Critical Care

Intravenous albumin is a human-derived blood product studied widely in a variety of patient populations. Despite its frequent use in critical care, few high-quality studies have demonstrated improvements in patient-important outcomes. It is important for intensivists to think critically about prescribing albumin and individualize the prescription for each patient, as albumin use is not without risk. Compared with crystalloids, albumin increases the risk of fluid overload and bleeding and infections in patients undergoing cardiac surgery.^1,2 In addition, albumin is costly, and its production is fraught with donor supply chain ethical concerns (the majority of albumin is derived from paid plasma donors).

brotra

Albumin use is highly variable between countries, hospitals, and even clinicians within the same specialty due to several factors, including the perception of minimal risk with albumin, concerns regarding insufficient short-term hemodynamic response to crystalloid, and lack of high-quality evidence to inform clinical practice. We will discuss when intensivists should consider albumin use (with prescription personalized to patient context) and when it should be avoided due to the concerns for patient harm.

An intensivist might consider albumin as a reasonable treatment option in patients with cirrhosis undergoing large volume paracentesis to prevent paracentesis-induced circulatory dysfunction, and in patients with cirrhosis and spontaneous bacterial peritonitis (SBP), as data suggests use in this setting leads to a reduction in mortality.³ Clinicians should be aware that even for these widely accepted albumin indications, which are supported by published guidelines, the certainty of evidence is low, recommendations are weak (conditional), and, therefore, albumin should always be personalized to the patient based on volume of paracentesis fluid removed, prior history of hypotension after procedures, and degree of renal dysfunction.⁴

stastuspicutritethichestosaposadaswawustohanogoswophiclotemugubrecraprutawrukuuagamodrocidivitrachiuobrewreduvivicrospithidocrerakuclokurapafracravouomivebrecabauadaphefrespawospafrichavosleraclovorikachapavupapropis

copishujetomubeswiuelidreuenocrodrovothanucrebupredotreroslodrobrishapricrobrolofropuclagikegiswuphomabishacloshasticledrocrojasurepopucrecibribanouimadedrechuuecoposlepodratrishipo

As with any intervention, the use of albumin is associated with risks. In patients undergoing on-pump cardiac surgery, the ALBICS study showed that albumin did not reduce the risk of major adverse events and, instead, increased risk of bleeding, resternotomy, and infection.² The ATTIRE trial showed that in patients hospitalized with decompensated cirrhosis and serum albumin <30 g/L, albumin failed to reduce infection, renal impairment, or mortality while increasing life-threatening adverse events, including pulmonary edema and fluid overload.¹ Similarly, in patients with cirrhosis and extraperitoneal infections, albumin showed no benefit in reducing renal impairment or mortality, and its use was associated with higher rates of pulmonary edema.⁶ Lastly, critically ill patients with traumatic brain injury (TBI) who received fluid resuscitation with albumin have been shown to experience higher mortality compared with saline.⁷ Thus, based on current evidence, intravenous albumin is not recommended for patients undergoing cardiac surgery (priming of the bypass circuit or volume replacement), patients hospitalized with decompensated cirrhosis and hypoalbuminemia, patients hospitalized with cirrhosis and extraperitoneal infections, and critically ill patients with TBI.⁴

sheketroslepakih

spavolecrusponosistulachufrisinusaswoguhalepifratrachuwipreshocifruphorebricobrivetrunadejaduguladuspidrothosporatogestewusluraphibritujoswosugokustiswawajosliswowoswiphicrabrapaswothivadeswashelegogawr

High-quality evidence is currently lacking in many clinical settings, and large randomized controlled trials are underway to provide further insights into the utility of albumin. These trials will address albumin use in the following: acute kidney injury requiring renal replacement therapy (ALTER-AKI, NCT04705896), inpatients with community-acquired pneumonia (NCT04071041), high-risk cardiac surgery (ACTRN1261900135516703), and septic shock (NCT03869385).

uupovouodefruprocrishechisosperukopanonisloslutefrafrofrijejoslacopujinasepisporechochagawrishakuswuprushoswadileprimagaspogufrutrepruclodrathaspikuwoswuslatrostastesapuprustoclebroswethewuphucredrobrespesulowroslokowrimac

Financial/nonfinancial disclosures

Nicole Relke: None. Mark Hewitt: None. Bram Rochwerg: None. Jeannie Callum: Research support from Canadian Blood Services and Octapharma.

References

1. China L, Freemantle N, Forrest E, et al. A randomized trial of albumin infusions in hospitalized patients with cirrhosis. N Engl J Med. 2021;384(9):808-817. doi:10.1056/NEJMoa2022166

2. Pesonen E, Vlasov H, Suojaranta R, et al. Effect of 4% albumin solution vs ringer acetate on major adverse events in patients undergoing cardiac surgery with cardiopulmonary bypass: a randomized clinical trial. JAMA. 2022;328(3):251-258. doi:10.1001/jama.2022.10461

3. Sort P, Navasa M, Arroyo V, et al. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. NEJM. 1999;341:403-409.

4. Callum J, Skubas NJ, Bathla A, et al. Use of intravenous albumin: a guideline from the international collaboration for transfusion medicine guidelines. Chest. 2024:S0012-3692(24)00285-X. doi:10.1016/j.chest.2024.02.049

5. Torp N. High doses of albumin increases mortality and complications in terlipressin treated patients with cirrhosis: insights from the ATTIRE trial. Paper presented at the AASLD; 2023; San Diego, CA. https://www.aasld.org/the-liver-meeting/high-doses-albumin-increases-mortality-and-complications-terlipressin-treated

6. Wong YJ, Qiu TY, Tam YC, Mohan BP, Gallegos-Orozco JF, Adler DG. Efficacy and safety of IV albumin for non-spontaneous bacterial peritonitis infection among patients with cirrhosis: a systematic review and meta-analysis. Dig Liver Dis. 2020;52(10):1137-1142. doi:10.1016/j.dld.2020.05.047

7. Myburgh J, Cooper JD, Finfer S, et al. Saline or albumin for fluid resuscitation in patients with traumatic brain injury. N Engl J Med. 2007;357(9):874-884.

Intravenous albumin is a human-derived blood product studied widely in a variety of patient populations. Despite its frequent use in critical care, few high-quality studies have demonstrated improvements in patient-important outcomes. It is important for intensivists to think critically about prescribing albumin and individualize the prescription for each patient, as albumin use is not without risk. Compared with crystalloids, albumin increases the risk of fluid overload and bleeding and infections in patients undergoing cardiac surgery.^1,2 In addition, albumin is costly, and its production is fraught with donor supply chain ethical concerns (the majority of albumin is derived from paid plasma donors).

brotra

Albumin use is highly variable between countries, hospitals, and even clinicians within the same specialty due to several factors, including the perception of minimal risk with albumin, concerns regarding insufficient short-term hemodynamic response to crystalloid, and lack of high-quality evidence to inform clinical practice. We will discuss when intensivists should consider albumin use (with prescription personalized to patient context) and when it should be avoided due to the concerns for patient harm.

An intensivist might consider albumin as a reasonable treatment option in patients with cirrhosis undergoing large volume paracentesis to prevent paracentesis-induced circulatory dysfunction, and in patients with cirrhosis and spontaneous bacterial peritonitis (SBP), as data suggests use in this setting leads to a reduction in mortality.³ Clinicians should be aware that even for these widely accepted albumin indications, which are supported by published guidelines, the certainty of evidence is low, recommendations are weak (conditional), and, therefore, albumin should always be personalized to the patient based on volume of paracentesis fluid removed, prior history of hypotension after procedures, and degree of renal dysfunction.⁴

stastuspicutritethichestosaposadaswawustohanogoswophiclotemugubrecraprutawrukuuagamodrocidivitrachiuobrewreduvivicrospithidocrerakuclokurapafracravouomivebrecabauadaphefrespawospafrichavosleraclovorikachapavupapropis

copishujetomubeswiuelidreuenocrodrovothanucrebupredotreroslodrobrishapricrobrolofropuclagikegiswuphomabishacloshasticledrocrojasurepopucrecibribanouimadedrechuuecoposlepodratrishipo

As with any intervention, the use of albumin is associated with risks. In patients undergoing on-pump cardiac surgery, the ALBICS study showed that albumin did not reduce the risk of major adverse events and, instead, increased risk of bleeding, resternotomy, and infection.² The ATTIRE trial showed that in patients hospitalized with decompensated cirrhosis and serum albumin <30 g/L, albumin failed to reduce infection, renal impairment, or mortality while increasing life-threatening adverse events, including pulmonary edema and fluid overload.¹ Similarly, in patients with cirrhosis and extraperitoneal infections, albumin showed no benefit in reducing renal impairment or mortality, and its use was associated with higher rates of pulmonary edema.⁶ Lastly, critically ill patients with traumatic brain injury (TBI) who received fluid resuscitation with albumin have been shown to experience higher mortality compared with saline.⁷ Thus, based on current evidence, intravenous albumin is not recommended for patients undergoing cardiac surgery (priming of the bypass circuit or volume replacement), patients hospitalized with decompensated cirrhosis and hypoalbuminemia, patients hospitalized with cirrhosis and extraperitoneal infections, and critically ill patients with TBI.⁴

sheketroslepakih

spavolecrusponosistulachufrisinusaswoguhalepifratrachuwipreshocifruphorebricobrivetrunadejaduguladuspidrothosporatogestewusluraphibritujoswosugokustiswawajosliswowoswiphicrabrapaswothivadeswashelegogawr

High-quality evidence is currently lacking in many clinical settings, and large randomized controlled trials are underway to provide further insights into the utility of albumin. These trials will address albumin use in the following: acute kidney injury requiring renal replacement therapy (ALTER-AKI, NCT04705896), inpatients with community-acquired pneumonia (NCT04071041), high-risk cardiac surgery (ACTRN1261900135516703), and septic shock (NCT03869385).

uupovouodefruprocrishechisosperukopanonisloslutefrafrofrijejoslacopujinasepisporechochagawrishakuswuprushoswadileprimagaspogufrutrepruclodrathaspikuwoswuslatrostastesapuprustoclebroswethewuphucredrobrespesulowroslokowrimac

Financial/nonfinancial disclosures

Nicole Relke: None. Mark Hewitt: None. Bram Rochwerg: None. Jeannie Callum: Research support from Canadian Blood Services and Octapharma.

References

1. China L, Freemantle N, Forrest E, et al. A randomized trial of albumin infusions in hospitalized patients with cirrhosis. N Engl J Med. 2021;384(9):808-817. doi:10.1056/NEJMoa2022166

2. Pesonen E, Vlasov H, Suojaranta R, et al. Effect of 4% albumin solution vs ringer acetate on major adverse events in patients undergoing cardiac surgery with cardiopulmonary bypass: a randomized clinical trial. JAMA. 2022;328(3):251-258. doi:10.1001/jama.2022.10461

3. Sort P, Navasa M, Arroyo V, et al. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. NEJM. 1999;341:403-409.

4. Callum J, Skubas NJ, Bathla A, et al. Use of intravenous albumin: a guideline from the international collaboration for transfusion medicine guidelines. Chest. 2024:S0012-3692(24)00285-X. doi:10.1016/j.chest.2024.02.049

5. Torp N. High doses of albumin increases mortality and complications in terlipressin treated patients with cirrhosis: insights from the ATTIRE trial. Paper presented at the AASLD; 2023; San Diego, CA. https://www.aasld.org/the-liver-meeting/high-doses-albumin-increases-mortality-and-complications-terlipressin-treated

6. Wong YJ, Qiu TY, Tam YC, Mohan BP, Gallegos-Orozco JF, Adler DG. Efficacy and safety of IV albumin for non-spontaneous bacterial peritonitis infection among patients with cirrhosis: a systematic review and meta-analysis. Dig Liver Dis. 2020;52(10):1137-1142. doi:10.1016/j.dld.2020.05.047

7. Myburgh J, Cooper JD, Finfer S, et al. Saline or albumin for fluid resuscitation in patients with traumatic brain injury. N Engl J Med. 2007;357(9):874-884.

Intravenous albumin is a human-derived blood product studied widely in a variety of patient populations. Despite its frequent use in critical care, few high-quality studies have demonstrated improvements in patient-important outcomes. It is important for intensivists to think critically about prescribing albumin and individualize the prescription for each patient, as albumin use is not without risk. Compared with crystalloids, albumin increases the risk of fluid overload and bleeding and infections in patients undergoing cardiac surgery.^1,2 In addition, albumin is costly, and its production is fraught with donor supply chain ethical concerns (the majority of albumin is derived from paid plasma donors).

brotra

Albumin use is highly variable between countries, hospitals, and even clinicians within the same specialty due to several factors, including the perception of minimal risk with albumin, concerns regarding insufficient short-term hemodynamic response to crystalloid, and lack of high-quality evidence to inform clinical practice. We will discuss when intensivists should consider albumin use (with prescription personalized to patient context) and when it should be avoided due to the concerns for patient harm.

An intensivist might consider albumin as a reasonable treatment option in patients with cirrhosis undergoing large volume paracentesis to prevent paracentesis-induced circulatory dysfunction, and in patients with cirrhosis and spontaneous bacterial peritonitis (SBP), as data suggests use in this setting leads to a reduction in mortality.³ Clinicians should be aware that even for these widely accepted albumin indications, which are supported by published guidelines, the certainty of evidence is low, recommendations are weak (conditional), and, therefore, albumin should always be personalized to the patient based on volume of paracentesis fluid removed, prior history of hypotension after procedures, and degree of renal dysfunction.⁴

stastuspicutritethichestosaposadaswawustohanogoswophiclotemugubrecraprutawrukuuagamodrocidivitrachiuobrewreduvivicrospithidocrerakuclokurapafracravouomivebrecabauadaphefrespawospafrichavosleraclovorikachapavupapropis

copishujetomubeswiuelidreuenocrodrovothanucrebupredotreroslodrobrishapricrobrolofropuclagikegiswuphomabishacloshasticledrocrojasurepopucrecibribanouimadedrechuuecoposlepodratrishipo

As with any intervention, the use of albumin is associated with risks. In patients undergoing on-pump cardiac surgery, the ALBICS study showed that albumin did not reduce the risk of major adverse events and, instead, increased risk of bleeding, resternotomy, and infection.² The ATTIRE trial showed that in patients hospitalized with decompensated cirrhosis and serum albumin <30 g/L, albumin failed to reduce infection, renal impairment, or mortality while increasing life-threatening adverse events, including pulmonary edema and fluid overload.¹ Similarly, in patients with cirrhosis and extraperitoneal infections, albumin showed no benefit in reducing renal impairment or mortality, and its use was associated with higher rates of pulmonary edema.⁶ Lastly, critically ill patients with traumatic brain injury (TBI) who received fluid resuscitation with albumin have been shown to experience higher mortality compared with saline.⁷ Thus, based on current evidence, intravenous albumin is not recommended for patients undergoing cardiac surgery (priming of the bypass circuit or volume replacement), patients hospitalized with decompensated cirrhosis and hypoalbuminemia, patients hospitalized with cirrhosis and extraperitoneal infections, and critically ill patients with TBI.⁴

sheketroslepakih

spavolecrusponosistulachufrisinusaswoguhalepifratrachuwipreshocifruphorebricobrivetrunadejaduguladuspidrothosporatogestewusluraphibritujoswosugokustiswawajosliswowoswiphicrabrapaswothivadeswashelegogawr

High-quality evidence is currently lacking in many clinical settings, and large randomized controlled trials are underway to provide further insights into the utility of albumin. These trials will address albumin use in the following: acute kidney injury requiring renal replacement therapy (ALTER-AKI, NCT04705896), inpatients with community-acquired pneumonia (NCT04071041), high-risk cardiac surgery (ACTRN1261900135516703), and septic shock (NCT03869385).

uupovouodefruprocrishechisosperukopanonisloslutefrafrofrijejoslacopujinasepisporechochagawrishakuswuprushoswadileprimagaspogufrutrepruclodrathaspikuwoswuslatrostastesapuprustoclebroswethewuphucredrobrespesulowroslokowrimac

Financial/nonfinancial disclosures

Nicole Relke: None. Mark Hewitt: None. Bram Rochwerg: None. Jeannie Callum: Research support from Canadian Blood Services and Octapharma.

References

1. China L, Freemantle N, Forrest E, et al. A randomized trial of albumin infusions in hospitalized patients with cirrhosis. N Engl J Med. 2021;384(9):808-817. doi:10.1056/NEJMoa2022166

2. Pesonen E, Vlasov H, Suojaranta R, et al. Effect of 4% albumin solution vs ringer acetate on major adverse events in patients undergoing cardiac surgery with cardiopulmonary bypass: a randomized clinical trial. JAMA. 2022;328(3):251-258. doi:10.1001/jama.2022.10461

3. Sort P, Navasa M, Arroyo V, et al. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. NEJM. 1999;341:403-409.

4. Callum J, Skubas NJ, Bathla A, et al. Use of intravenous albumin: a guideline from the international collaboration for transfusion medicine guidelines. Chest. 2024:S0012-3692(24)00285-X. doi:10.1016/j.chest.2024.02.049

5. Torp N. High doses of albumin increases mortality and complications in terlipressin treated patients with cirrhosis: insights from the ATTIRE trial. Paper presented at the AASLD; 2023; San Diego, CA. https://www.aasld.org/the-liver-meeting/high-doses-albumin-increases-mortality-and-complications-terlipressin-treated

6. Wong YJ, Qiu TY, Tam YC, Mohan BP, Gallegos-Orozco JF, Adler DG. Efficacy and safety of IV albumin for non-spontaneous bacterial peritonitis infection among patients with cirrhosis: a systematic review and meta-analysis. Dig Liver Dis. 2020;52(10):1137-1142. doi:10.1016/j.dld.2020.05.047

7. Myburgh J, Cooper JD, Finfer S, et al. Saline or albumin for fluid resuscitation in patients with traumatic brain injury. N Engl J Med. 2007;357(9):874-884.

CRITICAL CARE NETWORK

Mechanical Ventilation and Airways Management Section

Lung protective ventilation (LPV) is the cornerstone to minimizing ventilator-induced lung injury. Hence, LPV is associated with better survival in patients both with and without ARDS.^1,2,3 Continuous monitoring of the tidal volume, plateau pressure, and positive end-expiratory pressure (PEEP) is crucial to maintain LPV. Electrical impedance tomography (EIT) is a noninvasive, radiation-free, imaging method of the electrical conductivity distribution inside the human body.⁴ Integrating EIT into invasive mechanical ventilation allows imaging of the regional lung ventilation as affected by the mechanical ventilation settings as well as the patient position. It can also provide a personalized approach to determining the optimum ventilatory settings based on individual patient conditions.^5,6

Optimum PEEP titration is crucial to prevent lung collapse as well as overdistension. In a single-center, randomized, crossover pilot study of 12 patients, optimum PEEP titration was carried out using a high PEEP/FiO₂ table vs EIT in moderate to severe ARDS. The primary endpoint was the reduction of mechanical power, which was consistently lower in the EIT group.⁷ EIT also allows the assessment of regional compliance of the lungs. There are reports regarding the superiority of regional compliance of lung over global compliance in achieving better gas exchange, lung compliance, and weaning of mechanical ventilation.⁸ EIT could assess the patient’s response to prone positioning by illustrating the change in the functional residual capacity between supine and prone positioning.⁹ In addition, by visualization of the ventilated areas during spontaneous breathing and reduction of pressure support, EIT could help in weaning off the mechanical ventilation.¹⁰

pratroslubrestehuvulowiwupedidiwoswasheslahabirobepenelulabrameuucothowribretulislijitrefrataclatherifreshadahikigisiclujosposwoslupamerodrosa

In conclusion, EIT can be a tool to provide safe and personalized mechanical ventilation in patients with respiratory failure. However, there are limited data regarding its use and application, which might become an interesting subject for future clinical research.

– Akram M. Zaaqoq, MD, MPH

Member-at-Large


References

1. Amato MB, Barbas CS, Medeiros DM, et al. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med. 1998;338(6):347-354.

2. Brower RG, Matthay MA, Morris A, et al. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342(18):1301-1308.

3. Neto AS, Simonis FD, Barbas CSV, et al. Lung-protective ventilation with low tidal volumes and the occurrence of pulmonary complications in patients without acute respiratory distress syndrome: a systematic review and individual patient data analysis. Crit Care Med. 2015;43(10):2155-2163.

4. Adler A, Boyle A. Electrical impedance tomography: tissue properties to image measures. IEEE Trans Biomed Eng. 2017;64(11):2494-2504.

5. Jang GY, Ayoub G, Kim YE, et al. Integrated EIT system for functional lung ventilation imaging. Biomed Eng Online. 2019;18(1):83.

6. Sella N, Pettenuzzo T, Zarantonello F, et al. Electrical impedance tomography: a compass for the safe route to optimal PEEP. Respir Med. 2021;187:106555.

7. Jimenez JV, Munroe E, Weirauch AJ, et al. Electric impedance tomography-guided PEEP titration reduces mechanical power in ARDS: a randomized crossover pilot trial. Crit Care. 2023;27(1):21.

8. Costa ELV, Borges JB, Melo A, et al. Bedside estimation of recruitable alveolar collapse and hyperdistension by electrical impedance tomography. Intensive Care Med. 2009;35(6):1132-1137.9. Riera J, Pérez P, Cortés J, Roca O, Masclans JR, Rello J. Effect of high-flow nasal cannula and body position on end-expiratory lung volume: a cohort study using electrical impedance tomography. Respir Care. 2013;58(4):589-596.10. Wisse JJ, Goos TG, Jonkman AH, et al. Electrical impedance tomography as a monitoring tool during weaning from mechanical ventilation: an observational study during the spontaneous breathing trial. Respir Res. 2024;25(1):179.
 

CRITICAL CARE NETWORK

Mechanical Ventilation and Airways Management Section

Lung protective ventilation (LPV) is the cornerstone to minimizing ventilator-induced lung injury. Hence, LPV is associated with better survival in patients both with and without ARDS.^1,2,3 Continuous monitoring of the tidal volume, plateau pressure, and positive end-expiratory pressure (PEEP) is crucial to maintain LPV. Electrical impedance tomography (EIT) is a noninvasive, radiation-free, imaging method of the electrical conductivity distribution inside the human body.⁴ Integrating EIT into invasive mechanical ventilation allows imaging of the regional lung ventilation as affected by the mechanical ventilation settings as well as the patient position. It can also provide a personalized approach to determining the optimum ventilatory settings based on individual patient conditions.^5,6

Optimum PEEP titration is crucial to prevent lung collapse as well as overdistension. In a single-center, randomized, crossover pilot study of 12 patients, optimum PEEP titration was carried out using a high PEEP/FiO₂ table vs EIT in moderate to severe ARDS. The primary endpoint was the reduction of mechanical power, which was consistently lower in the EIT group.⁷ EIT also allows the assessment of regional compliance of the lungs. There are reports regarding the superiority of regional compliance of lung over global compliance in achieving better gas exchange, lung compliance, and weaning of mechanical ventilation.⁸ EIT could assess the patient’s response to prone positioning by illustrating the change in the functional residual capacity between supine and prone positioning.⁹ In addition, by visualization of the ventilated areas during spontaneous breathing and reduction of pressure support, EIT could help in weaning off the mechanical ventilation.¹⁰

pratroslubrestehuvulowiwupedidiwoswasheslahabirobepenelulabrameuucothowribretulislijitrefrataclatherifreshadahikigisiclujosposwoslupamerodrosa

In conclusion, EIT can be a tool to provide safe and personalized mechanical ventilation in patients with respiratory failure. However, there are limited data regarding its use and application, which might become an interesting subject for future clinical research.

– Akram M. Zaaqoq, MD, MPH

Member-at-Large


References

1. Amato MB, Barbas CS, Medeiros DM, et al. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med. 1998;338(6):347-354.

2. Brower RG, Matthay MA, Morris A, et al. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342(18):1301-1308.

3. Neto AS, Simonis FD, Barbas CSV, et al. Lung-protective ventilation with low tidal volumes and the occurrence of pulmonary complications in patients without acute respiratory distress syndrome: a systematic review and individual patient data analysis. Crit Care Med. 2015;43(10):2155-2163.

4. Adler A, Boyle A. Electrical impedance tomography: tissue properties to image measures. IEEE Trans Biomed Eng. 2017;64(11):2494-2504.

5. Jang GY, Ayoub G, Kim YE, et al. Integrated EIT system for functional lung ventilation imaging. Biomed Eng Online. 2019;18(1):83.

6. Sella N, Pettenuzzo T, Zarantonello F, et al. Electrical impedance tomography: a compass for the safe route to optimal PEEP. Respir Med. 2021;187:106555.

7. Jimenez JV, Munroe E, Weirauch AJ, et al. Electric impedance tomography-guided PEEP titration reduces mechanical power in ARDS: a randomized crossover pilot trial. Crit Care. 2023;27(1):21.

8. Costa ELV, Borges JB, Melo A, et al. Bedside estimation of recruitable alveolar collapse and hyperdistension by electrical impedance tomography. Intensive Care Med. 2009;35(6):1132-1137.9. Riera J, Pérez P, Cortés J, Roca O, Masclans JR, Rello J. Effect of high-flow nasal cannula and body position on end-expiratory lung volume: a cohort study using electrical impedance tomography. Respir Care. 2013;58(4):589-596.10. Wisse JJ, Goos TG, Jonkman AH, et al. Electrical impedance tomography as a monitoring tool during weaning from mechanical ventilation: an observational study during the spontaneous breathing trial. Respir Res. 2024;25(1):179.
 

CRITICAL CARE NETWORK

Mechanical Ventilation and Airways Management Section

Lung protective ventilation (LPV) is the cornerstone to minimizing ventilator-induced lung injury. Hence, LPV is associated with better survival in patients both with and without ARDS.^1,2,3 Continuous monitoring of the tidal volume, plateau pressure, and positive end-expiratory pressure (PEEP) is crucial to maintain LPV. Electrical impedance tomography (EIT) is a noninvasive, radiation-free, imaging method of the electrical conductivity distribution inside the human body.⁴ Integrating EIT into invasive mechanical ventilation allows imaging of the regional lung ventilation as affected by the mechanical ventilation settings as well as the patient position. It can also provide a personalized approach to determining the optimum ventilatory settings based on individual patient conditions.^5,6

Optimum PEEP titration is crucial to prevent lung collapse as well as overdistension. In a single-center, randomized, crossover pilot study of 12 patients, optimum PEEP titration was carried out using a high PEEP/FiO₂ table vs EIT in moderate to severe ARDS. The primary endpoint was the reduction of mechanical power, which was consistently lower in the EIT group.⁷ EIT also allows the assessment of regional compliance of the lungs. There are reports regarding the superiority of regional compliance of lung over global compliance in achieving better gas exchange, lung compliance, and weaning of mechanical ventilation.⁸ EIT could assess the patient’s response to prone positioning by illustrating the change in the functional residual capacity between supine and prone positioning.⁹ In addition, by visualization of the ventilated areas during spontaneous breathing and reduction of pressure support, EIT could help in weaning off the mechanical ventilation.¹⁰

pratroslubrestehuvulowiwupedidiwoswasheslahabirobepenelulabrameuucothowribretulislijitrefrataclatherifreshadahikigisiclujosposwoslupamerodrosa

In conclusion, EIT can be a tool to provide safe and personalized mechanical ventilation in patients with respiratory failure. However, there are limited data regarding its use and application, which might become an interesting subject for future clinical research.

– Akram M. Zaaqoq, MD, MPH

Member-at-Large


References

1. Amato MB, Barbas CS, Medeiros DM, et al. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med. 1998;338(6):347-354.

2. Brower RG, Matthay MA, Morris A, et al. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342(18):1301-1308.

3. Neto AS, Simonis FD, Barbas CSV, et al. Lung-protective ventilation with low tidal volumes and the occurrence of pulmonary complications in patients without acute respiratory distress syndrome: a systematic review and individual patient data analysis. Crit Care Med. 2015;43(10):2155-2163.

4. Adler A, Boyle A. Electrical impedance tomography: tissue properties to image measures. IEEE Trans Biomed Eng. 2017;64(11):2494-2504.

5. Jang GY, Ayoub G, Kim YE, et al. Integrated EIT system for functional lung ventilation imaging. Biomed Eng Online. 2019;18(1):83.

6. Sella N, Pettenuzzo T, Zarantonello F, et al. Electrical impedance tomography: a compass for the safe route to optimal PEEP. Respir Med. 2021;187:106555.

7. Jimenez JV, Munroe E, Weirauch AJ, et al. Electric impedance tomography-guided PEEP titration reduces mechanical power in ARDS: a randomized crossover pilot trial. Crit Care. 2023;27(1):21.

8. Costa ELV, Borges JB, Melo A, et al. Bedside estimation of recruitable alveolar collapse and hyperdistension by electrical impedance tomography. Intensive Care Med. 2009;35(6):1132-1137.9. Riera J, Pérez P, Cortés J, Roca O, Masclans JR, Rello J. Effect of high-flow nasal cannula and body position on end-expiratory lung volume: a cohort study using electrical impedance tomography. Respir Care. 2013;58(4):589-596.10. Wisse JJ, Goos TG, Jonkman AH, et al. Electrical impedance tomography as a monitoring tool during weaning from mechanical ventilation: an observational study during the spontaneous breathing trial. Respir Res. 2024;25(1):179.
 

A 47-year-old woman with a history of cirrhosis is admitted with an acute kidney injury and altered mental status. On the initial workup, there are no signs of infection, and dehydration is determined to be the cause of the kidney injury. There are signs of improvement in the kidney injury with hydration. On hospital day 3, the patient develops a fever (101.9 ^oF) with accompanying leukocytosis to 14,000. Concerned for infection, the team starts empiric broad spectrum antibiotics for presumed spontaneous bacterial peritonitis. The next day (hospital day 4), a rapid response evaluation is activated as the patient is demonstrating increasing confusion, hypotension with a systolic blood pressure of 70 mm Hg, and elevated lactic acid. The patient receives 1 L of normal saline and transfers to the ICU. The new critical care fellow, who has just read up on sepsis early management bundles, and specifically the Severe Sepsis and Septic Shock Management Bundle (SEP-1), is reviewing the chart and notices a history of multidrug-resistant organisms in her urine cultures from an admission 2 months ago. They ask of the transferring team, “When was time zero, and was the 3-hour bundle completed?”

Sepsis is recognized as a medical emergency, which, without a prompt response, causes significant morbidity and mortality. In the United States alone, more than 1.7 million adults develop sepsis, with approximately 270,000 deaths and $57 billion in aggregate costs annually.¹ The excessive cost, both of human life and monetary, has led to the commitment of significant resources to sepsis care. Improved recognition and timely intervention for sepsis have led to noteworthy improvement in mortality. Most of this effort has been directed toward patients with sepsis diagnosed in the emergency department (ED) who are presenting with community-onset sepsis (COS). A new entity, called hospital-onset sepsis (HOS), has been described recently, defined by the Centers for Disease Control and Prevention (CDC) as both infection and organ dysfunction developing more than 48 hours after hospital admission.²

roretruspuspujifregusuvebristehaslaswacrinajadushuprechidruprovefrunehuslorenulegugubrisucobrajinelecrunuvovewauenewecuthedrucruslospashuroprocrust

A systematic review of 51 studies found approximately 23.6% of all sepsis cases are HOS. The proportion of HOS is even higher (more than 45%) in patients admitted to the ICU with sepsis.³ The outcome for this group remains comparatively poor. The hospital mortality among patients with HOS is 35%, which increases to 52% with progression to septic shock compared with 25% with COS.³ Even after adjusting for baseline factors that make one prone to developing infection in the hospital, a patient developing HOS has three-times a higher risk of dying compared with a patient who never developed sepsis and two-times a higher risk of dying compared with patients with COS.⁴Furthermore, HOS utilizes more resources with significantly longer ICU and hospital stays and has five-times the hospital cost compared with COS.⁴

The two most crucial factors in improving sepsis outcomes, as identified by the Surviving Sepsis Campaign guidelines, are: 1) prompt identification and treatment within the first few hours of onset and 2) regular reevaluation of the patient’s response to treatment.

kalodusluneslehipospastowruslitupomodregobuslabaloshuwutromichuprosle

Prompt identification

Diagnosing sepsis in the patient who is hospitalized is challenging. Patients admitted to the hospital often have competing comorbidities, have existing organ failure, or are in a postoperative/intervention state that clouds the application and interpretation of vital sign triggers customarily used to identify sepsis. The positive predictive value for all existing sepsis definitions and diagnostic criteria is dismally low. ⁵ And while automated electronic sepsis alerts may improve processes of care, they still have poor positive predictive value and have not impacted patient-centered outcomes (mortality or length of stay). Furthermore, the causative microorganisms often associated with hospital-acquired infections are complex, are drug-resistant, and can have courses which further delay identification. Finally, cognitive errors, such as anchoring biases or premature diagnosis closure, can contribute to provider-level identification delays that are only further exacerbated by system issues, such as capacity constraints, staffing issues, and differing paces between wards that tend to impede time-sensitive evaluations and interventions. ^4,6,7

Management

The SEP-1 core measure uses a framework of early recognition of infection and completion of the sepsis bundles in a timely manner to improve outcomes. Patients with HOS are less likely than those with COS to receive Centers for Medicare & Medicaid Services SEP-1-compliant care, including timely blood culture collection, initial and repeat lactate testing, and fluid resuscitation.⁸ The Surviving Sepsis Campaign has explored barriers to managing HOS. Among caregivers, these include delay in recognition, poor communication regarding change in patient status, not prioritizing treatment for sepsis, failure to measure lactate, delayed or no antimicrobial administration, and inadequate fluid resuscitation. In one study, the adherence to SEP-1 for HOS was reported at 13% compared with 39.9% in COS. The differences in initial sepsis management included timing of antimicrobials and fluid resuscitation, which accounted for 23% of observed greater mortality risk among patients with HOS compared with COS.^6,8 It remains unclear how these recommendations should be applied and whether some of these recommendations confer the same benefits for patients with HOS as for those with COS. For example, administration of fluids conferred no additional benefit to patients with HOS, while rapid antimicrobial administration was shown to be associated with improved mortality in patients with HOS. Although, the optimal timing for treatment initiation and microbial coverage has not been established.

swujuloshespidrochesluphahechamudrabristosweroslacluwrehosiclawr

The path forward

Effective HOS management requires both individual and systematic approaches. How clinicians identify a patient with sepsis must be context-dependent. Although standard criteria exist for defining sepsis, the approach to a patient presenting to the ED from home should differ from that of a patient who has been hospitalized for several days, is postoperative, or is in the ICU on multiple forms of life support. Clinical medicine is context-dependent, and the same principles apply to sepsis management. To address the diagnostic uncertainty of the syndrome, providers must remain vigilant and maintain a clinical “iterative urgency” in diagnosing and managing sepsis. While machine learning algorithms have potential, they still rely on human intervention and interaction to navigate the complexities of HOS diagnosis.

At the system level, survival from sepsis is determined by the speed with which complex medical care is delivered and the effectiveness with which resources and personnel are mobilized and coordinated. The Hospital Sepsis Program Core Elements, released by the CDC, serves as an initial playbook to aid hospitals in establishing comprehensive sepsis improvement programs.

A second invaluable resource for hospitals in sepsis management is the rapid response team (RRT). Studies have shown that resolute RRTs can enhance patient outcomes and compliance with sepsis bundles; though, the composition and scope of these teams are crucial to their effectiveness. Responding to in-hospital emergencies and urgencies without conflicting responsibilities is an essential feature of a successful RRT. Often, they are familiar with bundles, protocols, and documentation, and members of these teams can offer clinical and/or technical expertise as well as support active participation and reengagement with bedside staff, which fosters trust and collaboration. This partnership is key, as these interactions instill a common mission and foster a culture of sepsis improvement that is required to achieve sustained success and improved patient outcomes.
 

Dr. Dugar is Director, Point-of-Care Ultrasound, Department of Critical Care, Respiratory Institute, Assistant Professor, Cleveland Clinic Lerner College of Medicine, Cleveland, OH. Dr. Jayaprakash is Associate Medical Director, Quality, Emergency Medicine, Physician Lead, Henry Ford Health Sepsis Program. Dr. Reilkoff is Executive Medical Director of Critical Care, M Health Fairview Intensive Care Units, Director of Acting Internship in Critical Care, University of Minnesota Medical School, Associate Professor of Medicine and Surgery, University of Minnesota. Dr. Duggal is Vice-Chair, Department of Critical Care, Respiratory Institute, Director, Critical Care Clinical Research, Associate Professor, Cleveland Clinic Lerner College of Medicine, Cleveland, OH
 

References

1. Singer M, Deutschman CS, Seymour CW, et al. The third international consensus definitions for sepsis and septic shock (sepsis-3). JAMA. 2016;315(8):801-810.

2. Ginestra JC, Coz Yataco AO, Dugar SP, Dettmer MR. Hospital-onset sepsis warrants expanded investigation and consideration as a unique clinical entity. Chest. 2024;S0012-3692(24):00039-4.

3. Markwart R, Saito H, Harder T, et al. Epidemiology and burden of sepsis acquired in hospitals and intensive care units: a systematic review and meta-analysis. Intensive Care Med. 2020;46(8):1536-1551.

4. Rhee C, Wang R, Zhang Z, et al. Epidemiology of hospital-onset versus community-onset sepsis in U.S. hospitals and association with mortality: a retrospective analysis using electronic clinical data. Crit Care Med. 2019;47(9):1169-1176.

5. Wong A, Otles E, Donnelly JP, et al. External validation of a widely implemented proprietary sepsis prediction model in hospitalized patients. JAMA Intern Med. 2021;181(8):1065-1070.

6. Baghdadi JD, Brook RH, Uslan DZ, et al. Association of a care bundle for early sepsis management with mortality among patients with hospital-onset or community-onset sepsis. JAMA Intern Med. 2020;180(5):707-716.

7. Baghdadi JD, Wong MD, Uslan DZ, et al. Adherence to the SEP-1 sepsis bundle in hospital-onset v. community-onset sepsis: a multicenter retrospective cohort study. J Gen Intern Med. 2020;35(4):1153-1160.

8. Basheer A. Patients with hospital-onset sepsis are less likely to receive sepsis bundle care than those with community-onset sepsis. Evid Based Nurs. 2021;24(3):99.
 

A 47-year-old woman with a history of cirrhosis is admitted with an acute kidney injury and altered mental status. On the initial workup, there are no signs of infection, and dehydration is determined to be the cause of the kidney injury. There are signs of improvement in the kidney injury with hydration. On hospital day 3, the patient develops a fever (101.9 ^oF) with accompanying leukocytosis to 14,000. Concerned for infection, the team starts empiric broad spectrum antibiotics for presumed spontaneous bacterial peritonitis. The next day (hospital day 4), a rapid response evaluation is activated as the patient is demonstrating increasing confusion, hypotension with a systolic blood pressure of 70 mm Hg, and elevated lactic acid. The patient receives 1 L of normal saline and transfers to the ICU. The new critical care fellow, who has just read up on sepsis early management bundles, and specifically the Severe Sepsis and Septic Shock Management Bundle (SEP-1), is reviewing the chart and notices a history of multidrug-resistant organisms in her urine cultures from an admission 2 months ago. They ask of the transferring team, “When was time zero, and was the 3-hour bundle completed?”

Sepsis is recognized as a medical emergency, which, without a prompt response, causes significant morbidity and mortality. In the United States alone, more than 1.7 million adults develop sepsis, with approximately 270,000 deaths and $57 billion in aggregate costs annually.¹ The excessive cost, both of human life and monetary, has led to the commitment of significant resources to sepsis care. Improved recognition and timely intervention for sepsis have led to noteworthy improvement in mortality. Most of this effort has been directed toward patients with sepsis diagnosed in the emergency department (ED) who are presenting with community-onset sepsis (COS). A new entity, called hospital-onset sepsis (HOS), has been described recently, defined by the Centers for Disease Control and Prevention (CDC) as both infection and organ dysfunction developing more than 48 hours after hospital admission.²

roretruspuspujifregusuvebristehaslaswacrinajadushuprechidruprovefrunehuslorenulegugubrisucobrajinelecrunuvovewauenewecuthedrucruslospashuroprocrust

A systematic review of 51 studies found approximately 23.6% of all sepsis cases are HOS. The proportion of HOS is even higher (more than 45%) in patients admitted to the ICU with sepsis.³ The outcome for this group remains comparatively poor. The hospital mortality among patients with HOS is 35%, which increases to 52% with progression to septic shock compared with 25% with COS.³ Even after adjusting for baseline factors that make one prone to developing infection in the hospital, a patient developing HOS has three-times a higher risk of dying compared with a patient who never developed sepsis and two-times a higher risk of dying compared with patients with COS.⁴Furthermore, HOS utilizes more resources with significantly longer ICU and hospital stays and has five-times the hospital cost compared with COS.⁴

The two most crucial factors in improving sepsis outcomes, as identified by the Surviving Sepsis Campaign guidelines, are: 1) prompt identification and treatment within the first few hours of onset and 2) regular reevaluation of the patient’s response to treatment.

kalodusluneslehipospastowruslitupomodregobuslabaloshuwutromichuprosle

Prompt identification

Diagnosing sepsis in the patient who is hospitalized is challenging. Patients admitted to the hospital often have competing comorbidities, have existing organ failure, or are in a postoperative/intervention state that clouds the application and interpretation of vital sign triggers customarily used to identify sepsis. The positive predictive value for all existing sepsis definitions and diagnostic criteria is dismally low. ⁵ And while automated electronic sepsis alerts may improve processes of care, they still have poor positive predictive value and have not impacted patient-centered outcomes (mortality or length of stay). Furthermore, the causative microorganisms often associated with hospital-acquired infections are complex, are drug-resistant, and can have courses which further delay identification. Finally, cognitive errors, such as anchoring biases or premature diagnosis closure, can contribute to provider-level identification delays that are only further exacerbated by system issues, such as capacity constraints, staffing issues, and differing paces between wards that tend to impede time-sensitive evaluations and interventions. ^4,6,7

Management

The SEP-1 core measure uses a framework of early recognition of infection and completion of the sepsis bundles in a timely manner to improve outcomes. Patients with HOS are less likely than those with COS to receive Centers for Medicare & Medicaid Services SEP-1-compliant care, including timely blood culture collection, initial and repeat lactate testing, and fluid resuscitation.⁸ The Surviving Sepsis Campaign has explored barriers to managing HOS. Among caregivers, these include delay in recognition, poor communication regarding change in patient status, not prioritizing treatment for sepsis, failure to measure lactate, delayed or no antimicrobial administration, and inadequate fluid resuscitation. In one study, the adherence to SEP-1 for HOS was reported at 13% compared with 39.9% in COS. The differences in initial sepsis management included timing of antimicrobials and fluid resuscitation, which accounted for 23% of observed greater mortality risk among patients with HOS compared with COS.^6,8 It remains unclear how these recommendations should be applied and whether some of these recommendations confer the same benefits for patients with HOS as for those with COS. For example, administration of fluids conferred no additional benefit to patients with HOS, while rapid antimicrobial administration was shown to be associated with improved mortality in patients with HOS. Although, the optimal timing for treatment initiation and microbial coverage has not been established.

swujuloshespidrochesluphahechamudrabristosweroslacluwrehosiclawr

The path forward

Effective HOS management requires both individual and systematic approaches. How clinicians identify a patient with sepsis must be context-dependent. Although standard criteria exist for defining sepsis, the approach to a patient presenting to the ED from home should differ from that of a patient who has been hospitalized for several days, is postoperative, or is in the ICU on multiple forms of life support. Clinical medicine is context-dependent, and the same principles apply to sepsis management. To address the diagnostic uncertainty of the syndrome, providers must remain vigilant and maintain a clinical “iterative urgency” in diagnosing and managing sepsis. While machine learning algorithms have potential, they still rely on human intervention and interaction to navigate the complexities of HOS diagnosis.

At the system level, survival from sepsis is determined by the speed with which complex medical care is delivered and the effectiveness with which resources and personnel are mobilized and coordinated. The Hospital Sepsis Program Core Elements, released by the CDC, serves as an initial playbook to aid hospitals in establishing comprehensive sepsis improvement programs.

A second invaluable resource for hospitals in sepsis management is the rapid response team (RRT). Studies have shown that resolute RRTs can enhance patient outcomes and compliance with sepsis bundles; though, the composition and scope of these teams are crucial to their effectiveness. Responding to in-hospital emergencies and urgencies without conflicting responsibilities is an essential feature of a successful RRT. Often, they are familiar with bundles, protocols, and documentation, and members of these teams can offer clinical and/or technical expertise as well as support active participation and reengagement with bedside staff, which fosters trust and collaboration. This partnership is key, as these interactions instill a common mission and foster a culture of sepsis improvement that is required to achieve sustained success and improved patient outcomes.
 

Dr. Dugar is Director, Point-of-Care Ultrasound, Department of Critical Care, Respiratory Institute, Assistant Professor, Cleveland Clinic Lerner College of Medicine, Cleveland, OH. Dr. Jayaprakash is Associate Medical Director, Quality, Emergency Medicine, Physician Lead, Henry Ford Health Sepsis Program. Dr. Reilkoff is Executive Medical Director of Critical Care, M Health Fairview Intensive Care Units, Director of Acting Internship in Critical Care, University of Minnesota Medical School, Associate Professor of Medicine and Surgery, University of Minnesota. Dr. Duggal is Vice-Chair, Department of Critical Care, Respiratory Institute, Director, Critical Care Clinical Research, Associate Professor, Cleveland Clinic Lerner College of Medicine, Cleveland, OH
 

References

1. Singer M, Deutschman CS, Seymour CW, et al. The third international consensus definitions for sepsis and septic shock (sepsis-3). JAMA. 2016;315(8):801-810.

2. Ginestra JC, Coz Yataco AO, Dugar SP, Dettmer MR. Hospital-onset sepsis warrants expanded investigation and consideration as a unique clinical entity. Chest. 2024;S0012-3692(24):00039-4.

3. Markwart R, Saito H, Harder T, et al. Epidemiology and burden of sepsis acquired in hospitals and intensive care units: a systematic review and meta-analysis. Intensive Care Med. 2020;46(8):1536-1551.

4. Rhee C, Wang R, Zhang Z, et al. Epidemiology of hospital-onset versus community-onset sepsis in U.S. hospitals and association with mortality: a retrospective analysis using electronic clinical data. Crit Care Med. 2019;47(9):1169-1176.

5. Wong A, Otles E, Donnelly JP, et al. External validation of a widely implemented proprietary sepsis prediction model in hospitalized patients. JAMA Intern Med. 2021;181(8):1065-1070.

6. Baghdadi JD, Brook RH, Uslan DZ, et al. Association of a care bundle for early sepsis management with mortality among patients with hospital-onset or community-onset sepsis. JAMA Intern Med. 2020;180(5):707-716.

7. Baghdadi JD, Wong MD, Uslan DZ, et al. Adherence to the SEP-1 sepsis bundle in hospital-onset v. community-onset sepsis: a multicenter retrospective cohort study. J Gen Intern Med. 2020;35(4):1153-1160.

8. Basheer A. Patients with hospital-onset sepsis are less likely to receive sepsis bundle care than those with community-onset sepsis. Evid Based Nurs. 2021;24(3):99.
 

A 47-year-old woman with a history of cirrhosis is admitted with an acute kidney injury and altered mental status. On the initial workup, there are no signs of infection, and dehydration is determined to be the cause of the kidney injury. There are signs of improvement in the kidney injury with hydration. On hospital day 3, the patient develops a fever (101.9 ^oF) with accompanying leukocytosis to 14,000. Concerned for infection, the team starts empiric broad spectrum antibiotics for presumed spontaneous bacterial peritonitis. The next day (hospital day 4), a rapid response evaluation is activated as the patient is demonstrating increasing confusion, hypotension with a systolic blood pressure of 70 mm Hg, and elevated lactic acid. The patient receives 1 L of normal saline and transfers to the ICU. The new critical care fellow, who has just read up on sepsis early management bundles, and specifically the Severe Sepsis and Septic Shock Management Bundle (SEP-1), is reviewing the chart and notices a history of multidrug-resistant organisms in her urine cultures from an admission 2 months ago. They ask of the transferring team, “When was time zero, and was the 3-hour bundle completed?”

Sepsis is recognized as a medical emergency, which, without a prompt response, causes significant morbidity and mortality. In the United States alone, more than 1.7 million adults develop sepsis, with approximately 270,000 deaths and $57 billion in aggregate costs annually.¹ The excessive cost, both of human life and monetary, has led to the commitment of significant resources to sepsis care. Improved recognition and timely intervention for sepsis have led to noteworthy improvement in mortality. Most of this effort has been directed toward patients with sepsis diagnosed in the emergency department (ED) who are presenting with community-onset sepsis (COS). A new entity, called hospital-onset sepsis (HOS), has been described recently, defined by the Centers for Disease Control and Prevention (CDC) as both infection and organ dysfunction developing more than 48 hours after hospital admission.²

roretruspuspujifregusuvebristehaslaswacrinajadushuprechidruprovefrunehuslorenulegugubrisucobrajinelecrunuvovewauenewecuthedrucruslospashuroprocrust

A systematic review of 51 studies found approximately 23.6% of all sepsis cases are HOS. The proportion of HOS is even higher (more than 45%) in patients admitted to the ICU with sepsis.³ The outcome for this group remains comparatively poor. The hospital mortality among patients with HOS is 35%, which increases to 52% with progression to septic shock compared with 25% with COS.³ Even after adjusting for baseline factors that make one prone to developing infection in the hospital, a patient developing HOS has three-times a higher risk of dying compared with a patient who never developed sepsis and two-times a higher risk of dying compared with patients with COS.⁴Furthermore, HOS utilizes more resources with significantly longer ICU and hospital stays and has five-times the hospital cost compared with COS.⁴

The two most crucial factors in improving sepsis outcomes, as identified by the Surviving Sepsis Campaign guidelines, are: 1) prompt identification and treatment within the first few hours of onset and 2) regular reevaluation of the patient’s response to treatment.

kalodusluneslehipospastowruslitupomodregobuslabaloshuwutromichuprosle

Prompt identification

Diagnosing sepsis in the patient who is hospitalized is challenging. Patients admitted to the hospital often have competing comorbidities, have existing organ failure, or are in a postoperative/intervention state that clouds the application and interpretation of vital sign triggers customarily used to identify sepsis. The positive predictive value for all existing sepsis definitions and diagnostic criteria is dismally low. ⁵ And while automated electronic sepsis alerts may improve processes of care, they still have poor positive predictive value and have not impacted patient-centered outcomes (mortality or length of stay). Furthermore, the causative microorganisms often associated with hospital-acquired infections are complex, are drug-resistant, and can have courses which further delay identification. Finally, cognitive errors, such as anchoring biases or premature diagnosis closure, can contribute to provider-level identification delays that are only further exacerbated by system issues, such as capacity constraints, staffing issues, and differing paces between wards that tend to impede time-sensitive evaluations and interventions. ^4,6,7

Management

The SEP-1 core measure uses a framework of early recognition of infection and completion of the sepsis bundles in a timely manner to improve outcomes. Patients with HOS are less likely than those with COS to receive Centers for Medicare & Medicaid Services SEP-1-compliant care, including timely blood culture collection, initial and repeat lactate testing, and fluid resuscitation.⁸ The Surviving Sepsis Campaign has explored barriers to managing HOS. Among caregivers, these include delay in recognition, poor communication regarding change in patient status, not prioritizing treatment for sepsis, failure to measure lactate, delayed or no antimicrobial administration, and inadequate fluid resuscitation. In one study, the adherence to SEP-1 for HOS was reported at 13% compared with 39.9% in COS. The differences in initial sepsis management included timing of antimicrobials and fluid resuscitation, which accounted for 23% of observed greater mortality risk among patients with HOS compared with COS.^6,8 It remains unclear how these recommendations should be applied and whether some of these recommendations confer the same benefits for patients with HOS as for those with COS. For example, administration of fluids conferred no additional benefit to patients with HOS, while rapid antimicrobial administration was shown to be associated with improved mortality in patients with HOS. Although, the optimal timing for treatment initiation and microbial coverage has not been established.

swujuloshespidrochesluphahechamudrabristosweroslacluwrehosiclawr

The path forward

Effective HOS management requires both individual and systematic approaches. How clinicians identify a patient with sepsis must be context-dependent. Although standard criteria exist for defining sepsis, the approach to a patient presenting to the ED from home should differ from that of a patient who has been hospitalized for several days, is postoperative, or is in the ICU on multiple forms of life support. Clinical medicine is context-dependent, and the same principles apply to sepsis management. To address the diagnostic uncertainty of the syndrome, providers must remain vigilant and maintain a clinical “iterative urgency” in diagnosing and managing sepsis. While machine learning algorithms have potential, they still rely on human intervention and interaction to navigate the complexities of HOS diagnosis.

At the system level, survival from sepsis is determined by the speed with which complex medical care is delivered and the effectiveness with which resources and personnel are mobilized and coordinated. The Hospital Sepsis Program Core Elements, released by the CDC, serves as an initial playbook to aid hospitals in establishing comprehensive sepsis improvement programs.

A second invaluable resource for hospitals in sepsis management is the rapid response team (RRT). Studies have shown that resolute RRTs can enhance patient outcomes and compliance with sepsis bundles; though, the composition and scope of these teams are crucial to their effectiveness. Responding to in-hospital emergencies and urgencies without conflicting responsibilities is an essential feature of a successful RRT. Often, they are familiar with bundles, protocols, and documentation, and members of these teams can offer clinical and/or technical expertise as well as support active participation and reengagement with bedside staff, which fosters trust and collaboration. This partnership is key, as these interactions instill a common mission and foster a culture of sepsis improvement that is required to achieve sustained success and improved patient outcomes.
 

Dr. Dugar is Director, Point-of-Care Ultrasound, Department of Critical Care, Respiratory Institute, Assistant Professor, Cleveland Clinic Lerner College of Medicine, Cleveland, OH. Dr. Jayaprakash is Associate Medical Director, Quality, Emergency Medicine, Physician Lead, Henry Ford Health Sepsis Program. Dr. Reilkoff is Executive Medical Director of Critical Care, M Health Fairview Intensive Care Units, Director of Acting Internship in Critical Care, University of Minnesota Medical School, Associate Professor of Medicine and Surgery, University of Minnesota. Dr. Duggal is Vice-Chair, Department of Critical Care, Respiratory Institute, Director, Critical Care Clinical Research, Associate Professor, Cleveland Clinic Lerner College of Medicine, Cleveland, OH
 

References

1. Singer M, Deutschman CS, Seymour CW, et al. The third international consensus definitions for sepsis and septic shock (sepsis-3). JAMA. 2016;315(8):801-810.

2. Ginestra JC, Coz Yataco AO, Dugar SP, Dettmer MR. Hospital-onset sepsis warrants expanded investigation and consideration as a unique clinical entity. Chest. 2024;S0012-3692(24):00039-4.

3. Markwart R, Saito H, Harder T, et al. Epidemiology and burden of sepsis acquired in hospitals and intensive care units: a systematic review and meta-analysis. Intensive Care Med. 2020;46(8):1536-1551.

4. Rhee C, Wang R, Zhang Z, et al. Epidemiology of hospital-onset versus community-onset sepsis in U.S. hospitals and association with mortality: a retrospective analysis using electronic clinical data. Crit Care Med. 2019;47(9):1169-1176.

5. Wong A, Otles E, Donnelly JP, et al. External validation of a widely implemented proprietary sepsis prediction model in hospitalized patients. JAMA Intern Med. 2021;181(8):1065-1070.

6. Baghdadi JD, Brook RH, Uslan DZ, et al. Association of a care bundle for early sepsis management with mortality among patients with hospital-onset or community-onset sepsis. JAMA Intern Med. 2020;180(5):707-716.

7. Baghdadi JD, Wong MD, Uslan DZ, et al. Adherence to the SEP-1 sepsis bundle in hospital-onset v. community-onset sepsis: a multicenter retrospective cohort study. J Gen Intern Med. 2020;35(4):1153-1160.

8. Basheer A. Patients with hospital-onset sepsis are less likely to receive sepsis bundle care than those with community-onset sepsis. Evid Based Nurs. 2021;24(3):99.
 

SAN DIEGO — Avoiding the use of antianaerobic antibiotics for empiric treatment of patients with sepsis can prevent depletion of beneficial bacteria in the gut microbiome and reduce both organ dysfunction and in-hospital mortality, a critical care specialists contends.

“You may not be personally moved by a 2- to 5-percent absolute difference in mortality, but sepsis is so common and so lethal that even small differences in outcomes can actually translate into enormous public health implications,” said Robert P. Dickson, MD a pulmonary and critical care specialist at the University of Michigan in Ann Arbor.

topudopikidivavohacrostaclostiwreclowrewodutrifruslebabrimikepawrosuclucrawogumeproswapachucrucluhiclugeuethedrorowestofraslislospebofrivulipribucluuauiprumospotheslothasecaluleclicifrauaspo

If instead of prescribing piperacillin-tazobactam (Zosyn; pip-tazo) for sepsis critical care specialists were to switch to cefepime “even if you make very conservative assumptions like a modest effect size, you’re still talking about [saving] thousands of lives a year,” he said in a scientific symposium at the American Thoracic Society’s international conference.

“This is why I say this isn’t really over the horizon; this is microbiome modulation that’s happening all the time,” he said.

Most patients with sepsis in a medical ICU with respiratory, urinary or bloodstream sources of infection do not have indications for antianaerobic antibiotics, and there are no head-to-head clinical trials demonstrating a benefit for one anti-sepsis antibiotic strategy over another he said.

“In contrast, every observational study between antianaerobic and non-antianaerobic shows benefits to the anaerobe-sparing [drugs], and it’s been shown with animal models too. So to my mind, it’s already practice changing. I need to be talked into giving antianaerobic antibiotics for septic patients” he said.
 

Targeting gut microbiota

There are three basic approaches to focusing on the gut microbiome as a therapeutic target. The hardest is attempting to engineer an ecosystem — a fiendishly complex task with unpredictable results that has never been shown to work in either the gut or in the ICU, Dr. Dickson said.

A second approach, the use of probiotics to repopulate the gut with beneficial bacteria, is largely futile in the ICU, as the large majority of patients are on antibiotics and can’t be safely weaned off of them while in critical care. In this situation, giving probiotics would be akin to try to repopulate a forest while a forest fire is raging, he said.

The third and easiest approach is to minimize dysbiosis — imbalance of organisms in the gut — in the first place.

Anaerobic bacteria in the gut have been shown in several different disease states and animals models to be protective against pneumonia, organ failure, and death.

To see whether antianaerobic antibiotics could increase risk for adverse outcomes in the ICU, Dr. Dickson and colleagues previously conducted a retrospective study of 3032 mechanically ventilated patients in their center who received antibiotics either with or without anaerobic coverage in the first 72 hours.

They found that patients treated with early antianaerobic antibiotics had decreased ventilator-associated pneumonia-free survival (hazard ratio [HR] 1.24), infection-free survival (HR 1.22), and overall survival (HR 1.14) compared with patients who received antibiotics without anaerobic cover (all comparisons statistically significant by confidence intervals).

In a subcohort of 116 patients for whom gut microbiota data compositions were available, those who received antianaerobic antibiotics had decreased initial gut bacterial density (P = .00038), increased microbiome expansion during hospitalization (P = .011), and domination of the microbiome by Enterobacteriaceae species (P = .045). They also found that Enterobacteriaceae were enriched among respiratory pathogens in antianaerobic treated patients, and that in murine models, treatment with antianaerobic antibiotics increased susceptibility to Enterobacteriaceae pneumonia and increased the risk of death from non-infectious injuries.
 

Pip-tazo vs. cefepime

In the ACORN (Antibiotic Choice on Renal Outcomes) trial, results of which were reported by this news organization in November 2023, there were no differences in the highest stage of acute kidney injury or death in the first 14 days between piperacillin-tazobactam and cefepime. Remarking on the results, lead investigator Edward T. Qian, MD, MSc from Vanderbilt University in Nashville, Tennessee, said “I think the big takeaway is that you should feel comfortable starting or using pip-tazo for your patients who are coming into the hospital and receiving empiric antibiotics for acute infection.”

But as Dr. Dickson’s group reported more recently in JAMA Internal Medicine, a 15-month pip-tazo shortage allowed the investigators to conduct a natural experiment comparing 90-day outcomes among 7569 patients with sepsis who received vancomycin plus either pip-tazo or cefepime.

They found in an instrumental variable analysis that piperacillin-tazobactam was associated with an absolute increase in mortality at 90 days of 5.0%, and that patients who received this antianaerobic antibiotic had 2.1 fewer organ failure–free days, 1.1 fewer ventilator-free days, and 1.5 fewer vasopressor-free days.

“Our study reveals the potential risks associated with empirical piperacillin-tazobactam in patients with sepsis without a specific indication for antianaerobic therapy. These findings should prompt reconsideration and further study of the widespread use of empirical antianaerobic antibiotics in sepsis,” the investigators concluded.
 

Who gets what?

In the question-and-answer at the end of the session, comoderator Christina Sarah Thornton, MD, PhD, FRCPC from the University of Calgary, Alberta, asked Dr. Dickson whether the question of antianaerobic overuse in the ICU “is a function that we aren’t able yet from a diagnostic perspective to identify the group that may need antianaerobes? Because we often don’t get culture data back in time for a critically ill patient. Do you think there could maybe be a more rapid diagnostic for these patients?”

He replied that “a lot of our problems would be solved if we had really good, reliable rapid diagnostics for infection,” but noted that most of the patients in the study mentioned above did not have indications for antianaerobics.

Asked by this reporter whether Dr. Dickson’s presentation changed her mind about the use of piperacillin-tazobactam in her patients, Dr. Thornton replied “Yes! It did for me.”

She noted that although in Canada respirologists don’t work in intensive care units, “it makes me wonder about just giving pip-tazo to patients that are really sick. It definitely changed my mind.”

The work of Dr. Dickson and colleagues is supported by National Institute of Health and Agency for Healthcare Research and Quality grants. He reported no other relevant disclosures. Dr. Thornton had no relevant disclosures.

SAN DIEGO — Avoiding the use of antianaerobic antibiotics for empiric treatment of patients with sepsis can prevent depletion of beneficial bacteria in the gut microbiome and reduce both organ dysfunction and in-hospital mortality, a critical care specialists contends.

“You may not be personally moved by a 2- to 5-percent absolute difference in mortality, but sepsis is so common and so lethal that even small differences in outcomes can actually translate into enormous public health implications,” said Robert P. Dickson, MD a pulmonary and critical care specialist at the University of Michigan in Ann Arbor.

topudopikidivavohacrostaclostiwreclowrewodutrifruslebabrimikepawrosuclucrawogumeproswapachucrucluhiclugeuethedrorowestofraslislospebofrivulipribucluuauiprumospotheslothasecaluleclicifrauaspo

If instead of prescribing piperacillin-tazobactam (Zosyn; pip-tazo) for sepsis critical care specialists were to switch to cefepime “even if you make very conservative assumptions like a modest effect size, you’re still talking about [saving] thousands of lives a year,” he said in a scientific symposium at the American Thoracic Society’s international conference.

“This is why I say this isn’t really over the horizon; this is microbiome modulation that’s happening all the time,” he said.

Most patients with sepsis in a medical ICU with respiratory, urinary or bloodstream sources of infection do not have indications for antianaerobic antibiotics, and there are no head-to-head clinical trials demonstrating a benefit for one anti-sepsis antibiotic strategy over another he said.

“In contrast, every observational study between antianaerobic and non-antianaerobic shows benefits to the anaerobe-sparing [drugs], and it’s been shown with animal models too. So to my mind, it’s already practice changing. I need to be talked into giving antianaerobic antibiotics for septic patients” he said.
 

Targeting gut microbiota

There are three basic approaches to focusing on the gut microbiome as a therapeutic target. The hardest is attempting to engineer an ecosystem — a fiendishly complex task with unpredictable results that has never been shown to work in either the gut or in the ICU, Dr. Dickson said.

A second approach, the use of probiotics to repopulate the gut with beneficial bacteria, is largely futile in the ICU, as the large majority of patients are on antibiotics and can’t be safely weaned off of them while in critical care. In this situation, giving probiotics would be akin to try to repopulate a forest while a forest fire is raging, he said.

The third and easiest approach is to minimize dysbiosis — imbalance of organisms in the gut — in the first place.

Anaerobic bacteria in the gut have been shown in several different disease states and animals models to be protective against pneumonia, organ failure, and death.

To see whether antianaerobic antibiotics could increase risk for adverse outcomes in the ICU, Dr. Dickson and colleagues previously conducted a retrospective study of 3032 mechanically ventilated patients in their center who received antibiotics either with or without anaerobic coverage in the first 72 hours.

They found that patients treated with early antianaerobic antibiotics had decreased ventilator-associated pneumonia-free survival (hazard ratio [HR] 1.24), infection-free survival (HR 1.22), and overall survival (HR 1.14) compared with patients who received antibiotics without anaerobic cover (all comparisons statistically significant by confidence intervals).

In a subcohort of 116 patients for whom gut microbiota data compositions were available, those who received antianaerobic antibiotics had decreased initial gut bacterial density (P = .00038), increased microbiome expansion during hospitalization (P = .011), and domination of the microbiome by Enterobacteriaceae species (P = .045). They also found that Enterobacteriaceae were enriched among respiratory pathogens in antianaerobic treated patients, and that in murine models, treatment with antianaerobic antibiotics increased susceptibility to Enterobacteriaceae pneumonia and increased the risk of death from non-infectious injuries.
 

Pip-tazo vs. cefepime

In the ACORN (Antibiotic Choice on Renal Outcomes) trial, results of which were reported by this news organization in November 2023, there were no differences in the highest stage of acute kidney injury or death in the first 14 days between piperacillin-tazobactam and cefepime. Remarking on the results, lead investigator Edward T. Qian, MD, MSc from Vanderbilt University in Nashville, Tennessee, said “I think the big takeaway is that you should feel comfortable starting or using pip-tazo for your patients who are coming into the hospital and receiving empiric antibiotics for acute infection.”

But as Dr. Dickson’s group reported more recently in JAMA Internal Medicine, a 15-month pip-tazo shortage allowed the investigators to conduct a natural experiment comparing 90-day outcomes among 7569 patients with sepsis who received vancomycin plus either pip-tazo or cefepime.

They found in an instrumental variable analysis that piperacillin-tazobactam was associated with an absolute increase in mortality at 90 days of 5.0%, and that patients who received this antianaerobic antibiotic had 2.1 fewer organ failure–free days, 1.1 fewer ventilator-free days, and 1.5 fewer vasopressor-free days.

“Our study reveals the potential risks associated with empirical piperacillin-tazobactam in patients with sepsis without a specific indication for antianaerobic therapy. These findings should prompt reconsideration and further study of the widespread use of empirical antianaerobic antibiotics in sepsis,” the investigators concluded.
 

Who gets what?

In the question-and-answer at the end of the session, comoderator Christina Sarah Thornton, MD, PhD, FRCPC from the University of Calgary, Alberta, asked Dr. Dickson whether the question of antianaerobic overuse in the ICU “is a function that we aren’t able yet from a diagnostic perspective to identify the group that may need antianaerobes? Because we often don’t get culture data back in time for a critically ill patient. Do you think there could maybe be a more rapid diagnostic for these patients?”

He replied that “a lot of our problems would be solved if we had really good, reliable rapid diagnostics for infection,” but noted that most of the patients in the study mentioned above did not have indications for antianaerobics.

Asked by this reporter whether Dr. Dickson’s presentation changed her mind about the use of piperacillin-tazobactam in her patients, Dr. Thornton replied “Yes! It did for me.”

She noted that although in Canada respirologists don’t work in intensive care units, “it makes me wonder about just giving pip-tazo to patients that are really sick. It definitely changed my mind.”

The work of Dr. Dickson and colleagues is supported by National Institute of Health and Agency for Healthcare Research and Quality grants. He reported no other relevant disclosures. Dr. Thornton had no relevant disclosures.

SAN DIEGO — Avoiding the use of antianaerobic antibiotics for empiric treatment of patients with sepsis can prevent depletion of beneficial bacteria in the gut microbiome and reduce both organ dysfunction and in-hospital mortality, a critical care specialists contends.

“You may not be personally moved by a 2- to 5-percent absolute difference in mortality, but sepsis is so common and so lethal that even small differences in outcomes can actually translate into enormous public health implications,” said Robert P. Dickson, MD a pulmonary and critical care specialist at the University of Michigan in Ann Arbor.

topudopikidivavohacrostaclostiwreclowrewodutrifruslebabrimikepawrosuclucrawogumeproswapachucrucluhiclugeuethedrorowestofraslislospebofrivulipribucluuauiprumospotheslothasecaluleclicifrauaspo

If instead of prescribing piperacillin-tazobactam (Zosyn; pip-tazo) for sepsis critical care specialists were to switch to cefepime “even if you make very conservative assumptions like a modest effect size, you’re still talking about [saving] thousands of lives a year,” he said in a scientific symposium at the American Thoracic Society’s international conference.

“This is why I say this isn’t really over the horizon; this is microbiome modulation that’s happening all the time,” he said.

Most patients with sepsis in a medical ICU with respiratory, urinary or bloodstream sources of infection do not have indications for antianaerobic antibiotics, and there are no head-to-head clinical trials demonstrating a benefit for one anti-sepsis antibiotic strategy over another he said.

“In contrast, every observational study between antianaerobic and non-antianaerobic shows benefits to the anaerobe-sparing [drugs], and it’s been shown with animal models too. So to my mind, it’s already practice changing. I need to be talked into giving antianaerobic antibiotics for septic patients” he said.
 

Targeting gut microbiota

There are three basic approaches to focusing on the gut microbiome as a therapeutic target. The hardest is attempting to engineer an ecosystem — a fiendishly complex task with unpredictable results that has never been shown to work in either the gut or in the ICU, Dr. Dickson said.

A second approach, the use of probiotics to repopulate the gut with beneficial bacteria, is largely futile in the ICU, as the large majority of patients are on antibiotics and can’t be safely weaned off of them while in critical care. In this situation, giving probiotics would be akin to try to repopulate a forest while a forest fire is raging, he said.

The third and easiest approach is to minimize dysbiosis — imbalance of organisms in the gut — in the first place.

Anaerobic bacteria in the gut have been shown in several different disease states and animals models to be protective against pneumonia, organ failure, and death.

To see whether antianaerobic antibiotics could increase risk for adverse outcomes in the ICU, Dr. Dickson and colleagues previously conducted a retrospective study of 3032 mechanically ventilated patients in their center who received antibiotics either with or without anaerobic coverage in the first 72 hours.

They found that patients treated with early antianaerobic antibiotics had decreased ventilator-associated pneumonia-free survival (hazard ratio [HR] 1.24), infection-free survival (HR 1.22), and overall survival (HR 1.14) compared with patients who received antibiotics without anaerobic cover (all comparisons statistically significant by confidence intervals).

In a subcohort of 116 patients for whom gut microbiota data compositions were available, those who received antianaerobic antibiotics had decreased initial gut bacterial density (P = .00038), increased microbiome expansion during hospitalization (P = .011), and domination of the microbiome by Enterobacteriaceae species (P = .045). They also found that Enterobacteriaceae were enriched among respiratory pathogens in antianaerobic treated patients, and that in murine models, treatment with antianaerobic antibiotics increased susceptibility to Enterobacteriaceae pneumonia and increased the risk of death from non-infectious injuries.
 

Pip-tazo vs. cefepime

In the ACORN (Antibiotic Choice on Renal Outcomes) trial, results of which were reported by this news organization in November 2023, there were no differences in the highest stage of acute kidney injury or death in the first 14 days between piperacillin-tazobactam and cefepime. Remarking on the results, lead investigator Edward T. Qian, MD, MSc from Vanderbilt University in Nashville, Tennessee, said “I think the big takeaway is that you should feel comfortable starting or using pip-tazo for your patients who are coming into the hospital and receiving empiric antibiotics for acute infection.”

But as Dr. Dickson’s group reported more recently in JAMA Internal Medicine, a 15-month pip-tazo shortage allowed the investigators to conduct a natural experiment comparing 90-day outcomes among 7569 patients with sepsis who received vancomycin plus either pip-tazo or cefepime.

They found in an instrumental variable analysis that piperacillin-tazobactam was associated with an absolute increase in mortality at 90 days of 5.0%, and that patients who received this antianaerobic antibiotic had 2.1 fewer organ failure–free days, 1.1 fewer ventilator-free days, and 1.5 fewer vasopressor-free days.

“Our study reveals the potential risks associated with empirical piperacillin-tazobactam in patients with sepsis without a specific indication for antianaerobic therapy. These findings should prompt reconsideration and further study of the widespread use of empirical antianaerobic antibiotics in sepsis,” the investigators concluded.
 

Who gets what?

In the question-and-answer at the end of the session, comoderator Christina Sarah Thornton, MD, PhD, FRCPC from the University of Calgary, Alberta, asked Dr. Dickson whether the question of antianaerobic overuse in the ICU “is a function that we aren’t able yet from a diagnostic perspective to identify the group that may need antianaerobes? Because we often don’t get culture data back in time for a critically ill patient. Do you think there could maybe be a more rapid diagnostic for these patients?”

He replied that “a lot of our problems would be solved if we had really good, reliable rapid diagnostics for infection,” but noted that most of the patients in the study mentioned above did not have indications for antianaerobics.

Asked by this reporter whether Dr. Dickson’s presentation changed her mind about the use of piperacillin-tazobactam in her patients, Dr. Thornton replied “Yes! It did for me.”

She noted that although in Canada respirologists don’t work in intensive care units, “it makes me wonder about just giving pip-tazo to patients that are really sick. It definitely changed my mind.”

The work of Dr. Dickson and colleagues is supported by National Institute of Health and Agency for Healthcare Research and Quality grants. He reported no other relevant disclosures. Dr. Thornton had no relevant disclosures.

Emergencies happen anywhere, anytime, and sometimes, medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series telling these stories.

Jennifer Suders, DO: We were in Florida with our 1-year-old daughter visiting my parents. They moved to an area called Hallandale Beach and live in a high-rise community with a few different pools and spas.

Dan and I were in the spa area at the gym. He was getting me to hurry up because we were supposed to meet my parents who were with our daughter. I was sort of moseying and taking my time.

We were walking by one of the pool decks to get into the building when I heard what sounded like a slap. My first thought was that maybe somebody was choking and someone was hitting their back. Choking has always been my biggest fear with our daughter.

I turned and saw some people who seemed frantic. I looked at Dan and started to ask, “Do you think they need help?” I don’t even think I got the whole sentence out before this mom whipped her head around. I’ll never forget her dark brown hair flying. She screamed, “HELP!”

Dan and I just ran. I let go of my backpack and iPad and water bottle. They scattered across the pool deck. I instantly had my phone in my hand dialing 911.

Daniel Suders, DO: That’s what they teach us, to call 911 first. I didn’t think of it in the moment, but Jenny did.

Jennifer Suders: There was a little boy lying on the ground. Totally gray. He looked about 3 years old. His mom was distraught. His grandparents were standing there in shock with his older brother who was around 5. He was scared and whimpering.

Dan and I got down on either side of the boy and checked for a pulse. We couldn’t feel anything. Dan started chest compressions. I was talking to the 911 operator, and then I gave two rescue breaths. We did a sternal rub.

I was kind of yelling in the boy’s face, trying to get him to respond. I tried English and Russian because there’s a big Russian community there, and my family speaks Russian. The grandma asked us if we knew what we were doing.

Daniel Suders: I think she asked if Jenny was a nurse.

Jennifer Suders: Common misconception. Suddenly, the boy started vomiting, and so much water poured out. We turned him on his side, and he had two or three more episodes of spitting up the water. After that, we could see the color start to come back into his face. His eyes started fluttering.

We thought he was probably coming back. But we were too scared to say that in case we were wrong, and he went back under. So, we just held him steady. We didn’t know what had happened, if he might have hit his head, so we needed to keep him still.

Daniel Suders: It was amazing when those eyes opened, and he started to wake up.

Jennifer Suders: It felt like my heart had stopped while I was waiting for his to start.

Daniel Suders: He was clutching his chest like it hurt and started calling for his mom. He was crying and wanting to get in his mom’s arms. We had to keep him from standing up and walking.

Jennifer Suders: He was clearly scared. There were all these strange faces around him. I kept looking at my phone, anxiously waiting for EMS to come. They got there about 8 or 9 minutes later.

At some point, the father walked in with their daughter, a baby under a year old. He was in shock, not knowing what was going on. The grandma explained that the boy had been jumping into the pool over and over with his brother. All of a sudden, they looked over, and he was just lying there, floating, face down. They were right there; they were watching him. It was just that quick.

Daniel Suders: They pulled him out right away, and that was a big thing on his side that it was caught so quickly. He didn’t have to wait long to start resuscitation.

Jennifer Suders: Once EMS got there and assessed him, they put him and his mom on the stretcher. I remember watching them wheel it through the double doors to get to the elevator. As soon as they were gone, I just turned around and broke down. I had been in doctor mode if you will. Straight to the point. No nonsense. Suddenly, I went back into civilian mode, and my emotions just bubbled up.

After we left, we went to meet my parents who had our kid. Dan just beelined toward her and scooped her up and wouldn’t let her go.

For the rest of the day, it was all I could think about. It took me a while to fall asleep that night, and it was the first thing I thought when I woke up the next morning. We were hopeful that the boy was going to be okay, but you never know. We didn’t call the hospital because with HIPAA, I didn’t know if they could tell us anything.

And then the next day — there they were. The family was back at the pool. The little boy was running around like nothing had happened. We were a little surprised. But I would hate for him to be scared of the pool for the rest of his life. His family was watching him like a hawk.

They told us that the boy and his mom had stayed overnight in the ER, but only as a precaution. He didn’t have any more vomiting. He was absolutely fine. They were incredibly grateful.

We got their names and exchanged numbers and took a picture. That’s all I wanted — a photo to remember them.

A day or so later, we saw them again at a nearby park. The boy was climbing trees and seemed completely normal. It was the best outcome we could have hoped for.

Daniel Suders: My biggest worry was any harm to his chest from the resuscitation, or of course how long he was without oxygen. But everyone says that kids are really resilient. I work with adults, so I don’t have a lot of experience.

As a hospitalist, we don’t always see a lot of success with CPR. It’s often an elderly person who just doesn’t have much of a chance. That same week before our vacation, I had lost a 90-year-old in the hospital. It was such a juxtaposition — a 3-year-old with their whole life in front of them. We were able to preserve that, and it was incredible.

Jennifer Suders: I’m a nephrologist, so my field is pretty calm. No big emergencies. We have patients on the floor, but if a code gets called, there’s a team that comes in from the intensive care unit. I always kind of wondered what I would do if I was presented with a scenario like this.

Daniel Suders: We have a lot of friends that do ER medicine, and I felt like those were the guys that really understood when we told them the story. One friend said to me, “By the time they get to us, they’re either in bad shape or they’re better already.” A lot depends on what happens in the field.

Jennifer Suders: I’m even more vigilant about pool safety now. I want to make sure parents know that drowning doesn›t look like flailing theatrics. It can be soundless. Three adults were right next to this little boy and didn›t realize until they looked down and saw him.

If we hadn’t been there, I don’t know if anyone would’ve been able to step in. No one else was medically trained. But I think the message is — you don’t have to be. Anyone can take a CPR class.

When I told my parents, my dad said, “Oh my gosh, I would’ve laid right down there next to that kid and passed out.” Without any training, it’s petrifying to see something like that.

I think about how we could have stayed in the gym longer and been too late. Or we could have gotten on the elevator earlier and been gone. Two minutes, and it would’ve been a story we heard later, not one we were a part of. It feels like we were at a true crossroads in that moment where that boy could have lived or died. And the stars aligned perfectly.

We had no medicine, no monitors, nothing but our hands and our breaths. And we helped a family continue their vacation rather than plan a funeral.

Jennifer Suders, DO, is a nephrologist at West Virginia University Medicine Wheeling Clinic. Daniel Suders, DO, is a hospitalist at West Virginia University Medicine Reynolds Memorial Hospital.

A version of this article appeared on Medscape.com .

Emergencies happen anywhere, anytime, and sometimes, medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series telling these stories.

Jennifer Suders, DO: We were in Florida with our 1-year-old daughter visiting my parents. They moved to an area called Hallandale Beach and live in a high-rise community with a few different pools and spas.

Dan and I were in the spa area at the gym. He was getting me to hurry up because we were supposed to meet my parents who were with our daughter. I was sort of moseying and taking my time.

We were walking by one of the pool decks to get into the building when I heard what sounded like a slap. My first thought was that maybe somebody was choking and someone was hitting their back. Choking has always been my biggest fear with our daughter.

I turned and saw some people who seemed frantic. I looked at Dan and started to ask, “Do you think they need help?” I don’t even think I got the whole sentence out before this mom whipped her head around. I’ll never forget her dark brown hair flying. She screamed, “HELP!”

Dan and I just ran. I let go of my backpack and iPad and water bottle. They scattered across the pool deck. I instantly had my phone in my hand dialing 911.

Daniel Suders, DO: That’s what they teach us, to call 911 first. I didn’t think of it in the moment, but Jenny did.

Jennifer Suders: There was a little boy lying on the ground. Totally gray. He looked about 3 years old. His mom was distraught. His grandparents were standing there in shock with his older brother who was around 5. He was scared and whimpering.

Dan and I got down on either side of the boy and checked for a pulse. We couldn’t feel anything. Dan started chest compressions. I was talking to the 911 operator, and then I gave two rescue breaths. We did a sternal rub.

I was kind of yelling in the boy’s face, trying to get him to respond. I tried English and Russian because there’s a big Russian community there, and my family speaks Russian. The grandma asked us if we knew what we were doing.

Daniel Suders: I think she asked if Jenny was a nurse.

Jennifer Suders: Common misconception. Suddenly, the boy started vomiting, and so much water poured out. We turned him on his side, and he had two or three more episodes of spitting up the water. After that, we could see the color start to come back into his face. His eyes started fluttering.

We thought he was probably coming back. But we were too scared to say that in case we were wrong, and he went back under. So, we just held him steady. We didn’t know what had happened, if he might have hit his head, so we needed to keep him still.

Daniel Suders: It was amazing when those eyes opened, and he started to wake up.

Jennifer Suders: It felt like my heart had stopped while I was waiting for his to start.

Daniel Suders: He was clutching his chest like it hurt and started calling for his mom. He was crying and wanting to get in his mom’s arms. We had to keep him from standing up and walking.

Jennifer Suders: He was clearly scared. There were all these strange faces around him. I kept looking at my phone, anxiously waiting for EMS to come. They got there about 8 or 9 minutes later.

At some point, the father walked in with their daughter, a baby under a year old. He was in shock, not knowing what was going on. The grandma explained that the boy had been jumping into the pool over and over with his brother. All of a sudden, they looked over, and he was just lying there, floating, face down. They were right there; they were watching him. It was just that quick.

Daniel Suders: They pulled him out right away, and that was a big thing on his side that it was caught so quickly. He didn’t have to wait long to start resuscitation.

Jennifer Suders: Once EMS got there and assessed him, they put him and his mom on the stretcher. I remember watching them wheel it through the double doors to get to the elevator. As soon as they were gone, I just turned around and broke down. I had been in doctor mode if you will. Straight to the point. No nonsense. Suddenly, I went back into civilian mode, and my emotions just bubbled up.

After we left, we went to meet my parents who had our kid. Dan just beelined toward her and scooped her up and wouldn’t let her go.

For the rest of the day, it was all I could think about. It took me a while to fall asleep that night, and it was the first thing I thought when I woke up the next morning. We were hopeful that the boy was going to be okay, but you never know. We didn’t call the hospital because with HIPAA, I didn’t know if they could tell us anything.

And then the next day — there they were. The family was back at the pool. The little boy was running around like nothing had happened. We were a little surprised. But I would hate for him to be scared of the pool for the rest of his life. His family was watching him like a hawk.

They told us that the boy and his mom had stayed overnight in the ER, but only as a precaution. He didn’t have any more vomiting. He was absolutely fine. They were incredibly grateful.

We got their names and exchanged numbers and took a picture. That’s all I wanted — a photo to remember them.

A day or so later, we saw them again at a nearby park. The boy was climbing trees and seemed completely normal. It was the best outcome we could have hoped for.

Daniel Suders: My biggest worry was any harm to his chest from the resuscitation, or of course how long he was without oxygen. But everyone says that kids are really resilient. I work with adults, so I don’t have a lot of experience.

As a hospitalist, we don’t always see a lot of success with CPR. It’s often an elderly person who just doesn’t have much of a chance. That same week before our vacation, I had lost a 90-year-old in the hospital. It was such a juxtaposition — a 3-year-old with their whole life in front of them. We were able to preserve that, and it was incredible.

Jennifer Suders: I’m a nephrologist, so my field is pretty calm. No big emergencies. We have patients on the floor, but if a code gets called, there’s a team that comes in from the intensive care unit. I always kind of wondered what I would do if I was presented with a scenario like this.

Daniel Suders: We have a lot of friends that do ER medicine, and I felt like those were the guys that really understood when we told them the story. One friend said to me, “By the time they get to us, they’re either in bad shape or they’re better already.” A lot depends on what happens in the field.

Jennifer Suders: I’m even more vigilant about pool safety now. I want to make sure parents know that drowning doesn›t look like flailing theatrics. It can be soundless. Three adults were right next to this little boy and didn›t realize until they looked down and saw him.

If we hadn’t been there, I don’t know if anyone would’ve been able to step in. No one else was medically trained. But I think the message is — you don’t have to be. Anyone can take a CPR class.

When I told my parents, my dad said, “Oh my gosh, I would’ve laid right down there next to that kid and passed out.” Without any training, it’s petrifying to see something like that.

I think about how we could have stayed in the gym longer and been too late. Or we could have gotten on the elevator earlier and been gone. Two minutes, and it would’ve been a story we heard later, not one we were a part of. It feels like we were at a true crossroads in that moment where that boy could have lived or died. And the stars aligned perfectly.

We had no medicine, no monitors, nothing but our hands and our breaths. And we helped a family continue their vacation rather than plan a funeral.

Jennifer Suders, DO, is a nephrologist at West Virginia University Medicine Wheeling Clinic. Daniel Suders, DO, is a hospitalist at West Virginia University Medicine Reynolds Memorial Hospital.

A version of this article appeared on Medscape.com .

Emergencies happen anywhere, anytime, and sometimes, medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series telling these stories.

Jennifer Suders, DO: We were in Florida with our 1-year-old daughter visiting my parents. They moved to an area called Hallandale Beach and live in a high-rise community with a few different pools and spas.

Dan and I were in the spa area at the gym. He was getting me to hurry up because we were supposed to meet my parents who were with our daughter. I was sort of moseying and taking my time.

We were walking by one of the pool decks to get into the building when I heard what sounded like a slap. My first thought was that maybe somebody was choking and someone was hitting their back. Choking has always been my biggest fear with our daughter.

I turned and saw some people who seemed frantic. I looked at Dan and started to ask, “Do you think they need help?” I don’t even think I got the whole sentence out before this mom whipped her head around. I’ll never forget her dark brown hair flying. She screamed, “HELP!”

Dan and I just ran. I let go of my backpack and iPad and water bottle. They scattered across the pool deck. I instantly had my phone in my hand dialing 911.

Daniel Suders, DO: That’s what they teach us, to call 911 first. I didn’t think of it in the moment, but Jenny did.

Jennifer Suders: There was a little boy lying on the ground. Totally gray. He looked about 3 years old. His mom was distraught. His grandparents were standing there in shock with his older brother who was around 5. He was scared and whimpering.

Dan and I got down on either side of the boy and checked for a pulse. We couldn’t feel anything. Dan started chest compressions. I was talking to the 911 operator, and then I gave two rescue breaths. We did a sternal rub.

I was kind of yelling in the boy’s face, trying to get him to respond. I tried English and Russian because there’s a big Russian community there, and my family speaks Russian. The grandma asked us if we knew what we were doing.

Daniel Suders: I think she asked if Jenny was a nurse.

Jennifer Suders: Common misconception. Suddenly, the boy started vomiting, and so much water poured out. We turned him on his side, and he had two or three more episodes of spitting up the water. After that, we could see the color start to come back into his face. His eyes started fluttering.

We thought he was probably coming back. But we were too scared to say that in case we were wrong, and he went back under. So, we just held him steady. We didn’t know what had happened, if he might have hit his head, so we needed to keep him still.

Daniel Suders: It was amazing when those eyes opened, and he started to wake up.

Jennifer Suders: It felt like my heart had stopped while I was waiting for his to start.

Daniel Suders: He was clutching his chest like it hurt and started calling for his mom. He was crying and wanting to get in his mom’s arms. We had to keep him from standing up and walking.

Jennifer Suders: He was clearly scared. There were all these strange faces around him. I kept looking at my phone, anxiously waiting for EMS to come. They got there about 8 or 9 minutes later.

At some point, the father walked in with their daughter, a baby under a year old. He was in shock, not knowing what was going on. The grandma explained that the boy had been jumping into the pool over and over with his brother. All of a sudden, they looked over, and he was just lying there, floating, face down. They were right there; they were watching him. It was just that quick.

Daniel Suders: They pulled him out right away, and that was a big thing on his side that it was caught so quickly. He didn’t have to wait long to start resuscitation.

Jennifer Suders: Once EMS got there and assessed him, they put him and his mom on the stretcher. I remember watching them wheel it through the double doors to get to the elevator. As soon as they were gone, I just turned around and broke down. I had been in doctor mode if you will. Straight to the point. No nonsense. Suddenly, I went back into civilian mode, and my emotions just bubbled up.

After we left, we went to meet my parents who had our kid. Dan just beelined toward her and scooped her up and wouldn’t let her go.

For the rest of the day, it was all I could think about. It took me a while to fall asleep that night, and it was the first thing I thought when I woke up the next morning. We were hopeful that the boy was going to be okay, but you never know. We didn’t call the hospital because with HIPAA, I didn’t know if they could tell us anything.

And then the next day — there they were. The family was back at the pool. The little boy was running around like nothing had happened. We were a little surprised. But I would hate for him to be scared of the pool for the rest of his life. His family was watching him like a hawk.

They told us that the boy and his mom had stayed overnight in the ER, but only as a precaution. He didn’t have any more vomiting. He was absolutely fine. They were incredibly grateful.

We got their names and exchanged numbers and took a picture. That’s all I wanted — a photo to remember them.

A day or so later, we saw them again at a nearby park. The boy was climbing trees and seemed completely normal. It was the best outcome we could have hoped for.

Daniel Suders: My biggest worry was any harm to his chest from the resuscitation, or of course how long he was without oxygen. But everyone says that kids are really resilient. I work with adults, so I don’t have a lot of experience.

As a hospitalist, we don’t always see a lot of success with CPR. It’s often an elderly person who just doesn’t have much of a chance. That same week before our vacation, I had lost a 90-year-old in the hospital. It was such a juxtaposition — a 3-year-old with their whole life in front of them. We were able to preserve that, and it was incredible.

Jennifer Suders: I’m a nephrologist, so my field is pretty calm. No big emergencies. We have patients on the floor, but if a code gets called, there’s a team that comes in from the intensive care unit. I always kind of wondered what I would do if I was presented with a scenario like this.

Daniel Suders: We have a lot of friends that do ER medicine, and I felt like those were the guys that really understood when we told them the story. One friend said to me, “By the time they get to us, they’re either in bad shape or they’re better already.” A lot depends on what happens in the field.

Jennifer Suders: I’m even more vigilant about pool safety now. I want to make sure parents know that drowning doesn›t look like flailing theatrics. It can be soundless. Three adults were right next to this little boy and didn›t realize until they looked down and saw him.

If we hadn’t been there, I don’t know if anyone would’ve been able to step in. No one else was medically trained. But I think the message is — you don’t have to be. Anyone can take a CPR class.

When I told my parents, my dad said, “Oh my gosh, I would’ve laid right down there next to that kid and passed out.” Without any training, it’s petrifying to see something like that.

I think about how we could have stayed in the gym longer and been too late. Or we could have gotten on the elevator earlier and been gone. Two minutes, and it would’ve been a story we heard later, not one we were a part of. It feels like we were at a true crossroads in that moment where that boy could have lived or died. And the stars aligned perfectly.

We had no medicine, no monitors, nothing but our hands and our breaths. And we helped a family continue their vacation rather than plan a funeral.

Jennifer Suders, DO, is a nephrologist at West Virginia University Medicine Wheeling Clinic. Daniel Suders, DO, is a hospitalist at West Virginia University Medicine Reynolds Memorial Hospital.

A version of this article appeared on Medscape.com .

Thoracic Oncology and Chest Procedures Network

Ultrasound and Chest Imaging Section

wiwisworuhokakadrasleuubaswucaswuclatrumuswopecruswefrerapefrephowraphidudibrefrucauovatrufrepephubrudepujupiphurokimupuwruwrasliprocurovarebustebichepruseshotheciuibudophemisweswechishitroslijuphastatrus

Historically, transesophageal ultrasound (TEE) has been regarded as a diagnostic and management tool for structural heart disease in relatively stable patients. However, TEE is more commonly being utilized by intensivists as a first-line tool in the diagnostics and management of patients in the ICU.

brabrugifrushiviprufripretagolusauokatreclerastostatrotasouashitroclupuverinukuvaloswekibrucheclebeuoneclaspubrovaueswivanowushushovirojo

TEE also provides ultrasonographic evaluation of the lungs through transesophageal lung ultrasound (TELUS). TELUS allows for visualization of all six traditional lung zones utilized in traditional lung ultrasound.⁵ Patients with severe acute respiratory distress syndrome may greatly benefit from TEE utilization. TEE enables early detection of right ventricular dysfunction, aids in fluid management, and assesses the severity of lung consolidation, thereby facilitating prompt utilization of prone positioning or adjustments in positive end-expiratory pressure.

Cardiac arrest is another unique opportunity for TEE utilization by providing real-time cardiac visualization during active cardiopulmonary resuscitation. This facilitates optimal chest compression positioning, early recognition of arrhythmia, timely identification of reversible cause, and procedural guidance for ECMO-assisted CPR.⁶ TEE is an invaluable tool for the modern-day intensivist, providing rapid and accurate assessments, and therefore holds the potential to become standard of care in the ICU.

References

1. Prager R, Bowdridge J, Pratte M, Cheng J, McInnes MD, Arntfield R. Indications, clinical impact, and complications of critical care transesophageal echocardiography: a scoping review. J Intensive Care Med. 2023;38(3):245-272. Preprint. Posted online July 19, 2022. PMID: 35854414; PMCID: PMC9806486. doi: 10.1177/08850666221115348

2. Hüttemann E, Schelenz C, Kara F, Chatzinikolaou K, Reinhart K. The use and safety of transoesophageal echocardiography in the general ICU – a minireview. Acta Anaesthesiol Scand. 2004;48(7):827-36. PMID: 15242426. doi: 10.1111/j.0001-5172.2004.00423.x

3. Mayo PH, Narasimhan M, Koenig S. Critical care transesophageal echocardiography. Chest. 2015;148(5):1323-1332. PMID: 26204465. doi: 10.1378/chest.15-0260

4. Prager R, Ainsworth C, Arntfield R. Critical care transesophageal echocardiography for the resuscitation of shock: an important diagnostic skill for the modern intensivist. Chest. 2023;163(2):268-269. PMID: 36759112. doi: 10.1016/j.chest.2022.09.001

5. Cavayas YA, Girard M, Desjardins G, Denault AY. Transesophageal lung ultrasonography: a novel technique for investigating hypoxemia. Can J Anaesth. 2016;63(11):1266-76. Preprint. Posted online July 29, 2016. PMID: 27473720. doi: 10.1007/s12630-016-0702-2

6. Teran F, Prats MI, Nelson BP, et al. Focused transesophageal echocardiography during cardiac arrest resuscitation: JACC review wopic of the Week. J Am Coll Cardiol. 2020;76(6):745-754. PMID: 32762909. doi: 10.1016/j.jacc.2020.05.074

Thoracic Oncology and Chest Procedures Network

Ultrasound and Chest Imaging Section

wiwisworuhokakadrasleuubaswucaswuclatrumuswopecruswefrerapefrephowraphidudibrefrucauovatrufrepephubrudepujupiphurokimupuwruwrasliprocurovarebustebichepruseshotheciuibudophemisweswechishitroslijuphastatrus

Historically, transesophageal ultrasound (TEE) has been regarded as a diagnostic and management tool for structural heart disease in relatively stable patients. However, TEE is more commonly being utilized by intensivists as a first-line tool in the diagnostics and management of patients in the ICU.

brabrugifrushiviprufripretagolusauokatreclerastostatrotasouashitroclupuverinukuvaloswekibrucheclebeuoneclaspubrovaueswivanowushushovirojo

TEE also provides ultrasonographic evaluation of the lungs through transesophageal lung ultrasound (TELUS). TELUS allows for visualization of all six traditional lung zones utilized in traditional lung ultrasound.⁵ Patients with severe acute respiratory distress syndrome may greatly benefit from TEE utilization. TEE enables early detection of right ventricular dysfunction, aids in fluid management, and assesses the severity of lung consolidation, thereby facilitating prompt utilization of prone positioning or adjustments in positive end-expiratory pressure.

Cardiac arrest is another unique opportunity for TEE utilization by providing real-time cardiac visualization during active cardiopulmonary resuscitation. This facilitates optimal chest compression positioning, early recognition of arrhythmia, timely identification of reversible cause, and procedural guidance for ECMO-assisted CPR.⁶ TEE is an invaluable tool for the modern-day intensivist, providing rapid and accurate assessments, and therefore holds the potential to become standard of care in the ICU.

References

1. Prager R, Bowdridge J, Pratte M, Cheng J, McInnes MD, Arntfield R. Indications, clinical impact, and complications of critical care transesophageal echocardiography: a scoping review. J Intensive Care Med. 2023;38(3):245-272. Preprint. Posted online July 19, 2022. PMID: 35854414; PMCID: PMC9806486. doi: 10.1177/08850666221115348

2. Hüttemann E, Schelenz C, Kara F, Chatzinikolaou K, Reinhart K. The use and safety of transoesophageal echocardiography in the general ICU – a minireview. Acta Anaesthesiol Scand. 2004;48(7):827-36. PMID: 15242426. doi: 10.1111/j.0001-5172.2004.00423.x

3. Mayo PH, Narasimhan M, Koenig S. Critical care transesophageal echocardiography. Chest. 2015;148(5):1323-1332. PMID: 26204465. doi: 10.1378/chest.15-0260

4. Prager R, Ainsworth C, Arntfield R. Critical care transesophageal echocardiography for the resuscitation of shock: an important diagnostic skill for the modern intensivist. Chest. 2023;163(2):268-269. PMID: 36759112. doi: 10.1016/j.chest.2022.09.001

5. Cavayas YA, Girard M, Desjardins G, Denault AY. Transesophageal lung ultrasonography: a novel technique for investigating hypoxemia. Can J Anaesth. 2016;63(11):1266-76. Preprint. Posted online July 29, 2016. PMID: 27473720. doi: 10.1007/s12630-016-0702-2

6. Teran F, Prats MI, Nelson BP, et al. Focused transesophageal echocardiography during cardiac arrest resuscitation: JACC review wopic of the Week. J Am Coll Cardiol. 2020;76(6):745-754. PMID: 32762909. doi: 10.1016/j.jacc.2020.05.074

Thoracic Oncology and Chest Procedures Network

Ultrasound and Chest Imaging Section

wiwisworuhokakadrasleuubaswucaswuclatrumuswopecruswefrerapefrephowraphidudibrefrucauovatrufrepephubrudepujupiphurokimupuwruwrasliprocurovarebustebichepruseshotheciuibudophemisweswechishitroslijuphastatrus

Historically, transesophageal ultrasound (TEE) has been regarded as a diagnostic and management tool for structural heart disease in relatively stable patients. However, TEE is more commonly being utilized by intensivists as a first-line tool in the diagnostics and management of patients in the ICU.

brabrugifrushiviprufripretagolusauokatreclerastostatrotasouashitroclupuverinukuvaloswekibrucheclebeuoneclaspubrovaueswivanowushushovirojo

TEE also provides ultrasonographic evaluation of the lungs through transesophageal lung ultrasound (TELUS). TELUS allows for visualization of all six traditional lung zones utilized in traditional lung ultrasound.⁵ Patients with severe acute respiratory distress syndrome may greatly benefit from TEE utilization. TEE enables early detection of right ventricular dysfunction, aids in fluid management, and assesses the severity of lung consolidation, thereby facilitating prompt utilization of prone positioning or adjustments in positive end-expiratory pressure.

Cardiac arrest is another unique opportunity for TEE utilization by providing real-time cardiac visualization during active cardiopulmonary resuscitation. This facilitates optimal chest compression positioning, early recognition of arrhythmia, timely identification of reversible cause, and procedural guidance for ECMO-assisted CPR.⁶ TEE is an invaluable tool for the modern-day intensivist, providing rapid and accurate assessments, and therefore holds the potential to become standard of care in the ICU.

References

1. Prager R, Bowdridge J, Pratte M, Cheng J, McInnes MD, Arntfield R. Indications, clinical impact, and complications of critical care transesophageal echocardiography: a scoping review. J Intensive Care Med. 2023;38(3):245-272. Preprint. Posted online July 19, 2022. PMID: 35854414; PMCID: PMC9806486. doi: 10.1177/08850666221115348

2. Hüttemann E, Schelenz C, Kara F, Chatzinikolaou K, Reinhart K. The use and safety of transoesophageal echocardiography in the general ICU – a minireview. Acta Anaesthesiol Scand. 2004;48(7):827-36. PMID: 15242426. doi: 10.1111/j.0001-5172.2004.00423.x

3. Mayo PH, Narasimhan M, Koenig S. Critical care transesophageal echocardiography. Chest. 2015;148(5):1323-1332. PMID: 26204465. doi: 10.1378/chest.15-0260

4. Prager R, Ainsworth C, Arntfield R. Critical care transesophageal echocardiography for the resuscitation of shock: an important diagnostic skill for the modern intensivist. Chest. 2023;163(2):268-269. PMID: 36759112. doi: 10.1016/j.chest.2022.09.001

5. Cavayas YA, Girard M, Desjardins G, Denault AY. Transesophageal lung ultrasonography: a novel technique for investigating hypoxemia. Can J Anaesth. 2016;63(11):1266-76. Preprint. Posted online July 29, 2016. PMID: 27473720. doi: 10.1007/s12630-016-0702-2

6. Teran F, Prats MI, Nelson BP, et al. Focused transesophageal echocardiography during cardiac arrest resuscitation: JACC review wopic of the Week. J Am Coll Cardiol. 2020;76(6):745-754. PMID: 32762909. doi: 10.1016/j.jacc.2020.05.074

peroshesuduphocraneslibriprastodrutojasuduclistetruclikinicrawushibrodrawajaba

Gotur_Deepa_TEXAS_web.jpg

Critical Care Network

Sepsis/Shock Section

The pendulum swings in favor of corticosteroids and endorses the colloquialism among intensivists that no patient shall die without steroids, especially as it relates to sepsis and septic shock.

In 2018, we saw divergence among randomized controlled trials in the use of glucocorticoids for adults with septic shock such that hydrocortisone without the use of fludrocortisone showed no 90-day mortality benefit; however, hydrocortisone with fludrocortisone showed a 90-day mortality benefit.^1,2 The Surviving Sepsis Guidelines in 2021 favored using low-dose corticosteroids in those with persistent vasopressor requirements in whom other core interventions had been instituted.
 

In 2023, a patient-level meta-analysis of low-dose hydrocortisone in adults with septic shock included seven trials and failed to demonstrate a mortality benefit by relative risk in those who received hydrocortisone compared with placebo. Separately, a network meta-analysis with hydrocortisone plus enteral fludrocortisone was associated with a 90-day all-cause mortality. Of the secondary outcomes, these results offered a possible association of hydrocortisone with a decreased risk of ICU mortality and with increased vasopressor-free days.³
 

The 2024 Society of Critical Care Medicine recently shared an update of focused guidelines on the use of corticosteroids in sepsis, acute respiratory distress syndrome, and community-acquired pneumonia. These included a conditional recommendation to administer corticosteroids for patients with septic shock but recommended against high-dose/short-duration administration of corticosteroids in these patients. These guidelines were supported by data from 46 randomized controlled trials, which showed that corticosteroid use may reduce hospital/long-term mortality and ICU/short-term mortality, as well as result in higher rates of shock reversal and reduced organ dysfunction.

With the results of these meta-analyses and randomized controlled trials, clinicians should consider low-dose corticosteroids paired with fludrocortisone as a tool in treating patients with septic shock given that the short- and long-term benefits may exceed any risks.
 

References

1. Venkatesh B, et al. Adjunctive glucocorticoid therapy in patients with septic shock. N Engl J Med. 2018;378:797-808.

2. Annane D, et al. Hydrocortisone plus fludrocortisone for adults with septic shock. N Engl J Med. 2018;378:809-818.

3. Pirracchio R, et al. Patient-level meta-analysis of low-dose hydrocortisone in adults with septic shock. NEJM Evid. 2023;2(6).

peroshesuduphocraneslibriprastodrutojasuduclistetruclikinicrawushibrodrawajaba

Gotur_Deepa_TEXAS_web.jpg

Critical Care Network

Sepsis/Shock Section

The pendulum swings in favor of corticosteroids and endorses the colloquialism among intensivists that no patient shall die without steroids, especially as it relates to sepsis and septic shock.

In 2018, we saw divergence among randomized controlled trials in the use of glucocorticoids for adults with septic shock such that hydrocortisone without the use of fludrocortisone showed no 90-day mortality benefit; however, hydrocortisone with fludrocortisone showed a 90-day mortality benefit.^1,2 The Surviving Sepsis Guidelines in 2021 favored using low-dose corticosteroids in those with persistent vasopressor requirements in whom other core interventions had been instituted.
 

In 2023, a patient-level meta-analysis of low-dose hydrocortisone in adults with septic shock included seven trials and failed to demonstrate a mortality benefit by relative risk in those who received hydrocortisone compared with placebo. Separately, a network meta-analysis with hydrocortisone plus enteral fludrocortisone was associated with a 90-day all-cause mortality. Of the secondary outcomes, these results offered a possible association of hydrocortisone with a decreased risk of ICU mortality and with increased vasopressor-free days.³
 

The 2024 Society of Critical Care Medicine recently shared an update of focused guidelines on the use of corticosteroids in sepsis, acute respiratory distress syndrome, and community-acquired pneumonia. These included a conditional recommendation to administer corticosteroids for patients with septic shock but recommended against high-dose/short-duration administration of corticosteroids in these patients. These guidelines were supported by data from 46 randomized controlled trials, which showed that corticosteroid use may reduce hospital/long-term mortality and ICU/short-term mortality, as well as result in higher rates of shock reversal and reduced organ dysfunction.

With the results of these meta-analyses and randomized controlled trials, clinicians should consider low-dose corticosteroids paired with fludrocortisone as a tool in treating patients with septic shock given that the short- and long-term benefits may exceed any risks.
 

References

1. Venkatesh B, et al. Adjunctive glucocorticoid therapy in patients with septic shock. N Engl J Med. 2018;378:797-808.

2. Annane D, et al. Hydrocortisone plus fludrocortisone for adults with septic shock. N Engl J Med. 2018;378:809-818.

3. Pirracchio R, et al. Patient-level meta-analysis of low-dose hydrocortisone in adults with septic shock. NEJM Evid. 2023;2(6).

peroshesuduphocraneslibriprastodrutojasuduclistetruclikinicrawushibrodrawajaba

Gotur_Deepa_TEXAS_web.jpg

Critical Care Network

Sepsis/Shock Section

The pendulum swings in favor of corticosteroids and endorses the colloquialism among intensivists that no patient shall die without steroids, especially as it relates to sepsis and septic shock.

In 2018, we saw divergence among randomized controlled trials in the use of glucocorticoids for adults with septic shock such that hydrocortisone without the use of fludrocortisone showed no 90-day mortality benefit; however, hydrocortisone with fludrocortisone showed a 90-day mortality benefit.^1,2 The Surviving Sepsis Guidelines in 2021 favored using low-dose corticosteroids in those with persistent vasopressor requirements in whom other core interventions had been instituted.
 

In 2023, a patient-level meta-analysis of low-dose hydrocortisone in adults with septic shock included seven trials and failed to demonstrate a mortality benefit by relative risk in those who received hydrocortisone compared with placebo. Separately, a network meta-analysis with hydrocortisone plus enteral fludrocortisone was associated with a 90-day all-cause mortality. Of the secondary outcomes, these results offered a possible association of hydrocortisone with a decreased risk of ICU mortality and with increased vasopressor-free days.³
 

The 2024 Society of Critical Care Medicine recently shared an update of focused guidelines on the use of corticosteroids in sepsis, acute respiratory distress syndrome, and community-acquired pneumonia. These included a conditional recommendation to administer corticosteroids for patients with septic shock but recommended against high-dose/short-duration administration of corticosteroids in these patients. These guidelines were supported by data from 46 randomized controlled trials, which showed that corticosteroid use may reduce hospital/long-term mortality and ICU/short-term mortality, as well as result in higher rates of shock reversal and reduced organ dysfunction.

With the results of these meta-analyses and randomized controlled trials, clinicians should consider low-dose corticosteroids paired with fludrocortisone as a tool in treating patients with septic shock given that the short- and long-term benefits may exceed any risks.
 

References

1. Venkatesh B, et al. Adjunctive glucocorticoid therapy in patients with septic shock. N Engl J Med. 2018;378:797-808.

2. Annane D, et al. Hydrocortisone plus fludrocortisone for adults with septic shock. N Engl J Med. 2018;378:809-818.

3. Pirracchio R, et al. Patient-level meta-analysis of low-dose hydrocortisone in adults with septic shock. NEJM Evid. 2023;2(6).

WIESBADEN, GERMANY — Crowded waiting rooms, long wait times, irritable patients, and aggression toward nursing staff and doctors are increasingly the reality in German emergency rooms. Clearly, emergencies belong in the emergency room. However, “In about half of all patients in the emergency room, there is no urgent medical emergency,” Norbert Schütz, MD, director of geriatrics and rheumatology at Helios Dr. Horst Schmidt Hospital in Wiesbaden, Germany, said at a press conference for the 130th Annual Meeting of the German Society of Internal Medicine (DGIM).

“In our daily medical practice, we repeatedly experience people either accessing our emergency departments and ambulances too quickly or lingering at home for too long when they have severe symptoms,” said Dr. Schütz, who organized the Patient Day during the Internist Congress.
 

DGIM Educates Patients

What is an emergency? “I think the public is quite well informed about conditions associated with loss of consciousness, severe pain, chest pain, or paralysis: Think stroke or heart attack. This is undoubtedly a success of recent years. The difficulty arises with everything in between. For instance, should I go to the hospital with severe headaches?” asked Dr. Schütz.

When is a patient a case for the emergency room, the physician on-call service, or the general practitioner? At the Patient Day in Wiesbaden, DGIM aims to educate and train interested parties with a dedicated lecture. The focus is on recognizing an emergency, specifically emergencies in children and mental illnesses.

“Our Patient Day aims to contribute to making the right decisions. We want to inform, answer questions, and alleviate fears,” said Dr. Schütz. Interested parties can refresh their emergency knowledge, tour ambulances, and have the equipment explained. The public also has the opportunity to learn about resuscitation techniques theoretically and practically.

“In general, the general practitioner should always be the first point of contact. They know their patients best and have the most background information,” explained Dr. Schütz. A trusting relationship is crucial for correctly assessing an unclear medical situation. “Should, for whatever reason, the general practitioner not be reachable, the physician on-call service can be reached,” said Dr. Schütz. It may happen, however, that neither the general practitioner nor the on-call physician is immediately available.
 

What Are Emergencies?

In cases of severe health impairment, urgency is required, and a severe emergency should be assumed in the following cases:

• Chest pain
• Circulatory disorder
• Disorders of consciousness
• Breathing difficulties
• Sudden weakness or numbness/paralysis
• Severe bleeding
• Allergic shock

“In such cases, the emergency departments of the hospitals are available around the clock, and if necessary, an emergency doctor should be present during transportation to the hospital,” said Dr. Schütz.

Classifying emergencies is challenging, especially with children. “Children often find it difficult to clearly categorize or describe symptoms,” said Dr. Schütz. A situation is critical if, for example, the child’s breathing or consciousness is impaired.

Mental emergencies pose a particular challenge for patients and relatives because the patient and relatives are often overwhelmed by the situation. If there are suicidal thoughts, the patient should present him- or herself immediately to an emergency room.

“Patients who come to the emergency room because they cannot get appointments with their general practitioner or specialist, for whatever reason, are no emergency. We also see this in the emergency room from time to time,” said Dr. Schütz. Emergency rooms are not intended for this purpose. “And generally, these are not emergencies.”
 

Four of 10 Cases

The number of patients in emergency rooms has steadily increased in recent years. Statistically, only 4 out of 10 cases are genuine emergencies, as detailed surveys of patients in the emergency rooms of northern German hospitals have shown.

In the PiNo Nord cross-sectional study, Martin Scherer, MD, of University Hospital Hamburg-Eppendorf in Hamburg, Germany, and his team examined the reasons why patients visit the emergency room. They interviewed 1175 patients in five hospitals and documented the medical diagnoses. Patients classified as “immediately” or “very urgently” in need of treatment were excluded.

The surveyed patients were on average 41.8 years old, 52.9% were men, and 54.7% of the patients indicated a low urgency of treatment. About 41% of the patients visited the emergency room on their own initiative, 17% stated they were referred or entrusted by their general practitioner, and 8% were referred by a specialist in the emergency room.

The strongest predictors for low subjective treatment urgency were musculoskeletal trauma (odds ratio [OR], 2.18), skin afflictions (OR, 2.15), and the unavailability of an open general practitioner’s office (OR, 1.70).

According to Dr. Scherer and his colleagues, the reasons for visiting an emergency room are diverse and can be based on the perceived structural conditions and individual patient preferences in addition to the urgency of the health problem.
 

This story was translated from the Medscape German edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

WIESBADEN, GERMANY — Crowded waiting rooms, long wait times, irritable patients, and aggression toward nursing staff and doctors are increasingly the reality in German emergency rooms. Clearly, emergencies belong in the emergency room. However, “In about half of all patients in the emergency room, there is no urgent medical emergency,” Norbert Schütz, MD, director of geriatrics and rheumatology at Helios Dr. Horst Schmidt Hospital in Wiesbaden, Germany, said at a press conference for the 130th Annual Meeting of the German Society of Internal Medicine (DGIM).

“In our daily medical practice, we repeatedly experience people either accessing our emergency departments and ambulances too quickly or lingering at home for too long when they have severe symptoms,” said Dr. Schütz, who organized the Patient Day during the Internist Congress.
 

DGIM Educates Patients

What is an emergency? “I think the public is quite well informed about conditions associated with loss of consciousness, severe pain, chest pain, or paralysis: Think stroke or heart attack. This is undoubtedly a success of recent years. The difficulty arises with everything in between. For instance, should I go to the hospital with severe headaches?” asked Dr. Schütz.

When is a patient a case for the emergency room, the physician on-call service, or the general practitioner? At the Patient Day in Wiesbaden, DGIM aims to educate and train interested parties with a dedicated lecture. The focus is on recognizing an emergency, specifically emergencies in children and mental illnesses.

“Our Patient Day aims to contribute to making the right decisions. We want to inform, answer questions, and alleviate fears,” said Dr. Schütz. Interested parties can refresh their emergency knowledge, tour ambulances, and have the equipment explained. The public also has the opportunity to learn about resuscitation techniques theoretically and practically.

“In general, the general practitioner should always be the first point of contact. They know their patients best and have the most background information,” explained Dr. Schütz. A trusting relationship is crucial for correctly assessing an unclear medical situation. “Should, for whatever reason, the general practitioner not be reachable, the physician on-call service can be reached,” said Dr. Schütz. It may happen, however, that neither the general practitioner nor the on-call physician is immediately available.
 

What Are Emergencies?

In cases of severe health impairment, urgency is required, and a severe emergency should be assumed in the following cases:

• Chest pain
• Circulatory disorder
• Disorders of consciousness
• Breathing difficulties
• Sudden weakness or numbness/paralysis
• Severe bleeding
• Allergic shock

“In such cases, the emergency departments of the hospitals are available around the clock, and if necessary, an emergency doctor should be present during transportation to the hospital,” said Dr. Schütz.

Classifying emergencies is challenging, especially with children. “Children often find it difficult to clearly categorize or describe symptoms,” said Dr. Schütz. A situation is critical if, for example, the child’s breathing or consciousness is impaired.

Mental emergencies pose a particular challenge for patients and relatives because the patient and relatives are often overwhelmed by the situation. If there are suicidal thoughts, the patient should present him- or herself immediately to an emergency room.

“Patients who come to the emergency room because they cannot get appointments with their general practitioner or specialist, for whatever reason, are no emergency. We also see this in the emergency room from time to time,” said Dr. Schütz. Emergency rooms are not intended for this purpose. “And generally, these are not emergencies.”
 

Four of 10 Cases

The number of patients in emergency rooms has steadily increased in recent years. Statistically, only 4 out of 10 cases are genuine emergencies, as detailed surveys of patients in the emergency rooms of northern German hospitals have shown.

In the PiNo Nord cross-sectional study, Martin Scherer, MD, of University Hospital Hamburg-Eppendorf in Hamburg, Germany, and his team examined the reasons why patients visit the emergency room. They interviewed 1175 patients in five hospitals and documented the medical diagnoses. Patients classified as “immediately” or “very urgently” in need of treatment were excluded.

The surveyed patients were on average 41.8 years old, 52.9% were men, and 54.7% of the patients indicated a low urgency of treatment. About 41% of the patients visited the emergency room on their own initiative, 17% stated they were referred or entrusted by their general practitioner, and 8% were referred by a specialist in the emergency room.

The strongest predictors for low subjective treatment urgency were musculoskeletal trauma (odds ratio [OR], 2.18), skin afflictions (OR, 2.15), and the unavailability of an open general practitioner’s office (OR, 1.70).

According to Dr. Scherer and his colleagues, the reasons for visiting an emergency room are diverse and can be based on the perceived structural conditions and individual patient preferences in addition to the urgency of the health problem.
 

This story was translated from the Medscape German edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

WIESBADEN, GERMANY — Crowded waiting rooms, long wait times, irritable patients, and aggression toward nursing staff and doctors are increasingly the reality in German emergency rooms. Clearly, emergencies belong in the emergency room. However, “In about half of all patients in the emergency room, there is no urgent medical emergency,” Norbert Schütz, MD, director of geriatrics and rheumatology at Helios Dr. Horst Schmidt Hospital in Wiesbaden, Germany, said at a press conference for the 130th Annual Meeting of the German Society of Internal Medicine (DGIM).

“In our daily medical practice, we repeatedly experience people either accessing our emergency departments and ambulances too quickly or lingering at home for too long when they have severe symptoms,” said Dr. Schütz, who organized the Patient Day during the Internist Congress.
 

DGIM Educates Patients

What is an emergency? “I think the public is quite well informed about conditions associated with loss of consciousness, severe pain, chest pain, or paralysis: Think stroke or heart attack. This is undoubtedly a success of recent years. The difficulty arises with everything in between. For instance, should I go to the hospital with severe headaches?” asked Dr. Schütz.

When is a patient a case for the emergency room, the physician on-call service, or the general practitioner? At the Patient Day in Wiesbaden, DGIM aims to educate and train interested parties with a dedicated lecture. The focus is on recognizing an emergency, specifically emergencies in children and mental illnesses.

“Our Patient Day aims to contribute to making the right decisions. We want to inform, answer questions, and alleviate fears,” said Dr. Schütz. Interested parties can refresh their emergency knowledge, tour ambulances, and have the equipment explained. The public also has the opportunity to learn about resuscitation techniques theoretically and practically.

“In general, the general practitioner should always be the first point of contact. They know their patients best and have the most background information,” explained Dr. Schütz. A trusting relationship is crucial for correctly assessing an unclear medical situation. “Should, for whatever reason, the general practitioner not be reachable, the physician on-call service can be reached,” said Dr. Schütz. It may happen, however, that neither the general practitioner nor the on-call physician is immediately available.
 

What Are Emergencies?

In cases of severe health impairment, urgency is required, and a severe emergency should be assumed in the following cases:

• Chest pain
• Circulatory disorder
• Disorders of consciousness
• Breathing difficulties
• Sudden weakness or numbness/paralysis
• Severe bleeding
• Allergic shock

“In such cases, the emergency departments of the hospitals are available around the clock, and if necessary, an emergency doctor should be present during transportation to the hospital,” said Dr. Schütz.

Classifying emergencies is challenging, especially with children. “Children often find it difficult to clearly categorize or describe symptoms,” said Dr. Schütz. A situation is critical if, for example, the child’s breathing or consciousness is impaired.

Mental emergencies pose a particular challenge for patients and relatives because the patient and relatives are often overwhelmed by the situation. If there are suicidal thoughts, the patient should present him- or herself immediately to an emergency room.

“Patients who come to the emergency room because they cannot get appointments with their general practitioner or specialist, for whatever reason, are no emergency. We also see this in the emergency room from time to time,” said Dr. Schütz. Emergency rooms are not intended for this purpose. “And generally, these are not emergencies.”
 

Four of 10 Cases

The number of patients in emergency rooms has steadily increased in recent years. Statistically, only 4 out of 10 cases are genuine emergencies, as detailed surveys of patients in the emergency rooms of northern German hospitals have shown.

In the PiNo Nord cross-sectional study, Martin Scherer, MD, of University Hospital Hamburg-Eppendorf in Hamburg, Germany, and his team examined the reasons why patients visit the emergency room. They interviewed 1175 patients in five hospitals and documented the medical diagnoses. Patients classified as “immediately” or “very urgently” in need of treatment were excluded.

The surveyed patients were on average 41.8 years old, 52.9% were men, and 54.7% of the patients indicated a low urgency of treatment. About 41% of the patients visited the emergency room on their own initiative, 17% stated they were referred or entrusted by their general practitioner, and 8% were referred by a specialist in the emergency room.

The strongest predictors for low subjective treatment urgency were musculoskeletal trauma (odds ratio [OR], 2.18), skin afflictions (OR, 2.15), and the unavailability of an open general practitioner’s office (OR, 1.70).

According to Dr. Scherer and his colleagues, the reasons for visiting an emergency room are diverse and can be based on the perceived structural conditions and individual patient preferences in addition to the urgency of the health problem.
 

This story was translated from the Medscape German edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Emergencies happen anywhere, anytime, and sometimes, medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series by this news organization that tells these stories.

It was my first night off after 12 days. It was a Friday night, and I went to a bar in Naples to get a beer with some friends. As it turned out, it wasn’t a night off after all.

As soon as we got inside, we heard over the speaker that they needed medical personnel and to please go to the left side of the bar. I thought it would be syncope or something like that.

I went over there and saw a woman holding up a man. He was basically leaning all over her. The light was low, and the music was pounding. I started to assess him and tried to get him to answer me. No response. I checked for pulses — nothing.

Now, I’m in a bar, right? It’s a cardiac arrest. The first thing you think is overdose or alcohol. I asked the woman if the man was doing any drugs. She said she didn’t know. Turns out they were both employees. He was a bouncer and a DJ.

The woman helped me lower him to the floor. I checked again for a pulse. Still nothing. I said, “Call 911,” and started compressions.

The difficult part was the place was completely dark. I knew where his body was on the floor. I could see his chest. But I couldn’t see his face at all.

It was also extremely loud with the music thumping. After a while, they finally shut it off.

Pretty soon, the security personnel from the bar brought me an automated external defibrillator, and it showed the man was having V-fib arrest. I shocked him. Still no pulse. I continued with cardiopulmonary resuscitation (CPR).

I hadn’t noticed, but lots of people were crowding around us. Somebody came up and said, “He’s my friend. He has a 9-year-old daughter. He can’t die. Let me help with the compressions.” I was like, “Go for it.”

The guy started kind of pushing on the man’s abdomen. He had no idea how to do compressions. I said, “Okay, let me take over again.”

Out of the crowd, nobody else volunteered to help. No one asked me, “Hey, what can I do?” Meanwhile, I found out later that someone was filming the whole thing on their phone.

But what the guy said about the man’s young daughter stayed in my brain. I thought, we need to keep going.

I did more compressions and shocked him again. Still no pulse. At that point, the police and emergency medical services showed up. They checked, nothing had changed, so they got him into the ambulance.

I asked one of the paramedics, “Where are you taking him? I can call ahead.”

But he said, “That’s HIPAA. We can’t tell you.” They also wouldn’t let me go with him in the ambulance.

“I have an active Florida license, and I work in the ICU [intensive care unit],” I said.

“No, we need to follow our protocol,” he replied.

I understood that, but I just wanted to help.

It was around 10:30 PM by then, and I was drenched in sweat. I had to go home. The first thing I did after taking a shower was open the computer and check my system. I needed to find out what happened to the guy.

I was looking for admissions, and I didn’t see him. I called the main hospital downtown and the one in North Naples. I couldn’t find him anywhere. I stayed up until almost 1:00 AM checking for his name. At that point I thought, okay, maybe he died.

The next night, Saturday, I was home and got a call from one of my colleagues. “Hey, were you in a bar yesterday? Did you do CPR on somebody?”

“How did you know?” I said.

He said the paramedics had described me — “a tall doctor with glasses who was a nice guy.” It was funny that he knew that was me.

He told me, “The guy’s alive. He’s sick and needs to be put on dialysis, but he’s alive.”

Apparently, the guy had gone to the emergency department at North Naples, and the doctors in the emergency room (ER) worked on him for over an hour. They did continuous CPR and shocked him for close to 40 minutes. They finally got his pulse back, and after that, he was transferred to the main hospital ICU. They didn’t admit him at the ER, which was why I couldn’t find his name.

On Sunday, I was checking my patients’ charts for the ICU that coming week. And there he was. I saw his name and the documentation by the ED that CPR was provided by a critical care doctor in the field. He was still alive. That gave me so much joy.

So, the man I had helped became my patient. When I saw him on Monday, he was intubated and needed dialysis. I finally saw his face and thought, Oh, so that’s what you look like. I hadn’t realized he was only 39 years old.

When he was awake, I explained to him I was the doctor that provided CPR at the bar. He was very grateful, but of course, he didn’t remember anything.

Eventually, I met his daughter, and she just said, “Thank you for allowing me to have my dad.”

The funny part is that he broke his leg. Well, that’s not funny, but no one had any idea how it happened. That was his only complaint. He was asking me, “Doctor, how did you break my leg?”

“Hey, I have no idea how you broke your leg,” I replied. “I was trying to save your life.”

He was in the hospital for almost a month but made a full recovery. The amazing part: After all the evaluations, he has no neurological deficits. He’s back to a normal life now.

They never found a cause for the cardiac arrest. I mean, he had an ejection fraction of 10%. All my money was on something drug related, but that wasn’t the case. They’d done a cardiac cut, and there was no obstruction. They couldn’t find a reason.

We’ve become friends. He still works as a DJ at the bar. He changed his name to “DJ the Survivor” or something like that.

Sometimes, he’ll text me: “Doctor, what are you doing? You want to come down to the bar?”

I’m like, “No. I don’t.”

It’s been more than a year, but I remember every detail. When you go into medicine, you dream that one day you’ll be able to say, “I saved somebody.”

He texted me a year later and told me he’s celebrating two birthdays now. He said, “I’m turning 1 year old today!”

I think about the value of life. How we can take it for granted. We think, I’m young, nothing is going to happen to me. But this guy was 39. He went to work and died that night.

I was able to help bring him back. That makes me thankful for every day.

Jose Valle Giler, MD, is a pulmonary, critical care, and sleep medicine physician at NCH Healthcare System in Naples, Florida.

A version of this article appeared on Medscape.com .

Emergencies happen anywhere, anytime, and sometimes, medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series by this news organization that tells these stories.

It was my first night off after 12 days. It was a Friday night, and I went to a bar in Naples to get a beer with some friends. As it turned out, it wasn’t a night off after all.

As soon as we got inside, we heard over the speaker that they needed medical personnel and to please go to the left side of the bar. I thought it would be syncope or something like that.

I went over there and saw a woman holding up a man. He was basically leaning all over her. The light was low, and the music was pounding. I started to assess him and tried to get him to answer me. No response. I checked for pulses — nothing.

Now, I’m in a bar, right? It’s a cardiac arrest. The first thing you think is overdose or alcohol. I asked the woman if the man was doing any drugs. She said she didn’t know. Turns out they were both employees. He was a bouncer and a DJ.

The woman helped me lower him to the floor. I checked again for a pulse. Still nothing. I said, “Call 911,” and started compressions.

The difficult part was the place was completely dark. I knew where his body was on the floor. I could see his chest. But I couldn’t see his face at all.

It was also extremely loud with the music thumping. After a while, they finally shut it off.

Pretty soon, the security personnel from the bar brought me an automated external defibrillator, and it showed the man was having V-fib arrest. I shocked him. Still no pulse. I continued with cardiopulmonary resuscitation (CPR).

I hadn’t noticed, but lots of people were crowding around us. Somebody came up and said, “He’s my friend. He has a 9-year-old daughter. He can’t die. Let me help with the compressions.” I was like, “Go for it.”

The guy started kind of pushing on the man’s abdomen. He had no idea how to do compressions. I said, “Okay, let me take over again.”

Out of the crowd, nobody else volunteered to help. No one asked me, “Hey, what can I do?” Meanwhile, I found out later that someone was filming the whole thing on their phone.

But what the guy said about the man’s young daughter stayed in my brain. I thought, we need to keep going.

I did more compressions and shocked him again. Still no pulse. At that point, the police and emergency medical services showed up. They checked, nothing had changed, so they got him into the ambulance.

I asked one of the paramedics, “Where are you taking him? I can call ahead.”

But he said, “That’s HIPAA. We can’t tell you.” They also wouldn’t let me go with him in the ambulance.

“I have an active Florida license, and I work in the ICU [intensive care unit],” I said.

“No, we need to follow our protocol,” he replied.

I understood that, but I just wanted to help.

It was around 10:30 PM by then, and I was drenched in sweat. I had to go home. The first thing I did after taking a shower was open the computer and check my system. I needed to find out what happened to the guy.

I was looking for admissions, and I didn’t see him. I called the main hospital downtown and the one in North Naples. I couldn’t find him anywhere. I stayed up until almost 1:00 AM checking for his name. At that point I thought, okay, maybe he died.

The next night, Saturday, I was home and got a call from one of my colleagues. “Hey, were you in a bar yesterday? Did you do CPR on somebody?”

“How did you know?” I said.

He said the paramedics had described me — “a tall doctor with glasses who was a nice guy.” It was funny that he knew that was me.

He told me, “The guy’s alive. He’s sick and needs to be put on dialysis, but he’s alive.”

Apparently, the guy had gone to the emergency department at North Naples, and the doctors in the emergency room (ER) worked on him for over an hour. They did continuous CPR and shocked him for close to 40 minutes. They finally got his pulse back, and after that, he was transferred to the main hospital ICU. They didn’t admit him at the ER, which was why I couldn’t find his name.

On Sunday, I was checking my patients’ charts for the ICU that coming week. And there he was. I saw his name and the documentation by the ED that CPR was provided by a critical care doctor in the field. He was still alive. That gave me so much joy.

So, the man I had helped became my patient. When I saw him on Monday, he was intubated and needed dialysis. I finally saw his face and thought, Oh, so that’s what you look like. I hadn’t realized he was only 39 years old.

When he was awake, I explained to him I was the doctor that provided CPR at the bar. He was very grateful, but of course, he didn’t remember anything.

Eventually, I met his daughter, and she just said, “Thank you for allowing me to have my dad.”

The funny part is that he broke his leg. Well, that’s not funny, but no one had any idea how it happened. That was his only complaint. He was asking me, “Doctor, how did you break my leg?”

“Hey, I have no idea how you broke your leg,” I replied. “I was trying to save your life.”

He was in the hospital for almost a month but made a full recovery. The amazing part: After all the evaluations, he has no neurological deficits. He’s back to a normal life now.

They never found a cause for the cardiac arrest. I mean, he had an ejection fraction of 10%. All my money was on something drug related, but that wasn’t the case. They’d done a cardiac cut, and there was no obstruction. They couldn’t find a reason.

We’ve become friends. He still works as a DJ at the bar. He changed his name to “DJ the Survivor” or something like that.

Sometimes, he’ll text me: “Doctor, what are you doing? You want to come down to the bar?”

I’m like, “No. I don’t.”

It’s been more than a year, but I remember every detail. When you go into medicine, you dream that one day you’ll be able to say, “I saved somebody.”

He texted me a year later and told me he’s celebrating two birthdays now. He said, “I’m turning 1 year old today!”

I think about the value of life. How we can take it for granted. We think, I’m young, nothing is going to happen to me. But this guy was 39. He went to work and died that night.

I was able to help bring him back. That makes me thankful for every day.

Jose Valle Giler, MD, is a pulmonary, critical care, and sleep medicine physician at NCH Healthcare System in Naples, Florida.

A version of this article appeared on Medscape.com .

Emergencies happen anywhere, anytime, and sometimes, medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series by this news organization that tells these stories.

It was my first night off after 12 days. It was a Friday night, and I went to a bar in Naples to get a beer with some friends. As it turned out, it wasn’t a night off after all.

As soon as we got inside, we heard over the speaker that they needed medical personnel and to please go to the left side of the bar. I thought it would be syncope or something like that.

I went over there and saw a woman holding up a man. He was basically leaning all over her. The light was low, and the music was pounding. I started to assess him and tried to get him to answer me. No response. I checked for pulses — nothing.

Now, I’m in a bar, right? It’s a cardiac arrest. The first thing you think is overdose or alcohol. I asked the woman if the man was doing any drugs. She said she didn’t know. Turns out they were both employees. He was a bouncer and a DJ.

The woman helped me lower him to the floor. I checked again for a pulse. Still nothing. I said, “Call 911,” and started compressions.

The difficult part was the place was completely dark. I knew where his body was on the floor. I could see his chest. But I couldn’t see his face at all.

It was also extremely loud with the music thumping. After a while, they finally shut it off.

Pretty soon, the security personnel from the bar brought me an automated external defibrillator, and it showed the man was having V-fib arrest. I shocked him. Still no pulse. I continued with cardiopulmonary resuscitation (CPR).

I hadn’t noticed, but lots of people were crowding around us. Somebody came up and said, “He’s my friend. He has a 9-year-old daughter. He can’t die. Let me help with the compressions.” I was like, “Go for it.”

The guy started kind of pushing on the man’s abdomen. He had no idea how to do compressions. I said, “Okay, let me take over again.”

Out of the crowd, nobody else volunteered to help. No one asked me, “Hey, what can I do?” Meanwhile, I found out later that someone was filming the whole thing on their phone.

But what the guy said about the man’s young daughter stayed in my brain. I thought, we need to keep going.

I did more compressions and shocked him again. Still no pulse. At that point, the police and emergency medical services showed up. They checked, nothing had changed, so they got him into the ambulance.

I asked one of the paramedics, “Where are you taking him? I can call ahead.”

But he said, “That’s HIPAA. We can’t tell you.” They also wouldn’t let me go with him in the ambulance.

“I have an active Florida license, and I work in the ICU [intensive care unit],” I said.

“No, we need to follow our protocol,” he replied.

I understood that, but I just wanted to help.

It was around 10:30 PM by then, and I was drenched in sweat. I had to go home. The first thing I did after taking a shower was open the computer and check my system. I needed to find out what happened to the guy.

I was looking for admissions, and I didn’t see him. I called the main hospital downtown and the one in North Naples. I couldn’t find him anywhere. I stayed up until almost 1:00 AM checking for his name. At that point I thought, okay, maybe he died.

The next night, Saturday, I was home and got a call from one of my colleagues. “Hey, were you in a bar yesterday? Did you do CPR on somebody?”

“How did you know?” I said.

He said the paramedics had described me — “a tall doctor with glasses who was a nice guy.” It was funny that he knew that was me.

He told me, “The guy’s alive. He’s sick and needs to be put on dialysis, but he’s alive.”

Apparently, the guy had gone to the emergency department at North Naples, and the doctors in the emergency room (ER) worked on him for over an hour. They did continuous CPR and shocked him for close to 40 minutes. They finally got his pulse back, and after that, he was transferred to the main hospital ICU. They didn’t admit him at the ER, which was why I couldn’t find his name.

On Sunday, I was checking my patients’ charts for the ICU that coming week. And there he was. I saw his name and the documentation by the ED that CPR was provided by a critical care doctor in the field. He was still alive. That gave me so much joy.

So, the man I had helped became my patient. When I saw him on Monday, he was intubated and needed dialysis. I finally saw his face and thought, Oh, so that’s what you look like. I hadn’t realized he was only 39 years old.

When he was awake, I explained to him I was the doctor that provided CPR at the bar. He was very grateful, but of course, he didn’t remember anything.

Eventually, I met his daughter, and she just said, “Thank you for allowing me to have my dad.”

The funny part is that he broke his leg. Well, that’s not funny, but no one had any idea how it happened. That was his only complaint. He was asking me, “Doctor, how did you break my leg?”

“Hey, I have no idea how you broke your leg,” I replied. “I was trying to save your life.”

He was in the hospital for almost a month but made a full recovery. The amazing part: After all the evaluations, he has no neurological deficits. He’s back to a normal life now.

They never found a cause for the cardiac arrest. I mean, he had an ejection fraction of 10%. All my money was on something drug related, but that wasn’t the case. They’d done a cardiac cut, and there was no obstruction. They couldn’t find a reason.

We’ve become friends. He still works as a DJ at the bar. He changed his name to “DJ the Survivor” or something like that.

Sometimes, he’ll text me: “Doctor, what are you doing? You want to come down to the bar?”

I’m like, “No. I don’t.”

It’s been more than a year, but I remember every detail. When you go into medicine, you dream that one day you’ll be able to say, “I saved somebody.”

He texted me a year later and told me he’s celebrating two birthdays now. He said, “I’m turning 1 year old today!”

I think about the value of life. How we can take it for granted. We think, I’m young, nothing is going to happen to me. But this guy was 39. He went to work and died that night.

I was able to help bring him back. That makes me thankful for every day.

Jose Valle Giler, MD, is a pulmonary, critical care, and sleep medicine physician at NCH Healthcare System in Naples, Florida.

A version of this article appeared on Medscape.com .

Kapoor_Aanchal_web.jpg

Critical Care Network

Nonrespiratory Critical Care Section

In patients with decompensated cirrhosis, there are multiple intrahepatic and extrahepatic factors contributing to hemodynamic alterations at baseline, including endothelial cell dysfunction, hepatic stellate cell activation promoting increase in vasoconstrictors, decrease in vasodilators, and angiogenesis leading to worsening of portal hypertension. Increased resistance to hepatic blood flow leads to increased production of nitric oxide and other vasodilators leading to splanchnic vasodilation, decreased effective blood volume, activation of the renin angiotensin system, sodium, and water retention. In addition to portal hypertension and splanchnic vasodilation, there is a decrease in systemic vascular resistance and hyperdynamic circulation with increased cardiac output. As cirrhosis progresses to the decompensated stage, patients may develop cirrhotic cardiomyopathy, characterized by impaired cardiac response to stress, manifesting as systolic and diastolic dysfunction, and electrophysiological abnormalities such as QT prolongation leading to hypotension and dysregulated response to fluid resuscitation.

DiRienzo_Vincent_web.jpg

Early recognition of septic shock in these patients can be challenging when using traditional criteria due to their baseline hypotension, tachycardia, systemic vasodilation, and propensity for volume overload with fluid resuscitation. Elevated lactate levels in acutely ill patients are an independent risk factor for mortality in patients with cirrhosis. However, lactate levels >2mmol/L need not necessarily define sepsis in these patients, as these patients have decreased lactate clearance. Understanding the intricate interplay between the cardiac pump, vascular tone, and afterload is essential in managing shock in these individuals. Aggressive volume resuscitation may not be well tolerated, emphasizing the need for frequent hemodynamic assessments and prompt initiation of vasopressors when indicated.

Kapoor_Aanchal_web.jpg

Critical Care Network

Nonrespiratory Critical Care Section

In patients with decompensated cirrhosis, there are multiple intrahepatic and extrahepatic factors contributing to hemodynamic alterations at baseline, including endothelial cell dysfunction, hepatic stellate cell activation promoting increase in vasoconstrictors, decrease in vasodilators, and angiogenesis leading to worsening of portal hypertension. Increased resistance to hepatic blood flow leads to increased production of nitric oxide and other vasodilators leading to splanchnic vasodilation, decreased effective blood volume, activation of the renin angiotensin system, sodium, and water retention. In addition to portal hypertension and splanchnic vasodilation, there is a decrease in systemic vascular resistance and hyperdynamic circulation with increased cardiac output. As cirrhosis progresses to the decompensated stage, patients may develop cirrhotic cardiomyopathy, characterized by impaired cardiac response to stress, manifesting as systolic and diastolic dysfunction, and electrophysiological abnormalities such as QT prolongation leading to hypotension and dysregulated response to fluid resuscitation.

DiRienzo_Vincent_web.jpg

Early recognition of septic shock in these patients can be challenging when using traditional criteria due to their baseline hypotension, tachycardia, systemic vasodilation, and propensity for volume overload with fluid resuscitation. Elevated lactate levels in acutely ill patients are an independent risk factor for mortality in patients with cirrhosis. However, lactate levels >2mmol/L need not necessarily define sepsis in these patients, as these patients have decreased lactate clearance. Understanding the intricate interplay between the cardiac pump, vascular tone, and afterload is essential in managing shock in these individuals. Aggressive volume resuscitation may not be well tolerated, emphasizing the need for frequent hemodynamic assessments and prompt initiation of vasopressors when indicated.

Kapoor_Aanchal_web.jpg

Critical Care Network

Nonrespiratory Critical Care Section

In patients with decompensated cirrhosis, there are multiple intrahepatic and extrahepatic factors contributing to hemodynamic alterations at baseline, including endothelial cell dysfunction, hepatic stellate cell activation promoting increase in vasoconstrictors, decrease in vasodilators, and angiogenesis leading to worsening of portal hypertension. Increased resistance to hepatic blood flow leads to increased production of nitric oxide and other vasodilators leading to splanchnic vasodilation, decreased effective blood volume, activation of the renin angiotensin system, sodium, and water retention. In addition to portal hypertension and splanchnic vasodilation, there is a decrease in systemic vascular resistance and hyperdynamic circulation with increased cardiac output. As cirrhosis progresses to the decompensated stage, patients may develop cirrhotic cardiomyopathy, characterized by impaired cardiac response to stress, manifesting as systolic and diastolic dysfunction, and electrophysiological abnormalities such as QT prolongation leading to hypotension and dysregulated response to fluid resuscitation.

DiRienzo_Vincent_web.jpg

Early recognition of septic shock in these patients can be challenging when using traditional criteria due to their baseline hypotension, tachycardia, systemic vasodilation, and propensity for volume overload with fluid resuscitation. Elevated lactate levels in acutely ill patients are an independent risk factor for mortality in patients with cirrhosis. However, lactate levels >2mmol/L need not necessarily define sepsis in these patients, as these patients have decreased lactate clearance. Understanding the intricate interplay between the cardiac pump, vascular tone, and afterload is essential in managing shock in these individuals. Aggressive volume resuscitation may not be well tolerated, emphasizing the need for frequent hemodynamic assessments and prompt initiation of vasopressors when indicated.