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Pseudomonas infection in patients with noncystic fibrosis bronchiectasis
Pseudomonas aeruginosa is a clinically important organism that infects patients with noncystic fibrosis bronchiectasis (NCFB). In the United States, the estimated prevalence of NCFB is 213 per 100,000 across all age groups and 813 per 100,000 in the over 65 age group.1 A retrospective cohort study suggests the incidence of NCFB as ascertained from International Classification of Diseases codes may significantly underestimate its true prevalence.2
As the incidence of patients with NCFB continues to increase, the impact of the Pseudomonas infection is expected to grow. A recent retrospective cohort study of commercial claims from IQVIA’s PharMetrics Plus database for the period 2006 to 2020 showed that patients with NCFB and Pseudomonas infection had on average 2.58 hospital admissions per year, with a mean length of stay of 9.94 (± 11.06) days, compared with 1.18 admissions per year, with a mean length of stay of 6.5 (± 8.42) days, in patients with Pseudomonas-negative NCFB. The same trend applied to 30-day readmissions and ICU admissions, 1.32 (± 2.51 days) vs 0.47 (± 1.30 days) and 0.95 (± 1.62 days) vs 0.33 (± 0.76 days), respectively. The differential cost of care per patient per year between patients with NCFB with and without Pseudomonas infection ranged from $55,225 to $315,901.3
Recent data from the United States Bronchiectasis Registry showed the probability of acquiring Pseudomonas aeruginosa was 3% annually.4 The prevalence of Pseudomonas infection in a large, geographically diverse cohort in the United States was quoted at 15%.5 A retrospective analysis of the European Bronchiectasis Registry database showed Pseudomonas infection was the most commonly isolated pathogen (21.8%).6
Given the high incidence and prevalence of NCFB, the high prevalence of Pseudomonas infection in patients with NCFB, and the associated costs and morbidity from infection, identifying effective treatments has become a priority. The British, Spanish (SEPAR), South African, and European bronchiectasis guidelines outline several antibiotic regimens meant to achieve eradication. Generally, there is induction with a (1) quinolone, (2) β-lactam + aminoglycoside, or (3) quinolone with an inhaled antibiotic followed by three months of maintenance inhaled antibiotics.7-10 SEPAR allows for retreatment for recurrence at any time during the first year with any regimen.
For chronic Pseudomonas infection, SEPAR recommends treatment with inhaled antibiotics for patients with more than two exacerbations or one hospitalization, while the threshold in the British and European guidelines is more than three exacerbations. Azithromycin may be used for those who are intolerant or allergic to the nebulized antibiotics. It is worth noting that in the United States, the antibiotics colistin, ciprofloxacin, aztreonam, gentamicin, and tobramycin are administered off label for this indication. A systematic review found a 10% rate of bronchospasm in the treated group compared with 2.3% in the control group, and premedication with albuterol is often needed.11
Unfortunately, the data supporting the listed eradication and suppressive regimens are weak. A systematic review and meta-analysis of six observational studies including 289 patients showed a 12-month eradication rate of only 40% (95% CI, 34-45; P < 0.00001; I2 = 0).12 These results are disappointing and identify a need for further research into the manner in which Pseudomonas infection interacts with the host lung.
We currently know Pseudomonas infection evades antibiotics and host defenses by accumulating mutations and deletions. These include loss-of-function mutations in mucA (mucoidy), lasR (quorum-sensing), mexS (regulates the antibiotic efflux pump), and other genes related to the production of the polysaccharides Psl and Pel (which contribute to biofilm formation).13 There may also be differences in low and high bacteria microbial networks that interact differently with host cytokines to create an unstable environment that predisposes to exacerbation.14
In an attempt to improve our eradication and suppression rates, investigators have begun to target specific aspects of Pseudomonas infection behavior. The GREAT-2 trial compares gremubamab (a bivalent, bispecific, monoclonal antibody targeting Psl exopolysaccharide and the type 3 secretion system component of PcrV) with placebo in patients with chronic Pseudomonas infection. A phase II trial with the phosphodiesterase inhibitor esifentrine, a phase III trial with a reversible DPP1 inhibitor called brensocatib (ASPEN), and a phase II trial with the CatC inhibitor BI 1291583 (Airleaf) are also being conducted. Each of these agents targets mediators of neutrophil inflammation.
In summary, NCFB with Pseudomonas infection is common and leads to an increase in costs, respiratory exacerbations, and hospitalizations. While eradication and suppression are recommended, they are difficult to achieve and require sustained durations of expensive medications that can be difficult to tolerate. Antibiotic therapies will continue to be studied (the ERASE randomized controlled trial to investigate the efficacy and safety of tobramycin to eradicate Pseudomonas infection is currently underway), but targeted therapies represent a promising new approach to combating this stubbornly resistant bacteria. The NCFB community will be watching closely to see whether medicines targeting molecular behavior and host interaction can achieve what antibiotic regimens thus far have not: consistent and sustainable eradication.
Dr. Green is Assistant Professor in Medicine, Medical Director, Bronchiectasis Program, UMass Chan/Baystate Health, Chest Infections Section, Member-at-Large
References
1. Weycker D, Hansen GL, Seifer FD. Prevalence and incidence of noncystic fibrosis bronchiectasis among US adults in 2013. Chron Respir Dis. 2017;14(4):377-384. doi: 10.1177/1479972317709649
2. Green O, Liautaud S, Knee A, Modahl L. Measuring accuracy of International Classification of Diseases codes in identification of patients with non-cystic fibrosis bronchiectasis. ERJ Open Res. 2024;10(2):00715-2023. doi: 10.1183/23120541.00715-2023
3. Franklin M, Minshall ME, Pontenani F, Devarajan S. Impact of Pseudomonas aeruginosa on resource utilization and costs in patients with exacerbated non-cystic fibrosis bronchiectasis. J Med Econ. 2024;27(1):671-677. doi: 10.1080/13696998.2024.2340382
4. Aksamit TR, Locantore N, Addrizzo-Harris D, et al. Five-year outcomes among U.S. bronchiectasis and NTM research registry patients. Am J Respir Crit Care Med. Accepted manuscript. Published online April 26, 2024.
5. Dean SG, Blakney RA, Ricotta EE, et al. Bronchiectasis-associated infections and outcomes in a large, geographically diverse electronic health record cohort in the United States. BMC Pulm Med. 2024;24(1):172. doi: 10.1186/s12890-024-02973-3
6. Chalmers JD, Polverino E, Crichton ML, et al. Bronchiectasis in Europe: data on disease characteristics from the European Bronchiectasis registry (EMBARC). Lancet Respir Med. 2023;11(7):637-649. doi: 10.1016/S2213-2600(23)00093-0
7. Polverino E, Goeminne PC, McDonnell MJ, et al. European Respiratory Society guidelines for the management of adult bronchiectasis. Eur Respir J. 2017;50(3):1700629. doi: 10.1183/13993003.00629-2017
8. Martínez-García MÁ, Máiz L, Olveira C, et al. Spanish guidelines on treatment of bronchiectasis in adults. Arch Bronconeumol. 2018;54(2):88-98. doi: 10.1016/j.arbres.2017.07.016
9. Hill AT, Sullivan AL, Chalmers JD, et al. British Thoracic Society guideline for bronchiectasis in adults. Thorax. 2019;74(Suppl 1):1-69. doi: 10.1136/thoraxjnl-2018-212463
10. Goolam Mahomed A, Maasdorp SD, Barnes R, et al. South African Thoracic Society position statement on the management of non-cystic fibrosis bronchiectasis in adults: 2023. Afr J Thorac Crit Care Med. 2023;29(2):10.7196/AJTCCM. 2023.v29i2.647. doi: 10.7196/AJTCCM.2023.v29i2.647
11. Brodt AM, Stovold E, Zhang L. Inhaled antibiotics for stable non-cystic fibrosis bronchiectasis: a systematic review. Eur Respir J. 2014;44(2):382-393. doi: 10.1183/09031936.00018414
12. Conceição M, Shteinberg M, Goeminne P, Altenburg J, Chalmers JD. Eradication treatment for Pseudomonas aeruginosa infection in adults with bronchiectasis: a systematic review and meta-analysis. Eur Respir Rev. 2024;33(171):230178. doi: 10.1183/16000617.0178-2023
13. Hilliam Y, Moore MP, Lamont IL, et al. Pseudomonas aeruginosa adaptation and diversification in the non-cystic fibrosis bronchiectasis lung. Eur Respir J. 2017;49(4):1602108. doi: 10.1183/13993003.02108-2016
14. Gramegna A, Kumar Narayana J, Amati F, et al. Microbial inflammatory networks in bronchiectasis exacerbators with Pseudomonas aeruginosa. Chest. 2023;164(1):65-68. doi: 10.1016/j.chest.2023.02.014
Pseudomonas aeruginosa is a clinically important organism that infects patients with noncystic fibrosis bronchiectasis (NCFB). In the United States, the estimated prevalence of NCFB is 213 per 100,000 across all age groups and 813 per 100,000 in the over 65 age group.1 A retrospective cohort study suggests the incidence of NCFB as ascertained from International Classification of Diseases codes may significantly underestimate its true prevalence.2
As the incidence of patients with NCFB continues to increase, the impact of the Pseudomonas infection is expected to grow. A recent retrospective cohort study of commercial claims from IQVIA’s PharMetrics Plus database for the period 2006 to 2020 showed that patients with NCFB and Pseudomonas infection had on average 2.58 hospital admissions per year, with a mean length of stay of 9.94 (± 11.06) days, compared with 1.18 admissions per year, with a mean length of stay of 6.5 (± 8.42) days, in patients with Pseudomonas-negative NCFB. The same trend applied to 30-day readmissions and ICU admissions, 1.32 (± 2.51 days) vs 0.47 (± 1.30 days) and 0.95 (± 1.62 days) vs 0.33 (± 0.76 days), respectively. The differential cost of care per patient per year between patients with NCFB with and without Pseudomonas infection ranged from $55,225 to $315,901.3
Recent data from the United States Bronchiectasis Registry showed the probability of acquiring Pseudomonas aeruginosa was 3% annually.4 The prevalence of Pseudomonas infection in a large, geographically diverse cohort in the United States was quoted at 15%.5 A retrospective analysis of the European Bronchiectasis Registry database showed Pseudomonas infection was the most commonly isolated pathogen (21.8%).6
Given the high incidence and prevalence of NCFB, the high prevalence of Pseudomonas infection in patients with NCFB, and the associated costs and morbidity from infection, identifying effective treatments has become a priority. The British, Spanish (SEPAR), South African, and European bronchiectasis guidelines outline several antibiotic regimens meant to achieve eradication. Generally, there is induction with a (1) quinolone, (2) β-lactam + aminoglycoside, or (3) quinolone with an inhaled antibiotic followed by three months of maintenance inhaled antibiotics.7-10 SEPAR allows for retreatment for recurrence at any time during the first year with any regimen.
For chronic Pseudomonas infection, SEPAR recommends treatment with inhaled antibiotics for patients with more than two exacerbations or one hospitalization, while the threshold in the British and European guidelines is more than three exacerbations. Azithromycin may be used for those who are intolerant or allergic to the nebulized antibiotics. It is worth noting that in the United States, the antibiotics colistin, ciprofloxacin, aztreonam, gentamicin, and tobramycin are administered off label for this indication. A systematic review found a 10% rate of bronchospasm in the treated group compared with 2.3% in the control group, and premedication with albuterol is often needed.11
Unfortunately, the data supporting the listed eradication and suppressive regimens are weak. A systematic review and meta-analysis of six observational studies including 289 patients showed a 12-month eradication rate of only 40% (95% CI, 34-45; P < 0.00001; I2 = 0).12 These results are disappointing and identify a need for further research into the manner in which Pseudomonas infection interacts with the host lung.
We currently know Pseudomonas infection evades antibiotics and host defenses by accumulating mutations and deletions. These include loss-of-function mutations in mucA (mucoidy), lasR (quorum-sensing), mexS (regulates the antibiotic efflux pump), and other genes related to the production of the polysaccharides Psl and Pel (which contribute to biofilm formation).13 There may also be differences in low and high bacteria microbial networks that interact differently with host cytokines to create an unstable environment that predisposes to exacerbation.14
In an attempt to improve our eradication and suppression rates, investigators have begun to target specific aspects of Pseudomonas infection behavior. The GREAT-2 trial compares gremubamab (a bivalent, bispecific, monoclonal antibody targeting Psl exopolysaccharide and the type 3 secretion system component of PcrV) with placebo in patients with chronic Pseudomonas infection. A phase II trial with the phosphodiesterase inhibitor esifentrine, a phase III trial with a reversible DPP1 inhibitor called brensocatib (ASPEN), and a phase II trial with the CatC inhibitor BI 1291583 (Airleaf) are also being conducted. Each of these agents targets mediators of neutrophil inflammation.
In summary, NCFB with Pseudomonas infection is common and leads to an increase in costs, respiratory exacerbations, and hospitalizations. While eradication and suppression are recommended, they are difficult to achieve and require sustained durations of expensive medications that can be difficult to tolerate. Antibiotic therapies will continue to be studied (the ERASE randomized controlled trial to investigate the efficacy and safety of tobramycin to eradicate Pseudomonas infection is currently underway), but targeted therapies represent a promising new approach to combating this stubbornly resistant bacteria. The NCFB community will be watching closely to see whether medicines targeting molecular behavior and host interaction can achieve what antibiotic regimens thus far have not: consistent and sustainable eradication.
Dr. Green is Assistant Professor in Medicine, Medical Director, Bronchiectasis Program, UMass Chan/Baystate Health, Chest Infections Section, Member-at-Large
References
1. Weycker D, Hansen GL, Seifer FD. Prevalence and incidence of noncystic fibrosis bronchiectasis among US adults in 2013. Chron Respir Dis. 2017;14(4):377-384. doi: 10.1177/1479972317709649
2. Green O, Liautaud S, Knee A, Modahl L. Measuring accuracy of International Classification of Diseases codes in identification of patients with non-cystic fibrosis bronchiectasis. ERJ Open Res. 2024;10(2):00715-2023. doi: 10.1183/23120541.00715-2023
3. Franklin M, Minshall ME, Pontenani F, Devarajan S. Impact of Pseudomonas aeruginosa on resource utilization and costs in patients with exacerbated non-cystic fibrosis bronchiectasis. J Med Econ. 2024;27(1):671-677. doi: 10.1080/13696998.2024.2340382
4. Aksamit TR, Locantore N, Addrizzo-Harris D, et al. Five-year outcomes among U.S. bronchiectasis and NTM research registry patients. Am J Respir Crit Care Med. Accepted manuscript. Published online April 26, 2024.
5. Dean SG, Blakney RA, Ricotta EE, et al. Bronchiectasis-associated infections and outcomes in a large, geographically diverse electronic health record cohort in the United States. BMC Pulm Med. 2024;24(1):172. doi: 10.1186/s12890-024-02973-3
6. Chalmers JD, Polverino E, Crichton ML, et al. Bronchiectasis in Europe: data on disease characteristics from the European Bronchiectasis registry (EMBARC). Lancet Respir Med. 2023;11(7):637-649. doi: 10.1016/S2213-2600(23)00093-0
7. Polverino E, Goeminne PC, McDonnell MJ, et al. European Respiratory Society guidelines for the management of adult bronchiectasis. Eur Respir J. 2017;50(3):1700629. doi: 10.1183/13993003.00629-2017
8. Martínez-García MÁ, Máiz L, Olveira C, et al. Spanish guidelines on treatment of bronchiectasis in adults. Arch Bronconeumol. 2018;54(2):88-98. doi: 10.1016/j.arbres.2017.07.016
9. Hill AT, Sullivan AL, Chalmers JD, et al. British Thoracic Society guideline for bronchiectasis in adults. Thorax. 2019;74(Suppl 1):1-69. doi: 10.1136/thoraxjnl-2018-212463
10. Goolam Mahomed A, Maasdorp SD, Barnes R, et al. South African Thoracic Society position statement on the management of non-cystic fibrosis bronchiectasis in adults: 2023. Afr J Thorac Crit Care Med. 2023;29(2):10.7196/AJTCCM. 2023.v29i2.647. doi: 10.7196/AJTCCM.2023.v29i2.647
11. Brodt AM, Stovold E, Zhang L. Inhaled antibiotics for stable non-cystic fibrosis bronchiectasis: a systematic review. Eur Respir J. 2014;44(2):382-393. doi: 10.1183/09031936.00018414
12. Conceição M, Shteinberg M, Goeminne P, Altenburg J, Chalmers JD. Eradication treatment for Pseudomonas aeruginosa infection in adults with bronchiectasis: a systematic review and meta-analysis. Eur Respir Rev. 2024;33(171):230178. doi: 10.1183/16000617.0178-2023
13. Hilliam Y, Moore MP, Lamont IL, et al. Pseudomonas aeruginosa adaptation and diversification in the non-cystic fibrosis bronchiectasis lung. Eur Respir J. 2017;49(4):1602108. doi: 10.1183/13993003.02108-2016
14. Gramegna A, Kumar Narayana J, Amati F, et al. Microbial inflammatory networks in bronchiectasis exacerbators with Pseudomonas aeruginosa. Chest. 2023;164(1):65-68. doi: 10.1016/j.chest.2023.02.014
Pseudomonas aeruginosa is a clinically important organism that infects patients with noncystic fibrosis bronchiectasis (NCFB). In the United States, the estimated prevalence of NCFB is 213 per 100,000 across all age groups and 813 per 100,000 in the over 65 age group.1 A retrospective cohort study suggests the incidence of NCFB as ascertained from International Classification of Diseases codes may significantly underestimate its true prevalence.2
As the incidence of patients with NCFB continues to increase, the impact of the Pseudomonas infection is expected to grow. A recent retrospective cohort study of commercial claims from IQVIA’s PharMetrics Plus database for the period 2006 to 2020 showed that patients with NCFB and Pseudomonas infection had on average 2.58 hospital admissions per year, with a mean length of stay of 9.94 (± 11.06) days, compared with 1.18 admissions per year, with a mean length of stay of 6.5 (± 8.42) days, in patients with Pseudomonas-negative NCFB. The same trend applied to 30-day readmissions and ICU admissions, 1.32 (± 2.51 days) vs 0.47 (± 1.30 days) and 0.95 (± 1.62 days) vs 0.33 (± 0.76 days), respectively. The differential cost of care per patient per year between patients with NCFB with and without Pseudomonas infection ranged from $55,225 to $315,901.3
Recent data from the United States Bronchiectasis Registry showed the probability of acquiring Pseudomonas aeruginosa was 3% annually.4 The prevalence of Pseudomonas infection in a large, geographically diverse cohort in the United States was quoted at 15%.5 A retrospective analysis of the European Bronchiectasis Registry database showed Pseudomonas infection was the most commonly isolated pathogen (21.8%).6
Given the high incidence and prevalence of NCFB, the high prevalence of Pseudomonas infection in patients with NCFB, and the associated costs and morbidity from infection, identifying effective treatments has become a priority. The British, Spanish (SEPAR), South African, and European bronchiectasis guidelines outline several antibiotic regimens meant to achieve eradication. Generally, there is induction with a (1) quinolone, (2) β-lactam + aminoglycoside, or (3) quinolone with an inhaled antibiotic followed by three months of maintenance inhaled antibiotics.7-10 SEPAR allows for retreatment for recurrence at any time during the first year with any regimen.
For chronic Pseudomonas infection, SEPAR recommends treatment with inhaled antibiotics for patients with more than two exacerbations or one hospitalization, while the threshold in the British and European guidelines is more than three exacerbations. Azithromycin may be used for those who are intolerant or allergic to the nebulized antibiotics. It is worth noting that in the United States, the antibiotics colistin, ciprofloxacin, aztreonam, gentamicin, and tobramycin are administered off label for this indication. A systematic review found a 10% rate of bronchospasm in the treated group compared with 2.3% in the control group, and premedication with albuterol is often needed.11
Unfortunately, the data supporting the listed eradication and suppressive regimens are weak. A systematic review and meta-analysis of six observational studies including 289 patients showed a 12-month eradication rate of only 40% (95% CI, 34-45; P < 0.00001; I2 = 0).12 These results are disappointing and identify a need for further research into the manner in which Pseudomonas infection interacts with the host lung.
We currently know Pseudomonas infection evades antibiotics and host defenses by accumulating mutations and deletions. These include loss-of-function mutations in mucA (mucoidy), lasR (quorum-sensing), mexS (regulates the antibiotic efflux pump), and other genes related to the production of the polysaccharides Psl and Pel (which contribute to biofilm formation).13 There may also be differences in low and high bacteria microbial networks that interact differently with host cytokines to create an unstable environment that predisposes to exacerbation.14
In an attempt to improve our eradication and suppression rates, investigators have begun to target specific aspects of Pseudomonas infection behavior. The GREAT-2 trial compares gremubamab (a bivalent, bispecific, monoclonal antibody targeting Psl exopolysaccharide and the type 3 secretion system component of PcrV) with placebo in patients with chronic Pseudomonas infection. A phase II trial with the phosphodiesterase inhibitor esifentrine, a phase III trial with a reversible DPP1 inhibitor called brensocatib (ASPEN), and a phase II trial with the CatC inhibitor BI 1291583 (Airleaf) are also being conducted. Each of these agents targets mediators of neutrophil inflammation.
In summary, NCFB with Pseudomonas infection is common and leads to an increase in costs, respiratory exacerbations, and hospitalizations. While eradication and suppression are recommended, they are difficult to achieve and require sustained durations of expensive medications that can be difficult to tolerate. Antibiotic therapies will continue to be studied (the ERASE randomized controlled trial to investigate the efficacy and safety of tobramycin to eradicate Pseudomonas infection is currently underway), but targeted therapies represent a promising new approach to combating this stubbornly resistant bacteria. The NCFB community will be watching closely to see whether medicines targeting molecular behavior and host interaction can achieve what antibiotic regimens thus far have not: consistent and sustainable eradication.
Dr. Green is Assistant Professor in Medicine, Medical Director, Bronchiectasis Program, UMass Chan/Baystate Health, Chest Infections Section, Member-at-Large
References
1. Weycker D, Hansen GL, Seifer FD. Prevalence and incidence of noncystic fibrosis bronchiectasis among US adults in 2013. Chron Respir Dis. 2017;14(4):377-384. doi: 10.1177/1479972317709649
2. Green O, Liautaud S, Knee A, Modahl L. Measuring accuracy of International Classification of Diseases codes in identification of patients with non-cystic fibrosis bronchiectasis. ERJ Open Res. 2024;10(2):00715-2023. doi: 10.1183/23120541.00715-2023
3. Franklin M, Minshall ME, Pontenani F, Devarajan S. Impact of Pseudomonas aeruginosa on resource utilization and costs in patients with exacerbated non-cystic fibrosis bronchiectasis. J Med Econ. 2024;27(1):671-677. doi: 10.1080/13696998.2024.2340382
4. Aksamit TR, Locantore N, Addrizzo-Harris D, et al. Five-year outcomes among U.S. bronchiectasis and NTM research registry patients. Am J Respir Crit Care Med. Accepted manuscript. Published online April 26, 2024.
5. Dean SG, Blakney RA, Ricotta EE, et al. Bronchiectasis-associated infections and outcomes in a large, geographically diverse electronic health record cohort in the United States. BMC Pulm Med. 2024;24(1):172. doi: 10.1186/s12890-024-02973-3
6. Chalmers JD, Polverino E, Crichton ML, et al. Bronchiectasis in Europe: data on disease characteristics from the European Bronchiectasis registry (EMBARC). Lancet Respir Med. 2023;11(7):637-649. doi: 10.1016/S2213-2600(23)00093-0
7. Polverino E, Goeminne PC, McDonnell MJ, et al. European Respiratory Society guidelines for the management of adult bronchiectasis. Eur Respir J. 2017;50(3):1700629. doi: 10.1183/13993003.00629-2017
8. Martínez-García MÁ, Máiz L, Olveira C, et al. Spanish guidelines on treatment of bronchiectasis in adults. Arch Bronconeumol. 2018;54(2):88-98. doi: 10.1016/j.arbres.2017.07.016
9. Hill AT, Sullivan AL, Chalmers JD, et al. British Thoracic Society guideline for bronchiectasis in adults. Thorax. 2019;74(Suppl 1):1-69. doi: 10.1136/thoraxjnl-2018-212463
10. Goolam Mahomed A, Maasdorp SD, Barnes R, et al. South African Thoracic Society position statement on the management of non-cystic fibrosis bronchiectasis in adults: 2023. Afr J Thorac Crit Care Med. 2023;29(2):10.7196/AJTCCM. 2023.v29i2.647. doi: 10.7196/AJTCCM.2023.v29i2.647
11. Brodt AM, Stovold E, Zhang L. Inhaled antibiotics for stable non-cystic fibrosis bronchiectasis: a systematic review. Eur Respir J. 2014;44(2):382-393. doi: 10.1183/09031936.00018414
12. Conceição M, Shteinberg M, Goeminne P, Altenburg J, Chalmers JD. Eradication treatment for Pseudomonas aeruginosa infection in adults with bronchiectasis: a systematic review and meta-analysis. Eur Respir Rev. 2024;33(171):230178. doi: 10.1183/16000617.0178-2023
13. Hilliam Y, Moore MP, Lamont IL, et al. Pseudomonas aeruginosa adaptation and diversification in the non-cystic fibrosis bronchiectasis lung. Eur Respir J. 2017;49(4):1602108. doi: 10.1183/13993003.02108-2016
14. Gramegna A, Kumar Narayana J, Amati F, et al. Microbial inflammatory networks in bronchiectasis exacerbators with Pseudomonas aeruginosa. Chest. 2023;164(1):65-68. doi: 10.1016/j.chest.2023.02.014
Sleep and athletic performance
Sleep Medicine Network
Respiratory-Related Sleep Disorders Section
Considering the recent Olympics, it is timely to review the importance of sleep for optimal athletic performance. When surveyed, 20% to 50% of athletes report poor or insufficient sleep, with consequences across four categories.1,2
Athletic performance: Objective measures of athletic performance, such as oxygen-carrying capacity during cardiopulmonary exercise and even sport-specific accuracy measures, like shooting percentage in basketball, have been shown to worsen with decreased sleep.
Decision-making: Insufficient sleep can impact split-second decisions in competition. In a study of male soccer players, sleep restriction negatively impacted perceptual abilities and reaction time. Traveling across time zones also appears to degrade performance; NBA players’ free-throw shooting worsens when they are jet-lagged.
Recovery and injury prevention: Getting less than eight hours of sleep may increase one’s chances of injury during performance. Sleepiness and insomnia are both independent risk factors for developing a concussion in college athletes and outperform more intuitive risk factors such as a history of prior concussion or participating in a high-risk sport. Impaired sleep directly alters secretion of growth hormone, cortisol, and proinflammatory cytokines—all of which can hinder recovery.
Mental health: Over a third of elite athletes are estimated to experience a mental health problem. A clear bidirectional relationship exists between mental health and sleep health, with important implications not only for optimal competitive mindset but also longevity and success over one’s career.
Although much of clinical sleep medicine focuses on pathology, we can also help our patients reach their athletic goals by strategizing ways to prioritize and improve sleep.
References
1. Cook JD, Charest J. Sleep and performance in professional athletes. Curr Sleep Med Rep. 2023;9(1):56-81.
2. Charest J, Grandner MA. Sleep and athletic performance: impacts on physical performance, mental performance, injury risk and recovery, and mental health. Sleep Med Clin. 2020;15(1):41-57.
Sleep Medicine Network
Respiratory-Related Sleep Disorders Section
Considering the recent Olympics, it is timely to review the importance of sleep for optimal athletic performance. When surveyed, 20% to 50% of athletes report poor or insufficient sleep, with consequences across four categories.1,2
Athletic performance: Objective measures of athletic performance, such as oxygen-carrying capacity during cardiopulmonary exercise and even sport-specific accuracy measures, like shooting percentage in basketball, have been shown to worsen with decreased sleep.
Decision-making: Insufficient sleep can impact split-second decisions in competition. In a study of male soccer players, sleep restriction negatively impacted perceptual abilities and reaction time. Traveling across time zones also appears to degrade performance; NBA players’ free-throw shooting worsens when they are jet-lagged.
Recovery and injury prevention: Getting less than eight hours of sleep may increase one’s chances of injury during performance. Sleepiness and insomnia are both independent risk factors for developing a concussion in college athletes and outperform more intuitive risk factors such as a history of prior concussion or participating in a high-risk sport. Impaired sleep directly alters secretion of growth hormone, cortisol, and proinflammatory cytokines—all of which can hinder recovery.
Mental health: Over a third of elite athletes are estimated to experience a mental health problem. A clear bidirectional relationship exists between mental health and sleep health, with important implications not only for optimal competitive mindset but also longevity and success over one’s career.
Although much of clinical sleep medicine focuses on pathology, we can also help our patients reach their athletic goals by strategizing ways to prioritize and improve sleep.
References
1. Cook JD, Charest J. Sleep and performance in professional athletes. Curr Sleep Med Rep. 2023;9(1):56-81.
2. Charest J, Grandner MA. Sleep and athletic performance: impacts on physical performance, mental performance, injury risk and recovery, and mental health. Sleep Med Clin. 2020;15(1):41-57.
Sleep Medicine Network
Respiratory-Related Sleep Disorders Section
Considering the recent Olympics, it is timely to review the importance of sleep for optimal athletic performance. When surveyed, 20% to 50% of athletes report poor or insufficient sleep, with consequences across four categories.1,2
Athletic performance: Objective measures of athletic performance, such as oxygen-carrying capacity during cardiopulmonary exercise and even sport-specific accuracy measures, like shooting percentage in basketball, have been shown to worsen with decreased sleep.
Decision-making: Insufficient sleep can impact split-second decisions in competition. In a study of male soccer players, sleep restriction negatively impacted perceptual abilities and reaction time. Traveling across time zones also appears to degrade performance; NBA players’ free-throw shooting worsens when they are jet-lagged.
Recovery and injury prevention: Getting less than eight hours of sleep may increase one’s chances of injury during performance. Sleepiness and insomnia are both independent risk factors for developing a concussion in college athletes and outperform more intuitive risk factors such as a history of prior concussion or participating in a high-risk sport. Impaired sleep directly alters secretion of growth hormone, cortisol, and proinflammatory cytokines—all of which can hinder recovery.
Mental health: Over a third of elite athletes are estimated to experience a mental health problem. A clear bidirectional relationship exists between mental health and sleep health, with important implications not only for optimal competitive mindset but also longevity and success over one’s career.
Although much of clinical sleep medicine focuses on pathology, we can also help our patients reach their athletic goals by strategizing ways to prioritize and improve sleep.
References
1. Cook JD, Charest J. Sleep and performance in professional athletes. Curr Sleep Med Rep. 2023;9(1):56-81.
2. Charest J, Grandner MA. Sleep and athletic performance: impacts on physical performance, mental performance, injury risk and recovery, and mental health. Sleep Med Clin. 2020;15(1):41-57.
The gas stove: Friend or foe?
Diffuse Lung Disease and Lung Transplant Network
Occupational and Environmental Health Section
The kitchen is considered the heart of the home, but recent discoveries have raised concerns about whether this beloved space might also pose hidden health risks. Gas stoves, present in 38% of U.S. homes, generate multiple pollutants including nitrogen dioxide (NO₂), a known respiratory irritant.1 Studies have identified a correlation between NO₂ levels and respiratory conditions, with children being particularly vulnerable.2 The association between domestic NO₂ exposure from gas stoves and conditions such as asthma has led to increased scrutiny of indoor air quality.
Studies have demonstrated that households using gas stoves have higher indoor NO₂ levels, with levels that far exceed the EPA national ambient air quality standards.3 While the predominance of studies have looked at a correlation with pediatric pulmonary processes, there is also evidence of increased lung function loss in patients who smoke and have COPD.4
Switching from gas to electric stoves is one proposed solution to mitigate exposure to NO₂. Evidence suggests that electric stoves significantly reduce indoor NO₂ levels, lowering the risk of respiratory illnesses.
Another proposed solution has been to utilize hoods; however, capture efficiency is variable and some recycle the air and return it indoors.5 While existing data indicates a connection between gas stove use and respiratory health risks, conclusive evidence examining the magnitude and mechanisms linking these factors to chronic lung diseases is still needed. Comprehensive studies will help determine whether the kitchen staple—a gas stove—is indeed a friend or a foe to our respiratory health.
References
1. U.S. Energy Information Administration, Appliances in U.S. homes, by household income, 2020. https://www.eia.gov/consumption/residential/data/2020/hc/pdf/HC%203.5.pdf. Accessed September 10, 2024.
2. Belanger K, Holford TR, Gent JF, Hill ME, Kezik JM, Leaderer BP. Household levels of nitrogen dioxide and pediatric asthma severity. Epidemiology. 2013;24(2):320-330.
3. Singer BC, Pass RZ, Delp WW, Lorenzetti DM, Maddalena RL. Pollutant concentrations and emission rates from natural gas cooking burners without and with range hood exhaust in nine California homes. Building and Environment. 2017;122:215-229.
4. Hansel NN, Woo H, Koehler K, et al. Indoor pollution and lung function decline in current and former smokers: SPIROMICS AIR. Am J Respir Crit Care Med. 2023;208(10):1042-1051.
5. Nassikas NJ, McCormack MC, Ewart G, et al. Indoor air sources of outdoor air pollution: health consequences, policy, and recommendations: an Official American Thoracic Society Workshop report. Ann Am Thorac Soc. 2024;21(3), 365-376.
Diffuse Lung Disease and Lung Transplant Network
Occupational and Environmental Health Section
The kitchen is considered the heart of the home, but recent discoveries have raised concerns about whether this beloved space might also pose hidden health risks. Gas stoves, present in 38% of U.S. homes, generate multiple pollutants including nitrogen dioxide (NO₂), a known respiratory irritant.1 Studies have identified a correlation between NO₂ levels and respiratory conditions, with children being particularly vulnerable.2 The association between domestic NO₂ exposure from gas stoves and conditions such as asthma has led to increased scrutiny of indoor air quality.
Studies have demonstrated that households using gas stoves have higher indoor NO₂ levels, with levels that far exceed the EPA national ambient air quality standards.3 While the predominance of studies have looked at a correlation with pediatric pulmonary processes, there is also evidence of increased lung function loss in patients who smoke and have COPD.4
Switching from gas to electric stoves is one proposed solution to mitigate exposure to NO₂. Evidence suggests that electric stoves significantly reduce indoor NO₂ levels, lowering the risk of respiratory illnesses.
Another proposed solution has been to utilize hoods; however, capture efficiency is variable and some recycle the air and return it indoors.5 While existing data indicates a connection between gas stove use and respiratory health risks, conclusive evidence examining the magnitude and mechanisms linking these factors to chronic lung diseases is still needed. Comprehensive studies will help determine whether the kitchen staple—a gas stove—is indeed a friend or a foe to our respiratory health.
References
1. U.S. Energy Information Administration, Appliances in U.S. homes, by household income, 2020. https://www.eia.gov/consumption/residential/data/2020/hc/pdf/HC%203.5.pdf. Accessed September 10, 2024.
2. Belanger K, Holford TR, Gent JF, Hill ME, Kezik JM, Leaderer BP. Household levels of nitrogen dioxide and pediatric asthma severity. Epidemiology. 2013;24(2):320-330.
3. Singer BC, Pass RZ, Delp WW, Lorenzetti DM, Maddalena RL. Pollutant concentrations and emission rates from natural gas cooking burners without and with range hood exhaust in nine California homes. Building and Environment. 2017;122:215-229.
4. Hansel NN, Woo H, Koehler K, et al. Indoor pollution and lung function decline in current and former smokers: SPIROMICS AIR. Am J Respir Crit Care Med. 2023;208(10):1042-1051.
5. Nassikas NJ, McCormack MC, Ewart G, et al. Indoor air sources of outdoor air pollution: health consequences, policy, and recommendations: an Official American Thoracic Society Workshop report. Ann Am Thorac Soc. 2024;21(3), 365-376.
Diffuse Lung Disease and Lung Transplant Network
Occupational and Environmental Health Section
The kitchen is considered the heart of the home, but recent discoveries have raised concerns about whether this beloved space might also pose hidden health risks. Gas stoves, present in 38% of U.S. homes, generate multiple pollutants including nitrogen dioxide (NO₂), a known respiratory irritant.1 Studies have identified a correlation between NO₂ levels and respiratory conditions, with children being particularly vulnerable.2 The association between domestic NO₂ exposure from gas stoves and conditions such as asthma has led to increased scrutiny of indoor air quality.
Studies have demonstrated that households using gas stoves have higher indoor NO₂ levels, with levels that far exceed the EPA national ambient air quality standards.3 While the predominance of studies have looked at a correlation with pediatric pulmonary processes, there is also evidence of increased lung function loss in patients who smoke and have COPD.4
Switching from gas to electric stoves is one proposed solution to mitigate exposure to NO₂. Evidence suggests that electric stoves significantly reduce indoor NO₂ levels, lowering the risk of respiratory illnesses.
Another proposed solution has been to utilize hoods; however, capture efficiency is variable and some recycle the air and return it indoors.5 While existing data indicates a connection between gas stove use and respiratory health risks, conclusive evidence examining the magnitude and mechanisms linking these factors to chronic lung diseases is still needed. Comprehensive studies will help determine whether the kitchen staple—a gas stove—is indeed a friend or a foe to our respiratory health.
References
1. U.S. Energy Information Administration, Appliances in U.S. homes, by household income, 2020. https://www.eia.gov/consumption/residential/data/2020/hc/pdf/HC%203.5.pdf. Accessed September 10, 2024.
2. Belanger K, Holford TR, Gent JF, Hill ME, Kezik JM, Leaderer BP. Household levels of nitrogen dioxide and pediatric asthma severity. Epidemiology. 2013;24(2):320-330.
3. Singer BC, Pass RZ, Delp WW, Lorenzetti DM, Maddalena RL. Pollutant concentrations and emission rates from natural gas cooking burners without and with range hood exhaust in nine California homes. Building and Environment. 2017;122:215-229.
4. Hansel NN, Woo H, Koehler K, et al. Indoor pollution and lung function decline in current and former smokers: SPIROMICS AIR. Am J Respir Crit Care Med. 2023;208(10):1042-1051.
5. Nassikas NJ, McCormack MC, Ewart G, et al. Indoor air sources of outdoor air pollution: health consequences, policy, and recommendations: an Official American Thoracic Society Workshop report. Ann Am Thorac Soc. 2024;21(3), 365-376.
Prediction models in sepsis
Critical Care Network
Sepsis/Shock Section
Early recognition is the linchpin of sepsis management, as mortality from sepsis increases by 4% to 9% for every hour that diagnosis and treatment are delayed.1,2 Artificial intelligence (AI) and machine learning (ML) are increasingly featured in discussions and publications about sepsis care. Already ML models are embedded in electronic medical records (EMR), driving best-practice advisories that are presented to users.3 Epic, the EMR that serves over half of patients in the US, offers its own proprietary cognitive computing model for early detection.
As ML permeates the critical care space, it is increasingly important that clinicians understand the limitations of these models. Recently Kamran et al (NEJM AI) evaluated the Epic sepsis model with disappointing results after excluding cases already recognized by clinicians. The model achieved a positive predictive value of 5%, and 80% of high-risk sepsis cases were missed.3
An application study by Lilly et al (CHEST) showed that an ML model for clinically actionable events was more accurate with less alarm burden when compared to biomedical monitor alarms or telemedicine systems.4 The clinical utility of this model, however, remains questionable; presumably by the time a patient monitor has alarmed, the term “early recognition” can no longer be applied. In this study a significantly elevated false-positive rate required clinicians to review all cases prior to action.
ML models seem to offer incredible potential to clinicians. How they fit into current practice, however, deserves careful consideration. It may be that we just are not there yet.
References
1. Sepsis Alliance. (2024, June 19). Septic shock. 2024. https://www.sepsis.org/sepsisand/septic-shock/. Accessed September 10, 2024.
2. Djikic M, Milenkovic M, Stojadinovic M, et al. The six scoring systems’ prognostic value in predicting 24-hour mortality in septic patients. Eur Rev Med Pharmacol Sci. 2024;28(12):3849-3859.
3. Kamran F, Tjandra D, Heiler A, et al. Evaluation of sepsis prediction models before onset of treatment. NEJM AI. 2024.
4. Lilly CM, Kirk D, Pessach IM, et al. Application of machine learning models to biomedical and information system signals from critically ill adults. CHEST. 2024;165(5):1139-1148.
Critical Care Network
Sepsis/Shock Section
Early recognition is the linchpin of sepsis management, as mortality from sepsis increases by 4% to 9% for every hour that diagnosis and treatment are delayed.1,2 Artificial intelligence (AI) and machine learning (ML) are increasingly featured in discussions and publications about sepsis care. Already ML models are embedded in electronic medical records (EMR), driving best-practice advisories that are presented to users.3 Epic, the EMR that serves over half of patients in the US, offers its own proprietary cognitive computing model for early detection.
As ML permeates the critical care space, it is increasingly important that clinicians understand the limitations of these models. Recently Kamran et al (NEJM AI) evaluated the Epic sepsis model with disappointing results after excluding cases already recognized by clinicians. The model achieved a positive predictive value of 5%, and 80% of high-risk sepsis cases were missed.3
An application study by Lilly et al (CHEST) showed that an ML model for clinically actionable events was more accurate with less alarm burden when compared to biomedical monitor alarms or telemedicine systems.4 The clinical utility of this model, however, remains questionable; presumably by the time a patient monitor has alarmed, the term “early recognition” can no longer be applied. In this study a significantly elevated false-positive rate required clinicians to review all cases prior to action.
ML models seem to offer incredible potential to clinicians. How they fit into current practice, however, deserves careful consideration. It may be that we just are not there yet.
References
1. Sepsis Alliance. (2024, June 19). Septic shock. 2024. https://www.sepsis.org/sepsisand/septic-shock/. Accessed September 10, 2024.
2. Djikic M, Milenkovic M, Stojadinovic M, et al. The six scoring systems’ prognostic value in predicting 24-hour mortality in septic patients. Eur Rev Med Pharmacol Sci. 2024;28(12):3849-3859.
3. Kamran F, Tjandra D, Heiler A, et al. Evaluation of sepsis prediction models before onset of treatment. NEJM AI. 2024.
4. Lilly CM, Kirk D, Pessach IM, et al. Application of machine learning models to biomedical and information system signals from critically ill adults. CHEST. 2024;165(5):1139-1148.
Critical Care Network
Sepsis/Shock Section
Early recognition is the linchpin of sepsis management, as mortality from sepsis increases by 4% to 9% for every hour that diagnosis and treatment are delayed.1,2 Artificial intelligence (AI) and machine learning (ML) are increasingly featured in discussions and publications about sepsis care. Already ML models are embedded in electronic medical records (EMR), driving best-practice advisories that are presented to users.3 Epic, the EMR that serves over half of patients in the US, offers its own proprietary cognitive computing model for early detection.
As ML permeates the critical care space, it is increasingly important that clinicians understand the limitations of these models. Recently Kamran et al (NEJM AI) evaluated the Epic sepsis model with disappointing results after excluding cases already recognized by clinicians. The model achieved a positive predictive value of 5%, and 80% of high-risk sepsis cases were missed.3
An application study by Lilly et al (CHEST) showed that an ML model for clinically actionable events was more accurate with less alarm burden when compared to biomedical monitor alarms or telemedicine systems.4 The clinical utility of this model, however, remains questionable; presumably by the time a patient monitor has alarmed, the term “early recognition” can no longer be applied. In this study a significantly elevated false-positive rate required clinicians to review all cases prior to action.
ML models seem to offer incredible potential to clinicians. How they fit into current practice, however, deserves careful consideration. It may be that we just are not there yet.
References
1. Sepsis Alliance. (2024, June 19). Septic shock. 2024. https://www.sepsis.org/sepsisand/septic-shock/. Accessed September 10, 2024.
2. Djikic M, Milenkovic M, Stojadinovic M, et al. The six scoring systems’ prognostic value in predicting 24-hour mortality in septic patients. Eur Rev Med Pharmacol Sci. 2024;28(12):3849-3859.
3. Kamran F, Tjandra D, Heiler A, et al. Evaluation of sepsis prediction models before onset of treatment. NEJM AI. 2024.
4. Lilly CM, Kirk D, Pessach IM, et al. Application of machine learning models to biomedical and information system signals from critically ill adults. CHEST. 2024;165(5):1139-1148.
Lung ultrasound: An indispensable yet underutilized tool
Thoracic Oncology and Chest Procedures Network
Ultrasound and Chest Imaging Section
An assessment using bedside thoracic ultrasound (TUS) improves diagnostic evaluation and therapeutic management in critically ill patients without undue risk. With changes in diagnosis occurring in 23% of cases and alterations in management in 39% of critically ill patients, TUS can improve length of stay, reduce complications, minimize delays in therapy, and lower hospitalization costs.1 Compared with its cardiac counterpart, attaining proficiency in lung ultrasound (LUS) is easier.2 Intensivists are at risk of forgoing mastering LUS in favor of developing more difficult skills. Proficiency in LUS is essential, as more than half of TUS evaluations are for respiratory complaints and most findings are pulmonary.1
A quick bedside assessment outperforms chest radiographs and available clinical scores in distinguishing pneumonia from atelectasis. The presence of dynamic air bronchograms within the consolidation is 45% sensitive and 99% specific for pneumonia over atelectasis.3 When air bronchograms are static, the presence of flow on color Doppler is 98% sensitive and 68% specific for pneumonia over atelectasis. Similarly, a closer look at the pleural lining shows more than the presence or absence of lung sliding. The presence of fragmentation, irregularity, or thickening of pleural lines provides 100% specificity in discriminating a noncardiogenic interstitial pathology from cardiogenic pulmonary edema.4
LUS is the workhorse and unsung hero of point-of-care ultrasound. In the last year, LUS has shown utility beyond evaluation for pneumothorax, pulmonary edema, and pleural effusion. Its potential impact on diagnosis and management is still growing. We just need to take a closer look.
References
1. Heldeweg M, Lopez Matta JE, Pisani L, Slot S. The impact of thoracic ultrasound on clinical management of critically ill patients (UltraMan): an international prospective observational study. Crit Care Med. 2023;51:357-364.
2. Kraaijenbrink BVC, Mousa A, Bos LD, et al. Defining basic (lung) ultrasound skills: not so basic after all? Intensive Care Med. 2022;48:628–629.
3. Haaksma M, Smit J, Heldeweg M, Nooitgedacht J, de Grooth H. Extended lung ultrasound to differentiate between pneumonia and atelectasis in critically ill patients: a diagnostic accuracy study. Crit Care Med. 2022;50:750-759.
4. Heldeweg M, Smit M, Kramer-Elliott S, et al. Lung ultrasound signs to diagnose and discriminate interstitial syndromes in ICU patients: a diagnostic accuracy study in two cohorts. Crit Care Med. 2022;50(11):1607-1617.
Thoracic Oncology and Chest Procedures Network
Ultrasound and Chest Imaging Section
An assessment using bedside thoracic ultrasound (TUS) improves diagnostic evaluation and therapeutic management in critically ill patients without undue risk. With changes in diagnosis occurring in 23% of cases and alterations in management in 39% of critically ill patients, TUS can improve length of stay, reduce complications, minimize delays in therapy, and lower hospitalization costs.1 Compared with its cardiac counterpart, attaining proficiency in lung ultrasound (LUS) is easier.2 Intensivists are at risk of forgoing mastering LUS in favor of developing more difficult skills. Proficiency in LUS is essential, as more than half of TUS evaluations are for respiratory complaints and most findings are pulmonary.1
A quick bedside assessment outperforms chest radiographs and available clinical scores in distinguishing pneumonia from atelectasis. The presence of dynamic air bronchograms within the consolidation is 45% sensitive and 99% specific for pneumonia over atelectasis.3 When air bronchograms are static, the presence of flow on color Doppler is 98% sensitive and 68% specific for pneumonia over atelectasis. Similarly, a closer look at the pleural lining shows more than the presence or absence of lung sliding. The presence of fragmentation, irregularity, or thickening of pleural lines provides 100% specificity in discriminating a noncardiogenic interstitial pathology from cardiogenic pulmonary edema.4
LUS is the workhorse and unsung hero of point-of-care ultrasound. In the last year, LUS has shown utility beyond evaluation for pneumothorax, pulmonary edema, and pleural effusion. Its potential impact on diagnosis and management is still growing. We just need to take a closer look.
References
1. Heldeweg M, Lopez Matta JE, Pisani L, Slot S. The impact of thoracic ultrasound on clinical management of critically ill patients (UltraMan): an international prospective observational study. Crit Care Med. 2023;51:357-364.
2. Kraaijenbrink BVC, Mousa A, Bos LD, et al. Defining basic (lung) ultrasound skills: not so basic after all? Intensive Care Med. 2022;48:628–629.
3. Haaksma M, Smit J, Heldeweg M, Nooitgedacht J, de Grooth H. Extended lung ultrasound to differentiate between pneumonia and atelectasis in critically ill patients: a diagnostic accuracy study. Crit Care Med. 2022;50:750-759.
4. Heldeweg M, Smit M, Kramer-Elliott S, et al. Lung ultrasound signs to diagnose and discriminate interstitial syndromes in ICU patients: a diagnostic accuracy study in two cohorts. Crit Care Med. 2022;50(11):1607-1617.
Thoracic Oncology and Chest Procedures Network
Ultrasound and Chest Imaging Section
An assessment using bedside thoracic ultrasound (TUS) improves diagnostic evaluation and therapeutic management in critically ill patients without undue risk. With changes in diagnosis occurring in 23% of cases and alterations in management in 39% of critically ill patients, TUS can improve length of stay, reduce complications, minimize delays in therapy, and lower hospitalization costs.1 Compared with its cardiac counterpart, attaining proficiency in lung ultrasound (LUS) is easier.2 Intensivists are at risk of forgoing mastering LUS in favor of developing more difficult skills. Proficiency in LUS is essential, as more than half of TUS evaluations are for respiratory complaints and most findings are pulmonary.1
A quick bedside assessment outperforms chest radiographs and available clinical scores in distinguishing pneumonia from atelectasis. The presence of dynamic air bronchograms within the consolidation is 45% sensitive and 99% specific for pneumonia over atelectasis.3 When air bronchograms are static, the presence of flow on color Doppler is 98% sensitive and 68% specific for pneumonia over atelectasis. Similarly, a closer look at the pleural lining shows more than the presence or absence of lung sliding. The presence of fragmentation, irregularity, or thickening of pleural lines provides 100% specificity in discriminating a noncardiogenic interstitial pathology from cardiogenic pulmonary edema.4
LUS is the workhorse and unsung hero of point-of-care ultrasound. In the last year, LUS has shown utility beyond evaluation for pneumothorax, pulmonary edema, and pleural effusion. Its potential impact on diagnosis and management is still growing. We just need to take a closer look.
References
1. Heldeweg M, Lopez Matta JE, Pisani L, Slot S. The impact of thoracic ultrasound on clinical management of critically ill patients (UltraMan): an international prospective observational study. Crit Care Med. 2023;51:357-364.
2. Kraaijenbrink BVC, Mousa A, Bos LD, et al. Defining basic (lung) ultrasound skills: not so basic after all? Intensive Care Med. 2022;48:628–629.
3. Haaksma M, Smit J, Heldeweg M, Nooitgedacht J, de Grooth H. Extended lung ultrasound to differentiate between pneumonia and atelectasis in critically ill patients: a diagnostic accuracy study. Crit Care Med. 2022;50:750-759.
4. Heldeweg M, Smit M, Kramer-Elliott S, et al. Lung ultrasound signs to diagnose and discriminate interstitial syndromes in ICU patients: a diagnostic accuracy study in two cohorts. Crit Care Med. 2022;50(11):1607-1617.
2025 Crohn’s & Colitis Congress® Abstract Submissions
The 2025 Crohn’s & Colitis Congress®, a partnership of the Crohn’s & Colitis Foundation and AGA, is now accepting original inflammatory bowel disease (IBD)-research abstract submissions through Oct. 16. Abstracts are free to submit and may be selected for in-person lectures or poster presentations. Accepted abstracts will also be co-published in AGA’s Gastroenterology (https://www.gastrojournal.org/) and the Crohn’s & Colitis Foundation’s Inflammatory Bowel Diseases (https://academic.oup.com/ibdjournal).
Be sure to review the abstract submission guidelines and submit by 9 p.m. EDT, Wednesday, Oct. 16.
Presenting authors will receive notification of acceptance on Monday, Dec. 9.
The Crohn’s & Colitis Congress will take place Feb. 6-8, 2025, in San Francisco, California. It brings together the community of multidisciplinary experts and colleagues to revolutionize prevention, care and outcomes for IBD patients.
Learn alongside your colleagues and discover how to provide the absolute best care to those suffering with Crohn’s disease and ulcerative colitis.
The 2025 Crohn’s & Colitis Congress®, a partnership of the Crohn’s & Colitis Foundation and AGA, is now accepting original inflammatory bowel disease (IBD)-research abstract submissions through Oct. 16. Abstracts are free to submit and may be selected for in-person lectures or poster presentations. Accepted abstracts will also be co-published in AGA’s Gastroenterology (https://www.gastrojournal.org/) and the Crohn’s & Colitis Foundation’s Inflammatory Bowel Diseases (https://academic.oup.com/ibdjournal).
Be sure to review the abstract submission guidelines and submit by 9 p.m. EDT, Wednesday, Oct. 16.
Presenting authors will receive notification of acceptance on Monday, Dec. 9.
The Crohn’s & Colitis Congress will take place Feb. 6-8, 2025, in San Francisco, California. It brings together the community of multidisciplinary experts and colleagues to revolutionize prevention, care and outcomes for IBD patients.
Learn alongside your colleagues and discover how to provide the absolute best care to those suffering with Crohn’s disease and ulcerative colitis.
The 2025 Crohn’s & Colitis Congress®, a partnership of the Crohn’s & Colitis Foundation and AGA, is now accepting original inflammatory bowel disease (IBD)-research abstract submissions through Oct. 16. Abstracts are free to submit and may be selected for in-person lectures or poster presentations. Accepted abstracts will also be co-published in AGA’s Gastroenterology (https://www.gastrojournal.org/) and the Crohn’s & Colitis Foundation’s Inflammatory Bowel Diseases (https://academic.oup.com/ibdjournal).
Be sure to review the abstract submission guidelines and submit by 9 p.m. EDT, Wednesday, Oct. 16.
Presenting authors will receive notification of acceptance on Monday, Dec. 9.
The Crohn’s & Colitis Congress will take place Feb. 6-8, 2025, in San Francisco, California. It brings together the community of multidisciplinary experts and colleagues to revolutionize prevention, care and outcomes for IBD patients.
Learn alongside your colleagues and discover how to provide the absolute best care to those suffering with Crohn’s disease and ulcerative colitis.
Meet Our 10 Editorial Fellows
We are excited to announce the 2024-25 participants, who will gain hands-on experience and mentorship working closely with the editors and staff at the AGA journals over the next year.
The 10 editorial fellows (2 per journal) will learn about the entire editorial process, from manuscript submission to peer review to acceptance. They will participate in discussions and conferences with the boards of editors, assist with manuscript review, and help disseminate articles via their social media platforms.
Clinical Gastroenterology and Hepatology
Robyn Jordan, MD, MPH
Johns Hopkins Hospital, Baltimore | USA
Daryl Ramai, MD, MPH, MSc
Brigham and Women’s Hospital, Boston | USA
Cellular and Molecular Gastroenterology and Hepatology
Kole H. Buckley, PhD
University of Pennsylvania Perelman School of Medicine, Philadelphia | USA
Lin Y. Hung, PhD
New York University | USA
Gastroenterology
Corey J. Ketchem, MD
University of Pennsylvania, Philadelphia | USA
Rishad Khan, MD
University of Toronto | Canada
Gastro Hep Advances
Sasha Kapil, MD
UT Southwestern Medical Center, Dallas | USA
June Tome, MD
Mayo Clinic, Rochester, Minnesota | USA
Techniques and Innovations in Gastrointestinal Endoscopy
Thomas Enke, MD
University of Colorado, Aurora | USA
Sami Elamin, MD
Harvard, Beth Israel Deaconess Medical Center, Boston | USA
We are excited to announce the 2024-25 participants, who will gain hands-on experience and mentorship working closely with the editors and staff at the AGA journals over the next year.
The 10 editorial fellows (2 per journal) will learn about the entire editorial process, from manuscript submission to peer review to acceptance. They will participate in discussions and conferences with the boards of editors, assist with manuscript review, and help disseminate articles via their social media platforms.
Clinical Gastroenterology and Hepatology
Robyn Jordan, MD, MPH
Johns Hopkins Hospital, Baltimore | USA
Daryl Ramai, MD, MPH, MSc
Brigham and Women’s Hospital, Boston | USA
Cellular and Molecular Gastroenterology and Hepatology
Kole H. Buckley, PhD
University of Pennsylvania Perelman School of Medicine, Philadelphia | USA
Lin Y. Hung, PhD
New York University | USA
Gastroenterology
Corey J. Ketchem, MD
University of Pennsylvania, Philadelphia | USA
Rishad Khan, MD
University of Toronto | Canada
Gastro Hep Advances
Sasha Kapil, MD
UT Southwestern Medical Center, Dallas | USA
June Tome, MD
Mayo Clinic, Rochester, Minnesota | USA
Techniques and Innovations in Gastrointestinal Endoscopy
Thomas Enke, MD
University of Colorado, Aurora | USA
Sami Elamin, MD
Harvard, Beth Israel Deaconess Medical Center, Boston | USA
We are excited to announce the 2024-25 participants, who will gain hands-on experience and mentorship working closely with the editors and staff at the AGA journals over the next year.
The 10 editorial fellows (2 per journal) will learn about the entire editorial process, from manuscript submission to peer review to acceptance. They will participate in discussions and conferences with the boards of editors, assist with manuscript review, and help disseminate articles via their social media platforms.
Clinical Gastroenterology and Hepatology
Robyn Jordan, MD, MPH
Johns Hopkins Hospital, Baltimore | USA
Daryl Ramai, MD, MPH, MSc
Brigham and Women’s Hospital, Boston | USA
Cellular and Molecular Gastroenterology and Hepatology
Kole H. Buckley, PhD
University of Pennsylvania Perelman School of Medicine, Philadelphia | USA
Lin Y. Hung, PhD
New York University | USA
Gastroenterology
Corey J. Ketchem, MD
University of Pennsylvania, Philadelphia | USA
Rishad Khan, MD
University of Toronto | Canada
Gastro Hep Advances
Sasha Kapil, MD
UT Southwestern Medical Center, Dallas | USA
June Tome, MD
Mayo Clinic, Rochester, Minnesota | USA
Techniques and Innovations in Gastrointestinal Endoscopy
Thomas Enke, MD
University of Colorado, Aurora | USA
Sami Elamin, MD
Harvard, Beth Israel Deaconess Medical Center, Boston | USA
Creating a Planned Gift That’s Meaningful To You
The AGA Research Foundation has helped make significant strides in advancing the treatment and cure of digestive diseases by funding talented investigators.
Planning your gift to benefit AGA Research Foundation in the future is an opportunity to express what matters to you. As an AGA member, you can work with the AGA Research Foundation to ensure that your planned gift is designated for a purpose that meets your goals for leaving a legacy—such as research awards, support for specific programs, or unrestricted gifts to help meet the Foundation’s mission.
In as little as one sentence in your will and/or trust, you can complete your gift: “I give to AGA Research Foundation, a nonprofit corporation currently located at 4930 Del Ray Avenue, Bethesda, MD 20814, or its successor thereto, _________ [written amount or percentage of the estate or description of property] for its unrestricted charitable use and purpose.”
If you have named the AGA Research Foundation in your will or trust, please let us know so we can ensure that your gift is used according to your wishes. Notifying us of your plans will enable us to plan for the use of your future gift. However, if you prefer to remain anonymous, we will keep your name and gift in strict confidence.
Please contact foundation@gastro.org for more information. If you are considering a planned gift, consult with your own legal and tax advisors.
The AGA Research Foundation has helped make significant strides in advancing the treatment and cure of digestive diseases by funding talented investigators.
Planning your gift to benefit AGA Research Foundation in the future is an opportunity to express what matters to you. As an AGA member, you can work with the AGA Research Foundation to ensure that your planned gift is designated for a purpose that meets your goals for leaving a legacy—such as research awards, support for specific programs, or unrestricted gifts to help meet the Foundation’s mission.
In as little as one sentence in your will and/or trust, you can complete your gift: “I give to AGA Research Foundation, a nonprofit corporation currently located at 4930 Del Ray Avenue, Bethesda, MD 20814, or its successor thereto, _________ [written amount or percentage of the estate or description of property] for its unrestricted charitable use and purpose.”
If you have named the AGA Research Foundation in your will or trust, please let us know so we can ensure that your gift is used according to your wishes. Notifying us of your plans will enable us to plan for the use of your future gift. However, if you prefer to remain anonymous, we will keep your name and gift in strict confidence.
Please contact foundation@gastro.org for more information. If you are considering a planned gift, consult with your own legal and tax advisors.
The AGA Research Foundation has helped make significant strides in advancing the treatment and cure of digestive diseases by funding talented investigators.
Planning your gift to benefit AGA Research Foundation in the future is an opportunity to express what matters to you. As an AGA member, you can work with the AGA Research Foundation to ensure that your planned gift is designated for a purpose that meets your goals for leaving a legacy—such as research awards, support for specific programs, or unrestricted gifts to help meet the Foundation’s mission.
In as little as one sentence in your will and/or trust, you can complete your gift: “I give to AGA Research Foundation, a nonprofit corporation currently located at 4930 Del Ray Avenue, Bethesda, MD 20814, or its successor thereto, _________ [written amount or percentage of the estate or description of property] for its unrestricted charitable use and purpose.”
If you have named the AGA Research Foundation in your will or trust, please let us know so we can ensure that your gift is used according to your wishes. Notifying us of your plans will enable us to plan for the use of your future gift. However, if you prefer to remain anonymous, we will keep your name and gift in strict confidence.
Please contact foundation@gastro.org for more information. If you are considering a planned gift, consult with your own legal and tax advisors.
Hospital to home tracheostomy care
SLEEP MEDICINE NETWORK
Home-Based Mechanical Ventilation and Neuromuscular Section
Technological improvement has enhanced our ability to support these patients with complex conditions in their home settings. However, clinical practice guidelines are lacking, and current practice relies on a consensus of expert opinions.1-3
Once a patient who has had a tracheostomy begins transitioning care to home, identifying caregivers is vital.
Caregivers need to be educated on daily tracheostomy care, airway clearance, and ventilator management.
Protocols to standardize this transition, such as the “Trach Trail” protocol, help reduce ICU readmissions with new tracheostomies (P = .05), eliminate predischarge mortality (P = .05), and may decrease ICU length of stay (P = 0.72).4 Standardized protocols for aspects of tracheostomy care, such as the “Go-Bag” from Boston Children’s Hospital, ensure that a consistent approach keeps providers, families, and patients familiar with their equipment and safety procedures, improving outcomes and decreasing tracheostomy-related adverse events.4-6
Understanding the landscape surrounding which equipment companies have trained field respiratory therapists is crucial. Airway clearance is key to improving ventilation and oxygenation and maintaining tracheostomy patency. Knowing the types of airway clearance modalities used for each patient remains critical.
Trach care may look substantially different for some populations, like patients in the neonatal ICU. Trach changes may happen more frequently. Speaking valve times may be gradually increased while planning for possible decannulation. Skin care involving granulation tissue and stoma complications is particularly important for this population. Active infants need well-fitting trach ties to balance enough support to maintain their trach without causing skin breakdown or discomfort. Securing the trach to prevent pulling or dislodgement as infants become more active is crucial as developmental milestones are achieved.
We hope national societies prioritize standardizing care for this vulnerable population while promoting additional high-quality, patient-centered outcomes in research studies. Implementation strategies to promote interprofessional teams to enhance education, communication, and outcomes will reduce health care disparities.
References
1. Am J Respir Crit Care Med Vol 161. pp Sherman JM, Davis S, Albamonte-Petrick S, et al. Care of the child with a chronic tracheostomy. This official statement of the American Thoracic Society was adopted by the ATS Board of Directors, July 1999. Am J Respir Crit Care Med. 2000;161(1):297-308. doi: 10.1164/ajrccm.161.1.ats1-00 297-308, 2000
2. Mitchell RB, Hussey HM, Setzen G, et al. Clinical consensus statement: tracheostomy care. Otolaryngol Head Neck Surg. 2013;148(1):6-20. Preprint. Posted online September 18, 2012. PMID: 22990518. doi: 10.1177/0194599812460376
3. Sterni LM, Collaco JM, Baker CD, et al; ATS Pediatric Chronic Home Ventilation Workgroup. An official American Thoracic Society clinical practice guideline: pediatric chronic home invasive ventilation. Am J Respir Crit Care Med. 2016;193(8):e16-35. PMID: 27082538; PMCID: PMC5439679. doi: 10.1164/rccm.201602-0276ST
4. Cherney RL, Pandian V, Ninan A, et al. The Trach Trail: a systems-based pathway to improve quality of tracheostomy care and interdisciplinary collaboration. Otolaryngol Head Neck Surg. 2020;163(2):232-243. doi: 10.1177/0194599820917427
5. Brown J. Tracheostomy to noninvasive ventilation: from acute care to home. Sleep Med Clin. 2020;15(4):593-598. doi: 10.1016/j.jsmc.2020.08.003
6. Kohn J, McKeon M, Munhall D, Blanchette S, Wells S, Watters K. Standardization of pediatric tracheostomy care with “Go-bags.” Int J Pediatr Otorhinolaryngol. 2019;121:154-156. doi: 10.1016/j.ijporl.2019.03.022
SLEEP MEDICINE NETWORK
Home-Based Mechanical Ventilation and Neuromuscular Section
Technological improvement has enhanced our ability to support these patients with complex conditions in their home settings. However, clinical practice guidelines are lacking, and current practice relies on a consensus of expert opinions.1-3
Once a patient who has had a tracheostomy begins transitioning care to home, identifying caregivers is vital.
Caregivers need to be educated on daily tracheostomy care, airway clearance, and ventilator management.
Protocols to standardize this transition, such as the “Trach Trail” protocol, help reduce ICU readmissions with new tracheostomies (P = .05), eliminate predischarge mortality (P = .05), and may decrease ICU length of stay (P = 0.72).4 Standardized protocols for aspects of tracheostomy care, such as the “Go-Bag” from Boston Children’s Hospital, ensure that a consistent approach keeps providers, families, and patients familiar with their equipment and safety procedures, improving outcomes and decreasing tracheostomy-related adverse events.4-6
Understanding the landscape surrounding which equipment companies have trained field respiratory therapists is crucial. Airway clearance is key to improving ventilation and oxygenation and maintaining tracheostomy patency. Knowing the types of airway clearance modalities used for each patient remains critical.
Trach care may look substantially different for some populations, like patients in the neonatal ICU. Trach changes may happen more frequently. Speaking valve times may be gradually increased while planning for possible decannulation. Skin care involving granulation tissue and stoma complications is particularly important for this population. Active infants need well-fitting trach ties to balance enough support to maintain their trach without causing skin breakdown or discomfort. Securing the trach to prevent pulling or dislodgement as infants become more active is crucial as developmental milestones are achieved.
We hope national societies prioritize standardizing care for this vulnerable population while promoting additional high-quality, patient-centered outcomes in research studies. Implementation strategies to promote interprofessional teams to enhance education, communication, and outcomes will reduce health care disparities.
References
1. Am J Respir Crit Care Med Vol 161. pp Sherman JM, Davis S, Albamonte-Petrick S, et al. Care of the child with a chronic tracheostomy. This official statement of the American Thoracic Society was adopted by the ATS Board of Directors, July 1999. Am J Respir Crit Care Med. 2000;161(1):297-308. doi: 10.1164/ajrccm.161.1.ats1-00 297-308, 2000
2. Mitchell RB, Hussey HM, Setzen G, et al. Clinical consensus statement: tracheostomy care. Otolaryngol Head Neck Surg. 2013;148(1):6-20. Preprint. Posted online September 18, 2012. PMID: 22990518. doi: 10.1177/0194599812460376
3. Sterni LM, Collaco JM, Baker CD, et al; ATS Pediatric Chronic Home Ventilation Workgroup. An official American Thoracic Society clinical practice guideline: pediatric chronic home invasive ventilation. Am J Respir Crit Care Med. 2016;193(8):e16-35. PMID: 27082538; PMCID: PMC5439679. doi: 10.1164/rccm.201602-0276ST
4. Cherney RL, Pandian V, Ninan A, et al. The Trach Trail: a systems-based pathway to improve quality of tracheostomy care and interdisciplinary collaboration. Otolaryngol Head Neck Surg. 2020;163(2):232-243. doi: 10.1177/0194599820917427
5. Brown J. Tracheostomy to noninvasive ventilation: from acute care to home. Sleep Med Clin. 2020;15(4):593-598. doi: 10.1016/j.jsmc.2020.08.003
6. Kohn J, McKeon M, Munhall D, Blanchette S, Wells S, Watters K. Standardization of pediatric tracheostomy care with “Go-bags.” Int J Pediatr Otorhinolaryngol. 2019;121:154-156. doi: 10.1016/j.ijporl.2019.03.022
SLEEP MEDICINE NETWORK
Home-Based Mechanical Ventilation and Neuromuscular Section
Technological improvement has enhanced our ability to support these patients with complex conditions in their home settings. However, clinical practice guidelines are lacking, and current practice relies on a consensus of expert opinions.1-3
Once a patient who has had a tracheostomy begins transitioning care to home, identifying caregivers is vital.
Caregivers need to be educated on daily tracheostomy care, airway clearance, and ventilator management.
Protocols to standardize this transition, such as the “Trach Trail” protocol, help reduce ICU readmissions with new tracheostomies (P = .05), eliminate predischarge mortality (P = .05), and may decrease ICU length of stay (P = 0.72).4 Standardized protocols for aspects of tracheostomy care, such as the “Go-Bag” from Boston Children’s Hospital, ensure that a consistent approach keeps providers, families, and patients familiar with their equipment and safety procedures, improving outcomes and decreasing tracheostomy-related adverse events.4-6
Understanding the landscape surrounding which equipment companies have trained field respiratory therapists is crucial. Airway clearance is key to improving ventilation and oxygenation and maintaining tracheostomy patency. Knowing the types of airway clearance modalities used for each patient remains critical.
Trach care may look substantially different for some populations, like patients in the neonatal ICU. Trach changes may happen more frequently. Speaking valve times may be gradually increased while planning for possible decannulation. Skin care involving granulation tissue and stoma complications is particularly important for this population. Active infants need well-fitting trach ties to balance enough support to maintain their trach without causing skin breakdown or discomfort. Securing the trach to prevent pulling or dislodgement as infants become more active is crucial as developmental milestones are achieved.
We hope national societies prioritize standardizing care for this vulnerable population while promoting additional high-quality, patient-centered outcomes in research studies. Implementation strategies to promote interprofessional teams to enhance education, communication, and outcomes will reduce health care disparities.
References
1. Am J Respir Crit Care Med Vol 161. pp Sherman JM, Davis S, Albamonte-Petrick S, et al. Care of the child with a chronic tracheostomy. This official statement of the American Thoracic Society was adopted by the ATS Board of Directors, July 1999. Am J Respir Crit Care Med. 2000;161(1):297-308. doi: 10.1164/ajrccm.161.1.ats1-00 297-308, 2000
2. Mitchell RB, Hussey HM, Setzen G, et al. Clinical consensus statement: tracheostomy care. Otolaryngol Head Neck Surg. 2013;148(1):6-20. Preprint. Posted online September 18, 2012. PMID: 22990518. doi: 10.1177/0194599812460376
3. Sterni LM, Collaco JM, Baker CD, et al; ATS Pediatric Chronic Home Ventilation Workgroup. An official American Thoracic Society clinical practice guideline: pediatric chronic home invasive ventilation. Am J Respir Crit Care Med. 2016;193(8):e16-35. PMID: 27082538; PMCID: PMC5439679. doi: 10.1164/rccm.201602-0276ST
4. Cherney RL, Pandian V, Ninan A, et al. The Trach Trail: a systems-based pathway to improve quality of tracheostomy care and interdisciplinary collaboration. Otolaryngol Head Neck Surg. 2020;163(2):232-243. doi: 10.1177/0194599820917427
5. Brown J. Tracheostomy to noninvasive ventilation: from acute care to home. Sleep Med Clin. 2020;15(4):593-598. doi: 10.1016/j.jsmc.2020.08.003
6. Kohn J, McKeon M, Munhall D, Blanchette S, Wells S, Watters K. Standardization of pediatric tracheostomy care with “Go-bags.” Int J Pediatr Otorhinolaryngol. 2019;121:154-156. doi: 10.1016/j.ijporl.2019.03.022
HALT early recognition is key
DIFFUSE LUNG DISEASE AND LUNG TRANSPLANT NETWORK
Lung Transplant Section
Hyperammonemia after lung transplantation (HALT) is a rare but serious complication occurring in 1% to 4% of patients with high morbidity and mortality. Early recognition is crucial, as mortality rates can reach 75%.1
HALT arises from excess ammonia production or decreased clearance and is often linked to infections by urea-splitting organisms, including mycoplasma and ureaplasma. Prompt, aggressive treatment is essential and typically includes dietary protein restriction, renal replacement therapy (ideally intermittent hemodialysis), bowel decontamination (lactulose, rifaximin, metronidazole, or neomycin), amino acids (arginine and levocarnitine), nitrogen scavengers (sodium phenylbutyrate or glycerol phenylbutyrate), and empiric antimicrobial coverage for urea-splitting organisms.2 Given concerns for calcineurin inhibitor-induced hyperammonemia, transition to an alternative agent may be considered.
Given the severe risks associated with HALT, vigilance is vital, particularly in intubated and sedated patients where monitoring of neurologic status is more challenging. Protocols may involve routine serum ammonia monitoring, polymerase chain reaction testing for mycoplasma and ureaplasma at the time of transplant or with postoperative bronchoscopy, and empiric antimicrobial treatment. No definitive ammonia threshold exists, but altered sensorium with elevated levels warrants immediate and more aggressive treatment with levels >75 μmol/L. Early testing and symptom recognition can significantly improve survival rates in this potentially devastating condition.
References
1. Leger RF, Silverman MS, Hauck ES, Guvakova KD. Hyperammonemia post lung transplantation: a review. Clin Med Insights Circ Respir Pulm Med. 2020;14:1179548420966234. doi:10.1177/1179548420966234
2. Chen C, Bain KB, Luppa JA. Hyperammonemia syndrome after lung transplantation: a single center experience. Transplantation. 2016;100(3):678-684. doi:10.1097/TP.0000000000000868
DIFFUSE LUNG DISEASE AND LUNG TRANSPLANT NETWORK
Lung Transplant Section
Hyperammonemia after lung transplantation (HALT) is a rare but serious complication occurring in 1% to 4% of patients with high morbidity and mortality. Early recognition is crucial, as mortality rates can reach 75%.1
HALT arises from excess ammonia production or decreased clearance and is often linked to infections by urea-splitting organisms, including mycoplasma and ureaplasma. Prompt, aggressive treatment is essential and typically includes dietary protein restriction, renal replacement therapy (ideally intermittent hemodialysis), bowel decontamination (lactulose, rifaximin, metronidazole, or neomycin), amino acids (arginine and levocarnitine), nitrogen scavengers (sodium phenylbutyrate or glycerol phenylbutyrate), and empiric antimicrobial coverage for urea-splitting organisms.2 Given concerns for calcineurin inhibitor-induced hyperammonemia, transition to an alternative agent may be considered.
Given the severe risks associated with HALT, vigilance is vital, particularly in intubated and sedated patients where monitoring of neurologic status is more challenging. Protocols may involve routine serum ammonia monitoring, polymerase chain reaction testing for mycoplasma and ureaplasma at the time of transplant or with postoperative bronchoscopy, and empiric antimicrobial treatment. No definitive ammonia threshold exists, but altered sensorium with elevated levels warrants immediate and more aggressive treatment with levels >75 μmol/L. Early testing and symptom recognition can significantly improve survival rates in this potentially devastating condition.
References
1. Leger RF, Silverman MS, Hauck ES, Guvakova KD. Hyperammonemia post lung transplantation: a review. Clin Med Insights Circ Respir Pulm Med. 2020;14:1179548420966234. doi:10.1177/1179548420966234
2. Chen C, Bain KB, Luppa JA. Hyperammonemia syndrome after lung transplantation: a single center experience. Transplantation. 2016;100(3):678-684. doi:10.1097/TP.0000000000000868
DIFFUSE LUNG DISEASE AND LUNG TRANSPLANT NETWORK
Lung Transplant Section
Hyperammonemia after lung transplantation (HALT) is a rare but serious complication occurring in 1% to 4% of patients with high morbidity and mortality. Early recognition is crucial, as mortality rates can reach 75%.1
HALT arises from excess ammonia production or decreased clearance and is often linked to infections by urea-splitting organisms, including mycoplasma and ureaplasma. Prompt, aggressive treatment is essential and typically includes dietary protein restriction, renal replacement therapy (ideally intermittent hemodialysis), bowel decontamination (lactulose, rifaximin, metronidazole, or neomycin), amino acids (arginine and levocarnitine), nitrogen scavengers (sodium phenylbutyrate or glycerol phenylbutyrate), and empiric antimicrobial coverage for urea-splitting organisms.2 Given concerns for calcineurin inhibitor-induced hyperammonemia, transition to an alternative agent may be considered.
Given the severe risks associated with HALT, vigilance is vital, particularly in intubated and sedated patients where monitoring of neurologic status is more challenging. Protocols may involve routine serum ammonia monitoring, polymerase chain reaction testing for mycoplasma and ureaplasma at the time of transplant or with postoperative bronchoscopy, and empiric antimicrobial treatment. No definitive ammonia threshold exists, but altered sensorium with elevated levels warrants immediate and more aggressive treatment with levels >75 μmol/L. Early testing and symptom recognition can significantly improve survival rates in this potentially devastating condition.
References
1. Leger RF, Silverman MS, Hauck ES, Guvakova KD. Hyperammonemia post lung transplantation: a review. Clin Med Insights Circ Respir Pulm Med. 2020;14:1179548420966234. doi:10.1177/1179548420966234
2. Chen C, Bain KB, Luppa JA. Hyperammonemia syndrome after lung transplantation: a single center experience. Transplantation. 2016;100(3):678-684. doi:10.1097/TP.0000000000000868