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Ventilator-Associated Pneumonia, Percutaneous Tracheostomy, and Antimicrobial Prophylaxis
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Pneumonia After Tracheotomy To the Editor: I read with interest Dr. Rello’s report (December 2003)1 on the incidence, etiology, and outcome of nosocomial pneumonia in ICU patients requiring percutaneous tracheotomy for mechanical ventilation. He showed that as many as 18% of patients acquired ventilator-associated pneumonia (VAP) after tracheotomy, most of them in the first week after the procedure. Unfortunately, the investigators did not compare the incidence of VAP in patients after tracheotomy with the incidence of nosocomial pneumonia in patients not receiving a tracheostoma. When the incidence of pneumonia in the latter group is as high as in the studied population, which very well might be the case, one can also say that prolonged mechanical ventilation predisposes to pneumonia. Thus, their conclusion—percutaneous tracheotomy predisposes to pneumonia—is not accurate. Furthermore, I was very much surprised to see that antimicrobial prophylaxis before tracheotomy—a single dose of amoxicilline-clavunate—was recommended. In addition, many patients received antibiotics before the procedure (80%). Antibiotic use may have predisposed to the high incidence of VAP, more than the procedure itself. It is not correct to state that the current findings suggest the need to select an antipseudomonal agent for prophylaxis; one can also suggest not administering antimicrobial prophylaxis. Marcus J. Schultz, MD, PhD University of Amsterdam Amsterdam, Netherlands Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail: [email protected]). Correspondence to: Marcus J. Schultz, MD, PhD, InternistIntensivist, Department of Intensive Care Medicine, Academic Medical Center, University of Amsterdam, Mail stop G3–206, Meibergdreef 9, 1105 AZ Amsterdam, Netherlands; e-mail: [email protected] 1382
Reference 1 Rello J, Lorente C, Diaz E, et al. Incidence, etiology, and outcome of nosocomial pneumonia in ICU patients requiring percutaneous tracheotomy for mechanical ventilation. Chest 2003; 124:2239 –2243
Ventilator-Associated Pneumonia, Percutaneous Tracheostomy, and Antimicrobial Prophylaxis To the Editor: Dr. Schultz raises pertinent concerns about the use of antimicrobial prophylaxis in patients who undergo percutaneous tracheostomies, and disagrees with our interpretation of the findings of ventilator-associated pneumonia (VAP) after percutaneous tracheostomy.1 Tracheostomy is an elective surgical procedure in patients with contaminated tracheal mucosa (present in all intubated patients). Therefore, we believe that administration of a -lactam in the interval of 2 h before the time of surgical incision is a correct indication.2 Antimicrobial prophylaxis should cover potential pathogens to decrease surgery-related infections. The most frequent isolates colonizing our patients prior to tracheotomy were nonfermentative Gram-negative bacilli, with Pseudomonas aeruginosa being identified as the most frequent responsible pathogen. Another patient acquired bacteremia by P aeruginosa during the procedure.1 Based on these findings, we suggested that surgical antimicrobials prescribed for tracheotomy prophylaxis in intubated patients should be active against P aeruginosa. Dr. Schultz also expressed concern that the incidence of VAP in patients with tracheotomy was not compared to patients not receiving a tracheostoma. The overall incidence of VAP in our ICU was 9.6% of intubated patients in the study period. In the current article, 18.1% of patients acquired VAP after percutaneous tracheotomy. These episodes occurred a median of 7 days after intubation, and most episodes occurred within the first 5 days after the procedure (Table 2).1 This percentage notably exceed the ⬍ 1% cumulative risk of acquiring pneumonia per day of mechanical ventilation, which is considered standard in intubated patients.3 Finally, Dr. Schultz indicates that antibiotic use in many patients before the procedure may have predisposed to the high incidence of VAP. However, in a cohort study4 focusing on episodes of pneumonia, prior antibiotic use showed a protective effect (relative risk, 0.1; 95% confidence interval, 0.01 to 0.71) within the first days after intubation. These findings agree with observations reported by Sirvent et al5 using a prophylactic antibiotic approach. Similarly, Cook et al6 estimated that exposure to antibiotics was associated with a risk ratio of 0.37 (95% confidence interval, 0.27 to 0.51) for development of VAP. A recent review article by Bonten et al7 confirmed these reports. Antibiotic exposure protects against pneumonia development within the first days of the intubation manipulation, especially Communications to the Editor
against flora present in the colonized airways, suggesting that risk factors vary depending of the exposure to risk (ie, length of ventilation).8 Our opinion on antimicrobial prophylaxis for VAP has been clearly stated in a recent editorial,9 and a randomized clinical trial to assess the effect of single-dose antibiotic administration as prophylaxis for VAP is highly recommended. Unfortunately, such evidence is lacking. Dr. Schultz suggests not using antimicrobial prophylaxis for percutaneous tracheotomies. However, as indicated before, prophylaxis for surgical neck procedures in intubated patients with colonized tracheal mucosa has a level 1 evidence. Until such studies are available, the extremely high incidence of VAP in the first days after the procedure, the distribution of pathogens, and the low predictive value of tracheal aspirates prior to tracheostomy1 suggest that prescription of a single dose of an antipseudomonal agent prior to the percutaneous tracheotomy is the most pertinent policy. Jordi Rello, MD, PhD Emili Diaz, MD, PhD Joan XXIII University Hospital Rovira & Virgili University Tarragona, Spain Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail: [email protected]). Correspondence to: Jordi Rello, MD, PhD, Critical Care Department, Joan XXIII University Hospital, Rovira & Virgili University, 43007 Tarragona, Spain; e-mail: [email protected]
References 1 Rello J, Lorente C, Diaz E, et al. Incidence, etiology, and outcome of nosocomial pneumonia in ICU patients requiring percutaneous tracheotomy for mechanical ventilation. Chest 2003; 124:2239 –2243 2 Classen DC, Evans RS, Pestotnik SL, et al. The timing of prophylactic administration of antibiotics and the risk of surgical-wound infection. N Engl J Med 1992; 326:281–286 3 Rello J, Diaz E. Pneumonia in the ICU. Crit Care Med 2003; 31:2544 –2551 4 Rello J, Dı´az E, Roque M, et al. Risk factors for developing pneumonia within forty-eight hours of intubation. Am J Respir Crit Care Med 1999; 159:1742–1746 5 Sirvent JM, Torres A, El-Ebiary M, et al. Protective effect of intravenously administered cefuroxime against nosocomial pneumonia in patients with structural coma. Am J Respir Crit Care Med 1997; 155:1729 –1734 6 Cook DJ, Walter SD, Cook RJ, et al. Incidence of and risk factors for ventilator-associated pneumonia in critically ill patients. Ann Intern Med 1998; 129:433– 440 7 Bonten MJM, Kollef MH, Hall JB. Risk factors for ventilatorassociated pneumonia: from epidemiology to patient management. Clin Infect Dis 2004; 38:1141–1149 8 Diaz O, Diaz E, Rello J. Risk factors for pneumonia in the intubated patient. Infect Dis Clin North Am 2003; 17:697–705 9 Diaz E, Rello J, Valles J. Antibiotic use and the risk of pneumonia: twenty years of studies, but where are we now? Clin Infect Dis 2004; 38:1409 –1411
Surgical Stress in ARDS Open-Lung Biopsy To the Editor: We read with great interest the recent case series by Patel and colleagues (January 2004).1 In their discussion about complicawww.chestjournal.org
tions after open-lung biopsy in patients with ARDS, however, they did not refer to the contribution of surgical stress to ARDS. Major surgery, including cardiovascular surgery with cramping of the aorta and resulting in ischemia/reperfusion of the lower body, sometimes causes a systemic inflammatory response leading to the development of fatal organ-system dysfunction such as ARDS.2,3 Tumor necrosis factor or other cytokines and chemokines play important roles in systemic inflammatory response syndrome.3 Enhanced release of proinflammatory cytokines and chemokines results in a trigger for the production of numerous other inflammatory mediators such as nitric oxide, adhesion molecules, and eicosanoids.2 Rajimakers et al4 demonstrated the strong correlation between an increase in circulatory interleukin-8 and pulmonary microvascular permeability related to aortic surgery. Indeed, we previously confirmed the pivotal roles of proinflammatory cytokines in murine acute lung injury induced by bacterial endotoxin, a similar condition for ARDS in humans.5 In particular, proinflammatory chemokines such as macrophage inflammatory protein-1, macrophage chemoattractant protein-1, and keratinocyte chemoattractant in the lung paralleled the magnitude of lung injury and neutrophilic inflammation in our experiments.5–7 Therefore, surgery itself may aggravate ARDS. As Patel and colleagues1 concluded, clinicians should give careful consideration to the selection of patients with ARDS. Ken-ichiro Inoue, MD Hirohisa Takano, MD, PhD Rie Yanagisawa, PhD Miho Sakurai National Institute for Environmental Studies Tsukuba, Japan Toshikazu Yoshikawa, MD, PhD Kyoto Prefectural University of Medicine Kyoto, Japan Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail: [email protected]). Correspondence to: Ken-ichiro Inoue, MD, Inhalation Toxicology Research Team, and Pathophysiology Research Team, National Institute for Environmental Studies, 16 –2 Onogawa, Tsukuba, 305-8506, Japan; e-mail: [email protected]
References 1 Patel SR, Karmpaliotis D, Ayas NT, et al. The role of open-lung biopsy in ARDS. Chest 2004; 125:197–202 2 Takezawa J. Surgical stress and acute lung injury [in Japanese]. Nippon Geka Gakkai Zasshi 1996; 97:739 –744 3 Endo S, Inada K, Sato N, et al. Cytokines in surgical stress [in Japanese]. Nippon Geka Gakkai Zasshi 1996; 97:708 –715 4 Raijmakers PG, Groeneveld AB, Rauwerda JA, et al. Transient increase in interleukin-8 and pulmonary microvascular permeability following aortic surgery. Am J Respir Crit Care Med 1995; 151:698 –705 5 Takano H, Yanagisawa R, Ichinose T, et al. Diesel exhaust particles enhance lung injury related to bacterial endotoxin through expression of proinflammatory cytokines, chemokines, and intercellular adhesion molecule-1. Am J Respir Crit Care Med 2002; 165:1329 –1335 6 Yanagisawa R, Takano H, Inoue K, et al. Enhancement of acute lung injury related to bacterial endotoxin by components of diesel exhaust particles. Thorax 2003; 58:605– 612 7 Inoue K, Takano H, Yanagisawa R, et al. Effect of 15-deoxydelta 12,14-prostaglandin J2 on acute lung injury induced by lipopolysaccharide in mice. Eur J Pharmacol 2003; 481:261– 269 CHEST / 126 / 4 / OCTOBER, 2004
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Pneumonia After Tracheotomy To the Editor: I read with interest Dr. Rello’s report (December 2003)1 on the incidence, etiology, and outcome of nosocomial pneumonia in ICU patients requiring percutaneous tracheotomy for mechanical ventilation. He showed that as many as 18% of patients acquired ventilator-associated pneumonia (VAP) after tracheotomy, most of them in the first week after the procedure. Unfortunately, the investigators did not compare the incidence of VAP in patients after tracheotomy with the incidence of nosocomial pneumonia in patients not receiving a tracheostoma. When the incidence of pneumonia in the latter group is as high as in the studied population, which very well might be the case, one can also say that prolonged mechanical ventilation predisposes to pneumonia. Thus, their conclusion—percutaneous tracheotomy predisposes to pneumonia—is not accurate. Furthermore, I was very much surprised to see that antimicrobial prophylaxis before tracheotomy—a single dose of amoxicilline-clavunate—was recommended. In addition, many patients received antibiotics before the procedure (80%). Antibiotic use may have predisposed to the high incidence of VAP, more than the procedure itself. It is not correct to state that the current findings suggest the need to select an antipseudomonal agent for prophylaxis; one can also suggest not administering antimicrobial prophylaxis. Marcus J. Schultz, MD, PhD University of Amsterdam Amsterdam, Netherlands Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail: [email protected]). Correspondence to: Marcus J. Schultz, MD, PhD, InternistIntensivist, Department of Intensive Care Medicine, Academic Medical Center, University of Amsterdam, Mail stop G3–206, Meibergdreef 9, 1105 AZ Amsterdam, Netherlands; e-mail: [email protected] 1382
Reference 1 Rello J, Lorente C, Diaz E, et al. Incidence, etiology, and outcome of nosocomial pneumonia in ICU patients requiring percutaneous tracheotomy for mechanical ventilation. Chest 2003; 124:2239 –2243
Ventilator-Associated Pneumonia, Percutaneous Tracheostomy, and Antimicrobial Prophylaxis To the Editor: Dr. Schultz raises pertinent concerns about the use of antimicrobial prophylaxis in patients who undergo percutaneous tracheostomies, and disagrees with our interpretation of the findings of ventilator-associated pneumonia (VAP) after percutaneous tracheostomy.1 Tracheostomy is an elective surgical procedure in patients with contaminated tracheal mucosa (present in all intubated patients). Therefore, we believe that administration of a -lactam in the interval of 2 h before the time of surgical incision is a correct indication.2 Antimicrobial prophylaxis should cover potential pathogens to decrease surgery-related infections. The most frequent isolates colonizing our patients prior to tracheotomy were nonfermentative Gram-negative bacilli, with Pseudomonas aeruginosa being identified as the most frequent responsible pathogen. Another patient acquired bacteremia by P aeruginosa during the procedure.1 Based on these findings, we suggested that surgical antimicrobials prescribed for tracheotomy prophylaxis in intubated patients should be active against P aeruginosa. Dr. Schultz also expressed concern that the incidence of VAP in patients with tracheotomy was not compared to patients not receiving a tracheostoma. The overall incidence of VAP in our ICU was 9.6% of intubated patients in the study period. In the current article, 18.1% of patients acquired VAP after percutaneous tracheotomy. These episodes occurred a median of 7 days after intubation, and most episodes occurred within the first 5 days after the procedure (Table 2).1 This percentage notably exceed the ⬍ 1% cumulative risk of acquiring pneumonia per day of mechanical ventilation, which is considered standard in intubated patients.3 Finally, Dr. Schultz indicates that antibiotic use in many patients before the procedure may have predisposed to the high incidence of VAP. However, in a cohort study4 focusing on episodes of pneumonia, prior antibiotic use showed a protective effect (relative risk, 0.1; 95% confidence interval, 0.01 to 0.71) within the first days after intubation. These findings agree with observations reported by Sirvent et al5 using a prophylactic antibiotic approach. Similarly, Cook et al6 estimated that exposure to antibiotics was associated with a risk ratio of 0.37 (95% confidence interval, 0.27 to 0.51) for development of VAP. A recent review article by Bonten et al7 confirmed these reports. Antibiotic exposure protects against pneumonia development within the first days of the intubation manipulation, especially Communications to the Editor
against flora present in the colonized airways, suggesting that risk factors vary depending of the exposure to risk (ie, length of ventilation).8 Our opinion on antimicrobial prophylaxis for VAP has been clearly stated in a recent editorial,9 and a randomized clinical trial to assess the effect of single-dose antibiotic administration as prophylaxis for VAP is highly recommended. Unfortunately, such evidence is lacking. Dr. Schultz suggests not using antimicrobial prophylaxis for percutaneous tracheotomies. However, as indicated before, prophylaxis for surgical neck procedures in intubated patients with colonized tracheal mucosa has a level 1 evidence. Until such studies are available, the extremely high incidence of VAP in the first days after the procedure, the distribution of pathogens, and the low predictive value of tracheal aspirates prior to tracheostomy1 suggest that prescription of a single dose of an antipseudomonal agent prior to the percutaneous tracheotomy is the most pertinent policy. Jordi Rello, MD, PhD Emili Diaz, MD, PhD Joan XXIII University Hospital Rovira & Virgili University Tarragona, Spain Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail: [email protected]). Correspondence to: Jordi Rello, MD, PhD, Critical Care Department, Joan XXIII University Hospital, Rovira & Virgili University, 43007 Tarragona, Spain; e-mail: [email protected]
References 1 Rello J, Lorente C, Diaz E, et al. Incidence, etiology, and outcome of nosocomial pneumonia in ICU patients requiring percutaneous tracheotomy for mechanical ventilation. Chest 2003; 124:2239 –2243 2 Classen DC, Evans RS, Pestotnik SL, et al. The timing of prophylactic administration of antibiotics and the risk of surgical-wound infection. N Engl J Med 1992; 326:281–286 3 Rello J, Diaz E. Pneumonia in the ICU. Crit Care Med 2003; 31:2544 –2551 4 Rello J, Dı´az E, Roque M, et al. Risk factors for developing pneumonia within forty-eight hours of intubation. Am J Respir Crit Care Med 1999; 159:1742–1746 5 Sirvent JM, Torres A, El-Ebiary M, et al. Protective effect of intravenously administered cefuroxime against nosocomial pneumonia in patients with structural coma. Am J Respir Crit Care Med 1997; 155:1729 –1734 6 Cook DJ, Walter SD, Cook RJ, et al. Incidence of and risk factors for ventilator-associated pneumonia in critically ill patients. Ann Intern Med 1998; 129:433– 440 7 Bonten MJM, Kollef MH, Hall JB. Risk factors for ventilatorassociated pneumonia: from epidemiology to patient management. Clin Infect Dis 2004; 38:1141–1149 8 Diaz O, Diaz E, Rello J. Risk factors for pneumonia in the intubated patient. Infect Dis Clin North Am 2003; 17:697–705 9 Diaz E, Rello J, Valles J. Antibiotic use and the risk of pneumonia: twenty years of studies, but where are we now? Clin Infect Dis 2004; 38:1409 –1411
Surgical Stress in ARDS Open-Lung Biopsy To the Editor: We read with great interest the recent case series by Patel and colleagues (January 2004).1 In their discussion about complicawww.chestjournal.org
tions after open-lung biopsy in patients with ARDS, however, they did not refer to the contribution of surgical stress to ARDS. Major surgery, including cardiovascular surgery with cramping of the aorta and resulting in ischemia/reperfusion of the lower body, sometimes causes a systemic inflammatory response leading to the development of fatal organ-system dysfunction such as ARDS.2,3 Tumor necrosis factor or other cytokines and chemokines play important roles in systemic inflammatory response syndrome.3 Enhanced release of proinflammatory cytokines and chemokines results in a trigger for the production of numerous other inflammatory mediators such as nitric oxide, adhesion molecules, and eicosanoids.2 Rajimakers et al4 demonstrated the strong correlation between an increase in circulatory interleukin-8 and pulmonary microvascular permeability related to aortic surgery. Indeed, we previously confirmed the pivotal roles of proinflammatory cytokines in murine acute lung injury induced by bacterial endotoxin, a similar condition for ARDS in humans.5 In particular, proinflammatory chemokines such as macrophage inflammatory protein-1, macrophage chemoattractant protein-1, and keratinocyte chemoattractant in the lung paralleled the magnitude of lung injury and neutrophilic inflammation in our experiments.5–7 Therefore, surgery itself may aggravate ARDS. As Patel and colleagues1 concluded, clinicians should give careful consideration to the selection of patients with ARDS. Ken-ichiro Inoue, MD Hirohisa Takano, MD, PhD Rie Yanagisawa, PhD Miho Sakurai National Institute for Environmental Studies Tsukuba, Japan Toshikazu Yoshikawa, MD, PhD Kyoto Prefectural University of Medicine Kyoto, Japan Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail: [email protected]). Correspondence to: Ken-ichiro Inoue, MD, Inhalation Toxicology Research Team, and Pathophysiology Research Team, National Institute for Environmental Studies, 16 –2 Onogawa, Tsukuba, 305-8506, Japan; e-mail: [email protected]
References 1 Patel SR, Karmpaliotis D, Ayas NT, et al. The role of open-lung biopsy in ARDS. Chest 2004; 125:197–202 2 Takezawa J. Surgical stress and acute lung injury [in Japanese]. Nippon Geka Gakkai Zasshi 1996; 97:739 –744 3 Endo S, Inada K, Sato N, et al. Cytokines in surgical stress [in Japanese]. Nippon Geka Gakkai Zasshi 1996; 97:708 –715 4 Raijmakers PG, Groeneveld AB, Rauwerda JA, et al. Transient increase in interleukin-8 and pulmonary microvascular permeability following aortic surgery. Am J Respir Crit Care Med 1995; 151:698 –705 5 Takano H, Yanagisawa R, Ichinose T, et al. Diesel exhaust particles enhance lung injury related to bacterial endotoxin through expression of proinflammatory cytokines, chemokines, and intercellular adhesion molecule-1. Am J Respir Crit Care Med 2002; 165:1329 –1335 6 Yanagisawa R, Takano H, Inoue K, et al. Enhancement of acute lung injury related to bacterial endotoxin by components of diesel exhaust particles. Thorax 2003; 58:605– 612 7 Inoue K, Takano H, Yanagisawa R, et al. Effect of 15-deoxydelta 12,14-prostaglandin J2 on acute lung injury induced by lipopolysaccharide in mice. Eur J Pharmacol 2003; 481:261– 269 CHEST / 126 / 4 / OCTOBER, 2004
1383