the Mobile App to scan the QR codes found in sponsors’ booths throughout the Exhibit Hall. When a multiple-choice question appears on the display, answer it. Correct answers earn 10 points. 

Vascular Live hosts innovative sessions about the latest products and development related to vascular surgery, in a theater-in-the-round setting during Thursday and Friday’s coffee breaks and lunch hours. These frequently are standing-room only, so be sure to arrive early for a good seat. (See the VAM Planner and the mobile app.)

The Exhibit Hall also is the place to be for coffee breaks, 10 a.m. and 3 p.m. Thursday and 9:30 a.m. and 3 p.m. Friday as well as lunch, at 12 p.m. Thursday and 12:15 p.m. Friday. Food stations offer box lunches – free to attendees, though tickets are required. And there are plenty of tables to permit sitting down and chatting with colleagues for a bit.

Industry participation in the VAM exhibits underwrites a significant portion of VAM, thereby allowing us to keep registration fees at a much lower rate than other industry meetings. Please support our industry partners. A complete list of exhibitors and their booth locations are found in the Connections on-site publication and in the Mobile App, VAM Planner and VAM website (vsweb.org/VAM19). 

The Exhibit Hall is an integral part of the Vascular Annual Meeting. All members of the vascular team, as well as other attendees, will be able to see a wide-ranging array of products of interest to vascular surgeons and their teams from dozens of vendors.

The VAM website (vsweb.org/VAM19) and mobile app offer a listing of exhibitors. A real-time floor plan (vsweb.org/FloorMap) helps attendees navigate the Exhibit Hall to find the products they most want to see.

Martin Allred

This year’s Exhibit Hall also will include the Office Vascular Care Pavilion, of interest particularly for those clinicians who perform procedures in outpatient and office-based settings. Five vendors currently plan to exhibit at the pavilion, and four presentations for office-based providers are scheduled. 

The Exhibit Hall on the lower level also hosts fun and games – literally. It’s the site for the Opening and Closing receptions, on Thursday and Friday evenings, respectively and the Scavenger Hunt. And attendees can also take advantage of non-CME learning opportunities, giveaways, training opportunities and networking potential.

The Opening Reception takes place from 5 to 6:30 p.m., coinciding with the Interactive Poster Session. The Closing Reception is from 4:30 to 5:30 p.m. Friday. It’s a great time to browse the exhibits, talk with vendors, meet up with friends and colleagues, sip on a beverage, and enjoy the food.

Participate in Scavenger Hunt

Games? That would be the Vascular Annual Meeting Scavenger Hunt, sure to be a hit with those with even a bit of a competitive streak. It’s simple and it’s fun. Just download the Mobile App to scan the QR codes found in sponsors’ booths throughout the Exhibit Hall. When a multiple-choice question appears on the display, answer it. Correct answers earn 10 points. 

Vascular Live hosts innovative sessions about the latest products and development related to vascular surgery, in a theater-in-the-round setting during Thursday and Friday’s coffee breaks and lunch hours. These frequently are standing-room only, so be sure to arrive early for a good seat. (See the VAM Planner and the mobile app.)

The Exhibit Hall also is the place to be for coffee breaks, 10 a.m. and 3 p.m. Thursday and 9:30 a.m. and 3 p.m. Friday as well as lunch, at 12 p.m. Thursday and 12:15 p.m. Friday. Food stations offer box lunches – free to attendees, though tickets are required. And there are plenty of tables to permit sitting down and chatting with colleagues for a bit.

Industry participation in the VAM exhibits underwrites a significant portion of VAM, thereby allowing us to keep registration fees at a much lower rate than other industry meetings. Please support our industry partners. A complete list of exhibitors and their booth locations are found in the Connections on-site publication and in the Mobile App, VAM Planner and VAM website (vsweb.org/VAM19). 

The Exhibit Hall is an integral part of the Vascular Annual Meeting. All members of the vascular team, as well as other attendees, will be able to see a wide-ranging array of products of interest to vascular surgeons and their teams from dozens of vendors.

The VAM website (vsweb.org/VAM19) and mobile app offer a listing of exhibitors. A real-time floor plan (vsweb.org/FloorMap) helps attendees navigate the Exhibit Hall to find the products they most want to see.

Martin Allred

This year’s Exhibit Hall also will include the Office Vascular Care Pavilion, of interest particularly for those clinicians who perform procedures in outpatient and office-based settings. Five vendors currently plan to exhibit at the pavilion, and four presentations for office-based providers are scheduled. 

The Exhibit Hall on the lower level also hosts fun and games – literally. It’s the site for the Opening and Closing receptions, on Thursday and Friday evenings, respectively and the Scavenger Hunt. And attendees can also take advantage of non-CME learning opportunities, giveaways, training opportunities and networking potential.

The Opening Reception takes place from 5 to 6:30 p.m., coinciding with the Interactive Poster Session. The Closing Reception is from 4:30 to 5:30 p.m. Friday. It’s a great time to browse the exhibits, talk with vendors, meet up with friends and colleagues, sip on a beverage, and enjoy the food.

Participate in Scavenger Hunt

Games? That would be the Vascular Annual Meeting Scavenger Hunt, sure to be a hit with those with even a bit of a competitive streak. It’s simple and it’s fun. Just download the Mobile App to scan the QR codes found in sponsors’ booths throughout the Exhibit Hall. When a multiple-choice question appears on the display, answer it. Correct answers earn 10 points. 

Vascular Live hosts innovative sessions about the latest products and development related to vascular surgery, in a theater-in-the-round setting during Thursday and Friday’s coffee breaks and lunch hours. These frequently are standing-room only, so be sure to arrive early for a good seat. (See the VAM Planner and the mobile app.)

The Exhibit Hall also is the place to be for coffee breaks, 10 a.m. and 3 p.m. Thursday and 9:30 a.m. and 3 p.m. Friday as well as lunch, at 12 p.m. Thursday and 12:15 p.m. Friday. Food stations offer box lunches – free to attendees, though tickets are required. And there are plenty of tables to permit sitting down and chatting with colleagues for a bit.

Industry participation in the VAM exhibits underwrites a significant portion of VAM, thereby allowing us to keep registration fees at a much lower rate than other industry meetings. Please support our industry partners. A complete list of exhibitors and their booth locations are found in the Connections on-site publication and in the Mobile App, VAM Planner and VAM website (vsweb.org/VAM19). 

This year’s VAM features an exhibit pavilion, special Vascular Live presentations, and a breakfast session geared specifically to clinicians who work in office and outpatient settings.

The Office Vascular Care Pavilion is in Exhibit Hall B, on the lower level of the Gaylord National Resort & Convention Center, across from the SVS Booth. Office Vascular Care Live presentations (not eligible for CME credit) include:
 

Thursday, June 13

12:30 to 1 p.m. OBL 101; Krishna M. Jain, MD

3 to 3:30 p.m. OBL Chatter, industry presentations by Cordis®, A Cardinal Health company, Philips and Vein Care iGuide
Sessions include: Coming to a town near you! Life Cycle of an OBL, Factors Influencing Behavior of an OBL, and Industry Partnership, sponsored by Cordis®, A Cardinal Health company
Keys to Success and Methods of Failure in Today’s OBL, David Baker, sponsored by Philips
 

Friday, June 14

12:30 to 1 p.m. OBL Tips and Tools; R. Clement Darling III, MD

3 to 3:30 p.m. OBL Quality and Safety; Robert G. Molnar, MD 

8:30 to 9:30 a.m. Ticket Required - The SVS also has a new member section focused on the move to outpatient and office-based settings, the Section on Outpatient and Office Vascular Care (SOOVC), which will hold its first meeting Friday in National Harbor 3. Tickets are available at Registration. Prospective members are welcome.

Saturday, June 15

6:30 to 8 a.m. Breakfast Session 9 will cover “Complications in Office-Based Procedures: Their Prevention and Management.” It is being presented in collaboration with the Outpatient Endovascular and Interventional Society. 

This year’s VAM features an exhibit pavilion, special Vascular Live presentations, and a breakfast session geared specifically to clinicians who work in office and outpatient settings.

The Office Vascular Care Pavilion is in Exhibit Hall B, on the lower level of the Gaylord National Resort & Convention Center, across from the SVS Booth. Office Vascular Care Live presentations (not eligible for CME credit) include:
 

Thursday, June 13

12:30 to 1 p.m. OBL 101; Krishna M. Jain, MD

3 to 3:30 p.m. OBL Chatter, industry presentations by Cordis®, A Cardinal Health company, Philips and Vein Care iGuide
Sessions include: Coming to a town near you! Life Cycle of an OBL, Factors Influencing Behavior of an OBL, and Industry Partnership, sponsored by Cordis®, A Cardinal Health company
Keys to Success and Methods of Failure in Today’s OBL, David Baker, sponsored by Philips
 

Friday, June 14

12:30 to 1 p.m. OBL Tips and Tools; R. Clement Darling III, MD

3 to 3:30 p.m. OBL Quality and Safety; Robert G. Molnar, MD 

8:30 to 9:30 a.m. Ticket Required - The SVS also has a new member section focused on the move to outpatient and office-based settings, the Section on Outpatient and Office Vascular Care (SOOVC), which will hold its first meeting Friday in National Harbor 3. Tickets are available at Registration. Prospective members are welcome.

Saturday, June 15

6:30 to 8 a.m. Breakfast Session 9 will cover “Complications in Office-Based Procedures: Their Prevention and Management.” It is being presented in collaboration with the Outpatient Endovascular and Interventional Society. 

This year’s VAM features an exhibit pavilion, special Vascular Live presentations, and a breakfast session geared specifically to clinicians who work in office and outpatient settings.

The Office Vascular Care Pavilion is in Exhibit Hall B, on the lower level of the Gaylord National Resort & Convention Center, across from the SVS Booth. Office Vascular Care Live presentations (not eligible for CME credit) include:
 

Thursday, June 13

12:30 to 1 p.m. OBL 101; Krishna M. Jain, MD

3 to 3:30 p.m. OBL Chatter, industry presentations by Cordis®, A Cardinal Health company, Philips and Vein Care iGuide
Sessions include: Coming to a town near you! Life Cycle of an OBL, Factors Influencing Behavior of an OBL, and Industry Partnership, sponsored by Cordis®, A Cardinal Health company
Keys to Success and Methods of Failure in Today’s OBL, David Baker, sponsored by Philips
 

Friday, June 14

12:30 to 1 p.m. OBL Tips and Tools; R. Clement Darling III, MD

3 to 3:30 p.m. OBL Quality and Safety; Robert G. Molnar, MD 

8:30 to 9:30 a.m. Ticket Required - The SVS also has a new member section focused on the move to outpatient and office-based settings, the Section on Outpatient and Office Vascular Care (SOOVC), which will hold its first meeting Friday in National Harbor 3. Tickets are available at Registration. Prospective members are welcome.

Saturday, June 15

6:30 to 8 a.m. Breakfast Session 9 will cover “Complications in Office-Based Procedures: Their Prevention and Management.” It is being presented in collaboration with the Outpatient Endovascular and Interventional Society. 

Nonhealing wounds in patients with diabetes are a major cause of morbidity and mortality in the United States and are increasing at an alarming rate. Equally concerning, the current “standard of care” leaves 70% of diabetic wounds unhealed. Given this substantial impact on patient outcomes and health care expenditure, a critical unmet need exists for improved understanding of the pathophysiology of diabetic wounds to develop effective treatments.

This year’s SVS Foundation’s Resident Research Award is being presented to Frank M. Davis, MD, of the University of Michigan, Ann Arbor, for his research on the epigenetic regulation of the prostaglandin pathway in macrophages during type 2 diabetic wound healing. Dr. Davis, and his mentor Katherine Gallagher, MD, also from the University of Michigan, investigated how impairments in the innate immune system in patients with diabetes promote chronic inflammation and impair wound healing.

Dr. Davis will present his award-winning research in the von Liebig Forum, Thursday, June 13, discussing the role of specific epigenetic enzymes in the dictation of macrophage phenotype in wound tissue. The talk will cover how diabetes alters those enzymes to influence a deleterious phenotype that promotes inflammation and delays wound healing. “Our laboratory specifically looks at the role of monocytes/macrophages in the inflammatory phase of wound healing and how perturbation in the local environment – such as those seen in diabetes – affects monocyte/macrophage phenotype and ultimately wound healing” said Dr. Davis.

The talk will specifically cover the cyclo-oxygenase (COX)-2/prostaglandin E₂ (PGE₂) axis. Using both a murine model and human wound samples Dr. Davis demonstrates that PGE₂ is substantially elevated in diabetic wound macrophages. Further, aberrant PGE₂ production in diabetic macrophages depended on epigenetic alterations to key enzymes in the PGE₂ pathway.

Specifically, MLL1, a histone methyltransferase, increased H3K4 trimethylation resulting in upregulation of PGE₂ in diabetic wound macrophages. Additionally, the authors found that augmentation to miR-29b and DNA methyltransferases in diabetic macrophage result in increased COX-2 expression. Overall, the increased COX-2/PGE₂ production in diabetic macrophages impairs bacterial killing, predisposing diabetic wounds to chronic infection.

“Our research provides insight into the prostaglandin E₂ axis and its role in macrophage inflammation, which has previously been an unrecognized pathway leading to delayed diabetic wound healing” added Dr. Gallagher.

Finally, in his presentation, Dr. Davis will discuss translational therapies as inhibition of the PGE₂ pathway through macrophage targeted nanoparticles decreased diabetic inflammation and improved healing. “Together, our results indicate the COX-2/PGE₂ pathway is a critical regulator of macrophage phenotype and impaired diabetic wound healing. This work identifies therapeutic targets for negating dysregulated inflammation in diabetic wounds and identifies macrophage-targeted local therapy as an effective means of improving wound healing,” Dr. Davis concluded.

Nonhealing wounds in patients with diabetes are a major cause of morbidity and mortality in the United States and are increasing at an alarming rate. Equally concerning, the current “standard of care” leaves 70% of diabetic wounds unhealed. Given this substantial impact on patient outcomes and health care expenditure, a critical unmet need exists for improved understanding of the pathophysiology of diabetic wounds to develop effective treatments.

This year’s SVS Foundation’s Resident Research Award is being presented to Frank M. Davis, MD, of the University of Michigan, Ann Arbor, for his research on the epigenetic regulation of the prostaglandin pathway in macrophages during type 2 diabetic wound healing. Dr. Davis, and his mentor Katherine Gallagher, MD, also from the University of Michigan, investigated how impairments in the innate immune system in patients with diabetes promote chronic inflammation and impair wound healing.

Dr. Davis will present his award-winning research in the von Liebig Forum, Thursday, June 13, discussing the role of specific epigenetic enzymes in the dictation of macrophage phenotype in wound tissue. The talk will cover how diabetes alters those enzymes to influence a deleterious phenotype that promotes inflammation and delays wound healing. “Our laboratory specifically looks at the role of monocytes/macrophages in the inflammatory phase of wound healing and how perturbation in the local environment – such as those seen in diabetes – affects monocyte/macrophage phenotype and ultimately wound healing” said Dr. Davis.

The talk will specifically cover the cyclo-oxygenase (COX)-2/prostaglandin E₂ (PGE₂) axis. Using both a murine model and human wound samples Dr. Davis demonstrates that PGE₂ is substantially elevated in diabetic wound macrophages. Further, aberrant PGE₂ production in diabetic macrophages depended on epigenetic alterations to key enzymes in the PGE₂ pathway.

Specifically, MLL1, a histone methyltransferase, increased H3K4 trimethylation resulting in upregulation of PGE₂ in diabetic wound macrophages. Additionally, the authors found that augmentation to miR-29b and DNA methyltransferases in diabetic macrophage result in increased COX-2 expression. Overall, the increased COX-2/PGE₂ production in diabetic macrophages impairs bacterial killing, predisposing diabetic wounds to chronic infection.

“Our research provides insight into the prostaglandin E₂ axis and its role in macrophage inflammation, which has previously been an unrecognized pathway leading to delayed diabetic wound healing” added Dr. Gallagher.

Finally, in his presentation, Dr. Davis will discuss translational therapies as inhibition of the PGE₂ pathway through macrophage targeted nanoparticles decreased diabetic inflammation and improved healing. “Together, our results indicate the COX-2/PGE₂ pathway is a critical regulator of macrophage phenotype and impaired diabetic wound healing. This work identifies therapeutic targets for negating dysregulated inflammation in diabetic wounds and identifies macrophage-targeted local therapy as an effective means of improving wound healing,” Dr. Davis concluded.

Nonhealing wounds in patients with diabetes are a major cause of morbidity and mortality in the United States and are increasing at an alarming rate. Equally concerning, the current “standard of care” leaves 70% of diabetic wounds unhealed. Given this substantial impact on patient outcomes and health care expenditure, a critical unmet need exists for improved understanding of the pathophysiology of diabetic wounds to develop effective treatments.

This year’s SVS Foundation’s Resident Research Award is being presented to Frank M. Davis, MD, of the University of Michigan, Ann Arbor, for his research on the epigenetic regulation of the prostaglandin pathway in macrophages during type 2 diabetic wound healing. Dr. Davis, and his mentor Katherine Gallagher, MD, also from the University of Michigan, investigated how impairments in the innate immune system in patients with diabetes promote chronic inflammation and impair wound healing.

Dr. Davis will present his award-winning research in the von Liebig Forum, Thursday, June 13, discussing the role of specific epigenetic enzymes in the dictation of macrophage phenotype in wound tissue. The talk will cover how diabetes alters those enzymes to influence a deleterious phenotype that promotes inflammation and delays wound healing. “Our laboratory specifically looks at the role of monocytes/macrophages in the inflammatory phase of wound healing and how perturbation in the local environment – such as those seen in diabetes – affects monocyte/macrophage phenotype and ultimately wound healing” said Dr. Davis.

The talk will specifically cover the cyclo-oxygenase (COX)-2/prostaglandin E₂ (PGE₂) axis. Using both a murine model and human wound samples Dr. Davis demonstrates that PGE₂ is substantially elevated in diabetic wound macrophages. Further, aberrant PGE₂ production in diabetic macrophages depended on epigenetic alterations to key enzymes in the PGE₂ pathway.

Specifically, MLL1, a histone methyltransferase, increased H3K4 trimethylation resulting in upregulation of PGE₂ in diabetic wound macrophages. Additionally, the authors found that augmentation to miR-29b and DNA methyltransferases in diabetic macrophage result in increased COX-2 expression. Overall, the increased COX-2/PGE₂ production in diabetic macrophages impairs bacterial killing, predisposing diabetic wounds to chronic infection.

“Our research provides insight into the prostaglandin E₂ axis and its role in macrophage inflammation, which has previously been an unrecognized pathway leading to delayed diabetic wound healing” added Dr. Gallagher.

Finally, in his presentation, Dr. Davis will discuss translational therapies as inhibition of the PGE₂ pathway through macrophage targeted nanoparticles decreased diabetic inflammation and improved healing. “Together, our results indicate the COX-2/PGE₂ pathway is a critical regulator of macrophage phenotype and impaired diabetic wound healing. This work identifies therapeutic targets for negating dysregulated inflammation in diabetic wounds and identifies macrophage-targeted local therapy as an effective means of improving wound healing,” Dr. Davis concluded.

Among patients with moderate to severe ulcerative colitis, a median of 1.4 years and up to 4.4 years of tofacitinib therapy was safe apart from a dose-related increase in risk of herpes zoster infection, according to an integrated analysis of data from five clinical trials.

clsgraphics/iStockphoto

Compared with placebo, a 5-mg twice-daily maintenance dose of tofacitinib (Xeljanz) produced a 2.1-fold greater risk of herpes zoster infection (95% confidence interval, 0.4-6.0), while a 10-mg, twice-daily dose produced a statistically significant 6.6-fold increase in incidence (95% CI, 3.2-12.2).

With the exception of the higher incidence rate of herpes zoster, “in the overall cohort, the safety profile of tofacitinib was generally similar to that of tumor necrosis factor inhibitor therapies,” wrote William J. Sandborn, MD, director of the inflammatory bowel disease center and professor of medicine, at the University of California, San Diego, and associates. The findings were published in Clinical Gastroenterology and Hepatology.

Tofacitinib is an oral, small-molecular Janus kinase inhibitor approved in the United States for treating moderate to severe ulcerative colitis, as well as rheumatoid and psoriatic arthritis. The recommended ulcerative colitis dose is 10 mg twice daily for at least 8 weeks (induction therapy) followed by 5 or 10 mg twice daily (maintenance). The safety of tofacitinib has been studied in patients with rheumatoid arthritis through 9 years of treatment. To begin a similar undertaking in ulcerative colitis, Dr. Sandborn and associates pooled data from three 8-week, double-blind, placebo-controlled induction trials, as well as one 52-week, double-blind, placebo-controlled maintenance trial and one ongoing open-label trial. All patients received twice-daily tofacitinib (5 mg or 10 mg) or placebo.

Among 1,157 tofacitinib recipients in the pooled analysis, 84% received an average of 10 mg twice daily. For every 100 person-years of tofacitinib exposure, there were an estimated 2.0 serious infections, 1.3 opportunistic infections, 4.1 herpes zoster infections, 1.4 malignancies (including nonmelanoma skin cancer, which had an incidence of 0.7), 0.2 major adverse cardiovascular events, and 0.2 gastrointestinal perforations. The likelihood of these events did not increase with time on tofacitinib, the researchers said.

Worsening ulcerative colitis was the most common serious adverse event for patients who received both induction and maintenance therapy. For patients on maintenance therapy, only herpes zoster infection had a higher incidence than placebo, which reached statistical significance at the 10-mg dose. These safety findings resemble those in rheumatoid arthritis trials of tofacitinib, and apart from herpes zoster, they also resemble safety data for vedolizumab (an integrin receptor antagonist), and anti-tumor necrosis factor agents in ulcerative colitis, the researchers wrote.

There were four deaths during the entire tofacitinib ulcerative colitis program, for an incidence rate of 0.2 per 100 person-years of exposure. All occurred in patients receiving 10 mg twice daily. Causes of death were dissecting aortic aneurysm, hepatic angiosarcoma, acute myeloid leukemia, and pulmonary embolism in a patient with cholangiocarcinoma that had metastasized to the peritoneum. Recently, concerns about pulmonary embolism have led the European Medicines Agency (EMA) to recommend against the use of 10-mg twice daily tofacitinib dose in patients at increased risk for pulmonary embolism.

“Compared with prior experience with tofacitinib in rheumatoid arthritis, no new or unexpected safety signals were identified,” the researchers concluded. “These safety findings support the long-term use of tofacitinib 5 and 10 mg twice daily in patients with moderately to severely active” ulcerative colitis.

Pfizer makes tofacitinib, funded the individual trials, and paid for medical writing. Dr. Sandborn disclosed grants, personal fees, and nonfinancial support from Pfizer and many other pharmaceutical companies.

SOURCE: Sandborn WJ et al. Clin Gastroenterol Hepatol. 2018 Nov 23. doi: 10.1016/j.cgh.2018.11.035.

Among patients with moderate to severe ulcerative colitis, a median of 1.4 years and up to 4.4 years of tofacitinib therapy was safe apart from a dose-related increase in risk of herpes zoster infection, according to an integrated analysis of data from five clinical trials.

clsgraphics/iStockphoto

Compared with placebo, a 5-mg twice-daily maintenance dose of tofacitinib (Xeljanz) produced a 2.1-fold greater risk of herpes zoster infection (95% confidence interval, 0.4-6.0), while a 10-mg, twice-daily dose produced a statistically significant 6.6-fold increase in incidence (95% CI, 3.2-12.2).

With the exception of the higher incidence rate of herpes zoster, “in the overall cohort, the safety profile of tofacitinib was generally similar to that of tumor necrosis factor inhibitor therapies,” wrote William J. Sandborn, MD, director of the inflammatory bowel disease center and professor of medicine, at the University of California, San Diego, and associates. The findings were published in Clinical Gastroenterology and Hepatology.

Tofacitinib is an oral, small-molecular Janus kinase inhibitor approved in the United States for treating moderate to severe ulcerative colitis, as well as rheumatoid and psoriatic arthritis. The recommended ulcerative colitis dose is 10 mg twice daily for at least 8 weeks (induction therapy) followed by 5 or 10 mg twice daily (maintenance). The safety of tofacitinib has been studied in patients with rheumatoid arthritis through 9 years of treatment. To begin a similar undertaking in ulcerative colitis, Dr. Sandborn and associates pooled data from three 8-week, double-blind, placebo-controlled induction trials, as well as one 52-week, double-blind, placebo-controlled maintenance trial and one ongoing open-label trial. All patients received twice-daily tofacitinib (5 mg or 10 mg) or placebo.

Among 1,157 tofacitinib recipients in the pooled analysis, 84% received an average of 10 mg twice daily. For every 100 person-years of tofacitinib exposure, there were an estimated 2.0 serious infections, 1.3 opportunistic infections, 4.1 herpes zoster infections, 1.4 malignancies (including nonmelanoma skin cancer, which had an incidence of 0.7), 0.2 major adverse cardiovascular events, and 0.2 gastrointestinal perforations. The likelihood of these events did not increase with time on tofacitinib, the researchers said.

Worsening ulcerative colitis was the most common serious adverse event for patients who received both induction and maintenance therapy. For patients on maintenance therapy, only herpes zoster infection had a higher incidence than placebo, which reached statistical significance at the 10-mg dose. These safety findings resemble those in rheumatoid arthritis trials of tofacitinib, and apart from herpes zoster, they also resemble safety data for vedolizumab (an integrin receptor antagonist), and anti-tumor necrosis factor agents in ulcerative colitis, the researchers wrote.

There were four deaths during the entire tofacitinib ulcerative colitis program, for an incidence rate of 0.2 per 100 person-years of exposure. All occurred in patients receiving 10 mg twice daily. Causes of death were dissecting aortic aneurysm, hepatic angiosarcoma, acute myeloid leukemia, and pulmonary embolism in a patient with cholangiocarcinoma that had metastasized to the peritoneum. Recently, concerns about pulmonary embolism have led the European Medicines Agency (EMA) to recommend against the use of 10-mg twice daily tofacitinib dose in patients at increased risk for pulmonary embolism.

“Compared with prior experience with tofacitinib in rheumatoid arthritis, no new or unexpected safety signals were identified,” the researchers concluded. “These safety findings support the long-term use of tofacitinib 5 and 10 mg twice daily in patients with moderately to severely active” ulcerative colitis.

Pfizer makes tofacitinib, funded the individual trials, and paid for medical writing. Dr. Sandborn disclosed grants, personal fees, and nonfinancial support from Pfizer and many other pharmaceutical companies.

SOURCE: Sandborn WJ et al. Clin Gastroenterol Hepatol. 2018 Nov 23. doi: 10.1016/j.cgh.2018.11.035.

Among patients with moderate to severe ulcerative colitis, a median of 1.4 years and up to 4.4 years of tofacitinib therapy was safe apart from a dose-related increase in risk of herpes zoster infection, according to an integrated analysis of data from five clinical trials.

clsgraphics/iStockphoto

Compared with placebo, a 5-mg twice-daily maintenance dose of tofacitinib (Xeljanz) produced a 2.1-fold greater risk of herpes zoster infection (95% confidence interval, 0.4-6.0), while a 10-mg, twice-daily dose produced a statistically significant 6.6-fold increase in incidence (95% CI, 3.2-12.2).

With the exception of the higher incidence rate of herpes zoster, “in the overall cohort, the safety profile of tofacitinib was generally similar to that of tumor necrosis factor inhibitor therapies,” wrote William J. Sandborn, MD, director of the inflammatory bowel disease center and professor of medicine, at the University of California, San Diego, and associates. The findings were published in Clinical Gastroenterology and Hepatology.

Tofacitinib is an oral, small-molecular Janus kinase inhibitor approved in the United States for treating moderate to severe ulcerative colitis, as well as rheumatoid and psoriatic arthritis. The recommended ulcerative colitis dose is 10 mg twice daily for at least 8 weeks (induction therapy) followed by 5 or 10 mg twice daily (maintenance). The safety of tofacitinib has been studied in patients with rheumatoid arthritis through 9 years of treatment. To begin a similar undertaking in ulcerative colitis, Dr. Sandborn and associates pooled data from three 8-week, double-blind, placebo-controlled induction trials, as well as one 52-week, double-blind, placebo-controlled maintenance trial and one ongoing open-label trial. All patients received twice-daily tofacitinib (5 mg or 10 mg) or placebo.

Among 1,157 tofacitinib recipients in the pooled analysis, 84% received an average of 10 mg twice daily. For every 100 person-years of tofacitinib exposure, there were an estimated 2.0 serious infections, 1.3 opportunistic infections, 4.1 herpes zoster infections, 1.4 malignancies (including nonmelanoma skin cancer, which had an incidence of 0.7), 0.2 major adverse cardiovascular events, and 0.2 gastrointestinal perforations. The likelihood of these events did not increase with time on tofacitinib, the researchers said.

Worsening ulcerative colitis was the most common serious adverse event for patients who received both induction and maintenance therapy. For patients on maintenance therapy, only herpes zoster infection had a higher incidence than placebo, which reached statistical significance at the 10-mg dose. These safety findings resemble those in rheumatoid arthritis trials of tofacitinib, and apart from herpes zoster, they also resemble safety data for vedolizumab (an integrin receptor antagonist), and anti-tumor necrosis factor agents in ulcerative colitis, the researchers wrote.

There were four deaths during the entire tofacitinib ulcerative colitis program, for an incidence rate of 0.2 per 100 person-years of exposure. All occurred in patients receiving 10 mg twice daily. Causes of death were dissecting aortic aneurysm, hepatic angiosarcoma, acute myeloid leukemia, and pulmonary embolism in a patient with cholangiocarcinoma that had metastasized to the peritoneum. Recently, concerns about pulmonary embolism have led the European Medicines Agency (EMA) to recommend against the use of 10-mg twice daily tofacitinib dose in patients at increased risk for pulmonary embolism.

“Compared with prior experience with tofacitinib in rheumatoid arthritis, no new or unexpected safety signals were identified,” the researchers concluded. “These safety findings support the long-term use of tofacitinib 5 and 10 mg twice daily in patients with moderately to severely active” ulcerative colitis.

Pfizer makes tofacitinib, funded the individual trials, and paid for medical writing. Dr. Sandborn disclosed grants, personal fees, and nonfinancial support from Pfizer and many other pharmaceutical companies.

SOURCE: Sandborn WJ et al. Clin Gastroenterol Hepatol. 2018 Nov 23. doi: 10.1016/j.cgh.2018.11.035.

Because of the increasing costs of prescription drugs and medical therapies, many patients are unable to afford the treatment they need that could improve their health or even save their lives. In the United States, drug manufacturers can set their own prices – a policy that has resulted in overall medicine costs being far higher than in other places around the globe. Increasingly, insurers are passing the costs along to patients through higher deductibles, and pharmaceutical companies are making record profits.

Something needs to change in order to achieve the right balance between maintaining pharmaceutical innovation and ensuring patients have proper access to treatments they need. Waiting for legislation, regulation, or the courts is not an effective short-term solution. Instead, hospitalists can take immediate actions to help by alleviating the costs for as many patients possible.
 

Historical context

Many might be wondering how prescription costs became so imbalanced in the first place. Here are a few important factors that played a role in the dramatic price increase of pharmaceuticals:

Entrance of generic drugs: Around 2012 the entrance of generic drugs caused major unexpected competition in the medical industry. During this time, many insurers were promoting the generic drugs and not allowing brand names to be covered when a generic substitute was available.

“Orphan drugs” and manufacturer pricing: In 2014, 33 new brand-name drugs were launched in the United States, and only 8 had a direct price competitor at the time they were introduced. In addition, manufacturers were free to set their prices. Over the past decade, introductory prices for brand name drugs have reached unprecedented levels. Furthermore, manufacturers use the patent protections to increase their prices every year, even when no significant improvements have been made to the drug.

Expiring patents: According to research, there are 182 drugs that no longer have patent protection or any associated generics available. This creates opportunities for manufacturers to maintain patent-era pricing or even engage in price gouging.

Lack of robust competition: Several high-priced blockbuster drugs hit the market to treat serious diseases, most of which do not have generic brand substitutes, which leaves only one option for patients – and it’s usually not affordable. According to research, more than 500 drugs have only one marketed generic. In addition, manufacturer mergers and acquisitions have occurred, which has led to a more concentrated and less competitive market for pricing.

Stricter Food and Drug Administration policies: American consumers have access to the safest and most advanced pharmaceutical system in the world, which requires several trials and testing before the drug can be approved and brought to the market. Despite the benefits of these strict procedures, the downside means higher costs for the brand and manufacturer that they will want to recoup through the price of the drug on the market.

Number of new drugs allowed to enter the market: New drugs that enter the market in the United States do so more quickly than in most other countries. Research shows the U.S. pharmaceutical market contributes to 45% of the global pharmaceutical market. The $76 billion in research and development that pharmaceutical companies claim overlooks the ways that U.S. employers and taxpayers pay for at least 44% through tax subsidies and credits. What makes it worse is that research shows most corporate research and development is directed at minimally innovative new drugs, using the system to secure patents and charge monopoly prices.

Compared with other high-income countries, the United States spends the most per capita on prescription drugs. While insured U.S. patients often pay little or nothing for generic prescriptions, they can be billed tens of thousands of dollars for certain high-priced medicines. The United States has the highest rate of insured patients skipping or not filling prescriptions because of cost. For example, the price of EpiPens, a drug delivery system that is crucial for persons experiencing life-threatening allergic reactions, has increased more than $500 in just 9 years.
 

How to alleviate rising drug costs

The good news is that hospitalists can do something about the high costs of pharmaceuticals.

Understand and offer alternative ways for drug intake: Many patients admitted to a hospital with severe infections are initially started with intravenous medications. Although conversion from intravenous to oral therapy is inappropriate for a patient who is critically ill or has an inability to absorb oral medications, every hospital will have a certain number of patients who are eligible for a switch from intravenous to oral therapy.

The World Health Organization (WHO) reports that the irrational use of medicines is a major problem worldwide, including antibiotics. Switching from IV to oral enables one to select a cheaper or older antibiotic that is as effective as the IV antibiotic. However, this requires breaking the belief that many physicians still have that IV medications’ bioavailability is stronger and creates less susceptibility to the illness reoccurring in the patient. For many medications, essentially the same amount of drug is found in the blood when given intravenously or orally. In addition, research has shown several benefits beyond cost reduction for oral over IV, such as earlier discharge and reduced risk of infections.

Limit unnecessary antibiotic prescriptions and consider antibiotics stewardship programs: The Center for Disease Control reports that one in three (47 million) antibiotic prescriptions are unnecessary. Most of these unnecessary antibiotics are prescribed for respiratory conditions caused by viruses including common colds, viral sore throats, bronchitis, and sinus and ear infections that do not respond to antibiotics. Although the White House released The National Action Plan for Combating Antibiotic-Resistant Bacteria (CARB) in 2015, which set a goal of reducing inappropriate outpatient antibiotic use by at least half by 2020, hospitalists can still do more by being extremely cautious with prescribing drugs to patients. Use appropriate consultants whenever necessary to suggest the right drug. For example, consider an infectious disease specialist to suggest the appropriate type and length of time for an antibiotic. In addition, hospital-based programs dedicated to improving antibiotic use, known as antibiotic stewardship programs (ASPs), have been shown to optimize the treatment of infections and reduce adverse events associated with antibiotic use.

Review labs and vitals carefully and encourage a higher level of patient care beyond the digital tools available: Studies have shown an oversight in an exam (a “miss”) can result in real consequences, including death. Our $3.4 trillion health care system is responsible for more than a quarter of a million deaths per year because of medical error. Much of that is a result of poorly coordinated care, poor communication, patients falling through the cracks, or knowledge not being transferred. “True clinical judgment is more than addressing the avalanche of blood work, imaging, and lab tests; it is about using human skills to understand where the patient is in the trajectory of a life and the disease, what the nature of the patient’s family and social circumstances is, and how much they want done,” wrote Dr. Abraham Verghese in the New York Times in 2018 (“How Tech Can Turn Doctors into Clerical Workers”). This also means understanding whether the patient is on any other type of medication and, as a result, having knowledge of possible consequences for drug interactions. Always look for safe medications or discontinue the use of any unnecessary drugs the patient is currently taking.

Allow pharmacies to automatically substitute less expensive equivalent drugs: When prescribing pharmaceuticals for patients, determine if there are any substitutes that can help alleviate costs while delivering equivalent care to the patient. This requires excellent ongoing communication with pharmacists and understanding the substitutes available, as well as any side effects or consequences.
 

Hospitalists can make a difference

There are many variables that play a role in rising pharmaceutical costs in the United States. One of the most significant is that there are no strategies in place to control pricing of drugs and the profits made by the pharmaceutical companies.

Although finding new drugs that can cure major life-threatening diseases or illnesses is important, so is ensuring that more patients have access to such drugs at a reasonable cost. While there are several ways that the government can and should help with enabling and supporting this balance, it most likely requires such large changes that it will take a long time. As a result, it is important for hospitalists to find effective short-term solutions that can be implemented right away to alleviate the rising costs of pharmaceuticals and provide proper patient care regardless of their economic status – all of which requires better research, analysis, and comparison before prescribing treatment to patients.
 

Dr. Kasarla is a hospitalist with APOGEE Physicians at Wise Surgical at Parkway in Fort Worth, Tex. He did his internal medicine residency at Mercy Hospital & Medical Center, Chicago. Contact him at madhukarreddy.kasarla@apogeephysicians.com. Dr. Devireddy is a hospitalist based at Sri Ramachandra Medical Centre, Porur, Tamilnadu, India. Contact her at drkirthireddy@gmail.com.

FURTHER READING

Olson and Sheiner (2017). “The Hutchins Center Explains: Prescription drug spending” Brooking.edu

Lo, Chris (2018). “Cost control: drug pricing policies around the world,” Pharmaceutical-Technology.com

Center for Disease Control and Prevention. (2016). 1 in 3 antibiotic prescriptions unnecessary. Retrieved Jan 31, 2019, from https://www.cdc.gov/media/releases/2016/p0503-unnecessary-prescriptions.html

Verghese, Abraham (2018). “How Tech Can Turn Doctors Into Clerical Workers” NYTimes.Com

Waxman, Corr, Martin et al (2017). “Getting to the Root of High Prescription Drug Prices” Commonwealthfund.org

American Council on Science and Health. (2018). Government Is The Big Reason EpiPen And Other Generics Are So Expensive. Retrieved Jan 31, 2019, from https://www.acsh.org/news/2018/06/23/government-big-reason-epipen-and-other-generics-are-so-expensive-13114

Statista. (2018). U.S. Pharmaceutical Industry – Statistics & Facts. Retrieved Jan 31, 2019, from https://www.statista.com/topics/1719/pharmaceutical-industry/

Because of the increasing costs of prescription drugs and medical therapies, many patients are unable to afford the treatment they need that could improve their health or even save their lives. In the United States, drug manufacturers can set their own prices – a policy that has resulted in overall medicine costs being far higher than in other places around the globe. Increasingly, insurers are passing the costs along to patients through higher deductibles, and pharmaceutical companies are making record profits.

Something needs to change in order to achieve the right balance between maintaining pharmaceutical innovation and ensuring patients have proper access to treatments they need. Waiting for legislation, regulation, or the courts is not an effective short-term solution. Instead, hospitalists can take immediate actions to help by alleviating the costs for as many patients possible.
 

Historical context

Many might be wondering how prescription costs became so imbalanced in the first place. Here are a few important factors that played a role in the dramatic price increase of pharmaceuticals:

Entrance of generic drugs: Around 2012 the entrance of generic drugs caused major unexpected competition in the medical industry. During this time, many insurers were promoting the generic drugs and not allowing brand names to be covered when a generic substitute was available.

“Orphan drugs” and manufacturer pricing: In 2014, 33 new brand-name drugs were launched in the United States, and only 8 had a direct price competitor at the time they were introduced. In addition, manufacturers were free to set their prices. Over the past decade, introductory prices for brand name drugs have reached unprecedented levels. Furthermore, manufacturers use the patent protections to increase their prices every year, even when no significant improvements have been made to the drug.

Expiring patents: According to research, there are 182 drugs that no longer have patent protection or any associated generics available. This creates opportunities for manufacturers to maintain patent-era pricing or even engage in price gouging.

Lack of robust competition: Several high-priced blockbuster drugs hit the market to treat serious diseases, most of which do not have generic brand substitutes, which leaves only one option for patients – and it’s usually not affordable. According to research, more than 500 drugs have only one marketed generic. In addition, manufacturer mergers and acquisitions have occurred, which has led to a more concentrated and less competitive market for pricing.

Stricter Food and Drug Administration policies: American consumers have access to the safest and most advanced pharmaceutical system in the world, which requires several trials and testing before the drug can be approved and brought to the market. Despite the benefits of these strict procedures, the downside means higher costs for the brand and manufacturer that they will want to recoup through the price of the drug on the market.

Number of new drugs allowed to enter the market: New drugs that enter the market in the United States do so more quickly than in most other countries. Research shows the U.S. pharmaceutical market contributes to 45% of the global pharmaceutical market. The $76 billion in research and development that pharmaceutical companies claim overlooks the ways that U.S. employers and taxpayers pay for at least 44% through tax subsidies and credits. What makes it worse is that research shows most corporate research and development is directed at minimally innovative new drugs, using the system to secure patents and charge monopoly prices.

Compared with other high-income countries, the United States spends the most per capita on prescription drugs. While insured U.S. patients often pay little or nothing for generic prescriptions, they can be billed tens of thousands of dollars for certain high-priced medicines. The United States has the highest rate of insured patients skipping or not filling prescriptions because of cost. For example, the price of EpiPens, a drug delivery system that is crucial for persons experiencing life-threatening allergic reactions, has increased more than $500 in just 9 years.
 

How to alleviate rising drug costs

The good news is that hospitalists can do something about the high costs of pharmaceuticals.

Understand and offer alternative ways for drug intake: Many patients admitted to a hospital with severe infections are initially started with intravenous medications. Although conversion from intravenous to oral therapy is inappropriate for a patient who is critically ill or has an inability to absorb oral medications, every hospital will have a certain number of patients who are eligible for a switch from intravenous to oral therapy.

The World Health Organization (WHO) reports that the irrational use of medicines is a major problem worldwide, including antibiotics. Switching from IV to oral enables one to select a cheaper or older antibiotic that is as effective as the IV antibiotic. However, this requires breaking the belief that many physicians still have that IV medications’ bioavailability is stronger and creates less susceptibility to the illness reoccurring in the patient. For many medications, essentially the same amount of drug is found in the blood when given intravenously or orally. In addition, research has shown several benefits beyond cost reduction for oral over IV, such as earlier discharge and reduced risk of infections.

Limit unnecessary antibiotic prescriptions and consider antibiotics stewardship programs: The Center for Disease Control reports that one in three (47 million) antibiotic prescriptions are unnecessary. Most of these unnecessary antibiotics are prescribed for respiratory conditions caused by viruses including common colds, viral sore throats, bronchitis, and sinus and ear infections that do not respond to antibiotics. Although the White House released The National Action Plan for Combating Antibiotic-Resistant Bacteria (CARB) in 2015, which set a goal of reducing inappropriate outpatient antibiotic use by at least half by 2020, hospitalists can still do more by being extremely cautious with prescribing drugs to patients. Use appropriate consultants whenever necessary to suggest the right drug. For example, consider an infectious disease specialist to suggest the appropriate type and length of time for an antibiotic. In addition, hospital-based programs dedicated to improving antibiotic use, known as antibiotic stewardship programs (ASPs), have been shown to optimize the treatment of infections and reduce adverse events associated with antibiotic use.

Review labs and vitals carefully and encourage a higher level of patient care beyond the digital tools available: Studies have shown an oversight in an exam (a “miss”) can result in real consequences, including death. Our $3.4 trillion health care system is responsible for more than a quarter of a million deaths per year because of medical error. Much of that is a result of poorly coordinated care, poor communication, patients falling through the cracks, or knowledge not being transferred. “True clinical judgment is more than addressing the avalanche of blood work, imaging, and lab tests; it is about using human skills to understand where the patient is in the trajectory of a life and the disease, what the nature of the patient’s family and social circumstances is, and how much they want done,” wrote Dr. Abraham Verghese in the New York Times in 2018 (“How Tech Can Turn Doctors into Clerical Workers”). This also means understanding whether the patient is on any other type of medication and, as a result, having knowledge of possible consequences for drug interactions. Always look for safe medications or discontinue the use of any unnecessary drugs the patient is currently taking.

Allow pharmacies to automatically substitute less expensive equivalent drugs: When prescribing pharmaceuticals for patients, determine if there are any substitutes that can help alleviate costs while delivering equivalent care to the patient. This requires excellent ongoing communication with pharmacists and understanding the substitutes available, as well as any side effects or consequences.
 

Hospitalists can make a difference

There are many variables that play a role in rising pharmaceutical costs in the United States. One of the most significant is that there are no strategies in place to control pricing of drugs and the profits made by the pharmaceutical companies.

Although finding new drugs that can cure major life-threatening diseases or illnesses is important, so is ensuring that more patients have access to such drugs at a reasonable cost. While there are several ways that the government can and should help with enabling and supporting this balance, it most likely requires such large changes that it will take a long time. As a result, it is important for hospitalists to find effective short-term solutions that can be implemented right away to alleviate the rising costs of pharmaceuticals and provide proper patient care regardless of their economic status – all of which requires better research, analysis, and comparison before prescribing treatment to patients.
 

Dr. Kasarla is a hospitalist with APOGEE Physicians at Wise Surgical at Parkway in Fort Worth, Tex. He did his internal medicine residency at Mercy Hospital & Medical Center, Chicago. Contact him at madhukarreddy.kasarla@apogeephysicians.com. Dr. Devireddy is a hospitalist based at Sri Ramachandra Medical Centre, Porur, Tamilnadu, India. Contact her at drkirthireddy@gmail.com.

FURTHER READING

Olson and Sheiner (2017). “The Hutchins Center Explains: Prescription drug spending” Brooking.edu

Lo, Chris (2018). “Cost control: drug pricing policies around the world,” Pharmaceutical-Technology.com

Center for Disease Control and Prevention. (2016). 1 in 3 antibiotic prescriptions unnecessary. Retrieved Jan 31, 2019, from https://www.cdc.gov/media/releases/2016/p0503-unnecessary-prescriptions.html

Verghese, Abraham (2018). “How Tech Can Turn Doctors Into Clerical Workers” NYTimes.Com

Waxman, Corr, Martin et al (2017). “Getting to the Root of High Prescription Drug Prices” Commonwealthfund.org

American Council on Science and Health. (2018). Government Is The Big Reason EpiPen And Other Generics Are So Expensive. Retrieved Jan 31, 2019, from https://www.acsh.org/news/2018/06/23/government-big-reason-epipen-and-other-generics-are-so-expensive-13114

Statista. (2018). U.S. Pharmaceutical Industry – Statistics & Facts. Retrieved Jan 31, 2019, from https://www.statista.com/topics/1719/pharmaceutical-industry/

Because of the increasing costs of prescription drugs and medical therapies, many patients are unable to afford the treatment they need that could improve their health or even save their lives. In the United States, drug manufacturers can set their own prices – a policy that has resulted in overall medicine costs being far higher than in other places around the globe. Increasingly, insurers are passing the costs along to patients through higher deductibles, and pharmaceutical companies are making record profits.

Something needs to change in order to achieve the right balance between maintaining pharmaceutical innovation and ensuring patients have proper access to treatments they need. Waiting for legislation, regulation, or the courts is not an effective short-term solution. Instead, hospitalists can take immediate actions to help by alleviating the costs for as many patients possible.
 

Historical context

Many might be wondering how prescription costs became so imbalanced in the first place. Here are a few important factors that played a role in the dramatic price increase of pharmaceuticals:

Entrance of generic drugs: Around 2012 the entrance of generic drugs caused major unexpected competition in the medical industry. During this time, many insurers were promoting the generic drugs and not allowing brand names to be covered when a generic substitute was available.

“Orphan drugs” and manufacturer pricing: In 2014, 33 new brand-name drugs were launched in the United States, and only 8 had a direct price competitor at the time they were introduced. In addition, manufacturers were free to set their prices. Over the past decade, introductory prices for brand name drugs have reached unprecedented levels. Furthermore, manufacturers use the patent protections to increase their prices every year, even when no significant improvements have been made to the drug.

Expiring patents: According to research, there are 182 drugs that no longer have patent protection or any associated generics available. This creates opportunities for manufacturers to maintain patent-era pricing or even engage in price gouging.

Lack of robust competition: Several high-priced blockbuster drugs hit the market to treat serious diseases, most of which do not have generic brand substitutes, which leaves only one option for patients – and it’s usually not affordable. According to research, more than 500 drugs have only one marketed generic. In addition, manufacturer mergers and acquisitions have occurred, which has led to a more concentrated and less competitive market for pricing.

Stricter Food and Drug Administration policies: American consumers have access to the safest and most advanced pharmaceutical system in the world, which requires several trials and testing before the drug can be approved and brought to the market. Despite the benefits of these strict procedures, the downside means higher costs for the brand and manufacturer that they will want to recoup through the price of the drug on the market.

Number of new drugs allowed to enter the market: New drugs that enter the market in the United States do so more quickly than in most other countries. Research shows the U.S. pharmaceutical market contributes to 45% of the global pharmaceutical market. The $76 billion in research and development that pharmaceutical companies claim overlooks the ways that U.S. employers and taxpayers pay for at least 44% through tax subsidies and credits. What makes it worse is that research shows most corporate research and development is directed at minimally innovative new drugs, using the system to secure patents and charge monopoly prices.

Compared with other high-income countries, the United States spends the most per capita on prescription drugs. While insured U.S. patients often pay little or nothing for generic prescriptions, they can be billed tens of thousands of dollars for certain high-priced medicines. The United States has the highest rate of insured patients skipping or not filling prescriptions because of cost. For example, the price of EpiPens, a drug delivery system that is crucial for persons experiencing life-threatening allergic reactions, has increased more than $500 in just 9 years.
 

How to alleviate rising drug costs

The good news is that hospitalists can do something about the high costs of pharmaceuticals.

Understand and offer alternative ways for drug intake: Many patients admitted to a hospital with severe infections are initially started with intravenous medications. Although conversion from intravenous to oral therapy is inappropriate for a patient who is critically ill or has an inability to absorb oral medications, every hospital will have a certain number of patients who are eligible for a switch from intravenous to oral therapy.

The World Health Organization (WHO) reports that the irrational use of medicines is a major problem worldwide, including antibiotics. Switching from IV to oral enables one to select a cheaper or older antibiotic that is as effective as the IV antibiotic. However, this requires breaking the belief that many physicians still have that IV medications’ bioavailability is stronger and creates less susceptibility to the illness reoccurring in the patient. For many medications, essentially the same amount of drug is found in the blood when given intravenously or orally. In addition, research has shown several benefits beyond cost reduction for oral over IV, such as earlier discharge and reduced risk of infections.

Limit unnecessary antibiotic prescriptions and consider antibiotics stewardship programs: The Center for Disease Control reports that one in three (47 million) antibiotic prescriptions are unnecessary. Most of these unnecessary antibiotics are prescribed for respiratory conditions caused by viruses including common colds, viral sore throats, bronchitis, and sinus and ear infections that do not respond to antibiotics. Although the White House released The National Action Plan for Combating Antibiotic-Resistant Bacteria (CARB) in 2015, which set a goal of reducing inappropriate outpatient antibiotic use by at least half by 2020, hospitalists can still do more by being extremely cautious with prescribing drugs to patients. Use appropriate consultants whenever necessary to suggest the right drug. For example, consider an infectious disease specialist to suggest the appropriate type and length of time for an antibiotic. In addition, hospital-based programs dedicated to improving antibiotic use, known as antibiotic stewardship programs (ASPs), have been shown to optimize the treatment of infections and reduce adverse events associated with antibiotic use.

Review labs and vitals carefully and encourage a higher level of patient care beyond the digital tools available: Studies have shown an oversight in an exam (a “miss”) can result in real consequences, including death. Our $3.4 trillion health care system is responsible for more than a quarter of a million deaths per year because of medical error. Much of that is a result of poorly coordinated care, poor communication, patients falling through the cracks, or knowledge not being transferred. “True clinical judgment is more than addressing the avalanche of blood work, imaging, and lab tests; it is about using human skills to understand where the patient is in the trajectory of a life and the disease, what the nature of the patient’s family and social circumstances is, and how much they want done,” wrote Dr. Abraham Verghese in the New York Times in 2018 (“How Tech Can Turn Doctors into Clerical Workers”). This also means understanding whether the patient is on any other type of medication and, as a result, having knowledge of possible consequences for drug interactions. Always look for safe medications or discontinue the use of any unnecessary drugs the patient is currently taking.

Allow pharmacies to automatically substitute less expensive equivalent drugs: When prescribing pharmaceuticals for patients, determine if there are any substitutes that can help alleviate costs while delivering equivalent care to the patient. This requires excellent ongoing communication with pharmacists and understanding the substitutes available, as well as any side effects or consequences.
 

Hospitalists can make a difference

There are many variables that play a role in rising pharmaceutical costs in the United States. One of the most significant is that there are no strategies in place to control pricing of drugs and the profits made by the pharmaceutical companies.

Although finding new drugs that can cure major life-threatening diseases or illnesses is important, so is ensuring that more patients have access to such drugs at a reasonable cost. While there are several ways that the government can and should help with enabling and supporting this balance, it most likely requires such large changes that it will take a long time. As a result, it is important for hospitalists to find effective short-term solutions that can be implemented right away to alleviate the rising costs of pharmaceuticals and provide proper patient care regardless of their economic status – all of which requires better research, analysis, and comparison before prescribing treatment to patients.
 

Dr. Kasarla is a hospitalist with APOGEE Physicians at Wise Surgical at Parkway in Fort Worth, Tex. He did his internal medicine residency at Mercy Hospital & Medical Center, Chicago. Contact him at madhukarreddy.kasarla@apogeephysicians.com. Dr. Devireddy is a hospitalist based at Sri Ramachandra Medical Centre, Porur, Tamilnadu, India. Contact her at drkirthireddy@gmail.com.

FURTHER READING

Olson and Sheiner (2017). “The Hutchins Center Explains: Prescription drug spending” Brooking.edu

Lo, Chris (2018). “Cost control: drug pricing policies around the world,” Pharmaceutical-Technology.com

Center for Disease Control and Prevention. (2016). 1 in 3 antibiotic prescriptions unnecessary. Retrieved Jan 31, 2019, from https://www.cdc.gov/media/releases/2016/p0503-unnecessary-prescriptions.html

Verghese, Abraham (2018). “How Tech Can Turn Doctors Into Clerical Workers” NYTimes.Com

Waxman, Corr, Martin et al (2017). “Getting to the Root of High Prescription Drug Prices” Commonwealthfund.org

American Council on Science and Health. (2018). Government Is The Big Reason EpiPen And Other Generics Are So Expensive. Retrieved Jan 31, 2019, from https://www.acsh.org/news/2018/06/23/government-big-reason-epipen-and-other-generics-are-so-expensive-13114

Statista. (2018). U.S. Pharmaceutical Industry – Statistics & Facts. Retrieved Jan 31, 2019, from https://www.statista.com/topics/1719/pharmaceutical-industry/

Almost 30 years ago a young woman made an appointment to see me. I had just started my internal medicine practice and almost all the patients who saw me were new to me. I assumed she was establishing care with me. Her first words to me were “Hello Dr. Paauw, I would like to interview you to see if you will be a good fit as my doctor.” We talked for the 40-minute appointment time. I asked her about her health, her life, and what she wanted out of both. We shared with each other that we both were parents of young children. When the appointment was over, she said she would really like for me to be her doctor. She told me that the main thing she appreciated about me was that I listened, and that her previous physician never sat down at her appointments and often had his hand on the door handle for much of the visit. Physicians and patients both agree that compassionate care is essential for good patient care, yet about half of patients and 60% of doctors believe it is lacking in our medical system.¹

Remember the golden first minutes

When you step in the room and greet the patient, make sure the first few minutes are about connecting with a new patient or reconnecting with a patient who has visited your office in the past. I often start by asking the patient to give me an update on how they are doing. This lets me know what is important to them. I do not touch the computer until after this initial check-in.

Use the computer as a bond to strengthen your patient relationship

Many studies have shown patients find the computer gets between the doctor and patient. It is especially problematic if it breaks eye contact with the patient. People are less likely to share scary, sensitive, or embarrassing information if someone is looking at a computer and typing. As you look up tests, radiology reports, or consultant notes, let the patient in on what you are doing. Explain why you are searching in the record, and if it helps make an important point, show your findings to the patient. Offer to print out results, so they have something to carry with them.

Explain what you are looking for and what you find on the physical exam

Being a patient is scary. We all want reassurance that our fears are not true. When you find normal findings on exam, share those with the patient. Hearing “your heart sounds good, your pulses are strong” really helps patients. Explaining what we are doing when we examine is also helpful. Explain why you are feeling for lymph nodes in the neck, why we percuss the abdomen. Patients are often fascinated by getting a window into how we are thinking. I usually have medical students with me, which offers another avenue to explaining the how and why behind the exam. In asking and explaining to students, the patient is also taught why we do what we do.

Make sure that we cover what they are afraid of, not just what their symptom is

Patients come in not just to get symptom relief but to rest their mind from their fears of what it could be. I find it helpful to ask the patient what they think is the cause of the problem, or if they are worried about any specific diagnosis. With certain symptoms this is particularly important (for example, headaches, fatigue, or abdominal pain).

None of these suggestions are easy to do in busy, time-pressured clinic visits. I have found though that when patients feel cared about, listened to and can have their fears addressed they value our advice more, and less time is needed to negotiate the plan, as it has been developed together.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at fpnews@mdedge.com.

Reference

Lown BA et al. Health Aff (Millwood). 2011 Sep;30(9):1772-8.

Almost 30 years ago a young woman made an appointment to see me. I had just started my internal medicine practice and almost all the patients who saw me were new to me. I assumed she was establishing care with me. Her first words to me were “Hello Dr. Paauw, I would like to interview you to see if you will be a good fit as my doctor.” We talked for the 40-minute appointment time. I asked her about her health, her life, and what she wanted out of both. We shared with each other that we both were parents of young children. When the appointment was over, she said she would really like for me to be her doctor. She told me that the main thing she appreciated about me was that I listened, and that her previous physician never sat down at her appointments and often had his hand on the door handle for much of the visit. Physicians and patients both agree that compassionate care is essential for good patient care, yet about half of patients and 60% of doctors believe it is lacking in our medical system.¹

Remember the golden first minutes

When you step in the room and greet the patient, make sure the first few minutes are about connecting with a new patient or reconnecting with a patient who has visited your office in the past. I often start by asking the patient to give me an update on how they are doing. This lets me know what is important to them. I do not touch the computer until after this initial check-in.

Use the computer as a bond to strengthen your patient relationship

Many studies have shown patients find the computer gets between the doctor and patient. It is especially problematic if it breaks eye contact with the patient. People are less likely to share scary, sensitive, or embarrassing information if someone is looking at a computer and typing. As you look up tests, radiology reports, or consultant notes, let the patient in on what you are doing. Explain why you are searching in the record, and if it helps make an important point, show your findings to the patient. Offer to print out results, so they have something to carry with them.

Explain what you are looking for and what you find on the physical exam

Being a patient is scary. We all want reassurance that our fears are not true. When you find normal findings on exam, share those with the patient. Hearing “your heart sounds good, your pulses are strong” really helps patients. Explaining what we are doing when we examine is also helpful. Explain why you are feeling for lymph nodes in the neck, why we percuss the abdomen. Patients are often fascinated by getting a window into how we are thinking. I usually have medical students with me, which offers another avenue to explaining the how and why behind the exam. In asking and explaining to students, the patient is also taught why we do what we do.

Make sure that we cover what they are afraid of, not just what their symptom is

Patients come in not just to get symptom relief but to rest their mind from their fears of what it could be. I find it helpful to ask the patient what they think is the cause of the problem, or if they are worried about any specific diagnosis. With certain symptoms this is particularly important (for example, headaches, fatigue, or abdominal pain).

None of these suggestions are easy to do in busy, time-pressured clinic visits. I have found though that when patients feel cared about, listened to and can have their fears addressed they value our advice more, and less time is needed to negotiate the plan, as it has been developed together.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at fpnews@mdedge.com.

Reference

Lown BA et al. Health Aff (Millwood). 2011 Sep;30(9):1772-8.

Almost 30 years ago a young woman made an appointment to see me. I had just started my internal medicine practice and almost all the patients who saw me were new to me. I assumed she was establishing care with me. Her first words to me were “Hello Dr. Paauw, I would like to interview you to see if you will be a good fit as my doctor.” We talked for the 40-minute appointment time. I asked her about her health, her life, and what she wanted out of both. We shared with each other that we both were parents of young children. When the appointment was over, she said she would really like for me to be her doctor. She told me that the main thing she appreciated about me was that I listened, and that her previous physician never sat down at her appointments and often had his hand on the door handle for much of the visit. Physicians and patients both agree that compassionate care is essential for good patient care, yet about half of patients and 60% of doctors believe it is lacking in our medical system.¹

Remember the golden first minutes

When you step in the room and greet the patient, make sure the first few minutes are about connecting with a new patient or reconnecting with a patient who has visited your office in the past. I often start by asking the patient to give me an update on how they are doing. This lets me know what is important to them. I do not touch the computer until after this initial check-in.

Use the computer as a bond to strengthen your patient relationship

Many studies have shown patients find the computer gets between the doctor and patient. It is especially problematic if it breaks eye contact with the patient. People are less likely to share scary, sensitive, or embarrassing information if someone is looking at a computer and typing. As you look up tests, radiology reports, or consultant notes, let the patient in on what you are doing. Explain why you are searching in the record, and if it helps make an important point, show your findings to the patient. Offer to print out results, so they have something to carry with them.

Explain what you are looking for and what you find on the physical exam

Being a patient is scary. We all want reassurance that our fears are not true. When you find normal findings on exam, share those with the patient. Hearing “your heart sounds good, your pulses are strong” really helps patients. Explaining what we are doing when we examine is also helpful. Explain why you are feeling for lymph nodes in the neck, why we percuss the abdomen. Patients are often fascinated by getting a window into how we are thinking. I usually have medical students with me, which offers another avenue to explaining the how and why behind the exam. In asking and explaining to students, the patient is also taught why we do what we do.

Make sure that we cover what they are afraid of, not just what their symptom is

Patients come in not just to get symptom relief but to rest their mind from their fears of what it could be. I find it helpful to ask the patient what they think is the cause of the problem, or if they are worried about any specific diagnosis. With certain symptoms this is particularly important (for example, headaches, fatigue, or abdominal pain).

None of these suggestions are easy to do in busy, time-pressured clinic visits. I have found though that when patients feel cared about, listened to and can have their fears addressed they value our advice more, and less time is needed to negotiate the plan, as it has been developed together.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at fpnews@mdedge.com.

Reference

Lown BA et al. Health Aff (Millwood). 2011 Sep;30(9):1772-8.

The Diagnosis: Erosive Adenomatosis of the Nipple 

Biopsy of the lesion revealed proliferative sections of glandular epithelium demonstrating apocrine differentiation, connecting to the epidermis and traversing throughout the entire dermis of the specimen (Figure). There were papillary projections of dilated ducts with a retained layer of myoepithelial cells surrounding the epithelial layers. Cytologic atypia was not appreciated. The patient was diagnosed with erosive adenomatosis of the nipple (EAN), also known as nipple adenoma. The lesion subsequently was treated and cleared with Mohs micrographic surgery (MMS). At 8-month follow-up there was no clinical recurrence of the lesion, and the patient was satisfied with the overall cosmetic appearance and conservation of the areola. The patient was followed clinically with annual breast examinations and mammography to monitor future recurrence. 

Erosive adenomatosis of the nipple is an uncommon benign proliferative process of the lactiferous ducts of the nipple. Recognizing EAN is important because it resembles malignant breast diseases such as Paget disease of the nipple and invasive breast carcinoma. Due to these similarities, early cases of EAN have resulted in unnecessary mastectomies before the benignity of the condition was established.¹ Accurate diagnosis is important to both the patient and the clinician for treatment planning as well as psychosocial consequences associated with the potential removal of this anatomically and cosmetically sensitive area. 

Reviewing the literature on EAN is complicated by the variety of terms used to describe this condition, including but not limited to nipple adenoma, nipple duct adenoma, papillary adenoma of the nipple, and florid papillomatosis of the nipple. In 1955, Jones² described EAN using the term florid papillomatosis of the nipple ducts. In 1962, Handley and Thackray¹ argued that adenoma of the nipple was a more descriptive term because it more closely described the appearance of a sweat gland adenoma. They reasoned that adenoma of the nipple is a separate process from ductal papilloma due to the adenomatous proliferation into the nipple stroma rather than the lumen of the nipple ducts.¹ The term adenoma of the nipple was further supported in 1965 by Taylor and Robertson.³ In 1959, Le Gal et al⁴ used the term erosive adenomatosis of the nipple to describe the erosive nature of nipple adenoma. The term nipple adenoma was published in the 2012 WHO Classification of Tumors of the Breast with 4 common histologic subtypes.^5,6  

Erosive adenomatosis of the nipple is clinically indistinguishable from Paget disease of the nipple, thus biopsy is essential for accurate diagnosis. In contrast to Paget disease, EAN tends to present in younger patients and progresses more slowly, and symptoms may be exacerbated around menstruation.¹ Case reports demonstrate that patients may wait years before seeking medical attention for EAN.^1,3,7,8 Presenting symptoms may include inflammation, crusting, nipple skin erosion, itching, and pain. Serous or sanguineous discharge from the lesions also is commonly reported. Palpation may reveal a small, hard, or elastic nodule within or underlying the nipple. In addition to Paget disease, EAN may resemble squamous cell carcinoma of the nipple, eczema, psoriasis, or a skin infection.⁶ Axillary lymphadenopathy is not present in the absence of a concomitant breast malignancy.⁸ On biopsy, nipple adenoma represents ductal proliferation of glandular structures within the stroma of the nipple that is well circumscribed but without borders. The erosive appearance of the lesion is produced by extensions of the glandular epithelium on the surface of the nipple.^1,6 Specific to EAN is the presence of 2 cell types: an inner columnar epithelium and an outer cuboidal myoepithelium. These 2 cell types are present in normal lactiferous ducts; however, normal ducts are highly organized compared to EAN.⁹  

After confirmation of EAN by nipple biopsy, complete surgical excision has been the gold standard for treatment, followed by reconstructive surgery.⁶ Handley and Thackray¹ advocated for total excision of the nipple and areola with an underlying wedge of breast tissue to facilitate wound closure. More recently, successful alternative forms of treatment have been utilized to minimize disfiguring surgery. Alternative treatments include MMS,⁸ cryotherapy,¹⁰ and nipple splitting enucleation.⁶ Treatment with MMS has resulted in nipple sparing with the least amount of surface area sacrificed (1.1 cm2).⁹ Our case and prior case reports demonstrate that the tissue sparing potential of MMS is appropriate for the treatment of EAN, though traditionally it has been reserved for more malignant tumors. Preserving this sensitive area is both cosmetically and psychologically advantageous for the patient and thus should be considered when reviewing treatment options for EAN. 

The Diagnosis: Erosive Adenomatosis of the Nipple 

Biopsy of the lesion revealed proliferative sections of glandular epithelium demonstrating apocrine differentiation, connecting to the epidermis and traversing throughout the entire dermis of the specimen (Figure). There were papillary projections of dilated ducts with a retained layer of myoepithelial cells surrounding the epithelial layers. Cytologic atypia was not appreciated. The patient was diagnosed with erosive adenomatosis of the nipple (EAN), also known as nipple adenoma. The lesion subsequently was treated and cleared with Mohs micrographic surgery (MMS). At 8-month follow-up there was no clinical recurrence of the lesion, and the patient was satisfied with the overall cosmetic appearance and conservation of the areola. The patient was followed clinically with annual breast examinations and mammography to monitor future recurrence. 

Erosive adenomatosis of the nipple is an uncommon benign proliferative process of the lactiferous ducts of the nipple. Recognizing EAN is important because it resembles malignant breast diseases such as Paget disease of the nipple and invasive breast carcinoma. Due to these similarities, early cases of EAN have resulted in unnecessary mastectomies before the benignity of the condition was established.¹ Accurate diagnosis is important to both the patient and the clinician for treatment planning as well as psychosocial consequences associated with the potential removal of this anatomically and cosmetically sensitive area. 

Reviewing the literature on EAN is complicated by the variety of terms used to describe this condition, including but not limited to nipple adenoma, nipple duct adenoma, papillary adenoma of the nipple, and florid papillomatosis of the nipple. In 1955, Jones² described EAN using the term florid papillomatosis of the nipple ducts. In 1962, Handley and Thackray¹ argued that adenoma of the nipple was a more descriptive term because it more closely described the appearance of a sweat gland adenoma. They reasoned that adenoma of the nipple is a separate process from ductal papilloma due to the adenomatous proliferation into the nipple stroma rather than the lumen of the nipple ducts.¹ The term adenoma of the nipple was further supported in 1965 by Taylor and Robertson.³ In 1959, Le Gal et al⁴ used the term erosive adenomatosis of the nipple to describe the erosive nature of nipple adenoma. The term nipple adenoma was published in the 2012 WHO Classification of Tumors of the Breast with 4 common histologic subtypes.^5,6  

Erosive adenomatosis of the nipple is clinically indistinguishable from Paget disease of the nipple, thus biopsy is essential for accurate diagnosis. In contrast to Paget disease, EAN tends to present in younger patients and progresses more slowly, and symptoms may be exacerbated around menstruation.¹ Case reports demonstrate that patients may wait years before seeking medical attention for EAN.^1,3,7,8 Presenting symptoms may include inflammation, crusting, nipple skin erosion, itching, and pain. Serous or sanguineous discharge from the lesions also is commonly reported. Palpation may reveal a small, hard, or elastic nodule within or underlying the nipple. In addition to Paget disease, EAN may resemble squamous cell carcinoma of the nipple, eczema, psoriasis, or a skin infection.⁶ Axillary lymphadenopathy is not present in the absence of a concomitant breast malignancy.⁸ On biopsy, nipple adenoma represents ductal proliferation of glandular structures within the stroma of the nipple that is well circumscribed but without borders. The erosive appearance of the lesion is produced by extensions of the glandular epithelium on the surface of the nipple.^1,6 Specific to EAN is the presence of 2 cell types: an inner columnar epithelium and an outer cuboidal myoepithelium. These 2 cell types are present in normal lactiferous ducts; however, normal ducts are highly organized compared to EAN.⁹  

After confirmation of EAN by nipple biopsy, complete surgical excision has been the gold standard for treatment, followed by reconstructive surgery.⁶ Handley and Thackray¹ advocated for total excision of the nipple and areola with an underlying wedge of breast tissue to facilitate wound closure. More recently, successful alternative forms of treatment have been utilized to minimize disfiguring surgery. Alternative treatments include MMS,⁸ cryotherapy,¹⁰ and nipple splitting enucleation.⁶ Treatment with MMS has resulted in nipple sparing with the least amount of surface area sacrificed (1.1 cm2).⁹ Our case and prior case reports demonstrate that the tissue sparing potential of MMS is appropriate for the treatment of EAN, though traditionally it has been reserved for more malignant tumors. Preserving this sensitive area is both cosmetically and psychologically advantageous for the patient and thus should be considered when reviewing treatment options for EAN. 

The Diagnosis: Erosive Adenomatosis of the Nipple 

Biopsy of the lesion revealed proliferative sections of glandular epithelium demonstrating apocrine differentiation, connecting to the epidermis and traversing throughout the entire dermis of the specimen (Figure). There were papillary projections of dilated ducts with a retained layer of myoepithelial cells surrounding the epithelial layers. Cytologic atypia was not appreciated. The patient was diagnosed with erosive adenomatosis of the nipple (EAN), also known as nipple adenoma. The lesion subsequently was treated and cleared with Mohs micrographic surgery (MMS). At 8-month follow-up there was no clinical recurrence of the lesion, and the patient was satisfied with the overall cosmetic appearance and conservation of the areola. The patient was followed clinically with annual breast examinations and mammography to monitor future recurrence. 

Erosive adenomatosis of the nipple is an uncommon benign proliferative process of the lactiferous ducts of the nipple. Recognizing EAN is important because it resembles malignant breast diseases such as Paget disease of the nipple and invasive breast carcinoma. Due to these similarities, early cases of EAN have resulted in unnecessary mastectomies before the benignity of the condition was established.¹ Accurate diagnosis is important to both the patient and the clinician for treatment planning as well as psychosocial consequences associated with the potential removal of this anatomically and cosmetically sensitive area. 

Reviewing the literature on EAN is complicated by the variety of terms used to describe this condition, including but not limited to nipple adenoma, nipple duct adenoma, papillary adenoma of the nipple, and florid papillomatosis of the nipple. In 1955, Jones² described EAN using the term florid papillomatosis of the nipple ducts. In 1962, Handley and Thackray¹ argued that adenoma of the nipple was a more descriptive term because it more closely described the appearance of a sweat gland adenoma. They reasoned that adenoma of the nipple is a separate process from ductal papilloma due to the adenomatous proliferation into the nipple stroma rather than the lumen of the nipple ducts.¹ The term adenoma of the nipple was further supported in 1965 by Taylor and Robertson.³ In 1959, Le Gal et al⁴ used the term erosive adenomatosis of the nipple to describe the erosive nature of nipple adenoma. The term nipple adenoma was published in the 2012 WHO Classification of Tumors of the Breast with 4 common histologic subtypes.^5,6  

Erosive adenomatosis of the nipple is clinically indistinguishable from Paget disease of the nipple, thus biopsy is essential for accurate diagnosis. In contrast to Paget disease, EAN tends to present in younger patients and progresses more slowly, and symptoms may be exacerbated around menstruation.¹ Case reports demonstrate that patients may wait years before seeking medical attention for EAN.^1,3,7,8 Presenting symptoms may include inflammation, crusting, nipple skin erosion, itching, and pain. Serous or sanguineous discharge from the lesions also is commonly reported. Palpation may reveal a small, hard, or elastic nodule within or underlying the nipple. In addition to Paget disease, EAN may resemble squamous cell carcinoma of the nipple, eczema, psoriasis, or a skin infection.⁶ Axillary lymphadenopathy is not present in the absence of a concomitant breast malignancy.⁸ On biopsy, nipple adenoma represents ductal proliferation of glandular structures within the stroma of the nipple that is well circumscribed but without borders. The erosive appearance of the lesion is produced by extensions of the glandular epithelium on the surface of the nipple.^1,6 Specific to EAN is the presence of 2 cell types: an inner columnar epithelium and an outer cuboidal myoepithelium. These 2 cell types are present in normal lactiferous ducts; however, normal ducts are highly organized compared to EAN.⁹  

After confirmation of EAN by nipple biopsy, complete surgical excision has been the gold standard for treatment, followed by reconstructive surgery.⁶ Handley and Thackray¹ advocated for total excision of the nipple and areola with an underlying wedge of breast tissue to facilitate wound closure. More recently, successful alternative forms of treatment have been utilized to minimize disfiguring surgery. Alternative treatments include MMS,⁸ cryotherapy,¹⁰ and nipple splitting enucleation.⁶ Treatment with MMS has resulted in nipple sparing with the least amount of surface area sacrificed (1.1 cm2).⁹ Our case and prior case reports demonstrate that the tissue sparing potential of MMS is appropriate for the treatment of EAN, though traditionally it has been reserved for more malignant tumors. Preserving this sensitive area is both cosmetically and psychologically advantageous for the patient and thus should be considered when reviewing treatment options for EAN. 

The flu virus uses a hemagglutinin (HA) protein to enter and infect cells. The “head” of the protein was thought to be safe from antibody attacks.

Turns out, it has a previously unsuspected chink in its armor. And researchers from National Institute of Allergy and Infectious Diseases may have found an “unexpected new target” for antiflu therapies. They discovered a naturally occurring human antibody (FluA-20) that—to their surprise—binds to the head of the HA protein at a site that was not thought to be vulnerable.

Using FluA-20 isolated from a patient who had received many influenza immunizations, the researchers showed that FluA-20 “reaches into” an otherwise inaccessible part of the HA trimer molecule and “rapidly disrupts” its integrity. In other words, FluA-20 causes it to fall apart, preventing the spread of virus.

Although the researchers also discovered that the window of opportunity is narrow (the region is only briefly exposed to antibody attack), unlike the rest of HA’s head, the open-access region varies little among influenza strains. The critical HA residues recognized by FluA-20, the researchers say, remain conserved across most subtypes of influenza A virus, which explains the antibody’s “extraordinary breadth.” In mouse studies, when used as prophylaxis or therapy, it protected against H1N1, N3N2, H5N1, and H7N9 subtypes.

In theory, the researchers say, direct strikes with antibody-based therapeutics against that part of the HA protein could be effective with many strains of influenza A virus, and—also theoretically—other influenza strains.

The flu virus uses a hemagglutinin (HA) protein to enter and infect cells. The “head” of the protein was thought to be safe from antibody attacks.

Turns out, it has a previously unsuspected chink in its armor. And researchers from National Institute of Allergy and Infectious Diseases may have found an “unexpected new target” for antiflu therapies. They discovered a naturally occurring human antibody (FluA-20) that—to their surprise—binds to the head of the HA protein at a site that was not thought to be vulnerable.

Using FluA-20 isolated from a patient who had received many influenza immunizations, the researchers showed that FluA-20 “reaches into” an otherwise inaccessible part of the HA trimer molecule and “rapidly disrupts” its integrity. In other words, FluA-20 causes it to fall apart, preventing the spread of virus.

Although the researchers also discovered that the window of opportunity is narrow (the region is only briefly exposed to antibody attack), unlike the rest of HA’s head, the open-access region varies little among influenza strains. The critical HA residues recognized by FluA-20, the researchers say, remain conserved across most subtypes of influenza A virus, which explains the antibody’s “extraordinary breadth.” In mouse studies, when used as prophylaxis or therapy, it protected against H1N1, N3N2, H5N1, and H7N9 subtypes.

In theory, the researchers say, direct strikes with antibody-based therapeutics against that part of the HA protein could be effective with many strains of influenza A virus, and—also theoretically—other influenza strains.

The flu virus uses a hemagglutinin (HA) protein to enter and infect cells. The “head” of the protein was thought to be safe from antibody attacks.

Turns out, it has a previously unsuspected chink in its armor. And researchers from National Institute of Allergy and Infectious Diseases may have found an “unexpected new target” for antiflu therapies. They discovered a naturally occurring human antibody (FluA-20) that—to their surprise—binds to the head of the HA protein at a site that was not thought to be vulnerable.

Using FluA-20 isolated from a patient who had received many influenza immunizations, the researchers showed that FluA-20 “reaches into” an otherwise inaccessible part of the HA trimer molecule and “rapidly disrupts” its integrity. In other words, FluA-20 causes it to fall apart, preventing the spread of virus.

Although the researchers also discovered that the window of opportunity is narrow (the region is only briefly exposed to antibody attack), unlike the rest of HA’s head, the open-access region varies little among influenza strains. The critical HA residues recognized by FluA-20, the researchers say, remain conserved across most subtypes of influenza A virus, which explains the antibody’s “extraordinary breadth.” In mouse studies, when used as prophylaxis or therapy, it protected against H1N1, N3N2, H5N1, and H7N9 subtypes.

In theory, the researchers say, direct strikes with antibody-based therapeutics against that part of the HA protein could be effective with many strains of influenza A virus, and—also theoretically—other influenza strains.