About a year ago, I had a patient come in who didn’t like me.

It seemed like a normal visit. My secretary had him fill out the usual forms and copied his insurance cards, and I took him back to my office. We do this many times, every day.

He came back to my office, and I asked him what brought him to my care.

Instead of starting his medical history, though, he immediately gave me a long list of complaints. He didn’t like my appearance. Or my secretary. Or my forms. Or us asking if he’d had any previous tests. Or the parking at my office. Or the phone system. Or a coffee stain in my building’s elevator carpeting.

A whole list of stuff, none actually related to his reason for coming in. I let him rant for a minute, thinking maybe he’d get to the point, but he just kept getting angrier and bringing up more grievances.

I finally interrupted him and said, “Sir, if you’re unhappy with me, you are welcome to end the appointment and leave now.” He told me he wasn’t going to pay for the visit (not that I would have charged him for it) and stomped out. My secretary shredded his info. There’s always other stuff that needs my attention, so I busied myself with that until the next appointment arrived.

Twenty years ago this probably would have really upset me. But today? Not at all.

Like most other doctors, I want to help people. I enjoy doing that. It’s why I’m here. But I’ve also learned that there are some people I’ll never be able to work with under any circumstances. Some will just never like me as a physician, my casual appearance, or small practice.

People like this guy happen a few times a year. Experience teaches that you can’t be everyone’s doctor, can’t make everyone happy, and can’t have them all like you. If they don’t, that’s part of life. You can’t predict interpersonal chemistry and worrying about such things isn’t good for your blood pressure. You can’t change others.

Ironically, the same gentleman called recently, saying he needed to get in with me now. My secretary called him back, reminded him of what happened last year and suggested he go elsewhere.

His response? “I didn’t like your office then and still don’t.”

I’m okay with that. You can’t please everyone. Sometimes it’s not even worth trying.

 

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

About a year ago, I had a patient come in who didn’t like me.

It seemed like a normal visit. My secretary had him fill out the usual forms and copied his insurance cards, and I took him back to my office. We do this many times, every day.

He came back to my office, and I asked him what brought him to my care.

Instead of starting his medical history, though, he immediately gave me a long list of complaints. He didn’t like my appearance. Or my secretary. Or my forms. Or us asking if he’d had any previous tests. Or the parking at my office. Or the phone system. Or a coffee stain in my building’s elevator carpeting.

A whole list of stuff, none actually related to his reason for coming in. I let him rant for a minute, thinking maybe he’d get to the point, but he just kept getting angrier and bringing up more grievances.

I finally interrupted him and said, “Sir, if you’re unhappy with me, you are welcome to end the appointment and leave now.” He told me he wasn’t going to pay for the visit (not that I would have charged him for it) and stomped out. My secretary shredded his info. There’s always other stuff that needs my attention, so I busied myself with that until the next appointment arrived.

Twenty years ago this probably would have really upset me. But today? Not at all.

Like most other doctors, I want to help people. I enjoy doing that. It’s why I’m here. But I’ve also learned that there are some people I’ll never be able to work with under any circumstances. Some will just never like me as a physician, my casual appearance, or small practice.

People like this guy happen a few times a year. Experience teaches that you can’t be everyone’s doctor, can’t make everyone happy, and can’t have them all like you. If they don’t, that’s part of life. You can’t predict interpersonal chemistry and worrying about such things isn’t good for your blood pressure. You can’t change others.

Ironically, the same gentleman called recently, saying he needed to get in with me now. My secretary called him back, reminded him of what happened last year and suggested he go elsewhere.

His response? “I didn’t like your office then and still don’t.”

I’m okay with that. You can’t please everyone. Sometimes it’s not even worth trying.

 

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

About a year ago, I had a patient come in who didn’t like me.

It seemed like a normal visit. My secretary had him fill out the usual forms and copied his insurance cards, and I took him back to my office. We do this many times, every day.

He came back to my office, and I asked him what brought him to my care.

Instead of starting his medical history, though, he immediately gave me a long list of complaints. He didn’t like my appearance. Or my secretary. Or my forms. Or us asking if he’d had any previous tests. Or the parking at my office. Or the phone system. Or a coffee stain in my building’s elevator carpeting.

A whole list of stuff, none actually related to his reason for coming in. I let him rant for a minute, thinking maybe he’d get to the point, but he just kept getting angrier and bringing up more grievances.

I finally interrupted him and said, “Sir, if you’re unhappy with me, you are welcome to end the appointment and leave now.” He told me he wasn’t going to pay for the visit (not that I would have charged him for it) and stomped out. My secretary shredded his info. There’s always other stuff that needs my attention, so I busied myself with that until the next appointment arrived.

Twenty years ago this probably would have really upset me. But today? Not at all.

Like most other doctors, I want to help people. I enjoy doing that. It’s why I’m here. But I’ve also learned that there are some people I’ll never be able to work with under any circumstances. Some will just never like me as a physician, my casual appearance, or small practice.

People like this guy happen a few times a year. Experience teaches that you can’t be everyone’s doctor, can’t make everyone happy, and can’t have them all like you. If they don’t, that’s part of life. You can’t predict interpersonal chemistry and worrying about such things isn’t good for your blood pressure. You can’t change others.

Ironically, the same gentleman called recently, saying he needed to get in with me now. My secretary called him back, reminded him of what happened last year and suggested he go elsewhere.

His response? “I didn’t like your office then and still don’t.”

I’m okay with that. You can’t please everyone. Sometimes it’s not even worth trying.

 

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

To the Editor:

It is not uncommon for patients with extensive dermal scarring to overheat due to the inability to regulate body temperature through evaporative heat loss, as lack of perspiration in areas of prior full-thickness skin injury is well known. One of the authors (C.M.H.) previously reported a case of a patient with considerable hypertrophic scarring after surviving an episode of toxic epidermal necrolysis that was likely precipitated by lamotrigine.¹ The patient initially presented to our clinic in consultation for laser therapy to improve the pliability and cosmetic appearance of the scars; however, approximately 3 weeks after initiating treatment with a fractional CO₂ laser, the patient noticed perspiration in areas where she once lacked the ability to perspire as well as improved functionality.¹ It was speculated that scar remodeling stimulated by the CO₂ fractional laser allowed new connections to form between eccrine ducts in the dermis and epidermis.²

These findings are even more notable in light of a study by Rittié et al³ that suggested the primary appendages of the skin involved in human wound healing are the eccrine sweat glands. The investigators were able to demonstrate that eccrine sweat glands are major contributors in reepithelialization and wound healing in humans; therefore, it is possible that stimulating these glands with the CO₂ laser may promote enhanced reepithelialization in addition to the reestablishment of perspiration and wound healing.³ Considering inadequate wound repair represents a substantial disturbance to the patient and health care system, this finding offers promise as a potential means to decrease morbidity in patients with dermal scarring from burns and traumatic injuries. We have since evaluated and treated 3 patients who demonstrated sweat regeneration following treatment with the fractional CO₂ laser (Table).

A 42-year-old man was our first patient to demonstrate functional scar improvement following bone marrow transplant for acute lymphoblastic leukemia complicated by chronic sclerodermoid graft-versus-host disease and subsequent extensive scarring on the chest and arms. Approximately 2 weeks after the first treatment with the fractional CO₂ laser, the patient began to notice the presence of sweat beads in the treated areas. In addition to the reestablishment of perspiration, the patient had perceived increased mobility with improved pliability and “softness” (as described by family members) in treated areas likely related to scar remodeling.

A 36-year-old wounded army veteran presented with burns to the face, arms, and chest affecting 49% of the body surface area. After only 1 treatment, the patient reported that he could subjectively tolerate 10°F more ambient temperature and work all day outside in south Texas when heat intolerance previously would allow him to work only 2 to 3 hours. Additionally, he noted increased mobility and chest wall expansion, which in combination contributed to overall increased exercise tolerance and enhanced quality of life.

A 35-year-old US Marine and firefighter with burns primarily on the chest and arms involving 35% body surface area experienced increased exercise tolerance and sweat regeneration, particularly on the chest after a single treatment with the fractional CO₂ laser but continued to experience improvement after a total of 3 treatments. Additionally, the cosmetic improvement was so substantial that the physician (C.M.H) had to review older photographs to verify the location of the scars.

We have now treated 3 patients with various mechanisms of injury and extensive scarring who noticed improved heat tolerance from sweat regeneration following fractional CO₂ laser therapy. At this point, we only have anecdotal evidence of subjective functional improvement, and further research is warranted to elucidate the exact mechanism of action to support our findings.

To the Editor:

It is not uncommon for patients with extensive dermal scarring to overheat due to the inability to regulate body temperature through evaporative heat loss, as lack of perspiration in areas of prior full-thickness skin injury is well known. One of the authors (C.M.H.) previously reported a case of a patient with considerable hypertrophic scarring after surviving an episode of toxic epidermal necrolysis that was likely precipitated by lamotrigine.¹ The patient initially presented to our clinic in consultation for laser therapy to improve the pliability and cosmetic appearance of the scars; however, approximately 3 weeks after initiating treatment with a fractional CO₂ laser, the patient noticed perspiration in areas where she once lacked the ability to perspire as well as improved functionality.¹ It was speculated that scar remodeling stimulated by the CO₂ fractional laser allowed new connections to form between eccrine ducts in the dermis and epidermis.²

These findings are even more notable in light of a study by Rittié et al³ that suggested the primary appendages of the skin involved in human wound healing are the eccrine sweat glands. The investigators were able to demonstrate that eccrine sweat glands are major contributors in reepithelialization and wound healing in humans; therefore, it is possible that stimulating these glands with the CO₂ laser may promote enhanced reepithelialization in addition to the reestablishment of perspiration and wound healing.³ Considering inadequate wound repair represents a substantial disturbance to the patient and health care system, this finding offers promise as a potential means to decrease morbidity in patients with dermal scarring from burns and traumatic injuries. We have since evaluated and treated 3 patients who demonstrated sweat regeneration following treatment with the fractional CO₂ laser (Table).

A 42-year-old man was our first patient to demonstrate functional scar improvement following bone marrow transplant for acute lymphoblastic leukemia complicated by chronic sclerodermoid graft-versus-host disease and subsequent extensive scarring on the chest and arms. Approximately 2 weeks after the first treatment with the fractional CO₂ laser, the patient began to notice the presence of sweat beads in the treated areas. In addition to the reestablishment of perspiration, the patient had perceived increased mobility with improved pliability and “softness” (as described by family members) in treated areas likely related to scar remodeling.

A 36-year-old wounded army veteran presented with burns to the face, arms, and chest affecting 49% of the body surface area. After only 1 treatment, the patient reported that he could subjectively tolerate 10°F more ambient temperature and work all day outside in south Texas when heat intolerance previously would allow him to work only 2 to 3 hours. Additionally, he noted increased mobility and chest wall expansion, which in combination contributed to overall increased exercise tolerance and enhanced quality of life.

A 35-year-old US Marine and firefighter with burns primarily on the chest and arms involving 35% body surface area experienced increased exercise tolerance and sweat regeneration, particularly on the chest after a single treatment with the fractional CO₂ laser but continued to experience improvement after a total of 3 treatments. Additionally, the cosmetic improvement was so substantial that the physician (C.M.H) had to review older photographs to verify the location of the scars.

We have now treated 3 patients with various mechanisms of injury and extensive scarring who noticed improved heat tolerance from sweat regeneration following fractional CO₂ laser therapy. At this point, we only have anecdotal evidence of subjective functional improvement, and further research is warranted to elucidate the exact mechanism of action to support our findings.

To the Editor:

It is not uncommon for patients with extensive dermal scarring to overheat due to the inability to regulate body temperature through evaporative heat loss, as lack of perspiration in areas of prior full-thickness skin injury is well known. One of the authors (C.M.H.) previously reported a case of a patient with considerable hypertrophic scarring after surviving an episode of toxic epidermal necrolysis that was likely precipitated by lamotrigine.¹ The patient initially presented to our clinic in consultation for laser therapy to improve the pliability and cosmetic appearance of the scars; however, approximately 3 weeks after initiating treatment with a fractional CO₂ laser, the patient noticed perspiration in areas where she once lacked the ability to perspire as well as improved functionality.¹ It was speculated that scar remodeling stimulated by the CO₂ fractional laser allowed new connections to form between eccrine ducts in the dermis and epidermis.²

These findings are even more notable in light of a study by Rittié et al³ that suggested the primary appendages of the skin involved in human wound healing are the eccrine sweat glands. The investigators were able to demonstrate that eccrine sweat glands are major contributors in reepithelialization and wound healing in humans; therefore, it is possible that stimulating these glands with the CO₂ laser may promote enhanced reepithelialization in addition to the reestablishment of perspiration and wound healing.³ Considering inadequate wound repair represents a substantial disturbance to the patient and health care system, this finding offers promise as a potential means to decrease morbidity in patients with dermal scarring from burns and traumatic injuries. We have since evaluated and treated 3 patients who demonstrated sweat regeneration following treatment with the fractional CO₂ laser (Table).

A 42-year-old man was our first patient to demonstrate functional scar improvement following bone marrow transplant for acute lymphoblastic leukemia complicated by chronic sclerodermoid graft-versus-host disease and subsequent extensive scarring on the chest and arms. Approximately 2 weeks after the first treatment with the fractional CO₂ laser, the patient began to notice the presence of sweat beads in the treated areas. In addition to the reestablishment of perspiration, the patient had perceived increased mobility with improved pliability and “softness” (as described by family members) in treated areas likely related to scar remodeling.

A 36-year-old wounded army veteran presented with burns to the face, arms, and chest affecting 49% of the body surface area. After only 1 treatment, the patient reported that he could subjectively tolerate 10°F more ambient temperature and work all day outside in south Texas when heat intolerance previously would allow him to work only 2 to 3 hours. Additionally, he noted increased mobility and chest wall expansion, which in combination contributed to overall increased exercise tolerance and enhanced quality of life.

A 35-year-old US Marine and firefighter with burns primarily on the chest and arms involving 35% body surface area experienced increased exercise tolerance and sweat regeneration, particularly on the chest after a single treatment with the fractional CO₂ laser but continued to experience improvement after a total of 3 treatments. Additionally, the cosmetic improvement was so substantial that the physician (C.M.H) had to review older photographs to verify the location of the scars.

We have now treated 3 patients with various mechanisms of injury and extensive scarring who noticed improved heat tolerance from sweat regeneration following fractional CO₂ laser therapy. At this point, we only have anecdotal evidence of subjective functional improvement, and further research is warranted to elucidate the exact mechanism of action to support our findings.

PARIS – A one-way endobronchial valve placed in the lungs of emphysema patients with hyperinflation provides acceptable safety and clinically significant improvement in lung function at 12 months, according to results from a multicenter trial presented as a late-breaker at the annual congress of the European Respiratory Society.

Ted Bosworth/MDedge News

Six-month results have been presented previously, but the 12-month results suggest that lung volume reduction associated with placement of the valves provides “durable effectiveness in appropriately selected hyperinflated emphysema patients,” according to Gerard Criner, MD, chair of the thoracic medicine department at Temple University, Philadelphia.

In this randomized controlled trial, called EMPROVE, 172 emphysema patients with severe dyspnea were randomized in a 2:1 fashion to receive a proprietary endobronchial valve or medical therapy alone. The valve, marketed under the brand name Spiration Valve System (SVS), is currently indicated for the treatment of air leaks after lung surgery.

“The valve serves to block airflow from edematous lungs with the objective of blocking hyperinflation and improving lung function,” Dr. Criner explained. The valves are retrievable, if necessary, with bronchoscopy.

High resolution computed tomography (HRCT) was used to identify emphysema obstruction and target valve placement to the most diseased lobes. The average number of valves placed per patient was slightly less than four. Most of the valves (70%) were placed in an upper lobe.

When reported at 6 months, the responder rate, defined as at least 15% improvement in forced expiratory volume in 1 second (FEV₁) was 36.8% and 10% in the SVS and control groups, respectively, a difference of 25.7% that Dr. Criner reported as statistically significant although he did not provide P values. At 12 months, the rates were 37.2% and 5.1%, respectively, demonstrating a persistent effect.

Thoracic adverse events were higher at both 6 months (31% vs. 11.9%) and 12 months (21.4% vs. 10.6%) in the treatment group relative to the control group. At 6 months, pneumothorax, which Dr. Criner characterized as “a recognized marker of target lobe volume reduction,” was the only event that occurred significantly more commonly (14.2% vs. 0%) in the SVS group.

Between 6 and 12 months, there were no pneumothorax events in either arm. The higher numerical rates of thoracic adverse events in the treatment arm were acute exacerbations (13.6% vs. 8.5%) and pneumonia in nontreated lobes (7.8% vs. 2.1%), but these rates were not statistically different.

At 6 months, there was a numerically higher rate of all-cause mortality in the treatment group (5.3% vs. 1.7%) but the rate was numerically lower between 6 and 12 months (2.9% vs. 6.4%). The differences were not significantly different at either time point or overall.

A significant reduction in hyperinflation favoring valve placement was accompanied by improvement in objective measures of lung function, such as FEV₁, and dyspnea, as measured with the Modified Medical Research Council (mMRC) Dyspnea Scale, at 6 and 12 months. These improvements translated into persistent quality of life benefits as measured with the St. George Respiratory Questionnaire (SGRQ). At 12 months, the SGRQ changes from baseline were a 5.5-point reduction and a four-point gain in the treatment and control groups, respectively. This absolute difference of 9.5 points is slightly more modest than the 13-point difference at 6 months (–8 vs. +5 points), but demonstrates a durable effect, Dr. Criner reported.

According to Dr. Criner, EMPROVE reinforces the principle that HRCT is effective “for selecting the lobe for therapy and which patients may benefit,” but the most important message from the 12-month results is persistent clinical benefit.

The endobronchial values “provide statistically and clinically meaningful improvements in FEV₁, reductions in lobe volume and dyspnea, and improvements in quality of life with an acceptable safety profile,” Dr. Criner reported.

On June 29, 2018, the Food and Drug Administration approved the first endobronchial valve for treatment of emphysema. This valve, marketed under the name Zephyr, was approved on the basis of the pivotal LIBERATE trial, also led by Dr. Criner and published earlier this year (Am J Respir Crit Care Med. 2018 May 22. doi: 10.1164/rccm.201803-0590OC.). The results of EMPROVE are consistent with previous evidence that a one-way valve, by preventing air from entering diseased lobes of patients with emphysema to exacerbate hyperinflation, improves lung function and reduces clinical symptoms.

Dr. Criner reports financial relationships with Olympus, the sponsor of this trial.

PARIS – A one-way endobronchial valve placed in the lungs of emphysema patients with hyperinflation provides acceptable safety and clinically significant improvement in lung function at 12 months, according to results from a multicenter trial presented as a late-breaker at the annual congress of the European Respiratory Society.

Ted Bosworth/MDedge News

Six-month results have been presented previously, but the 12-month results suggest that lung volume reduction associated with placement of the valves provides “durable effectiveness in appropriately selected hyperinflated emphysema patients,” according to Gerard Criner, MD, chair of the thoracic medicine department at Temple University, Philadelphia.

In this randomized controlled trial, called EMPROVE, 172 emphysema patients with severe dyspnea were randomized in a 2:1 fashion to receive a proprietary endobronchial valve or medical therapy alone. The valve, marketed under the brand name Spiration Valve System (SVS), is currently indicated for the treatment of air leaks after lung surgery.

“The valve serves to block airflow from edematous lungs with the objective of blocking hyperinflation and improving lung function,” Dr. Criner explained. The valves are retrievable, if necessary, with bronchoscopy.

High resolution computed tomography (HRCT) was used to identify emphysema obstruction and target valve placement to the most diseased lobes. The average number of valves placed per patient was slightly less than four. Most of the valves (70%) were placed in an upper lobe.

When reported at 6 months, the responder rate, defined as at least 15% improvement in forced expiratory volume in 1 second (FEV₁) was 36.8% and 10% in the SVS and control groups, respectively, a difference of 25.7% that Dr. Criner reported as statistically significant although he did not provide P values. At 12 months, the rates were 37.2% and 5.1%, respectively, demonstrating a persistent effect.

Thoracic adverse events were higher at both 6 months (31% vs. 11.9%) and 12 months (21.4% vs. 10.6%) in the treatment group relative to the control group. At 6 months, pneumothorax, which Dr. Criner characterized as “a recognized marker of target lobe volume reduction,” was the only event that occurred significantly more commonly (14.2% vs. 0%) in the SVS group.

Between 6 and 12 months, there were no pneumothorax events in either arm. The higher numerical rates of thoracic adverse events in the treatment arm were acute exacerbations (13.6% vs. 8.5%) and pneumonia in nontreated lobes (7.8% vs. 2.1%), but these rates were not statistically different.

At 6 months, there was a numerically higher rate of all-cause mortality in the treatment group (5.3% vs. 1.7%) but the rate was numerically lower between 6 and 12 months (2.9% vs. 6.4%). The differences were not significantly different at either time point or overall.

A significant reduction in hyperinflation favoring valve placement was accompanied by improvement in objective measures of lung function, such as FEV₁, and dyspnea, as measured with the Modified Medical Research Council (mMRC) Dyspnea Scale, at 6 and 12 months. These improvements translated into persistent quality of life benefits as measured with the St. George Respiratory Questionnaire (SGRQ). At 12 months, the SGRQ changes from baseline were a 5.5-point reduction and a four-point gain in the treatment and control groups, respectively. This absolute difference of 9.5 points is slightly more modest than the 13-point difference at 6 months (–8 vs. +5 points), but demonstrates a durable effect, Dr. Criner reported.

According to Dr. Criner, EMPROVE reinforces the principle that HRCT is effective “for selecting the lobe for therapy and which patients may benefit,” but the most important message from the 12-month results is persistent clinical benefit.

The endobronchial values “provide statistically and clinically meaningful improvements in FEV₁, reductions in lobe volume and dyspnea, and improvements in quality of life with an acceptable safety profile,” Dr. Criner reported.

On June 29, 2018, the Food and Drug Administration approved the first endobronchial valve for treatment of emphysema. This valve, marketed under the name Zephyr, was approved on the basis of the pivotal LIBERATE trial, also led by Dr. Criner and published earlier this year (Am J Respir Crit Care Med. 2018 May 22. doi: 10.1164/rccm.201803-0590OC.). The results of EMPROVE are consistent with previous evidence that a one-way valve, by preventing air from entering diseased lobes of patients with emphysema to exacerbate hyperinflation, improves lung function and reduces clinical symptoms.

Dr. Criner reports financial relationships with Olympus, the sponsor of this trial.

PARIS – A one-way endobronchial valve placed in the lungs of emphysema patients with hyperinflation provides acceptable safety and clinically significant improvement in lung function at 12 months, according to results from a multicenter trial presented as a late-breaker at the annual congress of the European Respiratory Society.

Ted Bosworth/MDedge News

Six-month results have been presented previously, but the 12-month results suggest that lung volume reduction associated with placement of the valves provides “durable effectiveness in appropriately selected hyperinflated emphysema patients,” according to Gerard Criner, MD, chair of the thoracic medicine department at Temple University, Philadelphia.

In this randomized controlled trial, called EMPROVE, 172 emphysema patients with severe dyspnea were randomized in a 2:1 fashion to receive a proprietary endobronchial valve or medical therapy alone. The valve, marketed under the brand name Spiration Valve System (SVS), is currently indicated for the treatment of air leaks after lung surgery.

“The valve serves to block airflow from edematous lungs with the objective of blocking hyperinflation and improving lung function,” Dr. Criner explained. The valves are retrievable, if necessary, with bronchoscopy.

High resolution computed tomography (HRCT) was used to identify emphysema obstruction and target valve placement to the most diseased lobes. The average number of valves placed per patient was slightly less than four. Most of the valves (70%) were placed in an upper lobe.

When reported at 6 months, the responder rate, defined as at least 15% improvement in forced expiratory volume in 1 second (FEV₁) was 36.8% and 10% in the SVS and control groups, respectively, a difference of 25.7% that Dr. Criner reported as statistically significant although he did not provide P values. At 12 months, the rates were 37.2% and 5.1%, respectively, demonstrating a persistent effect.

Thoracic adverse events were higher at both 6 months (31% vs. 11.9%) and 12 months (21.4% vs. 10.6%) in the treatment group relative to the control group. At 6 months, pneumothorax, which Dr. Criner characterized as “a recognized marker of target lobe volume reduction,” was the only event that occurred significantly more commonly (14.2% vs. 0%) in the SVS group.

Between 6 and 12 months, there were no pneumothorax events in either arm. The higher numerical rates of thoracic adverse events in the treatment arm were acute exacerbations (13.6% vs. 8.5%) and pneumonia in nontreated lobes (7.8% vs. 2.1%), but these rates were not statistically different.

At 6 months, there was a numerically higher rate of all-cause mortality in the treatment group (5.3% vs. 1.7%) but the rate was numerically lower between 6 and 12 months (2.9% vs. 6.4%). The differences were not significantly different at either time point or overall.

A significant reduction in hyperinflation favoring valve placement was accompanied by improvement in objective measures of lung function, such as FEV₁, and dyspnea, as measured with the Modified Medical Research Council (mMRC) Dyspnea Scale, at 6 and 12 months. These improvements translated into persistent quality of life benefits as measured with the St. George Respiratory Questionnaire (SGRQ). At 12 months, the SGRQ changes from baseline were a 5.5-point reduction and a four-point gain in the treatment and control groups, respectively. This absolute difference of 9.5 points is slightly more modest than the 13-point difference at 6 months (–8 vs. +5 points), but demonstrates a durable effect, Dr. Criner reported.

According to Dr. Criner, EMPROVE reinforces the principle that HRCT is effective “for selecting the lobe for therapy and which patients may benefit,” but the most important message from the 12-month results is persistent clinical benefit.

The endobronchial values “provide statistically and clinically meaningful improvements in FEV₁, reductions in lobe volume and dyspnea, and improvements in quality of life with an acceptable safety profile,” Dr. Criner reported.

On June 29, 2018, the Food and Drug Administration approved the first endobronchial valve for treatment of emphysema. This valve, marketed under the name Zephyr, was approved on the basis of the pivotal LIBERATE trial, also led by Dr. Criner and published earlier this year (Am J Respir Crit Care Med. 2018 May 22. doi: 10.1164/rccm.201803-0590OC.). The results of EMPROVE are consistent with previous evidence that a one-way valve, by preventing air from entering diseased lobes of patients with emphysema to exacerbate hyperinflation, improves lung function and reduces clinical symptoms.

Dr. Criner reports financial relationships with Olympus, the sponsor of this trial.

The FP made the presumptive diagnosis of a nodular basal cell carcinoma.

He explained the importance of performing a biopsy and obtained informed consent. On the same day of the patient’s visit, he injected 1% lidocaine with epinephrine under the lesion with a single stick of a 30 gauge needle. He knew that it was safe to use epinephrine on the nose, and that it would prevent excessive bleeding during the biopsy. Contrary to the myth frequently taught in medical school, the nose is a very vascular area. The physician performed a shave biopsy that removed the top of the lesion flush with the skin around it. (See the Watch & Learn video on “Shave biopsy.”)

The pathology report came back as a nodular basal cell carcinoma. On the following visit, the physician recommended Mohs surgery as a way to preserve the vital anatomy of the nasal ala and achieve the highest cure rate.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Karnes J, Usatine R. Basal cell carcinoma. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:989-998.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/.

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com.

The FP made the presumptive diagnosis of a nodular basal cell carcinoma.

He explained the importance of performing a biopsy and obtained informed consent. On the same day of the patient’s visit, he injected 1% lidocaine with epinephrine under the lesion with a single stick of a 30 gauge needle. He knew that it was safe to use epinephrine on the nose, and that it would prevent excessive bleeding during the biopsy. Contrary to the myth frequently taught in medical school, the nose is a very vascular area. The physician performed a shave biopsy that removed the top of the lesion flush with the skin around it. (See the Watch & Learn video on “Shave biopsy.”)

The pathology report came back as a nodular basal cell carcinoma. On the following visit, the physician recommended Mohs surgery as a way to preserve the vital anatomy of the nasal ala and achieve the highest cure rate.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Karnes J, Usatine R. Basal cell carcinoma. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:989-998.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/.

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com.

The FP made the presumptive diagnosis of a nodular basal cell carcinoma.

He explained the importance of performing a biopsy and obtained informed consent. On the same day of the patient’s visit, he injected 1% lidocaine with epinephrine under the lesion with a single stick of a 30 gauge needle. He knew that it was safe to use epinephrine on the nose, and that it would prevent excessive bleeding during the biopsy. Contrary to the myth frequently taught in medical school, the nose is a very vascular area. The physician performed a shave biopsy that removed the top of the lesion flush with the skin around it. (See the Watch & Learn video on “Shave biopsy.”)

The pathology report came back as a nodular basal cell carcinoma. On the following visit, the physician recommended Mohs surgery as a way to preserve the vital anatomy of the nasal ala and achieve the highest cure rate.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Karnes J, Usatine R. Basal cell carcinoma. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:989-998.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/.

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com.

SAN DIEGO – In the ICU, ultrasound has been shown to reduce the need for CT to evaluate potential pulmonary embolism. But in the ED, this strategy hasn’t worked out so far, according to Joseph Brown, MD, of the department of emergency medicine at the University of California, San Francisco.

Vidyard Video

Based on the data so far, the ED patients were less likely than the ICU patients to have another etiology identified on ultrasound that explained their symptoms. Further, ultrasound alone missed small subsegmental pulmonary emboli that were detected on subsequent CT scans in 2 of 11 patients.

The study is continuing, and Dr. Brown explains in this interview how ultrasound might be combined with other risk stratification measures to safely achieve reductions in CT scans.

SAN DIEGO – In the ICU, ultrasound has been shown to reduce the need for CT to evaluate potential pulmonary embolism. But in the ED, this strategy hasn’t worked out so far, according to Joseph Brown, MD, of the department of emergency medicine at the University of California, San Francisco.

Vidyard Video

Based on the data so far, the ED patients were less likely than the ICU patients to have another etiology identified on ultrasound that explained their symptoms. Further, ultrasound alone missed small subsegmental pulmonary emboli that were detected on subsequent CT scans in 2 of 11 patients.

The study is continuing, and Dr. Brown explains in this interview how ultrasound might be combined with other risk stratification measures to safely achieve reductions in CT scans.

SAN DIEGO – In the ICU, ultrasound has been shown to reduce the need for CT to evaluate potential pulmonary embolism. But in the ED, this strategy hasn’t worked out so far, according to Joseph Brown, MD, of the department of emergency medicine at the University of California, San Francisco.

Vidyard Video

Based on the data so far, the ED patients were less likely than the ICU patients to have another etiology identified on ultrasound that explained their symptoms. Further, ultrasound alone missed small subsegmental pulmonary emboli that were detected on subsequent CT scans in 2 of 11 patients.

The study is continuing, and Dr. Brown explains in this interview how ultrasound might be combined with other risk stratification measures to safely achieve reductions in CT scans.

She had fallen on a garden implement, lacerating her superficial femoral artery. She used her cell phone to call 911. Thanks to an alert EMS crew and the Stop the Bleed training they recently received, a tourniquet was placed without delay. She got to our trauma bay in about 15 minutes after the tourniquet was applied. Although the patient made it abundantly clear that she was in pain, she was stable with moderate tachycardia and a good blood pressure.

Our trauma team leaped into action. The leader took report from the EMS while two nurses and a second surgeon assessed the patient, got her clothes cut off, and applied monitors. A third nurse got a second IV going. Primary survey was done in less than 90 seconds. The patient then underwent a focused exam including a log roll for back injuries.

The leg wound was still oozing a bit, so a second tourniquet was called for and pressure applied until it could be acquired. The patient was given 5 mg of morphine sulfate, which calmed her down a bit. Labs and x-rays were done quickly. The nursing staff suggested a tetanus booster, and the second surgeon who had gotten a basic past medical history suggested vancomycin since the patient said she was allergic to penicillin. Fifteen minutes after she hit the trauma bay, she was on her way to the OR for exploration, debridement, and vascular repair of her injury.

This was all done by four M2 medical students and five N4 nursing students, none of whom had had previous experience with this type of trauma patient

The students were managing this trauma situation in the simulation center of their medical school with four staff watching. This was their second run through for the afternoon. At debriefing, they compared their work on the first trauma of the day (a stab wound to the right chest) to their second attempt. They were satisfied with their efforts and so were we, the faculty who ran the simulation. Comparing their response to those I’ve seen in real life, I’d say these students understood their roles and responsibilities as well as the sort of thrown-together teams I’ve seen at places where trauma is not the main focus. While these young men and women are in the early stage of training and not ready for a real-world trauma emergency, they have gained knowledge about this kind of situation that I didn’t see until I was in residency and beyond. The times they are a-changing.

A couple of days later I was in Rochester, Minn., attending an American College of Surgeons Advanced Education Institute (ACS/AEI) course on simulations. At the end of that course, we participants were challenged by a manikin in extremis. Everyone there was an expert, had an advanced degree, had some experience in simulation, or were surgeons interested in simulation. I found that, even though this was a simulation and the patient was only a pretend human being, my adrenal cortex performed almost as if I were doing a real resuscitation. Previous training I’d had on teamwork, crew resource management, and ACLS all kicked in, and we got it done. But interestingly, we weren’t perfect. We debriefed and found that, even at our level of experience and training, a simple simulation could be very instructive. Seeing/doing is believing.

High-tech skills in high-risk occupations are well served by simulation training. Much of the airline piloting training is done by simulation. It works well for aviation, nuclear reactors, high voltage line work, and medicine. Most of these disciplines have embraced simulation as an essential part of training. Simulation is part of many surgical training programs, but it has other uses.

When was the last time you practiced a trauma resuscitation, an ultrasound fine-needle biopsy, laparoscopic maneuvers, or an unusual technique that you seldom perform, but when needed, must be pulled off very well? Most of us taking this simulation course agreed that time, money, and ego may get in the way of maintaining those skills for those rare instances when they are needed. Surgeons might want to consider simulation to keep some of our rarely used skills from getting rusty.

If you’re going to make a costly error, I would very much like you to do it on a piece of plastic, not on a patient. There are no consequences for messing up a procedure on a manikin and this kind of practice might teach you something critical. Practicing reduces stress and improves the performance of those placed on the spot by real-life events. Do you think Captain “Sully” Sullenberger could have landed that airliner in the Hudson River safely if he hadn’t practiced with countless mind-numbingly complex simulations? Sure, luck plays a part, and innate ability plays a part. But skill, knowledge, and practice are your best bet when all the eyes in the room swivel to you in a moment of crisis.

You may think that simulators have to cost $100,000 and be completely realistic to do the job. That’s not true. A banana, orange, or stick of butter can be fabulous sims for a med student. Felt and cardboard can make a realistic cricothyroidotomy model.

Surgeons all over the country are using simulation training to learn how to be better without getting real blood on their shoes. If you haven’t participated in a training simulation recently, I double-dog dare you to try it and tell me you found it without merit. The ACS Surgical Simulation Summit is being held in March 2019 in Chicago. You might want to check that out.


Dr. Hughes is clinical professor in the department of surgery and director of medical education at the University of Kansas School of Medicine, Salina, and Coeditor of ACS Surgery News.

She had fallen on a garden implement, lacerating her superficial femoral artery. She used her cell phone to call 911. Thanks to an alert EMS crew and the Stop the Bleed training they recently received, a tourniquet was placed without delay. She got to our trauma bay in about 15 minutes after the tourniquet was applied. Although the patient made it abundantly clear that she was in pain, she was stable with moderate tachycardia and a good blood pressure.

Our trauma team leaped into action. The leader took report from the EMS while two nurses and a second surgeon assessed the patient, got her clothes cut off, and applied monitors. A third nurse got a second IV going. Primary survey was done in less than 90 seconds. The patient then underwent a focused exam including a log roll for back injuries.

The leg wound was still oozing a bit, so a second tourniquet was called for and pressure applied until it could be acquired. The patient was given 5 mg of morphine sulfate, which calmed her down a bit. Labs and x-rays were done quickly. The nursing staff suggested a tetanus booster, and the second surgeon who had gotten a basic past medical history suggested vancomycin since the patient said she was allergic to penicillin. Fifteen minutes after she hit the trauma bay, she was on her way to the OR for exploration, debridement, and vascular repair of her injury.

This was all done by four M2 medical students and five N4 nursing students, none of whom had had previous experience with this type of trauma patient

The students were managing this trauma situation in the simulation center of their medical school with four staff watching. This was their second run through for the afternoon. At debriefing, they compared their work on the first trauma of the day (a stab wound to the right chest) to their second attempt. They were satisfied with their efforts and so were we, the faculty who ran the simulation. Comparing their response to those I’ve seen in real life, I’d say these students understood their roles and responsibilities as well as the sort of thrown-together teams I’ve seen at places where trauma is not the main focus. While these young men and women are in the early stage of training and not ready for a real-world trauma emergency, they have gained knowledge about this kind of situation that I didn’t see until I was in residency and beyond. The times they are a-changing.

A couple of days later I was in Rochester, Minn., attending an American College of Surgeons Advanced Education Institute (ACS/AEI) course on simulations. At the end of that course, we participants were challenged by a manikin in extremis. Everyone there was an expert, had an advanced degree, had some experience in simulation, or were surgeons interested in simulation. I found that, even though this was a simulation and the patient was only a pretend human being, my adrenal cortex performed almost as if I were doing a real resuscitation. Previous training I’d had on teamwork, crew resource management, and ACLS all kicked in, and we got it done. But interestingly, we weren’t perfect. We debriefed and found that, even at our level of experience and training, a simple simulation could be very instructive. Seeing/doing is believing.

High-tech skills in high-risk occupations are well served by simulation training. Much of the airline piloting training is done by simulation. It works well for aviation, nuclear reactors, high voltage line work, and medicine. Most of these disciplines have embraced simulation as an essential part of training. Simulation is part of many surgical training programs, but it has other uses.

When was the last time you practiced a trauma resuscitation, an ultrasound fine-needle biopsy, laparoscopic maneuvers, or an unusual technique that you seldom perform, but when needed, must be pulled off very well? Most of us taking this simulation course agreed that time, money, and ego may get in the way of maintaining those skills for those rare instances when they are needed. Surgeons might want to consider simulation to keep some of our rarely used skills from getting rusty.

If you’re going to make a costly error, I would very much like you to do it on a piece of plastic, not on a patient. There are no consequences for messing up a procedure on a manikin and this kind of practice might teach you something critical. Practicing reduces stress and improves the performance of those placed on the spot by real-life events. Do you think Captain “Sully” Sullenberger could have landed that airliner in the Hudson River safely if he hadn’t practiced with countless mind-numbingly complex simulations? Sure, luck plays a part, and innate ability plays a part. But skill, knowledge, and practice are your best bet when all the eyes in the room swivel to you in a moment of crisis.

You may think that simulators have to cost $100,000 and be completely realistic to do the job. That’s not true. A banana, orange, or stick of butter can be fabulous sims for a med student. Felt and cardboard can make a realistic cricothyroidotomy model.

Surgeons all over the country are using simulation training to learn how to be better without getting real blood on their shoes. If you haven’t participated in a training simulation recently, I double-dog dare you to try it and tell me you found it without merit. The ACS Surgical Simulation Summit is being held in March 2019 in Chicago. You might want to check that out.


Dr. Hughes is clinical professor in the department of surgery and director of medical education at the University of Kansas School of Medicine, Salina, and Coeditor of ACS Surgery News.

She had fallen on a garden implement, lacerating her superficial femoral artery. She used her cell phone to call 911. Thanks to an alert EMS crew and the Stop the Bleed training they recently received, a tourniquet was placed without delay. She got to our trauma bay in about 15 minutes after the tourniquet was applied. Although the patient made it abundantly clear that she was in pain, she was stable with moderate tachycardia and a good blood pressure.

Our trauma team leaped into action. The leader took report from the EMS while two nurses and a second surgeon assessed the patient, got her clothes cut off, and applied monitors. A third nurse got a second IV going. Primary survey was done in less than 90 seconds. The patient then underwent a focused exam including a log roll for back injuries.

The leg wound was still oozing a bit, so a second tourniquet was called for and pressure applied until it could be acquired. The patient was given 5 mg of morphine sulfate, which calmed her down a bit. Labs and x-rays were done quickly. The nursing staff suggested a tetanus booster, and the second surgeon who had gotten a basic past medical history suggested vancomycin since the patient said she was allergic to penicillin. Fifteen minutes after she hit the trauma bay, she was on her way to the OR for exploration, debridement, and vascular repair of her injury.

This was all done by four M2 medical students and five N4 nursing students, none of whom had had previous experience with this type of trauma patient

The students were managing this trauma situation in the simulation center of their medical school with four staff watching. This was their second run through for the afternoon. At debriefing, they compared their work on the first trauma of the day (a stab wound to the right chest) to their second attempt. They were satisfied with their efforts and so were we, the faculty who ran the simulation. Comparing their response to those I’ve seen in real life, I’d say these students understood their roles and responsibilities as well as the sort of thrown-together teams I’ve seen at places where trauma is not the main focus. While these young men and women are in the early stage of training and not ready for a real-world trauma emergency, they have gained knowledge about this kind of situation that I didn’t see until I was in residency and beyond. The times they are a-changing.

A couple of days later I was in Rochester, Minn., attending an American College of Surgeons Advanced Education Institute (ACS/AEI) course on simulations. At the end of that course, we participants were challenged by a manikin in extremis. Everyone there was an expert, had an advanced degree, had some experience in simulation, or were surgeons interested in simulation. I found that, even though this was a simulation and the patient was only a pretend human being, my adrenal cortex performed almost as if I were doing a real resuscitation. Previous training I’d had on teamwork, crew resource management, and ACLS all kicked in, and we got it done. But interestingly, we weren’t perfect. We debriefed and found that, even at our level of experience and training, a simple simulation could be very instructive. Seeing/doing is believing.

High-tech skills in high-risk occupations are well served by simulation training. Much of the airline piloting training is done by simulation. It works well for aviation, nuclear reactors, high voltage line work, and medicine. Most of these disciplines have embraced simulation as an essential part of training. Simulation is part of many surgical training programs, but it has other uses.

When was the last time you practiced a trauma resuscitation, an ultrasound fine-needle biopsy, laparoscopic maneuvers, or an unusual technique that you seldom perform, but when needed, must be pulled off very well? Most of us taking this simulation course agreed that time, money, and ego may get in the way of maintaining those skills for those rare instances when they are needed. Surgeons might want to consider simulation to keep some of our rarely used skills from getting rusty.

If you’re going to make a costly error, I would very much like you to do it on a piece of plastic, not on a patient. There are no consequences for messing up a procedure on a manikin and this kind of practice might teach you something critical. Practicing reduces stress and improves the performance of those placed on the spot by real-life events. Do you think Captain “Sully” Sullenberger could have landed that airliner in the Hudson River safely if he hadn’t practiced with countless mind-numbingly complex simulations? Sure, luck plays a part, and innate ability plays a part. But skill, knowledge, and practice are your best bet when all the eyes in the room swivel to you in a moment of crisis.

You may think that simulators have to cost $100,000 and be completely realistic to do the job. That’s not true. A banana, orange, or stick of butter can be fabulous sims for a med student. Felt and cardboard can make a realistic cricothyroidotomy model.

Surgeons all over the country are using simulation training to learn how to be better without getting real blood on their shoes. If you haven’t participated in a training simulation recently, I double-dog dare you to try it and tell me you found it without merit. The ACS Surgical Simulation Summit is being held in March 2019 in Chicago. You might want to check that out.


Dr. Hughes is clinical professor in the department of surgery and director of medical education at the University of Kansas School of Medicine, Salina, and Coeditor of ACS Surgery News.

The American College of Chest Physicians® announced updates to the evidence-based guidelines on antithrombotic therapy for atrial fibrillation. The guideline panel submitted the manuscript, Antithrombotic Therapy for Atrial Fibrillation: CHEST Guideline and Expert Panel Report, for publication in the journal CHEST®.

Key recommendations and shifts from previous guidelines include:

• For patients with atrial fibrillation without valvular heart disease, including those with paroxysmal atrial fibrillation who are at low risk of stroke (eg, CHA2DS2VASc score of 0 in males or 1 in females), we suggest no antithrombotic therapy.

• For patients with a single non-sex CHA2DS2VASc stroke risk factor, we suggest oral anticoagulation rather than no therapy, aspirin or combination therapy with aspirin and clopidogrel.

• For those at high risk of stroke, we recommend oral anticoagulation rather than no therapy, aspirin or combination therapy with aspirin and clopidogrel.

• Where we recommend or suggest in favor of oral anticoagulation, we suggest using a novel oral anticoagulant (NOAC) rather than adjusted-dose vitamin K antagonist therapy. With the latter, it is important to aim for good quality anticoagulation control with a time in therapeutic range (TTR) >70%.

• Attention to modifiable bleeding risk factors should be made at each patient contact, and HAS-BLED score should be used to assess the risk of bleeding where high-risk patients (>=3) can be identified for earlier review and follow-up visits.

The complete guideline article is free to view in the Online First section of the journal CHEST.

The American College of Chest Physicians® announced updates to the evidence-based guidelines on antithrombotic therapy for atrial fibrillation. The guideline panel submitted the manuscript, Antithrombotic Therapy for Atrial Fibrillation: CHEST Guideline and Expert Panel Report, for publication in the journal CHEST®.

Key recommendations and shifts from previous guidelines include:

• For patients with atrial fibrillation without valvular heart disease, including those with paroxysmal atrial fibrillation who are at low risk of stroke (eg, CHA2DS2VASc score of 0 in males or 1 in females), we suggest no antithrombotic therapy.

• For patients with a single non-sex CHA2DS2VASc stroke risk factor, we suggest oral anticoagulation rather than no therapy, aspirin or combination therapy with aspirin and clopidogrel.

• For those at high risk of stroke, we recommend oral anticoagulation rather than no therapy, aspirin or combination therapy with aspirin and clopidogrel.

• Where we recommend or suggest in favor of oral anticoagulation, we suggest using a novel oral anticoagulant (NOAC) rather than adjusted-dose vitamin K antagonist therapy. With the latter, it is important to aim for good quality anticoagulation control with a time in therapeutic range (TTR) >70%.

• Attention to modifiable bleeding risk factors should be made at each patient contact, and HAS-BLED score should be used to assess the risk of bleeding where high-risk patients (>=3) can be identified for earlier review and follow-up visits.

The complete guideline article is free to view in the Online First section of the journal CHEST.

The American College of Chest Physicians® announced updates to the evidence-based guidelines on antithrombotic therapy for atrial fibrillation. The guideline panel submitted the manuscript, Antithrombotic Therapy for Atrial Fibrillation: CHEST Guideline and Expert Panel Report, for publication in the journal CHEST®.

Key recommendations and shifts from previous guidelines include:

• For patients with atrial fibrillation without valvular heart disease, including those with paroxysmal atrial fibrillation who are at low risk of stroke (eg, CHA2DS2VASc score of 0 in males or 1 in females), we suggest no antithrombotic therapy.

• For patients with a single non-sex CHA2DS2VASc stroke risk factor, we suggest oral anticoagulation rather than no therapy, aspirin or combination therapy with aspirin and clopidogrel.

• For those at high risk of stroke, we recommend oral anticoagulation rather than no therapy, aspirin or combination therapy with aspirin and clopidogrel.

• Where we recommend or suggest in favor of oral anticoagulation, we suggest using a novel oral anticoagulant (NOAC) rather than adjusted-dose vitamin K antagonist therapy. With the latter, it is important to aim for good quality anticoagulation control with a time in therapeutic range (TTR) >70%.

• Attention to modifiable bleeding risk factors should be made at each patient contact, and HAS-BLED score should be used to assess the risk of bleeding where high-risk patients (>=3) can be identified for earlier review and follow-up visits.

The complete guideline article is free to view in the Online First section of the journal CHEST.

Extracorporeal membrane oxygenation (ECMO) has become increasingly accepted as a rescue therapy for severe respiratory failure from a variety of conditions, though most commonly, the acute respiratory distress syndrome (ARDS) (Thiagarajan R, et al. ASAIO. 2017;63[1]:60). ECMO can provide respiratory or cardiorespiratory support for failing lungs, heart, or both. The most common ECMO configuration used in ARDS is venovenous ECMO, in which blood is withdrawn from a catheter placed in a central vein, pumped through a gas exchange device known as an oxygenator, and returned to the venous system via another catheter. The blood flowing through the oxygenator is separated from a continuous supply of oxygen-rich sweep gas by a semipermeable membrane, across which diffusion-mediated gas exchange occurs, so that the blood exiting it is rich in oxygen and low in carbon dioxide. As venovenous ECMO functions in series with the native circulation, the well-oxygenated blood exiting the ECMO circuit mixes with poorly oxygenated blood flowing through the lungs. Therefore, oxygenation is dependent on native cardiac output to achieve systemic oxygen delivery (Figure 1).

ECMO been used successfully in adults with ARDS since the early 1970s (Hill JD, et al. N Engl J Med. 1972;286[12]:629-34) but, until recently, was limited to small numbers of patients at select global centers and associated with a high-risk profile. In the last decade, however, driven by improvements in ECMO circuit components making the device safer and easier to use, encouraging worldwide experience during the 2009 influenza A (H1N1) pandemic (Davies A, et al. JAMA. 2009;302[17]1888-95), and publication of the Efficacy and Economic Assessment of Conventional Ventilatory Support versus Extracorporeal Membrane Oxygenation for Severe Adult Respiratory Failure (CESAR) trial (Peek GJ, et al. Lancet. 2009;374[9698]:1351-63), ECMO use has markedly increased.

Despite its rapid growth, however, rigorous evidence supporting the use of ECMO has been lacking. The CESAR trial, while impressive in execution, had methodological issues that limited the strength of its conclusions. CESAR was a pragmatic trial that randomized 180 adults with severe respiratory failure from multiple etiologies to conventional management or transfer to an experienced, ECMO-capable center. CESAR met its primary outcome of improved survival without disability in the ECMO-referred group (63% vs 47%, relative risk [RR] 0.69; 95% confidence interval [CI] 0.05 to 0.97, P=.03), but not all patients in that group ultimately received ECMO. In addition, the use of lung protective ventilation was significantly higher in the ECMO-referred group, making it difficult to separate its benefit from that of ECMO. A conservative interpretation is that CESAR showed the clinical benefit of treatment at an ECMO-capable center, experienced in the management of patients with severe respiratory failure.

Not until the release of the Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome (EOLIA) trial earlier this year (Combes A, et al. N Engl J Med. 2018;378[21]:1965-75), did a modern, randomized controlled trial evaluating the use of ECMO itself exist. The EOLIA trial addressed the limitations of CESAR and randomized adult patients with early, severe ARDS to conventional, standard of care management that included a protocolized lung protective strategy in the control group vs immediate initiation of ECMO combined with an ultra-lung protective strategy (targeting end-inspiratory plateau pressure ≤24 cmH2O) in the intervention group. The primary outcome was all-cause mortality at 60 days. Of note, patients enrolled in EOLIA met entry criteria despite greater than 90% of patients receiving neuromuscular blockade and around 60% treated with prone positioning at the time of randomization (importantly, 90% of control group patients ultimately underwent prone positioning).

EOLIA was powered to detect a 20% decrease in mortality in the ECMO group. Based on trial design and the results of the fourth interim analysis, the trial was stopped for futility to reach that endpoint after enrollment of 249 of a maximum 331 patients. Although a 20% mortality reduction was not achieved, 60-day mortality was notably lower in the ECMO-treated group (35% vs 46%, RR 0.76, 95% CI 0.55 to 1.04, P=.09). The key secondary outcome of risk of treatment failure (defined as death in the ECMO group and death or crossover to ECMO in the control group) favored the ECMO group with a RR for mortality of 0.62 (95% CI, 0.47 to 0.82; P<.001), as did other secondary endpoints such as days free of renal and other organ failure.

A major limitation of the trial was that 35 (28%) of control group patients ultimately crossed over to ECMO, which diluted the effect of ECMO observed in the intention-to-treat analysis. Crossover occurred at clinician discretion an average of 6.5 days after randomization and after stringent criteria for crossover was met. These patients were incredibly ill, with a median oxygen saturation of 77%, rapidly worsening inotropic scores, and lactic acidosis; nine individuals had already suffered cardiac arrest, and six had received ECMO as part of extracorporeal cardiopulmonary resuscitation (ECPR), the initiation of venoarterial ECMO during cardiac arrest in attempt to restore spontaneous circulation. Mortality was considerably worse in the crossover group than in conventionally managed cohort overall, and, notably, 33% of patients crossed over to ECMO still survived.

In order to estimate the effect of ECMO on survival times if crossover had not occurred, the authors performed a post-hoc, rank-preserving structural failure time analysis. Though this relies on some assessment regarding the effect of the treatment itself, it showed a hazard ratio for mortality in the ECMO group of 0.51 (95% CI 0.24 to 1.02, P=.055). Although the EOLIA trial was not positive by traditional interpretation, all three major analyses and all secondary endpoints suggest some degree of benefit in patients with severe ARDS managed with ECMO.

Importantly, ECMO was well tolerated (at least when performed at expert centers, as done in this trial). There were significantly more bleeding events and cases of severe thrombocytopenia in the ECMO-treated group, but massive hemorrhage, ischemic and hemorrhagic stroke, arrhythmias, and other complications were similar.

Where do we go from here? Based on the totality of information, it is reasonable to consider ECMO for cases of severe ARDS not responsive to conventional measures, such as a lung protective ventilator strategy, neuromuscular blockade, and prone positioning. Initiation of ECMO may be reasonable prior to implementation of standard of care therapies, in order to permit safe transfer to an experienced center from a center not able to provide them.

Two take-away points: First, it is important to recognize that much of the clinical benefit derived from ECMO may be beyond its ability to normalize gas exchange and be due, at least in part, to the fact that ECMO allows the enhancement of proven lung protective ventilatory strategies. Initiation of ECMO and the “lung rest” it permits reduce the mechanical power applied to the injured alveoli and may attenuate ventilator-induced lung injury, cytokine release, and multiorgan failure that portend poor clinical outcomes in ARDS. Second, ECMO in EOLIA was conducted at expert centers with relatively low rates of complications.

It is too early to know how the critical care community will view ECMO for ARDS in light of EOLIA as well as a growing body of global ECMO experience, or how its wider application may impact the distribution and organization of ECMO centers. Regardless, of paramount importance in using ECMO as a treatment modality is optimizing patient management both prior to and after its initiation.

Dr. Agerstrand is Assistant Professor of Medicine, Director of the Medical ECMO Program, Columbia University College of Physicians and Surgeons, New York-Presbyterian Hospital.


 

Extracorporeal membrane oxygenation (ECMO) has become increasingly accepted as a rescue therapy for severe respiratory failure from a variety of conditions, though most commonly, the acute respiratory distress syndrome (ARDS) (Thiagarajan R, et al. ASAIO. 2017;63[1]:60). ECMO can provide respiratory or cardiorespiratory support for failing lungs, heart, or both. The most common ECMO configuration used in ARDS is venovenous ECMO, in which blood is withdrawn from a catheter placed in a central vein, pumped through a gas exchange device known as an oxygenator, and returned to the venous system via another catheter. The blood flowing through the oxygenator is separated from a continuous supply of oxygen-rich sweep gas by a semipermeable membrane, across which diffusion-mediated gas exchange occurs, so that the blood exiting it is rich in oxygen and low in carbon dioxide. As venovenous ECMO functions in series with the native circulation, the well-oxygenated blood exiting the ECMO circuit mixes with poorly oxygenated blood flowing through the lungs. Therefore, oxygenation is dependent on native cardiac output to achieve systemic oxygen delivery (Figure 1).

ECMO been used successfully in adults with ARDS since the early 1970s (Hill JD, et al. N Engl J Med. 1972;286[12]:629-34) but, until recently, was limited to small numbers of patients at select global centers and associated with a high-risk profile. In the last decade, however, driven by improvements in ECMO circuit components making the device safer and easier to use, encouraging worldwide experience during the 2009 influenza A (H1N1) pandemic (Davies A, et al. JAMA. 2009;302[17]1888-95), and publication of the Efficacy and Economic Assessment of Conventional Ventilatory Support versus Extracorporeal Membrane Oxygenation for Severe Adult Respiratory Failure (CESAR) trial (Peek GJ, et al. Lancet. 2009;374[9698]:1351-63), ECMO use has markedly increased.

Despite its rapid growth, however, rigorous evidence supporting the use of ECMO has been lacking. The CESAR trial, while impressive in execution, had methodological issues that limited the strength of its conclusions. CESAR was a pragmatic trial that randomized 180 adults with severe respiratory failure from multiple etiologies to conventional management or transfer to an experienced, ECMO-capable center. CESAR met its primary outcome of improved survival without disability in the ECMO-referred group (63% vs 47%, relative risk [RR] 0.69; 95% confidence interval [CI] 0.05 to 0.97, P=.03), but not all patients in that group ultimately received ECMO. In addition, the use of lung protective ventilation was significantly higher in the ECMO-referred group, making it difficult to separate its benefit from that of ECMO. A conservative interpretation is that CESAR showed the clinical benefit of treatment at an ECMO-capable center, experienced in the management of patients with severe respiratory failure.

Not until the release of the Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome (EOLIA) trial earlier this year (Combes A, et al. N Engl J Med. 2018;378[21]:1965-75), did a modern, randomized controlled trial evaluating the use of ECMO itself exist. The EOLIA trial addressed the limitations of CESAR and randomized adult patients with early, severe ARDS to conventional, standard of care management that included a protocolized lung protective strategy in the control group vs immediate initiation of ECMO combined with an ultra-lung protective strategy (targeting end-inspiratory plateau pressure ≤24 cmH2O) in the intervention group. The primary outcome was all-cause mortality at 60 days. Of note, patients enrolled in EOLIA met entry criteria despite greater than 90% of patients receiving neuromuscular blockade and around 60% treated with prone positioning at the time of randomization (importantly, 90% of control group patients ultimately underwent prone positioning).

EOLIA was powered to detect a 20% decrease in mortality in the ECMO group. Based on trial design and the results of the fourth interim analysis, the trial was stopped for futility to reach that endpoint after enrollment of 249 of a maximum 331 patients. Although a 20% mortality reduction was not achieved, 60-day mortality was notably lower in the ECMO-treated group (35% vs 46%, RR 0.76, 95% CI 0.55 to 1.04, P=.09). The key secondary outcome of risk of treatment failure (defined as death in the ECMO group and death or crossover to ECMO in the control group) favored the ECMO group with a RR for mortality of 0.62 (95% CI, 0.47 to 0.82; P<.001), as did other secondary endpoints such as days free of renal and other organ failure.

A major limitation of the trial was that 35 (28%) of control group patients ultimately crossed over to ECMO, which diluted the effect of ECMO observed in the intention-to-treat analysis. Crossover occurred at clinician discretion an average of 6.5 days after randomization and after stringent criteria for crossover was met. These patients were incredibly ill, with a median oxygen saturation of 77%, rapidly worsening inotropic scores, and lactic acidosis; nine individuals had already suffered cardiac arrest, and six had received ECMO as part of extracorporeal cardiopulmonary resuscitation (ECPR), the initiation of venoarterial ECMO during cardiac arrest in attempt to restore spontaneous circulation. Mortality was considerably worse in the crossover group than in conventionally managed cohort overall, and, notably, 33% of patients crossed over to ECMO still survived.

In order to estimate the effect of ECMO on survival times if crossover had not occurred, the authors performed a post-hoc, rank-preserving structural failure time analysis. Though this relies on some assessment regarding the effect of the treatment itself, it showed a hazard ratio for mortality in the ECMO group of 0.51 (95% CI 0.24 to 1.02, P=.055). Although the EOLIA trial was not positive by traditional interpretation, all three major analyses and all secondary endpoints suggest some degree of benefit in patients with severe ARDS managed with ECMO.

Importantly, ECMO was well tolerated (at least when performed at expert centers, as done in this trial). There were significantly more bleeding events and cases of severe thrombocytopenia in the ECMO-treated group, but massive hemorrhage, ischemic and hemorrhagic stroke, arrhythmias, and other complications were similar.

Where do we go from here? Based on the totality of information, it is reasonable to consider ECMO for cases of severe ARDS not responsive to conventional measures, such as a lung protective ventilator strategy, neuromuscular blockade, and prone positioning. Initiation of ECMO may be reasonable prior to implementation of standard of care therapies, in order to permit safe transfer to an experienced center from a center not able to provide them.

Two take-away points: First, it is important to recognize that much of the clinical benefit derived from ECMO may be beyond its ability to normalize gas exchange and be due, at least in part, to the fact that ECMO allows the enhancement of proven lung protective ventilatory strategies. Initiation of ECMO and the “lung rest” it permits reduce the mechanical power applied to the injured alveoli and may attenuate ventilator-induced lung injury, cytokine release, and multiorgan failure that portend poor clinical outcomes in ARDS. Second, ECMO in EOLIA was conducted at expert centers with relatively low rates of complications.

It is too early to know how the critical care community will view ECMO for ARDS in light of EOLIA as well as a growing body of global ECMO experience, or how its wider application may impact the distribution and organization of ECMO centers. Regardless, of paramount importance in using ECMO as a treatment modality is optimizing patient management both prior to and after its initiation.

Dr. Agerstrand is Assistant Professor of Medicine, Director of the Medical ECMO Program, Columbia University College of Physicians and Surgeons, New York-Presbyterian Hospital.


 

Extracorporeal membrane oxygenation (ECMO) has become increasingly accepted as a rescue therapy for severe respiratory failure from a variety of conditions, though most commonly, the acute respiratory distress syndrome (ARDS) (Thiagarajan R, et al. ASAIO. 2017;63[1]:60). ECMO can provide respiratory or cardiorespiratory support for failing lungs, heart, or both. The most common ECMO configuration used in ARDS is venovenous ECMO, in which blood is withdrawn from a catheter placed in a central vein, pumped through a gas exchange device known as an oxygenator, and returned to the venous system via another catheter. The blood flowing through the oxygenator is separated from a continuous supply of oxygen-rich sweep gas by a semipermeable membrane, across which diffusion-mediated gas exchange occurs, so that the blood exiting it is rich in oxygen and low in carbon dioxide. As venovenous ECMO functions in series with the native circulation, the well-oxygenated blood exiting the ECMO circuit mixes with poorly oxygenated blood flowing through the lungs. Therefore, oxygenation is dependent on native cardiac output to achieve systemic oxygen delivery (Figure 1).

ECMO been used successfully in adults with ARDS since the early 1970s (Hill JD, et al. N Engl J Med. 1972;286[12]:629-34) but, until recently, was limited to small numbers of patients at select global centers and associated with a high-risk profile. In the last decade, however, driven by improvements in ECMO circuit components making the device safer and easier to use, encouraging worldwide experience during the 2009 influenza A (H1N1) pandemic (Davies A, et al. JAMA. 2009;302[17]1888-95), and publication of the Efficacy and Economic Assessment of Conventional Ventilatory Support versus Extracorporeal Membrane Oxygenation for Severe Adult Respiratory Failure (CESAR) trial (Peek GJ, et al. Lancet. 2009;374[9698]:1351-63), ECMO use has markedly increased.

Despite its rapid growth, however, rigorous evidence supporting the use of ECMO has been lacking. The CESAR trial, while impressive in execution, had methodological issues that limited the strength of its conclusions. CESAR was a pragmatic trial that randomized 180 adults with severe respiratory failure from multiple etiologies to conventional management or transfer to an experienced, ECMO-capable center. CESAR met its primary outcome of improved survival without disability in the ECMO-referred group (63% vs 47%, relative risk [RR] 0.69; 95% confidence interval [CI] 0.05 to 0.97, P=.03), but not all patients in that group ultimately received ECMO. In addition, the use of lung protective ventilation was significantly higher in the ECMO-referred group, making it difficult to separate its benefit from that of ECMO. A conservative interpretation is that CESAR showed the clinical benefit of treatment at an ECMO-capable center, experienced in the management of patients with severe respiratory failure.

Not until the release of the Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome (EOLIA) trial earlier this year (Combes A, et al. N Engl J Med. 2018;378[21]:1965-75), did a modern, randomized controlled trial evaluating the use of ECMO itself exist. The EOLIA trial addressed the limitations of CESAR and randomized adult patients with early, severe ARDS to conventional, standard of care management that included a protocolized lung protective strategy in the control group vs immediate initiation of ECMO combined with an ultra-lung protective strategy (targeting end-inspiratory plateau pressure ≤24 cmH2O) in the intervention group. The primary outcome was all-cause mortality at 60 days. Of note, patients enrolled in EOLIA met entry criteria despite greater than 90% of patients receiving neuromuscular blockade and around 60% treated with prone positioning at the time of randomization (importantly, 90% of control group patients ultimately underwent prone positioning).

EOLIA was powered to detect a 20% decrease in mortality in the ECMO group. Based on trial design and the results of the fourth interim analysis, the trial was stopped for futility to reach that endpoint after enrollment of 249 of a maximum 331 patients. Although a 20% mortality reduction was not achieved, 60-day mortality was notably lower in the ECMO-treated group (35% vs 46%, RR 0.76, 95% CI 0.55 to 1.04, P=.09). The key secondary outcome of risk of treatment failure (defined as death in the ECMO group and death or crossover to ECMO in the control group) favored the ECMO group with a RR for mortality of 0.62 (95% CI, 0.47 to 0.82; P<.001), as did other secondary endpoints such as days free of renal and other organ failure.

A major limitation of the trial was that 35 (28%) of control group patients ultimately crossed over to ECMO, which diluted the effect of ECMO observed in the intention-to-treat analysis. Crossover occurred at clinician discretion an average of 6.5 days after randomization and after stringent criteria for crossover was met. These patients were incredibly ill, with a median oxygen saturation of 77%, rapidly worsening inotropic scores, and lactic acidosis; nine individuals had already suffered cardiac arrest, and six had received ECMO as part of extracorporeal cardiopulmonary resuscitation (ECPR), the initiation of venoarterial ECMO during cardiac arrest in attempt to restore spontaneous circulation. Mortality was considerably worse in the crossover group than in conventionally managed cohort overall, and, notably, 33% of patients crossed over to ECMO still survived.

In order to estimate the effect of ECMO on survival times if crossover had not occurred, the authors performed a post-hoc, rank-preserving structural failure time analysis. Though this relies on some assessment regarding the effect of the treatment itself, it showed a hazard ratio for mortality in the ECMO group of 0.51 (95% CI 0.24 to 1.02, P=.055). Although the EOLIA trial was not positive by traditional interpretation, all three major analyses and all secondary endpoints suggest some degree of benefit in patients with severe ARDS managed with ECMO.

Importantly, ECMO was well tolerated (at least when performed at expert centers, as done in this trial). There were significantly more bleeding events and cases of severe thrombocytopenia in the ECMO-treated group, but massive hemorrhage, ischemic and hemorrhagic stroke, arrhythmias, and other complications were similar.

Where do we go from here? Based on the totality of information, it is reasonable to consider ECMO for cases of severe ARDS not responsive to conventional measures, such as a lung protective ventilator strategy, neuromuscular blockade, and prone positioning. Initiation of ECMO may be reasonable prior to implementation of standard of care therapies, in order to permit safe transfer to an experienced center from a center not able to provide them.

Two take-away points: First, it is important to recognize that much of the clinical benefit derived from ECMO may be beyond its ability to normalize gas exchange and be due, at least in part, to the fact that ECMO allows the enhancement of proven lung protective ventilatory strategies. Initiation of ECMO and the “lung rest” it permits reduce the mechanical power applied to the injured alveoli and may attenuate ventilator-induced lung injury, cytokine release, and multiorgan failure that portend poor clinical outcomes in ARDS. Second, ECMO in EOLIA was conducted at expert centers with relatively low rates of complications.

It is too early to know how the critical care community will view ECMO for ARDS in light of EOLIA as well as a growing body of global ECMO experience, or how its wider application may impact the distribution and organization of ECMO centers. Regardless, of paramount importance in using ECMO as a treatment modality is optimizing patient management both prior to and after its initiation.

Dr. Agerstrand is Assistant Professor of Medicine, Director of the Medical ECMO Program, Columbia University College of Physicians and Surgeons, New York-Presbyterian Hospital.


 

Due to significant interest in the pulmonary/critical care community, the National Board of Echocardiography (NBE) has opened registration for a board examination as a requirement for national level certification in advanced critical care echocardiography (ACCE). The examination has been developed by the National Board of Medical Examiners; CHEST and the other professional societies are well represented on the writing committee. The first examination is scheduled to be given on January 15, 2019.

The board of the NBE will be the final arbiter for other requirements for certification. We anticipate that these will be available in 2019.

A few essential questions about the certification:

1. Who will be eligible for certification in ACCE?

The policy of the NBE is that any licensed physician may take the examination. Passing the examination confers testamur status, which is only one of several requirements for certification. The board of the NBE will make the final decision as to how to define the clinical background of the candidate that will be required for certification.

2. What will be the requirements for demonstration of competence at image acquisition for ACCE?

Competence at ACCE requires that the intensivist be expert at image acquisition of a comprehensive image set. The board of the NBE will make the final decision as to what constitutes a full ACCE image set, how many studies must be performed by the candidate, and how the studies will be documented. Regarding the latter question, it is likely that there will be a need for identification of qualified mentors to guide the candidate through the process of demonstrating competence in image acquisition.

3. What resources exist to learn more about the examination?

For some suggestions regarding mastery of the cognitive base, Dr. Yonatan Greenstein has set up an independent website that has recommendations about study material and an example of the full ACCE image set (advancedcriticalcareecho.org). The NBE website has a list of subjects that will be covered in the examination. In addition to passing the examination, there will be other elements required for ACCE certification. The NBE has not yet made final decision on the additional requirements. As soon as they are available, they will be posted on the NBE website (echoboards.org).

There is keen interest amongst fellows and junior attendings in the NBE certification who are already competent in whole body ultrasonography. They see ACCE as a natural and necessary extension of their scope of practice, as a means of better helping their critically ill patients, and as a means of acquiring a unique skill that defines them as having a special skill compared with other intensivists. A smaller group of senior attending intensivists are primarily motivated by a well-defined practice-related need of skill at ACCE and/or a strong perception that knowledge of ACCE may directly improve their ability to care for the critically ill patient. Interest in certification extends across the various specialties that provide critical care services. The NBE has indicated that there has been a strong showing of registrations for the examination thus far.

We recommend that candidates for certification consider that passing the examination should be the priority. Collection of the image set may occur in parallel, as the two will complement each other. Preparation for the examination requires intensive study of the cognitive base of ACCE and mastery of image interpretation.

To aid in preparation for the ACCE examination, CHEST is offering a comprehensive review course, Advanced Critical Care Echocardiography Board Review Exam Course, being held at the CHEST Innovation, Simulation, and Training Center, December 7-8, 2018, in Glenview, Illinois.




 

Due to significant interest in the pulmonary/critical care community, the National Board of Echocardiography (NBE) has opened registration for a board examination as a requirement for national level certification in advanced critical care echocardiography (ACCE). The examination has been developed by the National Board of Medical Examiners; CHEST and the other professional societies are well represented on the writing committee. The first examination is scheduled to be given on January 15, 2019.

The board of the NBE will be the final arbiter for other requirements for certification. We anticipate that these will be available in 2019.

A few essential questions about the certification:

1. Who will be eligible for certification in ACCE?

The policy of the NBE is that any licensed physician may take the examination. Passing the examination confers testamur status, which is only one of several requirements for certification. The board of the NBE will make the final decision as to how to define the clinical background of the candidate that will be required for certification.

2. What will be the requirements for demonstration of competence at image acquisition for ACCE?

Competence at ACCE requires that the intensivist be expert at image acquisition of a comprehensive image set. The board of the NBE will make the final decision as to what constitutes a full ACCE image set, how many studies must be performed by the candidate, and how the studies will be documented. Regarding the latter question, it is likely that there will be a need for identification of qualified mentors to guide the candidate through the process of demonstrating competence in image acquisition.

3. What resources exist to learn more about the examination?

For some suggestions regarding mastery of the cognitive base, Dr. Yonatan Greenstein has set up an independent website that has recommendations about study material and an example of the full ACCE image set (advancedcriticalcareecho.org). The NBE website has a list of subjects that will be covered in the examination. In addition to passing the examination, there will be other elements required for ACCE certification. The NBE has not yet made final decision on the additional requirements. As soon as they are available, they will be posted on the NBE website (echoboards.org).

There is keen interest amongst fellows and junior attendings in the NBE certification who are already competent in whole body ultrasonography. They see ACCE as a natural and necessary extension of their scope of practice, as a means of better helping their critically ill patients, and as a means of acquiring a unique skill that defines them as having a special skill compared with other intensivists. A smaller group of senior attending intensivists are primarily motivated by a well-defined practice-related need of skill at ACCE and/or a strong perception that knowledge of ACCE may directly improve their ability to care for the critically ill patient. Interest in certification extends across the various specialties that provide critical care services. The NBE has indicated that there has been a strong showing of registrations for the examination thus far.

We recommend that candidates for certification consider that passing the examination should be the priority. Collection of the image set may occur in parallel, as the two will complement each other. Preparation for the examination requires intensive study of the cognitive base of ACCE and mastery of image interpretation.

To aid in preparation for the ACCE examination, CHEST is offering a comprehensive review course, Advanced Critical Care Echocardiography Board Review Exam Course, being held at the CHEST Innovation, Simulation, and Training Center, December 7-8, 2018, in Glenview, Illinois.




 

Due to significant interest in the pulmonary/critical care community, the National Board of Echocardiography (NBE) has opened registration for a board examination as a requirement for national level certification in advanced critical care echocardiography (ACCE). The examination has been developed by the National Board of Medical Examiners; CHEST and the other professional societies are well represented on the writing committee. The first examination is scheduled to be given on January 15, 2019.

The board of the NBE will be the final arbiter for other requirements for certification. We anticipate that these will be available in 2019.

A few essential questions about the certification:

1. Who will be eligible for certification in ACCE?

The policy of the NBE is that any licensed physician may take the examination. Passing the examination confers testamur status, which is only one of several requirements for certification. The board of the NBE will make the final decision as to how to define the clinical background of the candidate that will be required for certification.

2. What will be the requirements for demonstration of competence at image acquisition for ACCE?

Competence at ACCE requires that the intensivist be expert at image acquisition of a comprehensive image set. The board of the NBE will make the final decision as to what constitutes a full ACCE image set, how many studies must be performed by the candidate, and how the studies will be documented. Regarding the latter question, it is likely that there will be a need for identification of qualified mentors to guide the candidate through the process of demonstrating competence in image acquisition.

3. What resources exist to learn more about the examination?

For some suggestions regarding mastery of the cognitive base, Dr. Yonatan Greenstein has set up an independent website that has recommendations about study material and an example of the full ACCE image set (advancedcriticalcareecho.org). The NBE website has a list of subjects that will be covered in the examination. In addition to passing the examination, there will be other elements required for ACCE certification. The NBE has not yet made final decision on the additional requirements. As soon as they are available, they will be posted on the NBE website (echoboards.org).

There is keen interest amongst fellows and junior attendings in the NBE certification who are already competent in whole body ultrasonography. They see ACCE as a natural and necessary extension of their scope of practice, as a means of better helping their critically ill patients, and as a means of acquiring a unique skill that defines them as having a special skill compared with other intensivists. A smaller group of senior attending intensivists are primarily motivated by a well-defined practice-related need of skill at ACCE and/or a strong perception that knowledge of ACCE may directly improve their ability to care for the critically ill patient. Interest in certification extends across the various specialties that provide critical care services. The NBE has indicated that there has been a strong showing of registrations for the examination thus far.

We recommend that candidates for certification consider that passing the examination should be the priority. Collection of the image set may occur in parallel, as the two will complement each other. Preparation for the examination requires intensive study of the cognitive base of ACCE and mastery of image interpretation.

To aid in preparation for the ACCE examination, CHEST is offering a comprehensive review course, Advanced Critical Care Echocardiography Board Review Exam Course, being held at the CHEST Innovation, Simulation, and Training Center, December 7-8, 2018, in Glenview, Illinois.




 

Interventional Chest/Diagnostic Procedures

Endobronchial valve therapy receives FDA approval for bronchoscopic LVR

Lung volume reduction surgery (LVRS) is an established approach to improve exercise capacity and lung function in patients with heterogeneous emphysema and may confer survival benefit in patients with apical-predominant disease (Fishman, et al. N Engl J Med. 2003;348[21]:2059). Despite this, LVRS case numbers remain low due to patient and procedural morbidity. Bronchoscopic alternatives for LVRS have advanced considerably over the last decade with endobronchial valve (EBV) therapy emerging as a viable option for select subsets of patients with heterogeneous emphysema. Endobronchial valves are removable devices placed in segmental/subsegmental airways, which allow efflux of air during exhalation but close during inspiration, resulting in distal atelectasis in the absence of collateral ventilation.

The LIBERATE study, a multicenter randomized controlled trial demonstrated improvement in FEV1 ≥15% in 48% of patients after EBV placement compared with 17% of patients receiving standard medical therapy has resulted in FDA approval (Criner G, et al. Am J Respir Crit Care Med. 2018 May 22. doi: 10.1164/rccm.201803-0590OC. [Epub ahead of print]). Patients with EBV had improved subjective dyspnea scores, residual volume, and 6-minute walk distance; however, the pneumothorax rate was 27%.

All study patients with EBV underwent bronchoscopic evaluation for collateral ventilation using a proprietary digital system, which measures expiratory airflow in target airways to establish the presence of collateral ventilation. Previous data have demonstrated improved transplant-free survival when implanted EBVs result in atelectasis of the target lobe, which requires intact interlobar fissures (Garner, et al. Am J Respir Crit Care Med. 2016;194[4]:519). Ongoing clinical trials are attempting to clarify the role of EBV therapy in different phenotypes of COPD, including patients with homogenous emphysema. Long-term follow-up data will be important in determining the broader implementation of bronchoscopic lung volume reduction moving forward.

Vivek Murthy, MD
Jason A. Akulian, MD, FCCP
Steering Committee Members
 

Pediatric Chest Medicine

CFTR modulators

Cystic fibrosis (CF) is a progressive genetic disorder resulting in multiorgan disease with progressive respiratory decline. CF is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. This codes for the CFTR anion channel and contributes to the movement of salt in and out of the cell. CFTR dysfunction leads to thickened secretions in the lungs and other organs, such as the gut and pancreas. This leads to more lung infections and other organ dysfunction that ultimately leads to premature death.

Pulmonary Physiology, Function, and Rehabilitation

Wildfires, particulate matter, and lung function

In the last 3 decades, human-caused climate change contributed to wildfires in an additional 4.2 million hectares of land across the western US alone. Human impact on climate is responsible for nearly doubling the expected wildfire area (Abatzoglou, et al. PNAS. 2016;113:11770). Year 2017 saw the most destructive wildfires in California recorded to date, and over $2 billion dollars was spent by the US Forest Service, the most-expensive on record. Besides the devastating effects on the forestry and nearby communities, wildfires also generate a large amount of particulate matter (PM). In western US, wildfires contributed to 71.3% of total PM2.5 on days exceeding regulatory PM2.5 standards during 2004-2009 (Liu et al. Clim Change. 2016;138:655). Acute PM exposure is associated with respiratory health effects, such as exacerbation of asthma and COPD, increased ED visits and hospitalization for pneumonia, and increased mortality. Chronic PM2.5 exposure may also affect lung function. Cross-shift and cross-season FEV1 declined by 0.150 L and 0.104 L, respectively in forest firefighters (Betchley, et al. Am. J Ind Med. 1997;31:503). The Children’s Health Study conducted in California found that subjects who were exposed to the highest level of exposure to PM2.5 were five times more likely to have an FEV1 less than 80% of expected FEV1 when they reached 18 years of age than subjects exposed to the lowest level of PM2.5 (Gauderman et al. N Engl J Med. 2004;351:1057). Clinicians should educate patients and the public how to protect our environment and, when wildfires occur, how to protect themselves from exposure to PM.

Thomas W. DeCato, MD
Fellow-in-Training Committee Member

Yuh-Chin T. Huang, MD, FCCP
Steering Committee Member
 

Pulmonary Vascular Disease

Small increases in pulmonary pressures—big impact

Pulmonary hypertension (PH) is a progressive, life-limiting pulmonary vascular disease that is diagnosed hemodynamically by right-sided heart catheterization (RHC) and defined by a mean pulmonary artery pressure (mPAP) >25 mm Hg (Hoeper MM, et al. JACC. 2013;62(25 Suppl):D42).

The impact of PH on survival both in its “pure” form, pulmonary arterial hypertension, and in the setting of underlying cardiopulmonary disease, is well established. However, the clinical relevance of mildly elevated mPAP, defined as mPAP between 18 and 24 mm Hg, has been unclear until recently. Two large cohort studies have suggested that mild increases in mPAP are clinically relevant. A large retrospective analysis of hemodynamic data from 21,727 US veterans found mildly increased mPAP (19-24 mm Hg) was associated with increased hospitalization and decreased survival (Maron, et al. Circulation. 2016;133:1240).

While this population was skewed toward elderly men, a study from Vanderbilt University that included equal numbers of men and women showed similar results. Patients with mPAP 19-24 mm Hg experienced incrementally increased mortality (HR:1.31, P=.001). Importantly, in the subset of patients who underwent a repeat RHC in follow-up, 61% developed progressive increases of pulmonary pressures (>25 mm Hg) on follow-up RHC suggesting that the disease process may progress in a substantial proportion of patients (Assad, et al. JAMA Cardiol. 2017;2[1]):1361). Combined with prior data from smaller cohorts, these studies highlight the impact of mildly increased pulmonary pressures on outcomes. Given the dearth of available data regarding interventions for these patients, there is an urgent need to study to role of specific therapy for mildly elevated pulmonary pressures.

Vijay Balasubramanian, MD, FCCP
Steering Committee Member

Jean Elwing, MD, FCCP
Steering Committee Vice-Chair

Thoracic Oncology

Multiple tumor nodules in lung cancer diagnosis

Low dose CT (LDCT) scan screening for lung cancer is a recommended preventative modality for adults with a significant smoking history (Mayer et al. Ann Int Med. 2014;160(5):330). The screening approach aims to identify adults at significant risk for lung cancer. The goal is to discover lung cancers at low stage with benign mediastinal nodes for optimal treatment and potential for cure. In a minority, but significant number of cases, the LDCT demonstrates multiple lung nodules or masses confounding the attempt to adequately stage the tumor. Two tumors representing a primary cancer and separate malignant spread, namely, intra-pulmonary metastases, in the same lobe, different ipsilateral lobe, or contralateral lobe would be staged, respectively, as T3, T4, or M1a (Detterbeck et al. Chest. 2013;143(5):e191S). Clearly, if the two tumors are separate unique primary cancers, independent of one another, then at best they would be considered as multiple T1 tumors. The treatment modalities of and clinical survival outcomes for these multiple conditions would be markedly different.

The identification of additional tumors may be synchronous (at the same time of the primary discovery) or metachronous (at a later time than the primary discovery). The approach is basically the same. Two tumors with different histologic types, or having separate in-situ squamous cell carcinoma patterns, or disparate immunohistochemical or molecular expressions, or different genomic profiles or driver mutations may be considered as separate distinct primary malignancies (Detterbeck et al. J Thorac Oncol. 2016;11:639; Nicholson et al. J Thorac Oncol. 2017;13:205). Separate foci of ground-glass opacities with small solid central component indicative of minimally invasive adenocarcinoma may be designated as the highest T-stage. These cited and more challenging cases should be presented to a lung cancer tumor board with multiple specialties represented for analysis and judgment. The approach to diagnostic decision-making and clinical management should involve the expertise of all specialties in the lung cancer patient care team.

Arnold M. Schwartz, MD, PhD, FCCP
Steering Committee Member


















 

Interventional Chest/Diagnostic Procedures

Endobronchial valve therapy receives FDA approval for bronchoscopic LVR

Lung volume reduction surgery (LVRS) is an established approach to improve exercise capacity and lung function in patients with heterogeneous emphysema and may confer survival benefit in patients with apical-predominant disease (Fishman, et al. N Engl J Med. 2003;348[21]:2059). Despite this, LVRS case numbers remain low due to patient and procedural morbidity. Bronchoscopic alternatives for LVRS have advanced considerably over the last decade with endobronchial valve (EBV) therapy emerging as a viable option for select subsets of patients with heterogeneous emphysema. Endobronchial valves are removable devices placed in segmental/subsegmental airways, which allow efflux of air during exhalation but close during inspiration, resulting in distal atelectasis in the absence of collateral ventilation.

The LIBERATE study, a multicenter randomized controlled trial demonstrated improvement in FEV1 ≥15% in 48% of patients after EBV placement compared with 17% of patients receiving standard medical therapy has resulted in FDA approval (Criner G, et al. Am J Respir Crit Care Med. 2018 May 22. doi: 10.1164/rccm.201803-0590OC. [Epub ahead of print]). Patients with EBV had improved subjective dyspnea scores, residual volume, and 6-minute walk distance; however, the pneumothorax rate was 27%.

All study patients with EBV underwent bronchoscopic evaluation for collateral ventilation using a proprietary digital system, which measures expiratory airflow in target airways to establish the presence of collateral ventilation. Previous data have demonstrated improved transplant-free survival when implanted EBVs result in atelectasis of the target lobe, which requires intact interlobar fissures (Garner, et al. Am J Respir Crit Care Med. 2016;194[4]:519). Ongoing clinical trials are attempting to clarify the role of EBV therapy in different phenotypes of COPD, including patients with homogenous emphysema. Long-term follow-up data will be important in determining the broader implementation of bronchoscopic lung volume reduction moving forward.

Vivek Murthy, MD
Jason A. Akulian, MD, FCCP
Steering Committee Members
 

Pediatric Chest Medicine

CFTR modulators

Cystic fibrosis (CF) is a progressive genetic disorder resulting in multiorgan disease with progressive respiratory decline. CF is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. This codes for the CFTR anion channel and contributes to the movement of salt in and out of the cell. CFTR dysfunction leads to thickened secretions in the lungs and other organs, such as the gut and pancreas. This leads to more lung infections and other organ dysfunction that ultimately leads to premature death.

Pulmonary Physiology, Function, and Rehabilitation

Wildfires, particulate matter, and lung function

In the last 3 decades, human-caused climate change contributed to wildfires in an additional 4.2 million hectares of land across the western US alone. Human impact on climate is responsible for nearly doubling the expected wildfire area (Abatzoglou, et al. PNAS. 2016;113:11770). Year 2017 saw the most destructive wildfires in California recorded to date, and over $2 billion dollars was spent by the US Forest Service, the most-expensive on record. Besides the devastating effects on the forestry and nearby communities, wildfires also generate a large amount of particulate matter (PM). In western US, wildfires contributed to 71.3% of total PM2.5 on days exceeding regulatory PM2.5 standards during 2004-2009 (Liu et al. Clim Change. 2016;138:655). Acute PM exposure is associated with respiratory health effects, such as exacerbation of asthma and COPD, increased ED visits and hospitalization for pneumonia, and increased mortality. Chronic PM2.5 exposure may also affect lung function. Cross-shift and cross-season FEV1 declined by 0.150 L and 0.104 L, respectively in forest firefighters (Betchley, et al. Am. J Ind Med. 1997;31:503). The Children’s Health Study conducted in California found that subjects who were exposed to the highest level of exposure to PM2.5 were five times more likely to have an FEV1 less than 80% of expected FEV1 when they reached 18 years of age than subjects exposed to the lowest level of PM2.5 (Gauderman et al. N Engl J Med. 2004;351:1057). Clinicians should educate patients and the public how to protect our environment and, when wildfires occur, how to protect themselves from exposure to PM.

Thomas W. DeCato, MD
Fellow-in-Training Committee Member

Yuh-Chin T. Huang, MD, FCCP
Steering Committee Member
 

Pulmonary Vascular Disease

Small increases in pulmonary pressures—big impact

Pulmonary hypertension (PH) is a progressive, life-limiting pulmonary vascular disease that is diagnosed hemodynamically by right-sided heart catheterization (RHC) and defined by a mean pulmonary artery pressure (mPAP) >25 mm Hg (Hoeper MM, et al. JACC. 2013;62(25 Suppl):D42).

The impact of PH on survival both in its “pure” form, pulmonary arterial hypertension, and in the setting of underlying cardiopulmonary disease, is well established. However, the clinical relevance of mildly elevated mPAP, defined as mPAP between 18 and 24 mm Hg, has been unclear until recently. Two large cohort studies have suggested that mild increases in mPAP are clinically relevant. A large retrospective analysis of hemodynamic data from 21,727 US veterans found mildly increased mPAP (19-24 mm Hg) was associated with increased hospitalization and decreased survival (Maron, et al. Circulation. 2016;133:1240).

While this population was skewed toward elderly men, a study from Vanderbilt University that included equal numbers of men and women showed similar results. Patients with mPAP 19-24 mm Hg experienced incrementally increased mortality (HR:1.31, P=.001). Importantly, in the subset of patients who underwent a repeat RHC in follow-up, 61% developed progressive increases of pulmonary pressures (>25 mm Hg) on follow-up RHC suggesting that the disease process may progress in a substantial proportion of patients (Assad, et al. JAMA Cardiol. 2017;2[1]):1361). Combined with prior data from smaller cohorts, these studies highlight the impact of mildly increased pulmonary pressures on outcomes. Given the dearth of available data regarding interventions for these patients, there is an urgent need to study to role of specific therapy for mildly elevated pulmonary pressures.

Vijay Balasubramanian, MD, FCCP
Steering Committee Member

Jean Elwing, MD, FCCP
Steering Committee Vice-Chair

Thoracic Oncology

Multiple tumor nodules in lung cancer diagnosis

Low dose CT (LDCT) scan screening for lung cancer is a recommended preventative modality for adults with a significant smoking history (Mayer et al. Ann Int Med. 2014;160(5):330). The screening approach aims to identify adults at significant risk for lung cancer. The goal is to discover lung cancers at low stage with benign mediastinal nodes for optimal treatment and potential for cure. In a minority, but significant number of cases, the LDCT demonstrates multiple lung nodules or masses confounding the attempt to adequately stage the tumor. Two tumors representing a primary cancer and separate malignant spread, namely, intra-pulmonary metastases, in the same lobe, different ipsilateral lobe, or contralateral lobe would be staged, respectively, as T3, T4, or M1a (Detterbeck et al. Chest. 2013;143(5):e191S). Clearly, if the two tumors are separate unique primary cancers, independent of one another, then at best they would be considered as multiple T1 tumors. The treatment modalities of and clinical survival outcomes for these multiple conditions would be markedly different.

The identification of additional tumors may be synchronous (at the same time of the primary discovery) or metachronous (at a later time than the primary discovery). The approach is basically the same. Two tumors with different histologic types, or having separate in-situ squamous cell carcinoma patterns, or disparate immunohistochemical or molecular expressions, or different genomic profiles or driver mutations may be considered as separate distinct primary malignancies (Detterbeck et al. J Thorac Oncol. 2016;11:639; Nicholson et al. J Thorac Oncol. 2017;13:205). Separate foci of ground-glass opacities with small solid central component indicative of minimally invasive adenocarcinoma may be designated as the highest T-stage. These cited and more challenging cases should be presented to a lung cancer tumor board with multiple specialties represented for analysis and judgment. The approach to diagnostic decision-making and clinical management should involve the expertise of all specialties in the lung cancer patient care team.

Arnold M. Schwartz, MD, PhD, FCCP
Steering Committee Member


















 

Interventional Chest/Diagnostic Procedures

Endobronchial valve therapy receives FDA approval for bronchoscopic LVR

Lung volume reduction surgery (LVRS) is an established approach to improve exercise capacity and lung function in patients with heterogeneous emphysema and may confer survival benefit in patients with apical-predominant disease (Fishman, et al. N Engl J Med. 2003;348[21]:2059). Despite this, LVRS case numbers remain low due to patient and procedural morbidity. Bronchoscopic alternatives for LVRS have advanced considerably over the last decade with endobronchial valve (EBV) therapy emerging as a viable option for select subsets of patients with heterogeneous emphysema. Endobronchial valves are removable devices placed in segmental/subsegmental airways, which allow efflux of air during exhalation but close during inspiration, resulting in distal atelectasis in the absence of collateral ventilation.

The LIBERATE study, a multicenter randomized controlled trial demonstrated improvement in FEV1 ≥15% in 48% of patients after EBV placement compared with 17% of patients receiving standard medical therapy has resulted in FDA approval (Criner G, et al. Am J Respir Crit Care Med. 2018 May 22. doi: 10.1164/rccm.201803-0590OC. [Epub ahead of print]). Patients with EBV had improved subjective dyspnea scores, residual volume, and 6-minute walk distance; however, the pneumothorax rate was 27%.

All study patients with EBV underwent bronchoscopic evaluation for collateral ventilation using a proprietary digital system, which measures expiratory airflow in target airways to establish the presence of collateral ventilation. Previous data have demonstrated improved transplant-free survival when implanted EBVs result in atelectasis of the target lobe, which requires intact interlobar fissures (Garner, et al. Am J Respir Crit Care Med. 2016;194[4]:519). Ongoing clinical trials are attempting to clarify the role of EBV therapy in different phenotypes of COPD, including patients with homogenous emphysema. Long-term follow-up data will be important in determining the broader implementation of bronchoscopic lung volume reduction moving forward.

Vivek Murthy, MD
Jason A. Akulian, MD, FCCP
Steering Committee Members
 

Pediatric Chest Medicine

CFTR modulators

Cystic fibrosis (CF) is a progressive genetic disorder resulting in multiorgan disease with progressive respiratory decline. CF is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. This codes for the CFTR anion channel and contributes to the movement of salt in and out of the cell. CFTR dysfunction leads to thickened secretions in the lungs and other organs, such as the gut and pancreas. This leads to more lung infections and other organ dysfunction that ultimately leads to premature death.

Pulmonary Physiology, Function, and Rehabilitation

Wildfires, particulate matter, and lung function

In the last 3 decades, human-caused climate change contributed to wildfires in an additional 4.2 million hectares of land across the western US alone. Human impact on climate is responsible for nearly doubling the expected wildfire area (Abatzoglou, et al. PNAS. 2016;113:11770). Year 2017 saw the most destructive wildfires in California recorded to date, and over $2 billion dollars was spent by the US Forest Service, the most-expensive on record. Besides the devastating effects on the forestry and nearby communities, wildfires also generate a large amount of particulate matter (PM). In western US, wildfires contributed to 71.3% of total PM2.5 on days exceeding regulatory PM2.5 standards during 2004-2009 (Liu et al. Clim Change. 2016;138:655). Acute PM exposure is associated with respiratory health effects, such as exacerbation of asthma and COPD, increased ED visits and hospitalization for pneumonia, and increased mortality. Chronic PM2.5 exposure may also affect lung function. Cross-shift and cross-season FEV1 declined by 0.150 L and 0.104 L, respectively in forest firefighters (Betchley, et al. Am. J Ind Med. 1997;31:503). The Children’s Health Study conducted in California found that subjects who were exposed to the highest level of exposure to PM2.5 were five times more likely to have an FEV1 less than 80% of expected FEV1 when they reached 18 years of age than subjects exposed to the lowest level of PM2.5 (Gauderman et al. N Engl J Med. 2004;351:1057). Clinicians should educate patients and the public how to protect our environment and, when wildfires occur, how to protect themselves from exposure to PM.

Thomas W. DeCato, MD
Fellow-in-Training Committee Member

Yuh-Chin T. Huang, MD, FCCP
Steering Committee Member
 

Pulmonary Vascular Disease

Small increases in pulmonary pressures—big impact

Pulmonary hypertension (PH) is a progressive, life-limiting pulmonary vascular disease that is diagnosed hemodynamically by right-sided heart catheterization (RHC) and defined by a mean pulmonary artery pressure (mPAP) >25 mm Hg (Hoeper MM, et al. JACC. 2013;62(25 Suppl):D42).

The impact of PH on survival both in its “pure” form, pulmonary arterial hypertension, and in the setting of underlying cardiopulmonary disease, is well established. However, the clinical relevance of mildly elevated mPAP, defined as mPAP between 18 and 24 mm Hg, has been unclear until recently. Two large cohort studies have suggested that mild increases in mPAP are clinically relevant. A large retrospective analysis of hemodynamic data from 21,727 US veterans found mildly increased mPAP (19-24 mm Hg) was associated with increased hospitalization and decreased survival (Maron, et al. Circulation. 2016;133:1240).

While this population was skewed toward elderly men, a study from Vanderbilt University that included equal numbers of men and women showed similar results. Patients with mPAP 19-24 mm Hg experienced incrementally increased mortality (HR:1.31, P=.001). Importantly, in the subset of patients who underwent a repeat RHC in follow-up, 61% developed progressive increases of pulmonary pressures (>25 mm Hg) on follow-up RHC suggesting that the disease process may progress in a substantial proportion of patients (Assad, et al. JAMA Cardiol. 2017;2[1]):1361). Combined with prior data from smaller cohorts, these studies highlight the impact of mildly increased pulmonary pressures on outcomes. Given the dearth of available data regarding interventions for these patients, there is an urgent need to study to role of specific therapy for mildly elevated pulmonary pressures.

Vijay Balasubramanian, MD, FCCP
Steering Committee Member

Jean Elwing, MD, FCCP
Steering Committee Vice-Chair

Thoracic Oncology

Multiple tumor nodules in lung cancer diagnosis

Low dose CT (LDCT) scan screening for lung cancer is a recommended preventative modality for adults with a significant smoking history (Mayer et al. Ann Int Med. 2014;160(5):330). The screening approach aims to identify adults at significant risk for lung cancer. The goal is to discover lung cancers at low stage with benign mediastinal nodes for optimal treatment and potential for cure. In a minority, but significant number of cases, the LDCT demonstrates multiple lung nodules or masses confounding the attempt to adequately stage the tumor. Two tumors representing a primary cancer and separate malignant spread, namely, intra-pulmonary metastases, in the same lobe, different ipsilateral lobe, or contralateral lobe would be staged, respectively, as T3, T4, or M1a (Detterbeck et al. Chest. 2013;143(5):e191S). Clearly, if the two tumors are separate unique primary cancers, independent of one another, then at best they would be considered as multiple T1 tumors. The treatment modalities of and clinical survival outcomes for these multiple conditions would be markedly different.

The identification of additional tumors may be synchronous (at the same time of the primary discovery) or metachronous (at a later time than the primary discovery). The approach is basically the same. Two tumors with different histologic types, or having separate in-situ squamous cell carcinoma patterns, or disparate immunohistochemical or molecular expressions, or different genomic profiles or driver mutations may be considered as separate distinct primary malignancies (Detterbeck et al. J Thorac Oncol. 2016;11:639; Nicholson et al. J Thorac Oncol. 2017;13:205). Separate foci of ground-glass opacities with small solid central component indicative of minimally invasive adenocarcinoma may be designated as the highest T-stage. These cited and more challenging cases should be presented to a lung cancer tumor board with multiple specialties represented for analysis and judgment. The approach to diagnostic decision-making and clinical management should involve the expertise of all specialties in the lung cancer patient care team.

Arnold M. Schwartz, MD, PhD, FCCP
Steering Committee Member