Adding the poly (ADP-ribose) polymerase (PARP) inhibitor veliparib to platinum doublet chemotherapy modestly improved progression-free survival in a randomized, placebo-controlled, phase 2 trial of 128 patients with extensive-stage non–small cell lung cancer.

Improved progression-free survival (PFS) “did not translate into reduction in overall mortality for patients treated with veliparib. However, the improvement in the point estimate of PFS was quite modest at 6.1 months, compared with 5.5 months [in the placebo control arm],” wrote Taofeek K. Owonikoko, MD, PhD, of Emory University, Atlanta, together with his coinvestigators in the Journal of Clinical Oncology.

Preclinical studies suggest that veliparib helps potentiate standard chemotherapy of non–small cell lung cancer (NSCLC), but clinical trials have yielded mixed results for PARP inhibition in this cancer. Patients in this study had untreated, extensive-stage NSCLC and an Eastern Cooperative Oncology Group performance status of 0 or 1. They received four 3-week cycles of cisplatin-etoposide (75 mg/m² intravenously on day 1 and 100 mg/m² on days 1-3) plus either veliparib (100 mg orally twice per day on days 1-7) or placebo.

Grade 3 or higher lymphopenia and neutropenia were more common in the veliparib arm but did not reduce treatment delivery. After a median follow-up time of 18.5 months, overall response rate was 72% in the veliparib arm versus 66% in the control arm (P =.57). Median overall survival times were 10.3 months and 8.9 months, respectively (hazard ratio, 0.83; P = .17).

The unstratified HR for PFS favored the veliparib-doublet arm but did not reach statistical significance (0.75; P = .06). After stratifying patients by sex and serum lactate dehydrogenase levels, the HR for PFS favored veliparib-doublet chemotherapy (0.63; P = .01). However, veliparib showed a much stronger effect in the subgroup of men with abnormal lactate dehydrogenase levels (adjusted HR, 0.34; P less than .001), which violated the “proportional hazards within strata assumption” on which this model was based, rendering the overall stratified HR uninterpretable, the researchers wrote.

They added that, before pursuing a larger definitive clinical trial, they await results from the ongoing phase 2 M14-361 study, in which patients with extensive-stage NSCLC are receiving platinum doublet therapy with carboplatin-etoposide plus either veliparib or placebo.

Funders included the Eastern Cooperative Oncology Group–American College of Radiology Imaging Network Cancer Research Group and the National Cancer Institute. Dr. Owonikoko reported ties to Novartis, Astellas Pharma, Celgene, and several other pharmaceutical companies.

SOURCE: Owonikoko TK et al. J Clin Oncol. 2018 Dec 5. doi: 10.1200/JCO.18.00264.

Adding the poly (ADP-ribose) polymerase (PARP) inhibitor veliparib to platinum doublet chemotherapy modestly improved progression-free survival in a randomized, placebo-controlled, phase 2 trial of 128 patients with extensive-stage non–small cell lung cancer.

Improved progression-free survival (PFS) “did not translate into reduction in overall mortality for patients treated with veliparib. However, the improvement in the point estimate of PFS was quite modest at 6.1 months, compared with 5.5 months [in the placebo control arm],” wrote Taofeek K. Owonikoko, MD, PhD, of Emory University, Atlanta, together with his coinvestigators in the Journal of Clinical Oncology.

Preclinical studies suggest that veliparib helps potentiate standard chemotherapy of non–small cell lung cancer (NSCLC), but clinical trials have yielded mixed results for PARP inhibition in this cancer. Patients in this study had untreated, extensive-stage NSCLC and an Eastern Cooperative Oncology Group performance status of 0 or 1. They received four 3-week cycles of cisplatin-etoposide (75 mg/m² intravenously on day 1 and 100 mg/m² on days 1-3) plus either veliparib (100 mg orally twice per day on days 1-7) or placebo.

Grade 3 or higher lymphopenia and neutropenia were more common in the veliparib arm but did not reduce treatment delivery. After a median follow-up time of 18.5 months, overall response rate was 72% in the veliparib arm versus 66% in the control arm (P =.57). Median overall survival times were 10.3 months and 8.9 months, respectively (hazard ratio, 0.83; P = .17).

The unstratified HR for PFS favored the veliparib-doublet arm but did not reach statistical significance (0.75; P = .06). After stratifying patients by sex and serum lactate dehydrogenase levels, the HR for PFS favored veliparib-doublet chemotherapy (0.63; P = .01). However, veliparib showed a much stronger effect in the subgroup of men with abnormal lactate dehydrogenase levels (adjusted HR, 0.34; P less than .001), which violated the “proportional hazards within strata assumption” on which this model was based, rendering the overall stratified HR uninterpretable, the researchers wrote.

They added that, before pursuing a larger definitive clinical trial, they await results from the ongoing phase 2 M14-361 study, in which patients with extensive-stage NSCLC are receiving platinum doublet therapy with carboplatin-etoposide plus either veliparib or placebo.

Funders included the Eastern Cooperative Oncology Group–American College of Radiology Imaging Network Cancer Research Group and the National Cancer Institute. Dr. Owonikoko reported ties to Novartis, Astellas Pharma, Celgene, and several other pharmaceutical companies.

SOURCE: Owonikoko TK et al. J Clin Oncol. 2018 Dec 5. doi: 10.1200/JCO.18.00264.

Adding the poly (ADP-ribose) polymerase (PARP) inhibitor veliparib to platinum doublet chemotherapy modestly improved progression-free survival in a randomized, placebo-controlled, phase 2 trial of 128 patients with extensive-stage non–small cell lung cancer.

Improved progression-free survival (PFS) “did not translate into reduction in overall mortality for patients treated with veliparib. However, the improvement in the point estimate of PFS was quite modest at 6.1 months, compared with 5.5 months [in the placebo control arm],” wrote Taofeek K. Owonikoko, MD, PhD, of Emory University, Atlanta, together with his coinvestigators in the Journal of Clinical Oncology.

Preclinical studies suggest that veliparib helps potentiate standard chemotherapy of non–small cell lung cancer (NSCLC), but clinical trials have yielded mixed results for PARP inhibition in this cancer. Patients in this study had untreated, extensive-stage NSCLC and an Eastern Cooperative Oncology Group performance status of 0 or 1. They received four 3-week cycles of cisplatin-etoposide (75 mg/m² intravenously on day 1 and 100 mg/m² on days 1-3) plus either veliparib (100 mg orally twice per day on days 1-7) or placebo.

Grade 3 or higher lymphopenia and neutropenia were more common in the veliparib arm but did not reduce treatment delivery. After a median follow-up time of 18.5 months, overall response rate was 72% in the veliparib arm versus 66% in the control arm (P =.57). Median overall survival times were 10.3 months and 8.9 months, respectively (hazard ratio, 0.83; P = .17).

The unstratified HR for PFS favored the veliparib-doublet arm but did not reach statistical significance (0.75; P = .06). After stratifying patients by sex and serum lactate dehydrogenase levels, the HR for PFS favored veliparib-doublet chemotherapy (0.63; P = .01). However, veliparib showed a much stronger effect in the subgroup of men with abnormal lactate dehydrogenase levels (adjusted HR, 0.34; P less than .001), which violated the “proportional hazards within strata assumption” on which this model was based, rendering the overall stratified HR uninterpretable, the researchers wrote.

They added that, before pursuing a larger definitive clinical trial, they await results from the ongoing phase 2 M14-361 study, in which patients with extensive-stage NSCLC are receiving platinum doublet therapy with carboplatin-etoposide plus either veliparib or placebo.

Funders included the Eastern Cooperative Oncology Group–American College of Radiology Imaging Network Cancer Research Group and the National Cancer Institute. Dr. Owonikoko reported ties to Novartis, Astellas Pharma, Celgene, and several other pharmaceutical companies.

SOURCE: Owonikoko TK et al. J Clin Oncol. 2018 Dec 5. doi: 10.1200/JCO.18.00264.

The 2018-2019 flu season may have peaked as measures of influenza-like illness (ILI) activity dropped in the first week of the new year, according to the U.S. Centers for Disease Control and Prevention.

The proportion of outpatients visits for ILI dropped to 3.5% for the week ending Jan. 5, 2019, after reaching 4.0% the previous week. Outpatient ILI visits first topped the national baseline of 2.2% during the week ending Dec. 8, 2018, and have remained above that value for 5 consecutive weeks, the CDC’s influenza division said on Jan. 11.

Flu activity reported by the states reflects the national drop: 10 states came in at level 10 on the CDC’s 1-10 scale of activity for the week ending Jan. 5 – down from 12 the week before – and a total of 15 were in the high range from 8 to 10, compared with 19 the previous week, the CDC said. Two states, Mississippi and Texas, dropped from level 10 to level 7, which the CDC categorizes as moderate activity.

A total of 73 ILI-related deaths were reported during the week ending Dec. 29 (the latest with data available; reporting less than 68% complete), which already exceeds the 71 deaths reported for the week ending Dec. 22 (reporting 85% complete). Flu deaths totaled 437 through the first 13 weeks of the 2018-2019 season, compared with the 1,659 that occurred during weeks 1-13 of the very severe 2017-2018 season, CDC data show.

For the week ending Jan. 5, the CDC received reports of three flu-related pediatric deaths, all of which occurred the previous week. For the season so far, there have been 16 pediatric deaths, compared with 20 at this point in the 2017-2018 season.

Estimates released during the flu season for the first time show that between 6 and 7 million Americans have been infected since Oct. 1, 2018, and that 69,000-84,000 people have been hospitalized with the flu through Jan. 5, 2019. These cumulative totals have previously been available only at the end of the season, the CDC noted.

rfranki@mdedge.com

The 2018-2019 flu season may have peaked as measures of influenza-like illness (ILI) activity dropped in the first week of the new year, according to the U.S. Centers for Disease Control and Prevention.

The proportion of outpatients visits for ILI dropped to 3.5% for the week ending Jan. 5, 2019, after reaching 4.0% the previous week. Outpatient ILI visits first topped the national baseline of 2.2% during the week ending Dec. 8, 2018, and have remained above that value for 5 consecutive weeks, the CDC’s influenza division said on Jan. 11.

Flu activity reported by the states reflects the national drop: 10 states came in at level 10 on the CDC’s 1-10 scale of activity for the week ending Jan. 5 – down from 12 the week before – and a total of 15 were in the high range from 8 to 10, compared with 19 the previous week, the CDC said. Two states, Mississippi and Texas, dropped from level 10 to level 7, which the CDC categorizes as moderate activity.

A total of 73 ILI-related deaths were reported during the week ending Dec. 29 (the latest with data available; reporting less than 68% complete), which already exceeds the 71 deaths reported for the week ending Dec. 22 (reporting 85% complete). Flu deaths totaled 437 through the first 13 weeks of the 2018-2019 season, compared with the 1,659 that occurred during weeks 1-13 of the very severe 2017-2018 season, CDC data show.

For the week ending Jan. 5, the CDC received reports of three flu-related pediatric deaths, all of which occurred the previous week. For the season so far, there have been 16 pediatric deaths, compared with 20 at this point in the 2017-2018 season.

Estimates released during the flu season for the first time show that between 6 and 7 million Americans have been infected since Oct. 1, 2018, and that 69,000-84,000 people have been hospitalized with the flu through Jan. 5, 2019. These cumulative totals have previously been available only at the end of the season, the CDC noted.

rfranki@mdedge.com

The 2018-2019 flu season may have peaked as measures of influenza-like illness (ILI) activity dropped in the first week of the new year, according to the U.S. Centers for Disease Control and Prevention.

The proportion of outpatients visits for ILI dropped to 3.5% for the week ending Jan. 5, 2019, after reaching 4.0% the previous week. Outpatient ILI visits first topped the national baseline of 2.2% during the week ending Dec. 8, 2018, and have remained above that value for 5 consecutive weeks, the CDC’s influenza division said on Jan. 11.

Flu activity reported by the states reflects the national drop: 10 states came in at level 10 on the CDC’s 1-10 scale of activity for the week ending Jan. 5 – down from 12 the week before – and a total of 15 were in the high range from 8 to 10, compared with 19 the previous week, the CDC said. Two states, Mississippi and Texas, dropped from level 10 to level 7, which the CDC categorizes as moderate activity.

A total of 73 ILI-related deaths were reported during the week ending Dec. 29 (the latest with data available; reporting less than 68% complete), which already exceeds the 71 deaths reported for the week ending Dec. 22 (reporting 85% complete). Flu deaths totaled 437 through the first 13 weeks of the 2018-2019 season, compared with the 1,659 that occurred during weeks 1-13 of the very severe 2017-2018 season, CDC data show.

For the week ending Jan. 5, the CDC received reports of three flu-related pediatric deaths, all of which occurred the previous week. For the season so far, there have been 16 pediatric deaths, compared with 20 at this point in the 2017-2018 season.

Estimates released during the flu season for the first time show that between 6 and 7 million Americans have been infected since Oct. 1, 2018, and that 69,000-84,000 people have been hospitalized with the flu through Jan. 5, 2019. These cumulative totals have previously been available only at the end of the season, the CDC noted.

rfranki@mdedge.com

I suspect, like me, you have never put much stock in astrology. It just doesn’t feel like a good fit with our science-based training. But recent evidence suggests that maybe we should be paying more attention to the whether our patient is a Taurus or a Leo when we are hunting for a diagnosis.

patchareeporn_s/Getty Images

Three researchers from Harvard’s Schools of Medicine and Public Health have followed several hundred thousand children born between 2007 and 2009 until 2016 (“Attention deficit–hyperactivity disorder and month of school enrollment,” N Engl J Med. 2018;379:2122-30). Their data revealed that, in states with a Sept. 1 school entry cutoff, children born in August had rates of diagnosis and treatment of ADHD that were 34% higher than those born in other months.

Their findings could mean that astrology deserves a lot more credibility than we have been giving it. More likely it suggests that those of us committed to the health and education of children deserve a booby prize for objectivity. In a New York Times Op-Ed piece, the study’s investigators point out that their data show that the relative immaturity of the youngest children in a class too often is interpreted as a symptom of ADHD (“The Link Between August Birthdays and ADHD,” 2018 Nov 28. Jena AB et al.).

For many of us who practiced pediatrics before the ADHD phenomenon erupted, this new study substantiates our suspicion that the condition is currently being both overdiagnosed and overtreated. The data leave unanswered the question of whom or what is to blame for starting the epidemic. However, the study does suggest that physicians and educators deserve some culpability by failing to maintain their objectivity when interpreting childhood behavior.

I clearly can recall the first time I spoke to a group of teachers about the articles I had been reading that suggested a beneficial effect of treating “hyperactive” children with stimulant medication. The teachers uniformly were incredulous and repulsed by the counterintuitive notion of medicating children whom they saw as difficult, but not out of the broad range of age and developmental maturity they could expect to see in their classrooms.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@mdedge.com.

I suspect, like me, you have never put much stock in astrology. It just doesn’t feel like a good fit with our science-based training. But recent evidence suggests that maybe we should be paying more attention to the whether our patient is a Taurus or a Leo when we are hunting for a diagnosis.

patchareeporn_s/Getty Images

Three researchers from Harvard’s Schools of Medicine and Public Health have followed several hundred thousand children born between 2007 and 2009 until 2016 (“Attention deficit–hyperactivity disorder and month of school enrollment,” N Engl J Med. 2018;379:2122-30). Their data revealed that, in states with a Sept. 1 school entry cutoff, children born in August had rates of diagnosis and treatment of ADHD that were 34% higher than those born in other months.

Their findings could mean that astrology deserves a lot more credibility than we have been giving it. More likely it suggests that those of us committed to the health and education of children deserve a booby prize for objectivity. In a New York Times Op-Ed piece, the study’s investigators point out that their data show that the relative immaturity of the youngest children in a class too often is interpreted as a symptom of ADHD (“The Link Between August Birthdays and ADHD,” 2018 Nov 28. Jena AB et al.).

For many of us who practiced pediatrics before the ADHD phenomenon erupted, this new study substantiates our suspicion that the condition is currently being both overdiagnosed and overtreated. The data leave unanswered the question of whom or what is to blame for starting the epidemic. However, the study does suggest that physicians and educators deserve some culpability by failing to maintain their objectivity when interpreting childhood behavior.

I clearly can recall the first time I spoke to a group of teachers about the articles I had been reading that suggested a beneficial effect of treating “hyperactive” children with stimulant medication. The teachers uniformly were incredulous and repulsed by the counterintuitive notion of medicating children whom they saw as difficult, but not out of the broad range of age and developmental maturity they could expect to see in their classrooms.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@mdedge.com.

I suspect, like me, you have never put much stock in astrology. It just doesn’t feel like a good fit with our science-based training. But recent evidence suggests that maybe we should be paying more attention to the whether our patient is a Taurus or a Leo when we are hunting for a diagnosis.

patchareeporn_s/Getty Images

Three researchers from Harvard’s Schools of Medicine and Public Health have followed several hundred thousand children born between 2007 and 2009 until 2016 (“Attention deficit–hyperactivity disorder and month of school enrollment,” N Engl J Med. 2018;379:2122-30). Their data revealed that, in states with a Sept. 1 school entry cutoff, children born in August had rates of diagnosis and treatment of ADHD that were 34% higher than those born in other months.

Their findings could mean that astrology deserves a lot more credibility than we have been giving it. More likely it suggests that those of us committed to the health and education of children deserve a booby prize for objectivity. In a New York Times Op-Ed piece, the study’s investigators point out that their data show that the relative immaturity of the youngest children in a class too often is interpreted as a symptom of ADHD (“The Link Between August Birthdays and ADHD,” 2018 Nov 28. Jena AB et al.).

For many of us who practiced pediatrics before the ADHD phenomenon erupted, this new study substantiates our suspicion that the condition is currently being both overdiagnosed and overtreated. The data leave unanswered the question of whom or what is to blame for starting the epidemic. However, the study does suggest that physicians and educators deserve some culpability by failing to maintain their objectivity when interpreting childhood behavior.

I clearly can recall the first time I spoke to a group of teachers about the articles I had been reading that suggested a beneficial effect of treating “hyperactive” children with stimulant medication. The teachers uniformly were incredulous and repulsed by the counterintuitive notion of medicating children whom they saw as difficult, but not out of the broad range of age and developmental maturity they could expect to see in their classrooms.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@mdedge.com.

For more information about upcoming events and award deadlines, please visit http://agau.gastro.org and http://www.gastro.org/research-funding.

UPCOMING EVENTS

Feb. 16, 2019
AGA Regional Practice Skills Workshop – Ohio
The workshop provides fellows with insights on life in private practice, life in academia, and other career opportunities. Attendees will also gain practical knowledge on key topics such as contract negotiations, billing/coding, health care policy, and other topics that can help to enhance their career. Work/life balance and financial management as an early career professional are also addressed.
Columbus, OH

Feb. 20-21, 2019
Two-Day, In-Depth Coding Seminar by McVey Associates, Inc.
Become a certified GI coder with a two-day, in-depth training course provided by McVey Associates, Inc.
Hartford, CT

Feb. 21, 2019
Coding and Reimbursement Solutions by McVey Associates, Inc.
Improve the efficiency and performance of your practice by staying current on the latest reimbursement, coding, and compliance changes.
Richmond, VA

March 8-9, 2019
2019 Women’s Leadership Conference
The conference is specifically designed for women looking to advance their careers, further professional goals, enhance personal growth, and effectively network.
Bethesda, MD

March 8-10, 2019
FORWARD Program
AGA’s Fostering Opportunities Resulting in Workforce and Research Diversity (FORWARD) Program is a new initiative funded by NIH, supporting the career entry and development for underrepresented minority physician scientists in gastroenterology. The program provides concrete leadership and skill development that includes scientific manuscript and grant writing, research development, executive coaching, and more.
Bethesda, MD

March 8-10, 2019
Future Leaders Program
The Future Leaders Program provides a pathway within the organization to network, connect with mentors, develop leadership skills and learn about AGA’s governance and operations while advancing your career and supporting the profession.
Bethesda, MD

March 23–24, 2019
2019 Gut Microbiota for Health World SummitThe 2019 program will present the latest evidence on the interaction between diet, nutrition and the gut microbiome. Learn how diet and nutrition are being used in concert with traditional therapies to manage GI disorders.
Miami, FL

March 30, 2019
AGA Regional Practice Skills Workshop – Massachusetts
The workshop provides fellows with insights on life in private practice, life in academia and other career opportunities. Attendees will also gain practical knowledge on key topics such as contract negotiations, billing/coding, health care policy and other topics that can help to enhance their career. Work/life balance and financial management as an early career professional are also addressed.
Boston, MA

April 10-12, 2019
2019 AGA Tech Summit
By bringing together and fostering collaboration among innovators, entrepreneurs, clinicians, MedTech companies,regulatory agency representatives and venture capitalists, the Tech Summit helps ensure a pipeline of GI innovation that ultimately will improve delivery of care and patient outcomes.
San Francisco, CA

May 18-21, 2019
Digestive Disease Week (DDW)®
DDW^® is the world’s leading educational forum for academicians, clinicians, researchers, students and trainees working in gastroenterology, hepatology, GI endoscopy, gastrointestinal surgery and related fields. Whether you work in patient care, research, education or administration, the DDW program offers something for you. DDW is co-sponsored by AGA, AASLD, ASGE and SSAT.
San Diego, CA

AWARDS APPLICATION DEADLINES

AGA Fellow Abstract Award
This travel award provides nine $500 and one $1,000 prize to recipients who are MD, PhD, or equivalent fellows presenting posters/oral sessions at Digestive Disease Week^® (DDW).
Application Deadline: Feb. 15, 2019

AGA Moti L. & Kamla Rustgi International Travel Awards
This travel award provides two $750 prizes to recipients who are young basic, translational, or clinical investigators residing outside North America to support travel and related expenses to attend Digestive Disease Week^® (DDW).
Application Deadline: Feb. 15, 2019

AGA Student Abstract Award
This travel award provides nine $500 and one $1,000 prize to recipients who are high school, undergraduate, graduate, or medical students, or residents (residents up to year three postgraduate) presenting posters/oral sessions at Digestive Disease Week^® (DDW).
Application Deadline: Feb. 15, 2019

AGA-Gastric Cancer Foundation Ben Feinstein Memorial Research Scholar Award in Gastric Cancer
This award provides $100,000 per year for three years (total $300,000) to early career faculty (i.e., investigator, instructor, research associate, or equivalent) working toward an independent career in gastric cancer research. Research involving precancerous lesions will be considered if relevance to gastric cancer is explicitly outlined.
Application Deadline: Dec. 16, 2019

For more information about upcoming events and award deadlines, please visit http://agau.gastro.org and http://www.gastro.org/research-funding.

UPCOMING EVENTS

Feb. 16, 2019
AGA Regional Practice Skills Workshop – Ohio
The workshop provides fellows with insights on life in private practice, life in academia, and other career opportunities. Attendees will also gain practical knowledge on key topics such as contract negotiations, billing/coding, health care policy, and other topics that can help to enhance their career. Work/life balance and financial management as an early career professional are also addressed.
Columbus, OH

Feb. 20-21, 2019
Two-Day, In-Depth Coding Seminar by McVey Associates, Inc.
Become a certified GI coder with a two-day, in-depth training course provided by McVey Associates, Inc.
Hartford, CT

Feb. 21, 2019
Coding and Reimbursement Solutions by McVey Associates, Inc.
Improve the efficiency and performance of your practice by staying current on the latest reimbursement, coding, and compliance changes.
Richmond, VA

March 8-9, 2019
2019 Women’s Leadership Conference
The conference is specifically designed for women looking to advance their careers, further professional goals, enhance personal growth, and effectively network.
Bethesda, MD

March 8-10, 2019
FORWARD Program
AGA’s Fostering Opportunities Resulting in Workforce and Research Diversity (FORWARD) Program is a new initiative funded by NIH, supporting the career entry and development for underrepresented minority physician scientists in gastroenterology. The program provides concrete leadership and skill development that includes scientific manuscript and grant writing, research development, executive coaching, and more.
Bethesda, MD

March 8-10, 2019
Future Leaders Program
The Future Leaders Program provides a pathway within the organization to network, connect with mentors, develop leadership skills and learn about AGA’s governance and operations while advancing your career and supporting the profession.
Bethesda, MD

March 23–24, 2019
2019 Gut Microbiota for Health World SummitThe 2019 program will present the latest evidence on the interaction between diet, nutrition and the gut microbiome. Learn how diet and nutrition are being used in concert with traditional therapies to manage GI disorders.
Miami, FL

March 30, 2019
AGA Regional Practice Skills Workshop – Massachusetts
The workshop provides fellows with insights on life in private practice, life in academia and other career opportunities. Attendees will also gain practical knowledge on key topics such as contract negotiations, billing/coding, health care policy and other topics that can help to enhance their career. Work/life balance and financial management as an early career professional are also addressed.
Boston, MA

April 10-12, 2019
2019 AGA Tech Summit
By bringing together and fostering collaboration among innovators, entrepreneurs, clinicians, MedTech companies,regulatory agency representatives and venture capitalists, the Tech Summit helps ensure a pipeline of GI innovation that ultimately will improve delivery of care and patient outcomes.
San Francisco, CA

May 18-21, 2019
Digestive Disease Week (DDW)®
DDW^® is the world’s leading educational forum for academicians, clinicians, researchers, students and trainees working in gastroenterology, hepatology, GI endoscopy, gastrointestinal surgery and related fields. Whether you work in patient care, research, education or administration, the DDW program offers something for you. DDW is co-sponsored by AGA, AASLD, ASGE and SSAT.
San Diego, CA

AWARDS APPLICATION DEADLINES

AGA Fellow Abstract Award
This travel award provides nine $500 and one $1,000 prize to recipients who are MD, PhD, or equivalent fellows presenting posters/oral sessions at Digestive Disease Week^® (DDW).
Application Deadline: Feb. 15, 2019

AGA Moti L. & Kamla Rustgi International Travel Awards
This travel award provides two $750 prizes to recipients who are young basic, translational, or clinical investigators residing outside North America to support travel and related expenses to attend Digestive Disease Week^® (DDW).
Application Deadline: Feb. 15, 2019

AGA Student Abstract Award
This travel award provides nine $500 and one $1,000 prize to recipients who are high school, undergraduate, graduate, or medical students, or residents (residents up to year three postgraduate) presenting posters/oral sessions at Digestive Disease Week^® (DDW).
Application Deadline: Feb. 15, 2019

AGA-Gastric Cancer Foundation Ben Feinstein Memorial Research Scholar Award in Gastric Cancer
This award provides $100,000 per year for three years (total $300,000) to early career faculty (i.e., investigator, instructor, research associate, or equivalent) working toward an independent career in gastric cancer research. Research involving precancerous lesions will be considered if relevance to gastric cancer is explicitly outlined.
Application Deadline: Dec. 16, 2019

For more information about upcoming events and award deadlines, please visit http://agau.gastro.org and http://www.gastro.org/research-funding.

UPCOMING EVENTS

Feb. 16, 2019
AGA Regional Practice Skills Workshop – Ohio
The workshop provides fellows with insights on life in private practice, life in academia, and other career opportunities. Attendees will also gain practical knowledge on key topics such as contract negotiations, billing/coding, health care policy, and other topics that can help to enhance their career. Work/life balance and financial management as an early career professional are also addressed.
Columbus, OH

Feb. 20-21, 2019
Two-Day, In-Depth Coding Seminar by McVey Associates, Inc.
Become a certified GI coder with a two-day, in-depth training course provided by McVey Associates, Inc.
Hartford, CT

Feb. 21, 2019
Coding and Reimbursement Solutions by McVey Associates, Inc.
Improve the efficiency and performance of your practice by staying current on the latest reimbursement, coding, and compliance changes.
Richmond, VA

March 8-9, 2019
2019 Women’s Leadership Conference
The conference is specifically designed for women looking to advance their careers, further professional goals, enhance personal growth, and effectively network.
Bethesda, MD

March 8-10, 2019
FORWARD Program
AGA’s Fostering Opportunities Resulting in Workforce and Research Diversity (FORWARD) Program is a new initiative funded by NIH, supporting the career entry and development for underrepresented minority physician scientists in gastroenterology. The program provides concrete leadership and skill development that includes scientific manuscript and grant writing, research development, executive coaching, and more.
Bethesda, MD

March 8-10, 2019
Future Leaders Program
The Future Leaders Program provides a pathway within the organization to network, connect with mentors, develop leadership skills and learn about AGA’s governance and operations while advancing your career and supporting the profession.
Bethesda, MD

March 23–24, 2019
2019 Gut Microbiota for Health World SummitThe 2019 program will present the latest evidence on the interaction between diet, nutrition and the gut microbiome. Learn how diet and nutrition are being used in concert with traditional therapies to manage GI disorders.
Miami, FL

March 30, 2019
AGA Regional Practice Skills Workshop – Massachusetts
The workshop provides fellows with insights on life in private practice, life in academia and other career opportunities. Attendees will also gain practical knowledge on key topics such as contract negotiations, billing/coding, health care policy and other topics that can help to enhance their career. Work/life balance and financial management as an early career professional are also addressed.
Boston, MA

April 10-12, 2019
2019 AGA Tech Summit
By bringing together and fostering collaboration among innovators, entrepreneurs, clinicians, MedTech companies,regulatory agency representatives and venture capitalists, the Tech Summit helps ensure a pipeline of GI innovation that ultimately will improve delivery of care and patient outcomes.
San Francisco, CA

May 18-21, 2019
Digestive Disease Week (DDW)®
DDW^® is the world’s leading educational forum for academicians, clinicians, researchers, students and trainees working in gastroenterology, hepatology, GI endoscopy, gastrointestinal surgery and related fields. Whether you work in patient care, research, education or administration, the DDW program offers something for you. DDW is co-sponsored by AGA, AASLD, ASGE and SSAT.
San Diego, CA

AWARDS APPLICATION DEADLINES

AGA Fellow Abstract Award
This travel award provides nine $500 and one $1,000 prize to recipients who are MD, PhD, or equivalent fellows presenting posters/oral sessions at Digestive Disease Week^® (DDW).
Application Deadline: Feb. 15, 2019

AGA Moti L. & Kamla Rustgi International Travel Awards
This travel award provides two $750 prizes to recipients who are young basic, translational, or clinical investigators residing outside North America to support travel and related expenses to attend Digestive Disease Week^® (DDW).
Application Deadline: Feb. 15, 2019

AGA Student Abstract Award
This travel award provides nine $500 and one $1,000 prize to recipients who are high school, undergraduate, graduate, or medical students, or residents (residents up to year three postgraduate) presenting posters/oral sessions at Digestive Disease Week^® (DDW).
Application Deadline: Feb. 15, 2019

AGA-Gastric Cancer Foundation Ben Feinstein Memorial Research Scholar Award in Gastric Cancer
This award provides $100,000 per year for three years (total $300,000) to early career faculty (i.e., investigator, instructor, research associate, or equivalent) working toward an independent career in gastric cancer research. Research involving precancerous lesions will be considered if relevance to gastric cancer is explicitly outlined.
Application Deadline: Dec. 16, 2019

Gastroenterology

How to approach a patient with refractory or recurrent benign esophageal stricture. Siersema PD. 2019 Jan;156(1):7-10. doi.org/10.1053/j.gastro.2018.11.040

How to approach a patient with ampullary lesion. Kandler J; Neuhaus H. 2018 Dec;155(6):1670-6. doi.org/10.1053/j.gastro.2018.11.010

How to promote the academic success of junior faculty physicians in gastroenterology. Shaheen NJ; Sandler RS. 2018 Nov;155(5):1293-7. doi.org/10.1053/j.gastro.2018.10.006

Clin Gastro Hepatol

Screening and surveillance of varices in patients with cirrhosis. Jakab SS; Garcia-Tsao G. 2019 Jan;17(1):26-9. doi.org/10.1016/j.cgh.2018.03.012

Common gastrostomy feeding tube complications and troubleshooting. Sealock RJ; Munot K. 2018 Dec;16(12):1864-9. doi.org/10.1016/j.cgh.2018.07.037

Endobariatrics: A primer. Storm AC; Abu Dayyeh BK; Topazian M. 2018 Nov;16(11):1701-4. doi.org/10.1016/j.cgh.2018.03.009

AGA Perspectives

My experiences during AGA’s Advocacy Day: Facilitating change
Published on 12/05/2018 by Yamini Natarajan, MD.

Lessons learned from the AGA Future Leaders Program
Published on 12/05/2018 by Jennifer Weiss, MD, MS, AGAF.

Gastroenterology

How to approach a patient with refractory or recurrent benign esophageal stricture. Siersema PD. 2019 Jan;156(1):7-10. doi.org/10.1053/j.gastro.2018.11.040

How to approach a patient with ampullary lesion. Kandler J; Neuhaus H. 2018 Dec;155(6):1670-6. doi.org/10.1053/j.gastro.2018.11.010

How to promote the academic success of junior faculty physicians in gastroenterology. Shaheen NJ; Sandler RS. 2018 Nov;155(5):1293-7. doi.org/10.1053/j.gastro.2018.10.006

Clin Gastro Hepatol

Screening and surveillance of varices in patients with cirrhosis. Jakab SS; Garcia-Tsao G. 2019 Jan;17(1):26-9. doi.org/10.1016/j.cgh.2018.03.012

Common gastrostomy feeding tube complications and troubleshooting. Sealock RJ; Munot K. 2018 Dec;16(12):1864-9. doi.org/10.1016/j.cgh.2018.07.037

Endobariatrics: A primer. Storm AC; Abu Dayyeh BK; Topazian M. 2018 Nov;16(11):1701-4. doi.org/10.1016/j.cgh.2018.03.009

AGA Perspectives

My experiences during AGA’s Advocacy Day: Facilitating change
Published on 12/05/2018 by Yamini Natarajan, MD.

Lessons learned from the AGA Future Leaders Program
Published on 12/05/2018 by Jennifer Weiss, MD, MS, AGAF.

Gastroenterology

How to approach a patient with refractory or recurrent benign esophageal stricture. Siersema PD. 2019 Jan;156(1):7-10. doi.org/10.1053/j.gastro.2018.11.040

How to approach a patient with ampullary lesion. Kandler J; Neuhaus H. 2018 Dec;155(6):1670-6. doi.org/10.1053/j.gastro.2018.11.010

How to promote the academic success of junior faculty physicians in gastroenterology. Shaheen NJ; Sandler RS. 2018 Nov;155(5):1293-7. doi.org/10.1053/j.gastro.2018.10.006

Clin Gastro Hepatol

Screening and surveillance of varices in patients with cirrhosis. Jakab SS; Garcia-Tsao G. 2019 Jan;17(1):26-9. doi.org/10.1016/j.cgh.2018.03.012

Common gastrostomy feeding tube complications and troubleshooting. Sealock RJ; Munot K. 2018 Dec;16(12):1864-9. doi.org/10.1016/j.cgh.2018.07.037

Endobariatrics: A primer. Storm AC; Abu Dayyeh BK; Topazian M. 2018 Nov;16(11):1701-4. doi.org/10.1016/j.cgh.2018.03.009

AGA Perspectives

My experiences during AGA’s Advocacy Day: Facilitating change
Published on 12/05/2018 by Yamini Natarajan, MD.

Lessons learned from the AGA Future Leaders Program
Published on 12/05/2018 by Jennifer Weiss, MD, MS, AGAF.

Oncologists frequently alter their treatment recommendations based on reimbursement incentives, an analysis suggests.

Lead author Aaron P. Mitchell, MD, of Memorial Sloan Kettering Cancer Center, New York, and his colleagues conducted a systematic review of 18 studies that examined the association between reimbursement incentives and oncology care delivery. Researchers obtained study data through PubMed/MEDLINE, Web of Science, Proquest Health Management, Econlit, and Business Source Premier. There were no date restrictions on the data.

The majority of studies (15 of 18) showed an association between reimbursement and care delivery consistent with physician responsiveness to financial incentives. Specifically, the review suggests that self-referral arrangements may increase radiotherapy use and that profitability of systemic anticancer agents may affect physicians’ choice of cancer medication, according to the analysis published in JAMA Oncology.

Of the 18 studies, 4 found that physicians respond to reimbursement incentives by preferentially using more-profitable treatments over less-profitable treatments, while 1 found evidence that reimbursement may be associated with doctors’ surgical approach to breast cancer. Particularly, oncologists were more likely to use breast-conserving therapy plus adjuvant radiotherapy rather than mastectomy alone when either reimbursement for breast-conserving therapy was higher or payment for mastectomy was lower. However, the same study did not find a statistically significant increase in breast-conserving therapy without adjuvant radiotherapy in association with the same reimbursement differences.

Another analysis in the data set determined preference for administering treatment in a more-profitable hospital outpatient setting, compared with an office setting. Meanwhile, five studies found that physicians are more likely to use radiotherapy when they or their practices profited through self-referral for radiotherapy or when practicing in freestanding facilities. (Urology practices are able to bill for radiotherapy services when using the in-office referral exception to the Stark Law.) Two of the four studies found that self-referral for radiotherapy was associated with increased use of intensity-modulated radiotherapy, while one study found that self-referral was associated with both receipt of any active therapy (radiotherapy, surgery, cryotherapy, or androgen deprivation therapy) and with receipt of radiotherapy specifically.

In relation to cancer drugs, one study found that physicians decreased their use of medications that showed the greatest declines in profitability. Another study found that after changes in compensation for drug administration resulting from the Medicare Modernization Act of 2003, patients dying of cancer were less likely to receive systemic therapy within the last 30 days of life. Another study found that physicians used less irinotecan after the drug’s patent protection expired and a lower-cost, less-profitable generic alternative became available. In addition, there was a significant increase in office-based cystoscopic procedures following an increase in reimbursement for procedures performed in the office setting and the absence of a coincident change in procedures performed in the hospital or ambulatory surgery settings, where reimbursement did not change, one of the studies found.

The authors concluded that some oncologists may, in certain circumstances, alter treatment recommendations based on personal revenue considerations. Changing such practices could lower health care spending and prevent potentially inappropriate treatment.

The findings from the systematic review are not surprising, said Walter Stadler, MD, a professor at the University of Chicago and chief of the hematology/oncology section.

“Financial incentives are always going to influence physicians and you cannot fully prevent that,” he said in an interview. “We all like to believe, we are all completely altruistic, but physicians respond to the same financial pressures that anybody else responds to. We’re not unique in that way.”

Particularly, when two treatment modalities are equally efficacious, it makes sense that financial incentives may impact the doctor’s choice.

“There are always outliers, but physicians as a community are not necessarily going to do something that is directly harmful for patients based only on financial incentives,” he said. “But if there are two medically equivalent choices, than financial incentives will play a role.”

Dr. Wheeler has received research grant funding from Pfizer unrelated to this work. No other disclosures were reported.

SOURCE: Mitchell AP et al. JAMA Oncol. 2019 Jan 3. doi: 10.1001/jamaoncol.2018.6196.

Oncologists frequently alter their treatment recommendations based on reimbursement incentives, an analysis suggests.

Lead author Aaron P. Mitchell, MD, of Memorial Sloan Kettering Cancer Center, New York, and his colleagues conducted a systematic review of 18 studies that examined the association between reimbursement incentives and oncology care delivery. Researchers obtained study data through PubMed/MEDLINE, Web of Science, Proquest Health Management, Econlit, and Business Source Premier. There were no date restrictions on the data.

The majority of studies (15 of 18) showed an association between reimbursement and care delivery consistent with physician responsiveness to financial incentives. Specifically, the review suggests that self-referral arrangements may increase radiotherapy use and that profitability of systemic anticancer agents may affect physicians’ choice of cancer medication, according to the analysis published in JAMA Oncology.

Of the 18 studies, 4 found that physicians respond to reimbursement incentives by preferentially using more-profitable treatments over less-profitable treatments, while 1 found evidence that reimbursement may be associated with doctors’ surgical approach to breast cancer. Particularly, oncologists were more likely to use breast-conserving therapy plus adjuvant radiotherapy rather than mastectomy alone when either reimbursement for breast-conserving therapy was higher or payment for mastectomy was lower. However, the same study did not find a statistically significant increase in breast-conserving therapy without adjuvant radiotherapy in association with the same reimbursement differences.

Another analysis in the data set determined preference for administering treatment in a more-profitable hospital outpatient setting, compared with an office setting. Meanwhile, five studies found that physicians are more likely to use radiotherapy when they or their practices profited through self-referral for radiotherapy or when practicing in freestanding facilities. (Urology practices are able to bill for radiotherapy services when using the in-office referral exception to the Stark Law.) Two of the four studies found that self-referral for radiotherapy was associated with increased use of intensity-modulated radiotherapy, while one study found that self-referral was associated with both receipt of any active therapy (radiotherapy, surgery, cryotherapy, or androgen deprivation therapy) and with receipt of radiotherapy specifically.

In relation to cancer drugs, one study found that physicians decreased their use of medications that showed the greatest declines in profitability. Another study found that after changes in compensation for drug administration resulting from the Medicare Modernization Act of 2003, patients dying of cancer were less likely to receive systemic therapy within the last 30 days of life. Another study found that physicians used less irinotecan after the drug’s patent protection expired and a lower-cost, less-profitable generic alternative became available. In addition, there was a significant increase in office-based cystoscopic procedures following an increase in reimbursement for procedures performed in the office setting and the absence of a coincident change in procedures performed in the hospital or ambulatory surgery settings, where reimbursement did not change, one of the studies found.

The authors concluded that some oncologists may, in certain circumstances, alter treatment recommendations based on personal revenue considerations. Changing such practices could lower health care spending and prevent potentially inappropriate treatment.

The findings from the systematic review are not surprising, said Walter Stadler, MD, a professor at the University of Chicago and chief of the hematology/oncology section.

“Financial incentives are always going to influence physicians and you cannot fully prevent that,” he said in an interview. “We all like to believe, we are all completely altruistic, but physicians respond to the same financial pressures that anybody else responds to. We’re not unique in that way.”

Particularly, when two treatment modalities are equally efficacious, it makes sense that financial incentives may impact the doctor’s choice.

“There are always outliers, but physicians as a community are not necessarily going to do something that is directly harmful for patients based only on financial incentives,” he said. “But if there are two medically equivalent choices, than financial incentives will play a role.”

Dr. Wheeler has received research grant funding from Pfizer unrelated to this work. No other disclosures were reported.

SOURCE: Mitchell AP et al. JAMA Oncol. 2019 Jan 3. doi: 10.1001/jamaoncol.2018.6196.

Oncologists frequently alter their treatment recommendations based on reimbursement incentives, an analysis suggests.

Lead author Aaron P. Mitchell, MD, of Memorial Sloan Kettering Cancer Center, New York, and his colleagues conducted a systematic review of 18 studies that examined the association between reimbursement incentives and oncology care delivery. Researchers obtained study data through PubMed/MEDLINE, Web of Science, Proquest Health Management, Econlit, and Business Source Premier. There were no date restrictions on the data.

The majority of studies (15 of 18) showed an association between reimbursement and care delivery consistent with physician responsiveness to financial incentives. Specifically, the review suggests that self-referral arrangements may increase radiotherapy use and that profitability of systemic anticancer agents may affect physicians’ choice of cancer medication, according to the analysis published in JAMA Oncology.

Of the 18 studies, 4 found that physicians respond to reimbursement incentives by preferentially using more-profitable treatments over less-profitable treatments, while 1 found evidence that reimbursement may be associated with doctors’ surgical approach to breast cancer. Particularly, oncologists were more likely to use breast-conserving therapy plus adjuvant radiotherapy rather than mastectomy alone when either reimbursement for breast-conserving therapy was higher or payment for mastectomy was lower. However, the same study did not find a statistically significant increase in breast-conserving therapy without adjuvant radiotherapy in association with the same reimbursement differences.

Another analysis in the data set determined preference for administering treatment in a more-profitable hospital outpatient setting, compared with an office setting. Meanwhile, five studies found that physicians are more likely to use radiotherapy when they or their practices profited through self-referral for radiotherapy or when practicing in freestanding facilities. (Urology practices are able to bill for radiotherapy services when using the in-office referral exception to the Stark Law.) Two of the four studies found that self-referral for radiotherapy was associated with increased use of intensity-modulated radiotherapy, while one study found that self-referral was associated with both receipt of any active therapy (radiotherapy, surgery, cryotherapy, or androgen deprivation therapy) and with receipt of radiotherapy specifically.

In relation to cancer drugs, one study found that physicians decreased their use of medications that showed the greatest declines in profitability. Another study found that after changes in compensation for drug administration resulting from the Medicare Modernization Act of 2003, patients dying of cancer were less likely to receive systemic therapy within the last 30 days of life. Another study found that physicians used less irinotecan after the drug’s patent protection expired and a lower-cost, less-profitable generic alternative became available. In addition, there was a significant increase in office-based cystoscopic procedures following an increase in reimbursement for procedures performed in the office setting and the absence of a coincident change in procedures performed in the hospital or ambulatory surgery settings, where reimbursement did not change, one of the studies found.

The authors concluded that some oncologists may, in certain circumstances, alter treatment recommendations based on personal revenue considerations. Changing such practices could lower health care spending and prevent potentially inappropriate treatment.

The findings from the systematic review are not surprising, said Walter Stadler, MD, a professor at the University of Chicago and chief of the hematology/oncology section.

“Financial incentives are always going to influence physicians and you cannot fully prevent that,” he said in an interview. “We all like to believe, we are all completely altruistic, but physicians respond to the same financial pressures that anybody else responds to. We’re not unique in that way.”

Particularly, when two treatment modalities are equally efficacious, it makes sense that financial incentives may impact the doctor’s choice.

“There are always outliers, but physicians as a community are not necessarily going to do something that is directly harmful for patients based only on financial incentives,” he said. “But if there are two medically equivalent choices, than financial incentives will play a role.”

Dr. Wheeler has received research grant funding from Pfizer unrelated to this work. No other disclosures were reported.

SOURCE: Mitchell AP et al. JAMA Oncol. 2019 Jan 3. doi: 10.1001/jamaoncol.2018.6196.

We are in the middle of flu season, and many of our patients are coughing. Is it the flu or might the child have a secondary bacterial pneumonia? Let’s start with the history for a tip off. The course of flu and respiratory viral infections in general involves a typical pattern of timing for fever and cough.

DavidWhalen/Thinkstock

A late-developing fever or fever that subsides then recurs should raise concern. A prolonged cough or cough that subsides then recurs also should raise concern. The respiratory rate and chest retractions are key physical findings that can aid in distinguishing children with bacterial pneumonia. Rales and decreased breath sounds in lung segments are best heard with deep breaths.

What diagnostic laboratory and imaging tests should be used

Fortunately, rapid tests to detect influenza are available, and many providers have added those to their laboratory evaluation. A complete blood count and differential may be helpful. If a pulse oximeter is available, checking oxygen saturation might be helpful. The American Academy of Pediatrics community pneumonia guideline states that routine chest radiographs are not necessary for the confirmation of suspected community-acquired pneumonia (CAP) in patients well enough to be treated in the outpatient setting (Clin Inf Dis. 2011 Oct;53[7]:e25–e76). Blood cultures should not be performed routinely in nontoxic, fully immunized children with CAP managed in the outpatient setting.

What antibiotic should be used

Antimicrobial therapy is not routinely required for preschool-aged children with cough, even cough caused by CAP, because viral pathogens are responsible for the great majority of clinical disease. If the diagnosis of CAP is made, the AAP endorses amoxicillin as first-line therapy for previously healthy, appropriately immunized infants and preschool children with mild to moderate CAP suspected to be of bacterial origin. For previously healthy, appropriately immunized school-aged children and adolescents with mild to moderate CAP, amoxicillin is recommended for treatment of Streptococcus pneumoniae, the most prominent invasive bacterial pathogen.

However, the treatment paradigm is complicated because Mycoplasma pneumoniae also should be considered in management decisions. Children with signs and symptoms suspicious for M. pneumoniae should be tested to help guide antibiotic selection. This may be a simple bedside cold agglutinin test. The highest incidence of Mycoplasma pneumonia is in 5- to 20-year-olds (51% in 5- to 9-year-olds, 74% in 9- to 15-year-olds, and 3%-18% in adults with pneumonia), but 9% of CAP occurs in patients younger than 5 years old. The clinical features of Mycoplasma pneumonia resemble influenza: The patient has gradual onset of headache, malaise, fever, sore throat, and cough. Mycoplasma pneumonia has a similar incidence of productive cough, rales, and diarrhea as pneumococcal CAP, but with more frequent upper respiratory symptoms and a normal leukocyte count. Mycoplasma bronchopneumonia occurs 30 times more frequently than Mycoplasma lobar pneumonia. The radiologic features of Mycoplasma is typical of a bronchopneumonia, usually involving a single lobe, subsegmental atelectasis, peribronchial thickening, and streaky interstitial densities. While Mycoplasma pneumonia is usually self-limited, the duration of illness is shortened by oral treatment with doxycycline, erythromycin, clarithromycin, or azithromycin.
 

What is the appropriate duration of antimicrobial therapy

Recommendations by the AAP for CAP note that treatment courses of 10 days have been best studied, although shorter courses may be just as effective, particularly for mild disease managed on an outpatient basis.

When should children be hospitalized

Dr. Pichichero is a specialist in pediatric infectious diseases and director of the Research Institute at Rochester (N.Y.) General Hospital. He had no conflicts to declare. Email him at pdnews@mdedge.com.

We are in the middle of flu season, and many of our patients are coughing. Is it the flu or might the child have a secondary bacterial pneumonia? Let’s start with the history for a tip off. The course of flu and respiratory viral infections in general involves a typical pattern of timing for fever and cough.

DavidWhalen/Thinkstock

A late-developing fever or fever that subsides then recurs should raise concern. A prolonged cough or cough that subsides then recurs also should raise concern. The respiratory rate and chest retractions are key physical findings that can aid in distinguishing children with bacterial pneumonia. Rales and decreased breath sounds in lung segments are best heard with deep breaths.

What diagnostic laboratory and imaging tests should be used

Fortunately, rapid tests to detect influenza are available, and many providers have added those to their laboratory evaluation. A complete blood count and differential may be helpful. If a pulse oximeter is available, checking oxygen saturation might be helpful. The American Academy of Pediatrics community pneumonia guideline states that routine chest radiographs are not necessary for the confirmation of suspected community-acquired pneumonia (CAP) in patients well enough to be treated in the outpatient setting (Clin Inf Dis. 2011 Oct;53[7]:e25–e76). Blood cultures should not be performed routinely in nontoxic, fully immunized children with CAP managed in the outpatient setting.

What antibiotic should be used

Antimicrobial therapy is not routinely required for preschool-aged children with cough, even cough caused by CAP, because viral pathogens are responsible for the great majority of clinical disease. If the diagnosis of CAP is made, the AAP endorses amoxicillin as first-line therapy for previously healthy, appropriately immunized infants and preschool children with mild to moderate CAP suspected to be of bacterial origin. For previously healthy, appropriately immunized school-aged children and adolescents with mild to moderate CAP, amoxicillin is recommended for treatment of Streptococcus pneumoniae, the most prominent invasive bacterial pathogen.

However, the treatment paradigm is complicated because Mycoplasma pneumoniae also should be considered in management decisions. Children with signs and symptoms suspicious for M. pneumoniae should be tested to help guide antibiotic selection. This may be a simple bedside cold agglutinin test. The highest incidence of Mycoplasma pneumonia is in 5- to 20-year-olds (51% in 5- to 9-year-olds, 74% in 9- to 15-year-olds, and 3%-18% in adults with pneumonia), but 9% of CAP occurs in patients younger than 5 years old. The clinical features of Mycoplasma pneumonia resemble influenza: The patient has gradual onset of headache, malaise, fever, sore throat, and cough. Mycoplasma pneumonia has a similar incidence of productive cough, rales, and diarrhea as pneumococcal CAP, but with more frequent upper respiratory symptoms and a normal leukocyte count. Mycoplasma bronchopneumonia occurs 30 times more frequently than Mycoplasma lobar pneumonia. The radiologic features of Mycoplasma is typical of a bronchopneumonia, usually involving a single lobe, subsegmental atelectasis, peribronchial thickening, and streaky interstitial densities. While Mycoplasma pneumonia is usually self-limited, the duration of illness is shortened by oral treatment with doxycycline, erythromycin, clarithromycin, or azithromycin.
 

What is the appropriate duration of antimicrobial therapy

Recommendations by the AAP for CAP note that treatment courses of 10 days have been best studied, although shorter courses may be just as effective, particularly for mild disease managed on an outpatient basis.

When should children be hospitalized

Dr. Pichichero is a specialist in pediatric infectious diseases and director of the Research Institute at Rochester (N.Y.) General Hospital. He had no conflicts to declare. Email him at pdnews@mdedge.com.

We are in the middle of flu season, and many of our patients are coughing. Is it the flu or might the child have a secondary bacterial pneumonia? Let’s start with the history for a tip off. The course of flu and respiratory viral infections in general involves a typical pattern of timing for fever and cough.

DavidWhalen/Thinkstock

A late-developing fever or fever that subsides then recurs should raise concern. A prolonged cough or cough that subsides then recurs also should raise concern. The respiratory rate and chest retractions are key physical findings that can aid in distinguishing children with bacterial pneumonia. Rales and decreased breath sounds in lung segments are best heard with deep breaths.

What diagnostic laboratory and imaging tests should be used

Fortunately, rapid tests to detect influenza are available, and many providers have added those to their laboratory evaluation. A complete blood count and differential may be helpful. If a pulse oximeter is available, checking oxygen saturation might be helpful. The American Academy of Pediatrics community pneumonia guideline states that routine chest radiographs are not necessary for the confirmation of suspected community-acquired pneumonia (CAP) in patients well enough to be treated in the outpatient setting (Clin Inf Dis. 2011 Oct;53[7]:e25–e76). Blood cultures should not be performed routinely in nontoxic, fully immunized children with CAP managed in the outpatient setting.

What antibiotic should be used

Antimicrobial therapy is not routinely required for preschool-aged children with cough, even cough caused by CAP, because viral pathogens are responsible for the great majority of clinical disease. If the diagnosis of CAP is made, the AAP endorses amoxicillin as first-line therapy for previously healthy, appropriately immunized infants and preschool children with mild to moderate CAP suspected to be of bacterial origin. For previously healthy, appropriately immunized school-aged children and adolescents with mild to moderate CAP, amoxicillin is recommended for treatment of Streptococcus pneumoniae, the most prominent invasive bacterial pathogen.

However, the treatment paradigm is complicated because Mycoplasma pneumoniae also should be considered in management decisions. Children with signs and symptoms suspicious for M. pneumoniae should be tested to help guide antibiotic selection. This may be a simple bedside cold agglutinin test. The highest incidence of Mycoplasma pneumonia is in 5- to 20-year-olds (51% in 5- to 9-year-olds, 74% in 9- to 15-year-olds, and 3%-18% in adults with pneumonia), but 9% of CAP occurs in patients younger than 5 years old. The clinical features of Mycoplasma pneumonia resemble influenza: The patient has gradual onset of headache, malaise, fever, sore throat, and cough. Mycoplasma pneumonia has a similar incidence of productive cough, rales, and diarrhea as pneumococcal CAP, but with more frequent upper respiratory symptoms and a normal leukocyte count. Mycoplasma bronchopneumonia occurs 30 times more frequently than Mycoplasma lobar pneumonia. The radiologic features of Mycoplasma is typical of a bronchopneumonia, usually involving a single lobe, subsegmental atelectasis, peribronchial thickening, and streaky interstitial densities. While Mycoplasma pneumonia is usually self-limited, the duration of illness is shortened by oral treatment with doxycycline, erythromycin, clarithromycin, or azithromycin.
 

What is the appropriate duration of antimicrobial therapy

Recommendations by the AAP for CAP note that treatment courses of 10 days have been best studied, although shorter courses may be just as effective, particularly for mild disease managed on an outpatient basis.

When should children be hospitalized

Dr. Pichichero is a specialist in pediatric infectious diseases and director of the Research Institute at Rochester (N.Y.) General Hospital. He had no conflicts to declare. Email him at pdnews@mdedge.com.

During the holiday break I took some time to organize a lot of old family pictures: deleting duplicates, merging those I pulled off my dad’s computer when he died (which was over 5 years ago), importing ones I took with old digital cameras that were in separate folders ... a bunch of stuff. Some were even childhood pics of me that had been scanned into digital formats. Lots of gigabytes. Lots of time spent watching the little “importing” wheel spin.

Jokic/iStock/Getty Images Plus

As I scrolled through them – literally 5,891 pics and 679 videos – I watched as it became more than a bunch of photos. I watched myself grow up, go through medical school, get married, raise a family. My hair went from brown to gray and receding. My kids went from toddlers to young adults about to leave for college.

It was the story of my life. Without meaning to, it’s what the pictures had become.

It was late at night, but I kept scrolling back and forth. My parents, wife, and others aged in front of me.

Looking in the mirror, or seeing others each day, we never notice the slow changes that time brings. You don’t really see it just thumbing through old photos, either.

But here, in the photos app (something entirely undreamed of in my childhood), I was watching it like it was a movie. Even childhood pictures of my parents. Them dating and getting married. Holding me after bringing me home from the hospital.

I’m certainly not the first to have these thoughts, nor will I be the last. We all go through life in a somewhat organized yet haphazard way, and only when looking backward do we really see how far we’ve come ... often realizing we’re past the halfway point.

Not that this is a bad thing. I mean, that’s life on Earth. It has its good and bad, and aging is part of the rules for all of us.

I suppose you could look at this in terms of our profession. We all (or at least most of us) start out as hospital patients. As we get older and become doctors, hopefully we need to see our own kind less often while at the same time seeing others as patients. As time goes by, most of us start to need to see doctors again, and as we retire and stop practicing medicine, we move back toward being patients ourselves.

For me, the pictures bring back memories and strike emotions in the way hearing or reading stories never can. They give new life to long-forgotten thoughts. Happy and sad, but overall a feeling of contentment that, so far, I feel like I’ve done more good than bad, more right than wrong.

I hope I always feel that way.

I hope everyone else does, too.

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

During the holiday break I took some time to organize a lot of old family pictures: deleting duplicates, merging those I pulled off my dad’s computer when he died (which was over 5 years ago), importing ones I took with old digital cameras that were in separate folders ... a bunch of stuff. Some were even childhood pics of me that had been scanned into digital formats. Lots of gigabytes. Lots of time spent watching the little “importing” wheel spin.

Jokic/iStock/Getty Images Plus

As I scrolled through them – literally 5,891 pics and 679 videos – I watched as it became more than a bunch of photos. I watched myself grow up, go through medical school, get married, raise a family. My hair went from brown to gray and receding. My kids went from toddlers to young adults about to leave for college.

It was the story of my life. Without meaning to, it’s what the pictures had become.

It was late at night, but I kept scrolling back and forth. My parents, wife, and others aged in front of me.

Looking in the mirror, or seeing others each day, we never notice the slow changes that time brings. You don’t really see it just thumbing through old photos, either.

But here, in the photos app (something entirely undreamed of in my childhood), I was watching it like it was a movie. Even childhood pictures of my parents. Them dating and getting married. Holding me after bringing me home from the hospital.

I’m certainly not the first to have these thoughts, nor will I be the last. We all go through life in a somewhat organized yet haphazard way, and only when looking backward do we really see how far we’ve come ... often realizing we’re past the halfway point.

Not that this is a bad thing. I mean, that’s life on Earth. It has its good and bad, and aging is part of the rules for all of us.

I suppose you could look at this in terms of our profession. We all (or at least most of us) start out as hospital patients. As we get older and become doctors, hopefully we need to see our own kind less often while at the same time seeing others as patients. As time goes by, most of us start to need to see doctors again, and as we retire and stop practicing medicine, we move back toward being patients ourselves.

For me, the pictures bring back memories and strike emotions in the way hearing or reading stories never can. They give new life to long-forgotten thoughts. Happy and sad, but overall a feeling of contentment that, so far, I feel like I’ve done more good than bad, more right than wrong.

I hope I always feel that way.

I hope everyone else does, too.

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

During the holiday break I took some time to organize a lot of old family pictures: deleting duplicates, merging those I pulled off my dad’s computer when he died (which was over 5 years ago), importing ones I took with old digital cameras that were in separate folders ... a bunch of stuff. Some were even childhood pics of me that had been scanned into digital formats. Lots of gigabytes. Lots of time spent watching the little “importing” wheel spin.

Jokic/iStock/Getty Images Plus

As I scrolled through them – literally 5,891 pics and 679 videos – I watched as it became more than a bunch of photos. I watched myself grow up, go through medical school, get married, raise a family. My hair went from brown to gray and receding. My kids went from toddlers to young adults about to leave for college.

It was the story of my life. Without meaning to, it’s what the pictures had become.

It was late at night, but I kept scrolling back and forth. My parents, wife, and others aged in front of me.

Looking in the mirror, or seeing others each day, we never notice the slow changes that time brings. You don’t really see it just thumbing through old photos, either.

But here, in the photos app (something entirely undreamed of in my childhood), I was watching it like it was a movie. Even childhood pictures of my parents. Them dating and getting married. Holding me after bringing me home from the hospital.

I’m certainly not the first to have these thoughts, nor will I be the last. We all go through life in a somewhat organized yet haphazard way, and only when looking backward do we really see how far we’ve come ... often realizing we’re past the halfway point.

Not that this is a bad thing. I mean, that’s life on Earth. It has its good and bad, and aging is part of the rules for all of us.

I suppose you could look at this in terms of our profession. We all (or at least most of us) start out as hospital patients. As we get older and become doctors, hopefully we need to see our own kind less often while at the same time seeing others as patients. As time goes by, most of us start to need to see doctors again, and as we retire and stop practicing medicine, we move back toward being patients ourselves.

For me, the pictures bring back memories and strike emotions in the way hearing or reading stories never can. They give new life to long-forgotten thoughts. Happy and sad, but overall a feeling of contentment that, so far, I feel like I’ve done more good than bad, more right than wrong.

I hope I always feel that way.

I hope everyone else does, too.

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

Capnography is the measurement of the partial pressure of carbon dioxide (CO₂) in exhaled air.¹ It provides real-time information on ventilation (elimination of CO₂), perfusion (CO₂ transportation in vasculature), and metabolism (production of CO₂ via cellular metabolism).² The technology was originally developed in the 1970s to monitor general anesthesia patients; however, its reach has since broadened, with numerous applications currently in use and in development for the emergency provider (EP).³

Capnography exists in two configurations: a mainstream device that attaches directly to the hub of an endotracheal tube (ETT) and a side-stream device that measure levels via nasal or nasal-oral cannula.^1,3

Qualitative monitors use a colorimetric device that monitors the end-tidal CO₂ (EtCO₂) in exhaled gas and changes color depending on the amount of CO₂ present.^2,4 Expired CO₂ and H₂0 form carbonic acid, causing the specially treated litmus paper inside the device to change from purple to yellow.^2,4 Quantitative monitors display a capnogram, the waveform of expired CO₂ as a function of time; as well as the capnometer, which depicts the numerical EtCO₂ for each breath.⁴ In this overview, we will discuss the general interpretation of capnography and its specific uses in the ED.

The Capnogram

Just like the various stages of an electrocardiogram represent different phases of the cardiac cycle, different phases of a capnogram correspond to different phases of the respiratory cycle. Knowing how to analyze and interpret each phase will contribute to the utility of capnography. While there has been considerable ambiguity in the terminology related to the capnogram,^5-7 the most frequently referenced capnogram terminology consists of the following phases (Figure 1):

Phase I: represents beginning of exhalation, where the dead space is cleared from the upper airway.² This should be zero unless the patient is rebreathing CO₂-laden expired gas from either artificially increased dead space or hypoventilation.^2,8 A precipitous rise in both the baseline and EtCO₂ may indicate contamination of the sensor, such as with secretions or water vapor.^2,6

Phase II: rapid rise in exhaled as the CO₂ from the alveoli reaches the sensor.⁴ This rise should be steep, particularly when ventilation to perfusion (V/Q) is well matched. More V/Q heterogeneity, such as with COPD or asthma, leads to a more gradual slope.⁹ A more gradual phase 2 slope may also indicate a delay in CO₂ delivery to the sampling site, such as with bronchospasm or ETT kinking.²

Phase III: the expiratory plateau, which represents the CO₂ concentration approaching equilibrium from alveoli to nose. The plateau should be nearly horizontal.² If all alveoli had the same pCO₂, this plateau would be perfectly flat, but spatial and temporal mismatch in alveolar V/Q ratios result in variable exhaled CO₂. When there is substantial V/Q heterogeneity, the slope of the plateau will increase.^1,2,6

Phase IV: the initiation of inspiration, which should be a nearly vertical drop to a baseline. If prolonged or bleeding into the expiratory phase, consider a leak in the expiratory portion of the circuit, such as an ETT tube cuff leak.²

Phase 0: the inspiratory segment

Another important part of the capnogram is the alpha angle. This is the angle of transition between Phase II and Phase III. The combination of a prolonged phase II and steeper phase III leads to a more obtuse alpha angle and will have a “shark-fin” appearance to the capnogram. This suggests an obstructive process, such as asthma or COPD (Figure 2).^1,2,6

Standard Uses

Intubation

Capnography, along with visualizing ETT placement through the vocal cords, is the standard of care for confirming correct placement during intubation.^4,10,11 Alternative signs of endotracheal intubation, such as chest wall movement, auscultation, condensation of water vapor in the tube lumen, or pulse oximetry, are less accurate.¹²

While not ideal, correct ETT placement can be confirmed qualitatively using a colorimetric device.¹³ Upon correct placement, the resultant exhalation of CO₂ will change the paper color from purple to yellow (indicating EtCO₂ values > 15 mm Hg).^2,4 Without this color change, tube placement should be verified to rule out esophageal intubation. Unfortunately, qualitative capnography has false positives and negatives that limit its utility in the ED, and this method should be avoided if quantitative capnography is available.

With quantitative capnography, obtaining the typical box-waveform on the capnogram reflects endotracheal intubation. In comparison, a flat capnogram is more indicative of an esophageal intubation (Figure 3).¹⁰ While other things may cause this waveform, such as technical malfunction or complete airway obstruction distal to the tube, tube placement confirmation to rule out esophageal intubation would be the first step to troubleshooting this waveform. In addition, if the ETT is placed in the hypopharynx above the vocal cords, the waveform may initially appear appropriate but will likely become erratic appearing over time.¹⁰

Quantitative capnography does have some limitations. For example, a main-stem bronchus intubation would still likely demonstrate normal-appearing capnography, so secondary strategies and a confirmatory chest x-ray are still indicated. False-negative ETCO₂ readings can occur in low CO₂ elimination states, such as cardiac arrest, pulmonary embolus, or pulmonary edema, while false-positives can theoretically occur after ingestion of large amounts of carbonated liquids or contamination of the sensor with stomach contents or acidic drugs.¹⁰ However, many of these misleading results can be caught by simply checking for an appropriate waveform.

Cardiac Arrest

Capnography has numerous uses in the monitoring, management, and prognostication of intubated patients in cardiac arrest.^1,3,4,10,14 Under normal conditions, EtCO₂ is 35-40 mm Hg. While the body still makes CO₂ during cardiac arrest, it will not reach the alveoli without circulating blood.¹⁰ Without CPR, CO₂ accumulates peripherally and won’t reach the lungs, causing EtCO₂ to approach zero. This means that EtCO₂ correlates directly with cardiac output during CPR, as long as ventilation remains constant.

This means the effectiveness of cardiac chest compression can be assessed in intubated patients using EtCO₂, with higher values during CPR correlated with increased return of spontaneous circulation (ROSC) and survival.^14-18 Using EtCO₂ monitoring during cardiac arrest may improve outcomes,¹⁹ and the American Heart Association (AHA) recommends monitoring capnography during cardiac arrest to assess compression efficacy.^10,20 EtCO₂ >20 mm Hg is considered optimal, while EtCO₂ <10-15 mm Hg is considered suboptimal.^4,10,16 In a recent meta-analysis, the average EtCO₂ was 13.1 mm Hg in those who did not obtain ROSC, compared to 25.8 mm Hg in those who did.²¹ As such, goal EtCO₂ for effective compressions may be even higher in future recommendations. If EtCO₂ is low, either compression technique should be improved or a different operator should do compressions. Every 1 cm increase in depth will increase EtCO₂ by approximately 1.4 mm Hg.16 Interestingly, compression rate is not a significant predictor of EtCO₂ over the dynamic range of chest compression delivery.¹⁶

An abrupt increase in EtCO₂ is an early indicator of ROSC.^{10,14-16,22,23} A return of a perfusing rhythm will increase cardiac output. This allows for accumulated peripheral CO₂ to reach the lungs, subsequently causing a rapid rise in EtCO₂.²⁴ It is important to note that when it comes to evaluating for ROSC, the actual numbers are less important than the change from pre- to post-ROSC. Providers should look for a jump of at least 10 mm Hg on capnometry.4 Nevertheless, an abrupt rise in EtCO₂ is a non-sensitive marker for ROSC (33%, 95% CI 22-47% in one multicenter cross-sectional study), meaning that the lack of an abrupt rise of EtCO₂ may not necessarily mean a lack of ROSC.²³

The EtCO₂ level may help guide decision-making in assessing whether continued resuscitation in cardiac arrest is futile. Values <10 mm Hg after 20 minutes of active resuscitation have consistently demonstrated minimal chance of survival.^17,25,26 In one study, an EtCO₂ of <10 mm Hg at 20 minutes had a sensitivity, specificity, PPV, and NPV of 100% for death in PEA arrest.¹⁷ However, determination of the specific EtCO₂ cutoff and the timing is still an area of research with a final consensus pending.^17,18,25-30 One recent study suggested that even 3 min with EtCO₂ <10 mm Hg could be an appropriate cutoff to cease resuscitation efforts.²⁷

Unfortunately, there is a large amount of heterogeneity in the available literature using capnography to assess for ROSC and in guiding resuscitation efforts. EtCO₂ should not be used as the only factor in the determination to cease resuscitation. In addition, the AHA recommends that EtCO₂ for prognostication should be limited to intubated patients only.²⁰

It is important to note that while cardiac output is the largest factor for EtCO₂ in arrest, other physiologic and iatrogenic causes may affect EtCO₂ during resuscitation. For example, there is considerable variation in EtCO₂ with changes in ventilation rate.⁴ Measured CO₂ may be significantly lower with manual instead of mechanical ventilation, likely due to over-ventilation that not only reduces alveolar CO₂ but also causes excess intra-thoracic pressure, reducing venous return.²¹ For these reasons, use caution when using EtCO₂ during manual ventilation of an intubated patient in cardiac arrest. In addition, administration of epinephrine may cause a small decrease in EtCO₂, although the effect may vary for each individual.^10,31 Sodium bicarbonate can also cause a transient increase in CO₂ due to its conversion into CO₂ and H₂O.¹⁰

Procedural Sedation

Capnography is being used with increasing frequency to monitor patients during procedural sedation; it is now considered standard of care in many settings.³² Although rare, hypoventilation is a risk of procedural sedation.³³ Typically, respiratory depression during procedural sedation is diagnosed with non-invasive pulse oximetry and visual inspection.³⁴ However, capnography has been shown to identify respiratory depression, airway obstruction, apnea, and laryngospasm earlier than pulse oximetry, allowing the provider to intervene quicker.^34,35 Unlike pulse oximetry, the capnogram also remains stable during patient motion and is reliable in low-perfusion states.³⁶

There are two distinct types of hypoventilation detected by capnography. Bradypneic hypoventilation (type 1), which is characterized by a decreased respiratory rate, results in a decreased expiratory time and a subsequent rise in EtCO₂.³⁶ This is depicted on capnography by a high EtCO₂ and longer waveform, and is commonly observed after oversedation with opioids (Figure 4).³⁶ In contrast, hypopneic hypoventilation (type 2) occurs with low tidal volumes but a normal respiratory rate.³⁶ Type 2 is graphically represented by a suddenly lower ETCO₂ with otherwise normal waveform and occurs most commonly with sedative-hypnotic drugs (Figure 5).³⁶ Seeing either type during procedural sedation should alert the clinician to assess for airway obstruction, consider supplemental oxygen, cease drug administration or reduce dosing, and consider reversal if appropriate.³⁶

There is some debate as to the utility of capnography for procedural sedation. While it is clear that capnography decreases the incidence of hypoxia, some studies suggest that it may not reduce patient-centered outcomes such as adverse respiratory events, neurologic injury, aspiration, or death compared to standard monitoring.^35,37,38 However, pulse oximetry alone can suffer response delay, while EtCO₂ can rapidly detect hypoventilation.³⁹

Potential Uses/Applications

Respiratory Distress

Capnography can provide dynamic monitoring in patients with acute respiratory distress. Measuring EtCO₂ with each breath provides instantaneous feedback on the clinical status of the patient and has numerous specific uses.^1,3,4

Determining the etiology of respiratory distress in either the obtunded patient or those with multiple comorbidities can be a challenge. Vital sign abnormalities and physical exam findings can overlap in numerous conditions, which may only further obscure the diagnosis. Since different etiologies for respiratory disease require different management modalities, anything that can help clue in to the specific cause can be beneficial. As discussed above, obstructive diseases such as COPD or asthma demonstrate a “shark-fin appearance” on capnogram due to both V/Q heterogeneity and a prolonged expiratory phase due to airway constriction, which will contrast to the typical box-waveform in other conditions (Figure 2).^1,2,6 Some studies have been able differentiate COPD from congestive heart failure (CHF) by waveform analysis alone, though this was primarily done via computer algorithms.⁴⁰ Seeing the shark-fin (or the lack thereof) can help guide management of respiratory distress in conjunction with the remainder of the initial assessment.

Monitoring capnography can help with management and disposition in those with COPD or asthma. During exacerbations, EtCO₂ levels may initially drop as the patient hyperventilates to compensate.¹ It is not until ventilation becomes less effective that EtCO₂ levels begin to rise. This may occur before hypoxia sets in and can prompt the clinician to escalate ventilation strategies. In addition, the normalization of the “shark-fin” obstructive pattern towards the more typical box-form wave may indicate effective treatment, though more data is needed before it can be recommended.⁴¹ One of the advantages of this technique would be that it is independent of patient effort, unlike peak-flow monitoring.

EtCO₂ can be beneficial even before patients get to the ED. In one study, prehospital patients presenting with asthma or COPD who were found to have EtCO₂ of >50 mm Hg or <28 mm Hg, representing the upper and lower limits in the study, had greater rates of intubation, critical care admission, and mortality.⁴² The patients in this cohort with higher EtCO₂ were likely tiring after prolonged hyperventilation and therefore would be more likely to need ventilatory support. Those on the lower end were likely hyperventilating and had not yet tired out. It is important to note that while arrival EtCO₂ levels may aid in determining the more critically ill, post-treatment levels were not found to have a statistical difference in determining disposition in patients with asthma or COPD.⁴³

Caution is advised when attempting to use EtCO₂ to approximate an arterial blood gas CO₂ (PaCO₂). While EtCO₂ can correlate with PaCO₂ within 5 mm Hg in greater than 80% of patients with dyspnea,⁴⁴ large discrepancies are common depending on the disease state.⁴⁵ In general, the EtCO₂ should always be lower than the PaCO₂ due to the contribution to the ETCO₂ from dead space, which has a low CO₂ content due to lack of perfusion.

Sepsis

EtCO₂ may help identify septic patients given its inverse relationship with lactate levels.^46-49 In conditions of poor tissue perfusion, lactate builds up. This begins to make the blood acidotic in the form of newly acquired anions, with a resultant anion gap metabolic acidosis. The body then tries to acutely compensate for this by hyperventilating, resulting in the observed lowering of EtCO₂. Since lactate is a predictor of mortality in sepsis,⁵⁰ and monitoring lactate clearance to evaluate resuscitation efforts in sepsis is recommended,⁵¹ EtCO₂ could play a similar role. One group in particular has demonstrated that, when used with SIRS criteria, abnormally low prehospital EtCO₂ levels is predictive of sepsis and inhospital mortality, and is more predictive than SIRS criteria alone.^48,50 That said, EtCO₂ was not associated with lactate temporally at 3 and 6 hours,⁵¹ so it should not be used to guide resuscitation like a lactate clearance. It appears that EtCO₂ may be helpful for triage in sepsis, but more study is needed to determine the exact role particularly given most of the available research involves multiple studies from one group.^47,48,52

Diabetic Ketoacidosis

Initial bicarbonate levels and venous pH are associated with low EtCO₂ readings in diabetic ketoacidosis (DKA).^54,55 This could have many practical uses, in particular for patients presenting with hyperglycemia to rule out DKA. One study demonstrated that a blood glucose >250 mg/dL and capnography of >24.5 mm Hg had 90% sensitivity for excluding DKA.⁵⁵ A value of 35 mm Hg or greater demonstrated 100% sensitivity for excluding DKA in patients with initial glucose >550 mg/dL,⁵⁶ though this blood glucose is not practical, as this excludes many patients the EP would seek to rule out DKA (recall that blood glucose only has to be >250 mg/dL for the diagnosis). Smaller studies focused on the pediatric population found a 100% sensitivity marker for DKA varied from >30 to >36 mm Hg.^57,58 Clearly a role exists, but no study has demonstrated sufficient sensitivity for ruling out DKA with EtCO₂ and blood glucose alone within the framework of clinically relevant values.

Trauma

As described above, low EtCO₂ is inversely correlated with lactate.⁴⁶ Because of this, it could theoretically be a marker of hypoperfusion in trauma. Initial EtCO₂ values <25 mm Hg have been associated with mortality and hemorrhage in intubated trauma patients,⁵⁹ as well as mortality prior to discharge in nonintubated trauma patients.⁶⁰ However, it did not demonstrate added clinical utility when combined with Glasgow Coma Scale (GCS) score, systolic blood pressure, and age in predicting severe injury.⁶¹

Pulmonary Embolism

A pulmonary embolism (PE) causes a blockage in blood flow to alveoli, which results in a decrease in CO₂ transportation to the alveoli and thus lower EtCO₂, while also widening the gradient between PaCO₂ and EtCO₂.³⁷ Because of this, it has a theoretical role in the diagnosis of PE, though numerous studies have demonstrated that EtCO₂ alone is not sensitive nor specific enough for this role.^62-66 In a recent meta-analysis, a pretest probability of 10% could lead to a posttest probability of 3% using capnography.⁶² While further study is needed before recommendation, this indicates that capnography could obviate the need for imaging in low to intermediate risk patients either after a positive D-Dimer or instead of obtaining a D-dimer.^62-64

Simply measuring an initial EtCO₂ as a triage vital sign may have added benefit to the EP, and consideration could be made for making this a policy in your ED. One study demonstrated that abnormal initial EtCO₂ (outside of 35-45 mm Hg) was predictive of admisison (RR 2.5, 95% CI 1.5-4.0).⁶⁷ An abnormal EtCO₂ (outside of 31-41 mm Hg for this study) was 93% sensitive (95% CI 79-98%), with expectedly low specificity of 44% (95% CI 41-48%) for mortality prior to discharge.⁴⁷ This potential vital sign may be treated similarly to tachycardia; while an abnormal heart rate should increase a clinician’s concern for a pathological condition, it needs to be taken in context of the situation to accurately interpret it.

Summary

Capnography has numerous uses in the ED in both intubated and spontaneously breathing patients. Quantitative capnography is the standard of care for confirming endotracheal intubation. It is recommended as an aide in maximizing chest compressions during cardiac arrest and can assist in prognostication. It rapidly identifies hypoventilation during procedural sedation. It also has many more potential applications that continue to be explored in areas such as respiratory distress, sepsis, trauma, DKA, and PE. Ultimately, capnography should always be used in association with the remainder of the clinical assessment.

Capnography is the measurement of the partial pressure of carbon dioxide (CO₂) in exhaled air.¹ It provides real-time information on ventilation (elimination of CO₂), perfusion (CO₂ transportation in vasculature), and metabolism (production of CO₂ via cellular metabolism).² The technology was originally developed in the 1970s to monitor general anesthesia patients; however, its reach has since broadened, with numerous applications currently in use and in development for the emergency provider (EP).³

Capnography exists in two configurations: a mainstream device that attaches directly to the hub of an endotracheal tube (ETT) and a side-stream device that measure levels via nasal or nasal-oral cannula.^1,3

Qualitative monitors use a colorimetric device that monitors the end-tidal CO₂ (EtCO₂) in exhaled gas and changes color depending on the amount of CO₂ present.^2,4 Expired CO₂ and H₂0 form carbonic acid, causing the specially treated litmus paper inside the device to change from purple to yellow.^2,4 Quantitative monitors display a capnogram, the waveform of expired CO₂ as a function of time; as well as the capnometer, which depicts the numerical EtCO₂ for each breath.⁴ In this overview, we will discuss the general interpretation of capnography and its specific uses in the ED.

The Capnogram

Just like the various stages of an electrocardiogram represent different phases of the cardiac cycle, different phases of a capnogram correspond to different phases of the respiratory cycle. Knowing how to analyze and interpret each phase will contribute to the utility of capnography. While there has been considerable ambiguity in the terminology related to the capnogram,^5-7 the most frequently referenced capnogram terminology consists of the following phases (Figure 1):

Phase I: represents beginning of exhalation, where the dead space is cleared from the upper airway.² This should be zero unless the patient is rebreathing CO₂-laden expired gas from either artificially increased dead space or hypoventilation.^2,8 A precipitous rise in both the baseline and EtCO₂ may indicate contamination of the sensor, such as with secretions or water vapor.^2,6

Phase II: rapid rise in exhaled as the CO₂ from the alveoli reaches the sensor.⁴ This rise should be steep, particularly when ventilation to perfusion (V/Q) is well matched. More V/Q heterogeneity, such as with COPD or asthma, leads to a more gradual slope.⁹ A more gradual phase 2 slope may also indicate a delay in CO₂ delivery to the sampling site, such as with bronchospasm or ETT kinking.²

Phase III: the expiratory plateau, which represents the CO₂ concentration approaching equilibrium from alveoli to nose. The plateau should be nearly horizontal.² If all alveoli had the same pCO₂, this plateau would be perfectly flat, but spatial and temporal mismatch in alveolar V/Q ratios result in variable exhaled CO₂. When there is substantial V/Q heterogeneity, the slope of the plateau will increase.^1,2,6

Phase IV: the initiation of inspiration, which should be a nearly vertical drop to a baseline. If prolonged or bleeding into the expiratory phase, consider a leak in the expiratory portion of the circuit, such as an ETT tube cuff leak.²

Phase 0: the inspiratory segment

Another important part of the capnogram is the alpha angle. This is the angle of transition between Phase II and Phase III. The combination of a prolonged phase II and steeper phase III leads to a more obtuse alpha angle and will have a “shark-fin” appearance to the capnogram. This suggests an obstructive process, such as asthma or COPD (Figure 2).^1,2,6

Standard Uses

Intubation

Capnography, along with visualizing ETT placement through the vocal cords, is the standard of care for confirming correct placement during intubation.^4,10,11 Alternative signs of endotracheal intubation, such as chest wall movement, auscultation, condensation of water vapor in the tube lumen, or pulse oximetry, are less accurate.¹²

While not ideal, correct ETT placement can be confirmed qualitatively using a colorimetric device.¹³ Upon correct placement, the resultant exhalation of CO₂ will change the paper color from purple to yellow (indicating EtCO₂ values > 15 mm Hg).^2,4 Without this color change, tube placement should be verified to rule out esophageal intubation. Unfortunately, qualitative capnography has false positives and negatives that limit its utility in the ED, and this method should be avoided if quantitative capnography is available.

With quantitative capnography, obtaining the typical box-waveform on the capnogram reflects endotracheal intubation. In comparison, a flat capnogram is more indicative of an esophageal intubation (Figure 3).¹⁰ While other things may cause this waveform, such as technical malfunction or complete airway obstruction distal to the tube, tube placement confirmation to rule out esophageal intubation would be the first step to troubleshooting this waveform. In addition, if the ETT is placed in the hypopharynx above the vocal cords, the waveform may initially appear appropriate but will likely become erratic appearing over time.¹⁰

Quantitative capnography does have some limitations. For example, a main-stem bronchus intubation would still likely demonstrate normal-appearing capnography, so secondary strategies and a confirmatory chest x-ray are still indicated. False-negative ETCO₂ readings can occur in low CO₂ elimination states, such as cardiac arrest, pulmonary embolus, or pulmonary edema, while false-positives can theoretically occur after ingestion of large amounts of carbonated liquids or contamination of the sensor with stomach contents or acidic drugs.¹⁰ However, many of these misleading results can be caught by simply checking for an appropriate waveform.

Cardiac Arrest

Capnography has numerous uses in the monitoring, management, and prognostication of intubated patients in cardiac arrest.^1,3,4,10,14 Under normal conditions, EtCO₂ is 35-40 mm Hg. While the body still makes CO₂ during cardiac arrest, it will not reach the alveoli without circulating blood.¹⁰ Without CPR, CO₂ accumulates peripherally and won’t reach the lungs, causing EtCO₂ to approach zero. This means that EtCO₂ correlates directly with cardiac output during CPR, as long as ventilation remains constant.

This means the effectiveness of cardiac chest compression can be assessed in intubated patients using EtCO₂, with higher values during CPR correlated with increased return of spontaneous circulation (ROSC) and survival.^14-18 Using EtCO₂ monitoring during cardiac arrest may improve outcomes,¹⁹ and the American Heart Association (AHA) recommends monitoring capnography during cardiac arrest to assess compression efficacy.^10,20 EtCO₂ >20 mm Hg is considered optimal, while EtCO₂ <10-15 mm Hg is considered suboptimal.^4,10,16 In a recent meta-analysis, the average EtCO₂ was 13.1 mm Hg in those who did not obtain ROSC, compared to 25.8 mm Hg in those who did.²¹ As such, goal EtCO₂ for effective compressions may be even higher in future recommendations. If EtCO₂ is low, either compression technique should be improved or a different operator should do compressions. Every 1 cm increase in depth will increase EtCO₂ by approximately 1.4 mm Hg.16 Interestingly, compression rate is not a significant predictor of EtCO₂ over the dynamic range of chest compression delivery.¹⁶

An abrupt increase in EtCO₂ is an early indicator of ROSC.^{10,14-16,22,23} A return of a perfusing rhythm will increase cardiac output. This allows for accumulated peripheral CO₂ to reach the lungs, subsequently causing a rapid rise in EtCO₂.²⁴ It is important to note that when it comes to evaluating for ROSC, the actual numbers are less important than the change from pre- to post-ROSC. Providers should look for a jump of at least 10 mm Hg on capnometry.4 Nevertheless, an abrupt rise in EtCO₂ is a non-sensitive marker for ROSC (33%, 95% CI 22-47% in one multicenter cross-sectional study), meaning that the lack of an abrupt rise of EtCO₂ may not necessarily mean a lack of ROSC.²³

The EtCO₂ level may help guide decision-making in assessing whether continued resuscitation in cardiac arrest is futile. Values <10 mm Hg after 20 minutes of active resuscitation have consistently demonstrated minimal chance of survival.^17,25,26 In one study, an EtCO₂ of <10 mm Hg at 20 minutes had a sensitivity, specificity, PPV, and NPV of 100% for death in PEA arrest.¹⁷ However, determination of the specific EtCO₂ cutoff and the timing is still an area of research with a final consensus pending.^17,18,25-30 One recent study suggested that even 3 min with EtCO₂ <10 mm Hg could be an appropriate cutoff to cease resuscitation efforts.²⁷

Unfortunately, there is a large amount of heterogeneity in the available literature using capnography to assess for ROSC and in guiding resuscitation efforts. EtCO₂ should not be used as the only factor in the determination to cease resuscitation. In addition, the AHA recommends that EtCO₂ for prognostication should be limited to intubated patients only.²⁰

It is important to note that while cardiac output is the largest factor for EtCO₂ in arrest, other physiologic and iatrogenic causes may affect EtCO₂ during resuscitation. For example, there is considerable variation in EtCO₂ with changes in ventilation rate.⁴ Measured CO₂ may be significantly lower with manual instead of mechanical ventilation, likely due to over-ventilation that not only reduces alveolar CO₂ but also causes excess intra-thoracic pressure, reducing venous return.²¹ For these reasons, use caution when using EtCO₂ during manual ventilation of an intubated patient in cardiac arrest. In addition, administration of epinephrine may cause a small decrease in EtCO₂, although the effect may vary for each individual.^10,31 Sodium bicarbonate can also cause a transient increase in CO₂ due to its conversion into CO₂ and H₂O.¹⁰

Procedural Sedation

Capnography is being used with increasing frequency to monitor patients during procedural sedation; it is now considered standard of care in many settings.³² Although rare, hypoventilation is a risk of procedural sedation.³³ Typically, respiratory depression during procedural sedation is diagnosed with non-invasive pulse oximetry and visual inspection.³⁴ However, capnography has been shown to identify respiratory depression, airway obstruction, apnea, and laryngospasm earlier than pulse oximetry, allowing the provider to intervene quicker.^34,35 Unlike pulse oximetry, the capnogram also remains stable during patient motion and is reliable in low-perfusion states.³⁶

There are two distinct types of hypoventilation detected by capnography. Bradypneic hypoventilation (type 1), which is characterized by a decreased respiratory rate, results in a decreased expiratory time and a subsequent rise in EtCO₂.³⁶ This is depicted on capnography by a high EtCO₂ and longer waveform, and is commonly observed after oversedation with opioids (Figure 4).³⁶ In contrast, hypopneic hypoventilation (type 2) occurs with low tidal volumes but a normal respiratory rate.³⁶ Type 2 is graphically represented by a suddenly lower ETCO₂ with otherwise normal waveform and occurs most commonly with sedative-hypnotic drugs (Figure 5).³⁶ Seeing either type during procedural sedation should alert the clinician to assess for airway obstruction, consider supplemental oxygen, cease drug administration or reduce dosing, and consider reversal if appropriate.³⁶

There is some debate as to the utility of capnography for procedural sedation. While it is clear that capnography decreases the incidence of hypoxia, some studies suggest that it may not reduce patient-centered outcomes such as adverse respiratory events, neurologic injury, aspiration, or death compared to standard monitoring.^35,37,38 However, pulse oximetry alone can suffer response delay, while EtCO₂ can rapidly detect hypoventilation.³⁹

Potential Uses/Applications

Respiratory Distress

Capnography can provide dynamic monitoring in patients with acute respiratory distress. Measuring EtCO₂ with each breath provides instantaneous feedback on the clinical status of the patient and has numerous specific uses.^1,3,4

Determining the etiology of respiratory distress in either the obtunded patient or those with multiple comorbidities can be a challenge. Vital sign abnormalities and physical exam findings can overlap in numerous conditions, which may only further obscure the diagnosis. Since different etiologies for respiratory disease require different management modalities, anything that can help clue in to the specific cause can be beneficial. As discussed above, obstructive diseases such as COPD or asthma demonstrate a “shark-fin appearance” on capnogram due to both V/Q heterogeneity and a prolonged expiratory phase due to airway constriction, which will contrast to the typical box-waveform in other conditions (Figure 2).^1,2,6 Some studies have been able differentiate COPD from congestive heart failure (CHF) by waveform analysis alone, though this was primarily done via computer algorithms.⁴⁰ Seeing the shark-fin (or the lack thereof) can help guide management of respiratory distress in conjunction with the remainder of the initial assessment.

Monitoring capnography can help with management and disposition in those with COPD or asthma. During exacerbations, EtCO₂ levels may initially drop as the patient hyperventilates to compensate.¹ It is not until ventilation becomes less effective that EtCO₂ levels begin to rise. This may occur before hypoxia sets in and can prompt the clinician to escalate ventilation strategies. In addition, the normalization of the “shark-fin” obstructive pattern towards the more typical box-form wave may indicate effective treatment, though more data is needed before it can be recommended.⁴¹ One of the advantages of this technique would be that it is independent of patient effort, unlike peak-flow monitoring.

EtCO₂ can be beneficial even before patients get to the ED. In one study, prehospital patients presenting with asthma or COPD who were found to have EtCO₂ of >50 mm Hg or <28 mm Hg, representing the upper and lower limits in the study, had greater rates of intubation, critical care admission, and mortality.⁴² The patients in this cohort with higher EtCO₂ were likely tiring after prolonged hyperventilation and therefore would be more likely to need ventilatory support. Those on the lower end were likely hyperventilating and had not yet tired out. It is important to note that while arrival EtCO₂ levels may aid in determining the more critically ill, post-treatment levels were not found to have a statistical difference in determining disposition in patients with asthma or COPD.⁴³

Caution is advised when attempting to use EtCO₂ to approximate an arterial blood gas CO₂ (PaCO₂). While EtCO₂ can correlate with PaCO₂ within 5 mm Hg in greater than 80% of patients with dyspnea,⁴⁴ large discrepancies are common depending on the disease state.⁴⁵ In general, the EtCO₂ should always be lower than the PaCO₂ due to the contribution to the ETCO₂ from dead space, which has a low CO₂ content due to lack of perfusion.

Sepsis

EtCO₂ may help identify septic patients given its inverse relationship with lactate levels.^46-49 In conditions of poor tissue perfusion, lactate builds up. This begins to make the blood acidotic in the form of newly acquired anions, with a resultant anion gap metabolic acidosis. The body then tries to acutely compensate for this by hyperventilating, resulting in the observed lowering of EtCO₂. Since lactate is a predictor of mortality in sepsis,⁵⁰ and monitoring lactate clearance to evaluate resuscitation efforts in sepsis is recommended,⁵¹ EtCO₂ could play a similar role. One group in particular has demonstrated that, when used with SIRS criteria, abnormally low prehospital EtCO₂ levels is predictive of sepsis and inhospital mortality, and is more predictive than SIRS criteria alone.^48,50 That said, EtCO₂ was not associated with lactate temporally at 3 and 6 hours,⁵¹ so it should not be used to guide resuscitation like a lactate clearance. It appears that EtCO₂ may be helpful for triage in sepsis, but more study is needed to determine the exact role particularly given most of the available research involves multiple studies from one group.^47,48,52

Diabetic Ketoacidosis

Initial bicarbonate levels and venous pH are associated with low EtCO₂ readings in diabetic ketoacidosis (DKA).^54,55 This could have many practical uses, in particular for patients presenting with hyperglycemia to rule out DKA. One study demonstrated that a blood glucose >250 mg/dL and capnography of >24.5 mm Hg had 90% sensitivity for excluding DKA.⁵⁵ A value of 35 mm Hg or greater demonstrated 100% sensitivity for excluding DKA in patients with initial glucose >550 mg/dL,⁵⁶ though this blood glucose is not practical, as this excludes many patients the EP would seek to rule out DKA (recall that blood glucose only has to be >250 mg/dL for the diagnosis). Smaller studies focused on the pediatric population found a 100% sensitivity marker for DKA varied from >30 to >36 mm Hg.^57,58 Clearly a role exists, but no study has demonstrated sufficient sensitivity for ruling out DKA with EtCO₂ and blood glucose alone within the framework of clinically relevant values.

Trauma

As described above, low EtCO₂ is inversely correlated with lactate.⁴⁶ Because of this, it could theoretically be a marker of hypoperfusion in trauma. Initial EtCO₂ values <25 mm Hg have been associated with mortality and hemorrhage in intubated trauma patients,⁵⁹ as well as mortality prior to discharge in nonintubated trauma patients.⁶⁰ However, it did not demonstrate added clinical utility when combined with Glasgow Coma Scale (GCS) score, systolic blood pressure, and age in predicting severe injury.⁶¹

Pulmonary Embolism

A pulmonary embolism (PE) causes a blockage in blood flow to alveoli, which results in a decrease in CO₂ transportation to the alveoli and thus lower EtCO₂, while also widening the gradient between PaCO₂ and EtCO₂.³⁷ Because of this, it has a theoretical role in the diagnosis of PE, though numerous studies have demonstrated that EtCO₂ alone is not sensitive nor specific enough for this role.^62-66 In a recent meta-analysis, a pretest probability of 10% could lead to a posttest probability of 3% using capnography.⁶² While further study is needed before recommendation, this indicates that capnography could obviate the need for imaging in low to intermediate risk patients either after a positive D-Dimer or instead of obtaining a D-dimer.^62-64

Simply measuring an initial EtCO₂ as a triage vital sign may have added benefit to the EP, and consideration could be made for making this a policy in your ED. One study demonstrated that abnormal initial EtCO₂ (outside of 35-45 mm Hg) was predictive of admisison (RR 2.5, 95% CI 1.5-4.0).⁶⁷ An abnormal EtCO₂ (outside of 31-41 mm Hg for this study) was 93% sensitive (95% CI 79-98%), with expectedly low specificity of 44% (95% CI 41-48%) for mortality prior to discharge.⁴⁷ This potential vital sign may be treated similarly to tachycardia; while an abnormal heart rate should increase a clinician’s concern for a pathological condition, it needs to be taken in context of the situation to accurately interpret it.

Summary

Capnography has numerous uses in the ED in both intubated and spontaneously breathing patients. Quantitative capnography is the standard of care for confirming endotracheal intubation. It is recommended as an aide in maximizing chest compressions during cardiac arrest and can assist in prognostication. It rapidly identifies hypoventilation during procedural sedation. It also has many more potential applications that continue to be explored in areas such as respiratory distress, sepsis, trauma, DKA, and PE. Ultimately, capnography should always be used in association with the remainder of the clinical assessment.

Capnography is the measurement of the partial pressure of carbon dioxide (CO₂) in exhaled air.¹ It provides real-time information on ventilation (elimination of CO₂), perfusion (CO₂ transportation in vasculature), and metabolism (production of CO₂ via cellular metabolism).² The technology was originally developed in the 1970s to monitor general anesthesia patients; however, its reach has since broadened, with numerous applications currently in use and in development for the emergency provider (EP).³

Capnography exists in two configurations: a mainstream device that attaches directly to the hub of an endotracheal tube (ETT) and a side-stream device that measure levels via nasal or nasal-oral cannula.^1,3

Qualitative monitors use a colorimetric device that monitors the end-tidal CO₂ (EtCO₂) in exhaled gas and changes color depending on the amount of CO₂ present.^2,4 Expired CO₂ and H₂0 form carbonic acid, causing the specially treated litmus paper inside the device to change from purple to yellow.^2,4 Quantitative monitors display a capnogram, the waveform of expired CO₂ as a function of time; as well as the capnometer, which depicts the numerical EtCO₂ for each breath.⁴ In this overview, we will discuss the general interpretation of capnography and its specific uses in the ED.

The Capnogram

Just like the various stages of an electrocardiogram represent different phases of the cardiac cycle, different phases of a capnogram correspond to different phases of the respiratory cycle. Knowing how to analyze and interpret each phase will contribute to the utility of capnography. While there has been considerable ambiguity in the terminology related to the capnogram,^5-7 the most frequently referenced capnogram terminology consists of the following phases (Figure 1):

Phase I: represents beginning of exhalation, where the dead space is cleared from the upper airway.² This should be zero unless the patient is rebreathing CO₂-laden expired gas from either artificially increased dead space or hypoventilation.^2,8 A precipitous rise in both the baseline and EtCO₂ may indicate contamination of the sensor, such as with secretions or water vapor.^2,6

Phase II: rapid rise in exhaled as the CO₂ from the alveoli reaches the sensor.⁴ This rise should be steep, particularly when ventilation to perfusion (V/Q) is well matched. More V/Q heterogeneity, such as with COPD or asthma, leads to a more gradual slope.⁹ A more gradual phase 2 slope may also indicate a delay in CO₂ delivery to the sampling site, such as with bronchospasm or ETT kinking.²

Phase III: the expiratory plateau, which represents the CO₂ concentration approaching equilibrium from alveoli to nose. The plateau should be nearly horizontal.² If all alveoli had the same pCO₂, this plateau would be perfectly flat, but spatial and temporal mismatch in alveolar V/Q ratios result in variable exhaled CO₂. When there is substantial V/Q heterogeneity, the slope of the plateau will increase.^1,2,6

Phase IV: the initiation of inspiration, which should be a nearly vertical drop to a baseline. If prolonged or bleeding into the expiratory phase, consider a leak in the expiratory portion of the circuit, such as an ETT tube cuff leak.²

Phase 0: the inspiratory segment

Another important part of the capnogram is the alpha angle. This is the angle of transition between Phase II and Phase III. The combination of a prolonged phase II and steeper phase III leads to a more obtuse alpha angle and will have a “shark-fin” appearance to the capnogram. This suggests an obstructive process, such as asthma or COPD (Figure 2).^1,2,6

Standard Uses

Intubation

Capnography, along with visualizing ETT placement through the vocal cords, is the standard of care for confirming correct placement during intubation.^4,10,11 Alternative signs of endotracheal intubation, such as chest wall movement, auscultation, condensation of water vapor in the tube lumen, or pulse oximetry, are less accurate.¹²

While not ideal, correct ETT placement can be confirmed qualitatively using a colorimetric device.¹³ Upon correct placement, the resultant exhalation of CO₂ will change the paper color from purple to yellow (indicating EtCO₂ values > 15 mm Hg).^2,4 Without this color change, tube placement should be verified to rule out esophageal intubation. Unfortunately, qualitative capnography has false positives and negatives that limit its utility in the ED, and this method should be avoided if quantitative capnography is available.

With quantitative capnography, obtaining the typical box-waveform on the capnogram reflects endotracheal intubation. In comparison, a flat capnogram is more indicative of an esophageal intubation (Figure 3).¹⁰ While other things may cause this waveform, such as technical malfunction or complete airway obstruction distal to the tube, tube placement confirmation to rule out esophageal intubation would be the first step to troubleshooting this waveform. In addition, if the ETT is placed in the hypopharynx above the vocal cords, the waveform may initially appear appropriate but will likely become erratic appearing over time.¹⁰

Quantitative capnography does have some limitations. For example, a main-stem bronchus intubation would still likely demonstrate normal-appearing capnography, so secondary strategies and a confirmatory chest x-ray are still indicated. False-negative ETCO₂ readings can occur in low CO₂ elimination states, such as cardiac arrest, pulmonary embolus, or pulmonary edema, while false-positives can theoretically occur after ingestion of large amounts of carbonated liquids or contamination of the sensor with stomach contents or acidic drugs.¹⁰ However, many of these misleading results can be caught by simply checking for an appropriate waveform.

Cardiac Arrest

Capnography has numerous uses in the monitoring, management, and prognostication of intubated patients in cardiac arrest.^1,3,4,10,14 Under normal conditions, EtCO₂ is 35-40 mm Hg. While the body still makes CO₂ during cardiac arrest, it will not reach the alveoli without circulating blood.¹⁰ Without CPR, CO₂ accumulates peripherally and won’t reach the lungs, causing EtCO₂ to approach zero. This means that EtCO₂ correlates directly with cardiac output during CPR, as long as ventilation remains constant.

This means the effectiveness of cardiac chest compression can be assessed in intubated patients using EtCO₂, with higher values during CPR correlated with increased return of spontaneous circulation (ROSC) and survival.^14-18 Using EtCO₂ monitoring during cardiac arrest may improve outcomes,¹⁹ and the American Heart Association (AHA) recommends monitoring capnography during cardiac arrest to assess compression efficacy.^10,20 EtCO₂ >20 mm Hg is considered optimal, while EtCO₂ <10-15 mm Hg is considered suboptimal.^4,10,16 In a recent meta-analysis, the average EtCO₂ was 13.1 mm Hg in those who did not obtain ROSC, compared to 25.8 mm Hg in those who did.²¹ As such, goal EtCO₂ for effective compressions may be even higher in future recommendations. If EtCO₂ is low, either compression technique should be improved or a different operator should do compressions. Every 1 cm increase in depth will increase EtCO₂ by approximately 1.4 mm Hg.16 Interestingly, compression rate is not a significant predictor of EtCO₂ over the dynamic range of chest compression delivery.¹⁶

An abrupt increase in EtCO₂ is an early indicator of ROSC.^{10,14-16,22,23} A return of a perfusing rhythm will increase cardiac output. This allows for accumulated peripheral CO₂ to reach the lungs, subsequently causing a rapid rise in EtCO₂.²⁴ It is important to note that when it comes to evaluating for ROSC, the actual numbers are less important than the change from pre- to post-ROSC. Providers should look for a jump of at least 10 mm Hg on capnometry.4 Nevertheless, an abrupt rise in EtCO₂ is a non-sensitive marker for ROSC (33%, 95% CI 22-47% in one multicenter cross-sectional study), meaning that the lack of an abrupt rise of EtCO₂ may not necessarily mean a lack of ROSC.²³

The EtCO₂ level may help guide decision-making in assessing whether continued resuscitation in cardiac arrest is futile. Values <10 mm Hg after 20 minutes of active resuscitation have consistently demonstrated minimal chance of survival.^17,25,26 In one study, an EtCO₂ of <10 mm Hg at 20 minutes had a sensitivity, specificity, PPV, and NPV of 100% for death in PEA arrest.¹⁷ However, determination of the specific EtCO₂ cutoff and the timing is still an area of research with a final consensus pending.^17,18,25-30 One recent study suggested that even 3 min with EtCO₂ <10 mm Hg could be an appropriate cutoff to cease resuscitation efforts.²⁷

Unfortunately, there is a large amount of heterogeneity in the available literature using capnography to assess for ROSC and in guiding resuscitation efforts. EtCO₂ should not be used as the only factor in the determination to cease resuscitation. In addition, the AHA recommends that EtCO₂ for prognostication should be limited to intubated patients only.²⁰

It is important to note that while cardiac output is the largest factor for EtCO₂ in arrest, other physiologic and iatrogenic causes may affect EtCO₂ during resuscitation. For example, there is considerable variation in EtCO₂ with changes in ventilation rate.⁴ Measured CO₂ may be significantly lower with manual instead of mechanical ventilation, likely due to over-ventilation that not only reduces alveolar CO₂ but also causes excess intra-thoracic pressure, reducing venous return.²¹ For these reasons, use caution when using EtCO₂ during manual ventilation of an intubated patient in cardiac arrest. In addition, administration of epinephrine may cause a small decrease in EtCO₂, although the effect may vary for each individual.^10,31 Sodium bicarbonate can also cause a transient increase in CO₂ due to its conversion into CO₂ and H₂O.¹⁰

Procedural Sedation

Capnography is being used with increasing frequency to monitor patients during procedural sedation; it is now considered standard of care in many settings.³² Although rare, hypoventilation is a risk of procedural sedation.³³ Typically, respiratory depression during procedural sedation is diagnosed with non-invasive pulse oximetry and visual inspection.³⁴ However, capnography has been shown to identify respiratory depression, airway obstruction, apnea, and laryngospasm earlier than pulse oximetry, allowing the provider to intervene quicker.^34,35 Unlike pulse oximetry, the capnogram also remains stable during patient motion and is reliable in low-perfusion states.³⁶

There are two distinct types of hypoventilation detected by capnography. Bradypneic hypoventilation (type 1), which is characterized by a decreased respiratory rate, results in a decreased expiratory time and a subsequent rise in EtCO₂.³⁶ This is depicted on capnography by a high EtCO₂ and longer waveform, and is commonly observed after oversedation with opioids (Figure 4).³⁶ In contrast, hypopneic hypoventilation (type 2) occurs with low tidal volumes but a normal respiratory rate.³⁶ Type 2 is graphically represented by a suddenly lower ETCO₂ with otherwise normal waveform and occurs most commonly with sedative-hypnotic drugs (Figure 5).³⁶ Seeing either type during procedural sedation should alert the clinician to assess for airway obstruction, consider supplemental oxygen, cease drug administration or reduce dosing, and consider reversal if appropriate.³⁶

There is some debate as to the utility of capnography for procedural sedation. While it is clear that capnography decreases the incidence of hypoxia, some studies suggest that it may not reduce patient-centered outcomes such as adverse respiratory events, neurologic injury, aspiration, or death compared to standard monitoring.^35,37,38 However, pulse oximetry alone can suffer response delay, while EtCO₂ can rapidly detect hypoventilation.³⁹

Potential Uses/Applications

Respiratory Distress

Capnography can provide dynamic monitoring in patients with acute respiratory distress. Measuring EtCO₂ with each breath provides instantaneous feedback on the clinical status of the patient and has numerous specific uses.^1,3,4

Determining the etiology of respiratory distress in either the obtunded patient or those with multiple comorbidities can be a challenge. Vital sign abnormalities and physical exam findings can overlap in numerous conditions, which may only further obscure the diagnosis. Since different etiologies for respiratory disease require different management modalities, anything that can help clue in to the specific cause can be beneficial. As discussed above, obstructive diseases such as COPD or asthma demonstrate a “shark-fin appearance” on capnogram due to both V/Q heterogeneity and a prolonged expiratory phase due to airway constriction, which will contrast to the typical box-waveform in other conditions (Figure 2).^1,2,6 Some studies have been able differentiate COPD from congestive heart failure (CHF) by waveform analysis alone, though this was primarily done via computer algorithms.⁴⁰ Seeing the shark-fin (or the lack thereof) can help guide management of respiratory distress in conjunction with the remainder of the initial assessment.

Monitoring capnography can help with management and disposition in those with COPD or asthma. During exacerbations, EtCO₂ levels may initially drop as the patient hyperventilates to compensate.¹ It is not until ventilation becomes less effective that EtCO₂ levels begin to rise. This may occur before hypoxia sets in and can prompt the clinician to escalate ventilation strategies. In addition, the normalization of the “shark-fin” obstructive pattern towards the more typical box-form wave may indicate effective treatment, though more data is needed before it can be recommended.⁴¹ One of the advantages of this technique would be that it is independent of patient effort, unlike peak-flow monitoring.

EtCO₂ can be beneficial even before patients get to the ED. In one study, prehospital patients presenting with asthma or COPD who were found to have EtCO₂ of >50 mm Hg or <28 mm Hg, representing the upper and lower limits in the study, had greater rates of intubation, critical care admission, and mortality.⁴² The patients in this cohort with higher EtCO₂ were likely tiring after prolonged hyperventilation and therefore would be more likely to need ventilatory support. Those on the lower end were likely hyperventilating and had not yet tired out. It is important to note that while arrival EtCO₂ levels may aid in determining the more critically ill, post-treatment levels were not found to have a statistical difference in determining disposition in patients with asthma or COPD.⁴³

Caution is advised when attempting to use EtCO₂ to approximate an arterial blood gas CO₂ (PaCO₂). While EtCO₂ can correlate with PaCO₂ within 5 mm Hg in greater than 80% of patients with dyspnea,⁴⁴ large discrepancies are common depending on the disease state.⁴⁵ In general, the EtCO₂ should always be lower than the PaCO₂ due to the contribution to the ETCO₂ from dead space, which has a low CO₂ content due to lack of perfusion.

Sepsis

EtCO₂ may help identify septic patients given its inverse relationship with lactate levels.^46-49 In conditions of poor tissue perfusion, lactate builds up. This begins to make the blood acidotic in the form of newly acquired anions, with a resultant anion gap metabolic acidosis. The body then tries to acutely compensate for this by hyperventilating, resulting in the observed lowering of EtCO₂. Since lactate is a predictor of mortality in sepsis,⁵⁰ and monitoring lactate clearance to evaluate resuscitation efforts in sepsis is recommended,⁵¹ EtCO₂ could play a similar role. One group in particular has demonstrated that, when used with SIRS criteria, abnormally low prehospital EtCO₂ levels is predictive of sepsis and inhospital mortality, and is more predictive than SIRS criteria alone.^48,50 That said, EtCO₂ was not associated with lactate temporally at 3 and 6 hours,⁵¹ so it should not be used to guide resuscitation like a lactate clearance. It appears that EtCO₂ may be helpful for triage in sepsis, but more study is needed to determine the exact role particularly given most of the available research involves multiple studies from one group.^47,48,52

Diabetic Ketoacidosis

Initial bicarbonate levels and venous pH are associated with low EtCO₂ readings in diabetic ketoacidosis (DKA).^54,55 This could have many practical uses, in particular for patients presenting with hyperglycemia to rule out DKA. One study demonstrated that a blood glucose >250 mg/dL and capnography of >24.5 mm Hg had 90% sensitivity for excluding DKA.⁵⁵ A value of 35 mm Hg or greater demonstrated 100% sensitivity for excluding DKA in patients with initial glucose >550 mg/dL,⁵⁶ though this blood glucose is not practical, as this excludes many patients the EP would seek to rule out DKA (recall that blood glucose only has to be >250 mg/dL for the diagnosis). Smaller studies focused on the pediatric population found a 100% sensitivity marker for DKA varied from >30 to >36 mm Hg.^57,58 Clearly a role exists, but no study has demonstrated sufficient sensitivity for ruling out DKA with EtCO₂ and blood glucose alone within the framework of clinically relevant values.

Trauma

As described above, low EtCO₂ is inversely correlated with lactate.⁴⁶ Because of this, it could theoretically be a marker of hypoperfusion in trauma. Initial EtCO₂ values <25 mm Hg have been associated with mortality and hemorrhage in intubated trauma patients,⁵⁹ as well as mortality prior to discharge in nonintubated trauma patients.⁶⁰ However, it did not demonstrate added clinical utility when combined with Glasgow Coma Scale (GCS) score, systolic blood pressure, and age in predicting severe injury.⁶¹

Pulmonary Embolism

A pulmonary embolism (PE) causes a blockage in blood flow to alveoli, which results in a decrease in CO₂ transportation to the alveoli and thus lower EtCO₂, while also widening the gradient between PaCO₂ and EtCO₂.³⁷ Because of this, it has a theoretical role in the diagnosis of PE, though numerous studies have demonstrated that EtCO₂ alone is not sensitive nor specific enough for this role.^62-66 In a recent meta-analysis, a pretest probability of 10% could lead to a posttest probability of 3% using capnography.⁶² While further study is needed before recommendation, this indicates that capnography could obviate the need for imaging in low to intermediate risk patients either after a positive D-Dimer or instead of obtaining a D-dimer.^62-64

Simply measuring an initial EtCO₂ as a triage vital sign may have added benefit to the EP, and consideration could be made for making this a policy in your ED. One study demonstrated that abnormal initial EtCO₂ (outside of 35-45 mm Hg) was predictive of admisison (RR 2.5, 95% CI 1.5-4.0).⁶⁷ An abnormal EtCO₂ (outside of 31-41 mm Hg for this study) was 93% sensitive (95% CI 79-98%), with expectedly low specificity of 44% (95% CI 41-48%) for mortality prior to discharge.⁴⁷ This potential vital sign may be treated similarly to tachycardia; while an abnormal heart rate should increase a clinician’s concern for a pathological condition, it needs to be taken in context of the situation to accurately interpret it.

Summary

Capnography has numerous uses in the ED in both intubated and spontaneously breathing patients. Quantitative capnography is the standard of care for confirming endotracheal intubation. It is recommended as an aide in maximizing chest compressions during cardiac arrest and can assist in prognostication. It rapidly identifies hypoventilation during procedural sedation. It also has many more potential applications that continue to be explored in areas such as respiratory distress, sepsis, trauma, DKA, and PE. Ultimately, capnography should always be used in association with the remainder of the clinical assessment.

“Parenthood in the United States has become much more demanding than it used to be.” It is hard to argue with this opening sentence in Clair Cain Miller’s op-ed piece titled “The Relentlessness of Modern Parenting,” published in the Dec. 25, 2018, electronic edition of the New York Times. But just in case you don’t agree with her premise, she lays out her case with evidence that parents in this country are investing more time, attention, and money into raising their children than was the norm several decades ago. She goes on to describe how this “intensive parenting” is taking its toll on parents on both sides of our nation’s widening economic divide. I’m sure you have seen it in your office in the tired faces and stooped shoulders of your patients’ parents. You may even be struggling yourself to find the time and energy to be the parent you believe your children need and deserve.

ftwitty/Getty Images

While there is debate on whether “parent” is inherently a verb or a noun (“Parent is a Noun, Not a Verb,” Cliff Price, the Australian Family Association; “Parent is a Verb – and we All do it,” Zaeli Kane, mother.ly), it is clear that “parenting” used as a verb has become one of the hot topics in pediatrics over the last quarter century and with it an epidemic of parental anxiety. What are the driving forces behind this shift in attitude? How has a relatively relaxed nature-will-take-its-course philosophy become an anxiety-provoking, stress-inducing phenomenon that will inevitably result in a disturbed and disappointed adult without a parent’s relentless attention to creating a nurturing and optimally stimulating environment?

Of course, parents have always worried about the health of their children and hope that they will be successful, regardless of how one defines success. But this natural parental concern seems to have gotten out of hand.

Is it because North Americans are having fewer children? Is it because in smaller families children become adults with little or no practical experience with hands-on child rearing? Are parents reacting to the predictions that the next generation may not be able to earn enough to match their parents’ lifestyle?

How much blame should fall on those of us who market ourselves as child health experts? Have we failed to put the research supporting the importance of early life experiences in the proper perspective? Are our recommendations creating unrealistic goals for parents? The American Academy of Pediatrics advice on breastfeeding duration and room sharing come to mind immediately. How realistic is it for parents to coview the majority of television shows their children are watching?

On one hand, we are beginning to realize that free play is important, but for years pediatricians have been one of the loudest voices supporting playground and toy safety. These two initiatives can certainly coexist, but I fear that at times we have begun to sound a bit like that annoying parent who is constantly warning his or her child, “Don’t do that, you’ll hurt yourself?”

Have we become the worry merchants? As a marketing strategy it seems to be working well. If we generate enough advice that supports an intensive parenting style, we can fill our waiting rooms with families struggling to meet the expectations we have been promoting.

A child can thrive without intensive parenting as long as he feels loved and he has been provided an environment with sensible limits to keep him safe. It is our job to help parents create that child-friendly discipline structure and then encourage them to step back.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@mdedge.com.

“Parenthood in the United States has become much more demanding than it used to be.” It is hard to argue with this opening sentence in Clair Cain Miller’s op-ed piece titled “The Relentlessness of Modern Parenting,” published in the Dec. 25, 2018, electronic edition of the New York Times. But just in case you don’t agree with her premise, she lays out her case with evidence that parents in this country are investing more time, attention, and money into raising their children than was the norm several decades ago. She goes on to describe how this “intensive parenting” is taking its toll on parents on both sides of our nation’s widening economic divide. I’m sure you have seen it in your office in the tired faces and stooped shoulders of your patients’ parents. You may even be struggling yourself to find the time and energy to be the parent you believe your children need and deserve.

ftwitty/Getty Images

While there is debate on whether “parent” is inherently a verb or a noun (“Parent is a Noun, Not a Verb,” Cliff Price, the Australian Family Association; “Parent is a Verb – and we All do it,” Zaeli Kane, mother.ly), it is clear that “parenting” used as a verb has become one of the hot topics in pediatrics over the last quarter century and with it an epidemic of parental anxiety. What are the driving forces behind this shift in attitude? How has a relatively relaxed nature-will-take-its-course philosophy become an anxiety-provoking, stress-inducing phenomenon that will inevitably result in a disturbed and disappointed adult without a parent’s relentless attention to creating a nurturing and optimally stimulating environment?

Of course, parents have always worried about the health of their children and hope that they will be successful, regardless of how one defines success. But this natural parental concern seems to have gotten out of hand.

Is it because North Americans are having fewer children? Is it because in smaller families children become adults with little or no practical experience with hands-on child rearing? Are parents reacting to the predictions that the next generation may not be able to earn enough to match their parents’ lifestyle?

How much blame should fall on those of us who market ourselves as child health experts? Have we failed to put the research supporting the importance of early life experiences in the proper perspective? Are our recommendations creating unrealistic goals for parents? The American Academy of Pediatrics advice on breastfeeding duration and room sharing come to mind immediately. How realistic is it for parents to coview the majority of television shows their children are watching?

On one hand, we are beginning to realize that free play is important, but for years pediatricians have been one of the loudest voices supporting playground and toy safety. These two initiatives can certainly coexist, but I fear that at times we have begun to sound a bit like that annoying parent who is constantly warning his or her child, “Don’t do that, you’ll hurt yourself?”

Have we become the worry merchants? As a marketing strategy it seems to be working well. If we generate enough advice that supports an intensive parenting style, we can fill our waiting rooms with families struggling to meet the expectations we have been promoting.

A child can thrive without intensive parenting as long as he feels loved and he has been provided an environment with sensible limits to keep him safe. It is our job to help parents create that child-friendly discipline structure and then encourage them to step back.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@mdedge.com.

“Parenthood in the United States has become much more demanding than it used to be.” It is hard to argue with this opening sentence in Clair Cain Miller’s op-ed piece titled “The Relentlessness of Modern Parenting,” published in the Dec. 25, 2018, electronic edition of the New York Times. But just in case you don’t agree with her premise, she lays out her case with evidence that parents in this country are investing more time, attention, and money into raising their children than was the norm several decades ago. She goes on to describe how this “intensive parenting” is taking its toll on parents on both sides of our nation’s widening economic divide. I’m sure you have seen it in your office in the tired faces and stooped shoulders of your patients’ parents. You may even be struggling yourself to find the time and energy to be the parent you believe your children need and deserve.

ftwitty/Getty Images

While there is debate on whether “parent” is inherently a verb or a noun (“Parent is a Noun, Not a Verb,” Cliff Price, the Australian Family Association; “Parent is a Verb – and we All do it,” Zaeli Kane, mother.ly), it is clear that “parenting” used as a verb has become one of the hot topics in pediatrics over the last quarter century and with it an epidemic of parental anxiety. What are the driving forces behind this shift in attitude? How has a relatively relaxed nature-will-take-its-course philosophy become an anxiety-provoking, stress-inducing phenomenon that will inevitably result in a disturbed and disappointed adult without a parent’s relentless attention to creating a nurturing and optimally stimulating environment?

Of course, parents have always worried about the health of their children and hope that they will be successful, regardless of how one defines success. But this natural parental concern seems to have gotten out of hand.

Is it because North Americans are having fewer children? Is it because in smaller families children become adults with little or no practical experience with hands-on child rearing? Are parents reacting to the predictions that the next generation may not be able to earn enough to match their parents’ lifestyle?

How much blame should fall on those of us who market ourselves as child health experts? Have we failed to put the research supporting the importance of early life experiences in the proper perspective? Are our recommendations creating unrealistic goals for parents? The American Academy of Pediatrics advice on breastfeeding duration and room sharing come to mind immediately. How realistic is it for parents to coview the majority of television shows their children are watching?

On one hand, we are beginning to realize that free play is important, but for years pediatricians have been one of the loudest voices supporting playground and toy safety. These two initiatives can certainly coexist, but I fear that at times we have begun to sound a bit like that annoying parent who is constantly warning his or her child, “Don’t do that, you’ll hurt yourself?”

Have we become the worry merchants? As a marketing strategy it seems to be working well. If we generate enough advice that supports an intensive parenting style, we can fill our waiting rooms with families struggling to meet the expectations we have been promoting.

A child can thrive without intensive parenting as long as he feels loved and he has been provided an environment with sensible limits to keep him safe. It is our job to help parents create that child-friendly discipline structure and then encourage them to step back.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@mdedge.com.