Journal of Critical Care 29 (2014) 463–464
Contents lists available at ScienceDirect
Journal of Critical Care journal homepage: www.jccjournal.org
Comment to the Letter to the Editor We thank Dr Esquinas et al [1] for their comments and interest in our work. In our study, noninvasive mechanical ventilation (NIV) was initially applied to all chronic obstructive pulmonary disease (COPD) patients with hypercapnic respiratory failure except when absolutely contraindicated, then all patients were intubated for invasive mechanical ventilation (IMV). Contraindications of NIV were defined as (1) “absolute,” respiratory arrest and unable to fit mask and (2) “relative,” medically unstable (hypotensive shock, uncontrolled cardiac ischemia or arrhythmia, and uncontrolled copious upper gastrointestinal bleeding), agitation, uncooperativeness, inability to protect airway, impaired swallowing, excessive secretions not managed by secretion clearance techniques, multiple (≥ 2) organ failure, and recent upper airway or upper gastrointestinal surgery [2,3]. The definition of NIV failure in hypercapnic patients was no pH improvement, no change or a rise in breathing frequency after 1 to 2 hours, and lack of cooperation. For hypoxic COPD patients, NIV failure was considered as no or a minimal rise in PaO2/fractionated inspired oxygen (FiO2) after 1 to 2 hours (b 200) [4]. All NIV failure patients were intubated for IMV unless patients/relatives did not consent to intubation. Invasive mechanical ventilation was applied in the presence of absolute or relative contraindications for NIV, as mentioned above. Noninvasive mechanical ventilation was applied intermittently for periods of 1 to 4 hours, and initial arterial blood gases (ABG) samples were obtained at the end of the first hour. The duration of each session was determined by ABG value improvement, although ABGs were not determined in the article, consciousness level, and patient compliance. According to patients’ tolerance and clinical improvement, NIV duration can be lasted to 4 hours; on the other hand, agitate patients, to expectorate, to drip water, or to increase patient compliance after 1 hour of NIV, 1 or 2 hours interruptions could be given. The clinical importance in time of intubation for IMV (1 vs 4 hours) was not analyzed in the present study. Furthermore, intermittent continuous positive airway pressure was not applied due to presence of hypercapnia. Arterial blood gases were not given except PaO2/FiO2. As mentioned above, PaO2/FiO2 less than 200 or no rise could be the clue for NIV failure and consider to IMV; however, COPD patients with IMV had PaO2/FiO2 more than 150 along with improvement of chest radiology; extubation was considered seriously. Noninvasive mechanical ventilation was then applied in cases of moderate respiratory distress after extubation if there was no contraindication [4]. Fractionated inspired oxygen was adjusted to maintain oxygen saturation at 90% with NIV or IMV. Pressure support with NIV could prevent the increase in carbon dioxide. Pseudomonas aeruginosa was the was the most frequent pathogen in our cohort. P aeruginosa is an uncommon cause of CAP but listed as a pathogen of severe CAP and CAP in patients with COPD [5-7]. Esquinas and Koksal indicated that the microorganism may have colonized during
0883-9441/$ – see front matter © 2014 Elsevier Inc. All rights reserved.
previous hospitalizations in our patients. That point of view may have a practical value for some patients because these microorganisms may have persisted in the flora of patients for extended periods [8]. Thus, if an infection develops in the community in due course of life in a patient with significant comorbidities like COPD, one cannot be exactly sure if the infecting microorganism is truly a community-acquired pathogen. However in clinical terms, we included patients with pneumonia acquired in the community and excluded cases with nosocomial or health care–associated pneumonias. This was noted in the methods section of our article. Moreover, only the culture results obtained from blood samples and quantitative respiratory secretions, which is a very strong indicator of true pathogens [9], were included in this study. The data related to sputum cultures, which may disclose confusing results due to colonizers were excluded from the study. Thus, our microbiological data indicated true pathogens, which caused infection in the community setting. Finally, in our study, we did not aim to determine whether concomitant CAP and COPD are at greater risk of death. Therefore, our study does not contradict with the study of Snijders et al [10].
Aykut Cilli, MD Department of Pulmonary Diseases School of Medicine Akdeniz University Antalya, Turkey Zuhal Karakurt, MD Respiratory Intensive Care Unit Süreyyapasa Chest Diseases and Thoracic Surgery Education and Research Hospital Istanbul, Turkey Hakan Erdem, MD Department of Infectious Diseases and Clinical Microbiology GATA Haydarpasa Training Hospital Istanbul, Turkey http://dx.doi.org/10.1016/j.jcrc.2014.02.001 References [1] Esquinas, Papadakos, Koksal. Mortality in community-acquired pneumonia associated with chronic obstructive pulmonary disease: Some reflections about this overly complex issue. J Crit Care 2014;29:461–2. [2] Nava S, Hill N. Non-invasive ventilation in acute respiratory failure. Lancet 2009;374:250–9. [3] Ambrosino N, Vagheggini G. Noninvasive positive pressure ventilation in the acute care setting: where are we? Eur Respir J 2008;31:874–86. [4] Boles JM, Bion J, Connors A, et al. Weaning from mechanical ventilation. Eur Respir J 2007;29:1033–56.
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Letters/Editorials / Journal of Critical Care 29 (2014) 463–464
[5] Futijani S, Sun HY, Yu VL, et al. Pneumonia due to Pseudomonas aeruginosa: part I: epidemiology, clinical diagnosis, and source. Chest 2011;139:909–19. [6] Rello J, Rodriguez A, Torres A, et al. Implications of COPD in patients admitted to the intensive care unit by community-acquired pneumonia. Eur Respir J 2006;27:1210–6. [7] Khawaja A, Zubairi ABS, Durrani FK, et al. Etiology and outcome of severe community acquired pneumonia in immunocompetent adults. BMC Infect Dis 2013;13:94.
[8] Montgomerie JZ, Morrow JW. Long-term pseudomonas colonization in spinal cord injury patients. Am J Epidemiol 1980;112:508–17. [9] El Solh AA, Akinnusi ME, Pineda LA, Mankowski CR. Diagnostic yield of quantitative endotracheal aspirates in patients with severe nursing homeacquired pneumonia. Crit Care 2007;11:R57. [10] Snijders D, van der Eerden M, de Graaff C, et al. The influence of COPD on mortality and severity scoring in community-acquired pneumonia. Respiration 2010;79:46–53.
Contents lists available at ScienceDirect
Journal of Critical Care journal homepage: www.jccjournal.org
Comment to the Letter to the Editor We thank Dr Esquinas et al [1] for their comments and interest in our work. In our study, noninvasive mechanical ventilation (NIV) was initially applied to all chronic obstructive pulmonary disease (COPD) patients with hypercapnic respiratory failure except when absolutely contraindicated, then all patients were intubated for invasive mechanical ventilation (IMV). Contraindications of NIV were defined as (1) “absolute,” respiratory arrest and unable to fit mask and (2) “relative,” medically unstable (hypotensive shock, uncontrolled cardiac ischemia or arrhythmia, and uncontrolled copious upper gastrointestinal bleeding), agitation, uncooperativeness, inability to protect airway, impaired swallowing, excessive secretions not managed by secretion clearance techniques, multiple (≥ 2) organ failure, and recent upper airway or upper gastrointestinal surgery [2,3]. The definition of NIV failure in hypercapnic patients was no pH improvement, no change or a rise in breathing frequency after 1 to 2 hours, and lack of cooperation. For hypoxic COPD patients, NIV failure was considered as no or a minimal rise in PaO2/fractionated inspired oxygen (FiO2) after 1 to 2 hours (b 200) [4]. All NIV failure patients were intubated for IMV unless patients/relatives did not consent to intubation. Invasive mechanical ventilation was applied in the presence of absolute or relative contraindications for NIV, as mentioned above. Noninvasive mechanical ventilation was applied intermittently for periods of 1 to 4 hours, and initial arterial blood gases (ABG) samples were obtained at the end of the first hour. The duration of each session was determined by ABG value improvement, although ABGs were not determined in the article, consciousness level, and patient compliance. According to patients’ tolerance and clinical improvement, NIV duration can be lasted to 4 hours; on the other hand, agitate patients, to expectorate, to drip water, or to increase patient compliance after 1 hour of NIV, 1 or 2 hours interruptions could be given. The clinical importance in time of intubation for IMV (1 vs 4 hours) was not analyzed in the present study. Furthermore, intermittent continuous positive airway pressure was not applied due to presence of hypercapnia. Arterial blood gases were not given except PaO2/FiO2. As mentioned above, PaO2/FiO2 less than 200 or no rise could be the clue for NIV failure and consider to IMV; however, COPD patients with IMV had PaO2/FiO2 more than 150 along with improvement of chest radiology; extubation was considered seriously. Noninvasive mechanical ventilation was then applied in cases of moderate respiratory distress after extubation if there was no contraindication [4]. Fractionated inspired oxygen was adjusted to maintain oxygen saturation at 90% with NIV or IMV. Pressure support with NIV could prevent the increase in carbon dioxide. Pseudomonas aeruginosa was the was the most frequent pathogen in our cohort. P aeruginosa is an uncommon cause of CAP but listed as a pathogen of severe CAP and CAP in patients with COPD [5-7]. Esquinas and Koksal indicated that the microorganism may have colonized during
0883-9441/$ – see front matter © 2014 Elsevier Inc. All rights reserved.
previous hospitalizations in our patients. That point of view may have a practical value for some patients because these microorganisms may have persisted in the flora of patients for extended periods [8]. Thus, if an infection develops in the community in due course of life in a patient with significant comorbidities like COPD, one cannot be exactly sure if the infecting microorganism is truly a community-acquired pathogen. However in clinical terms, we included patients with pneumonia acquired in the community and excluded cases with nosocomial or health care–associated pneumonias. This was noted in the methods section of our article. Moreover, only the culture results obtained from blood samples and quantitative respiratory secretions, which is a very strong indicator of true pathogens [9], were included in this study. The data related to sputum cultures, which may disclose confusing results due to colonizers were excluded from the study. Thus, our microbiological data indicated true pathogens, which caused infection in the community setting. Finally, in our study, we did not aim to determine whether concomitant CAP and COPD are at greater risk of death. Therefore, our study does not contradict with the study of Snijders et al [10].
Aykut Cilli, MD Department of Pulmonary Diseases School of Medicine Akdeniz University Antalya, Turkey Zuhal Karakurt, MD Respiratory Intensive Care Unit Süreyyapasa Chest Diseases and Thoracic Surgery Education and Research Hospital Istanbul, Turkey Hakan Erdem, MD Department of Infectious Diseases and Clinical Microbiology GATA Haydarpasa Training Hospital Istanbul, Turkey http://dx.doi.org/10.1016/j.jcrc.2014.02.001 References [1] Esquinas, Papadakos, Koksal. Mortality in community-acquired pneumonia associated with chronic obstructive pulmonary disease: Some reflections about this overly complex issue. J Crit Care 2014;29:461–2. [2] Nava S, Hill N. Non-invasive ventilation in acute respiratory failure. Lancet 2009;374:250–9. [3] Ambrosino N, Vagheggini G. Noninvasive positive pressure ventilation in the acute care setting: where are we? Eur Respir J 2008;31:874–86. [4] Boles JM, Bion J, Connors A, et al. Weaning from mechanical ventilation. Eur Respir J 2007;29:1033–56.
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Letters/Editorials / Journal of Critical Care 29 (2014) 463–464
[5] Futijani S, Sun HY, Yu VL, et al. Pneumonia due to Pseudomonas aeruginosa: part I: epidemiology, clinical diagnosis, and source. Chest 2011;139:909–19. [6] Rello J, Rodriguez A, Torres A, et al. Implications of COPD in patients admitted to the intensive care unit by community-acquired pneumonia. Eur Respir J 2006;27:1210–6. [7] Khawaja A, Zubairi ABS, Durrani FK, et al. Etiology and outcome of severe community acquired pneumonia in immunocompetent adults. BMC Infect Dis 2013;13:94.
[8] Montgomerie JZ, Morrow JW. Long-term pseudomonas colonization in spinal cord injury patients. Am J Epidemiol 1980;112:508–17. [9] El Solh AA, Akinnusi ME, Pineda LA, Mankowski CR. Diagnostic yield of quantitative endotracheal aspirates in patients with severe nursing homeacquired pneumonia. Crit Care 2007;11:R57. [10] Snijders D, van der Eerden M, de Graaff C, et al. The influence of COPD on mortality and severity scoring in community-acquired pneumonia. Respiration 2010;79:46–53.
