Online Letters to the Editor
ACs was 59% radial and 41% femoral. In the RCT by Timsit et al (7) published in 2012 were included 1,879 patients and 4,163 IVC, 1,962 CVC (47%), and 2,201 AC (53%). The distribution per site between CVCs was 37% jugular, 29% subclavian, and 34% femoral. The distribution per vascular access between ACs was 65% radial and 35% femoral. In the RCT by Maki et al (8) were included 1,401 IVC; however, the distribution of vascular access was not reported in this RCT published as abstract in a congress. Thus, the number of AC is important to exclude them from the conclusion and to say that the use of chlorhexidine-impregnated dressing could reduce the risk of CVC colonization and CVC-bloodstream infection. However, the conclusion of the meta-analysis saying that the use of chlorhexidine-impregnated dressing could reduce the risk of IVC colonization and IVC-bloodstream infection suggests that this effect is in all IVC accessed. In my opinion, the findings of the meta-analysis by Safdar et al (1) suggest that chlorhexidine-impregnated dressing may be another measure to prevent IVC-bloodstream infection. However, it could be interesting to analyze if the preventive effect of chlorhexidine-impregnated dressing to reduce the risk of IVCbloodstream infection is present in all IVC accesses; this would help us in taking decision and to optimize the distribution of healthcare cost. The author has disclosed that he does not have any potential conflicts of interest. Leonardo Lorente, MD, PhD, Intensive Care Unit, Hospital Universitario de Canarias, La Laguna, Santa Cruz de Tenerife, Spain
REFERENCES
1. Safdar N, O’Horo JC, Ghufran A, et al: Chlorhexidine-Impregnated Dressing for Prevention of Catheter-Related Bloodstream Infection: A Meta-Analysis. Crit Care Med 2014; 42:1703–1713 2. Mahjoub Y, Dupont H: Chlorhexidine-impregnated dressing: An efficient weapon against catheter-related bloodstream infection? Crit Care Med 2014; 42:1742–1743 3. Lorente L, Jiménez A, Martín MM, et al: Lower catheter-related bloodstream infection in arterial than in venous femoral catheter. Eur J Clin Microbiol Infect Dis 2012; 31:487–490 4. Lorente L, Santacreu R, Martín MM, et al: Arterial catheter-related infection of 2,949 catheters. Crit Care 2006; 10:R83 5. Lorente L, Henry C, Martín MM, et al: Central venous catheter-related infection in a prospective and observational study of 2,595 catheters. Crit Care 2005; 9:R631–R635 6. Timsit JF, Schwebel C, Bouadma L, et al; Dressing Study Group: Chlorhexidine-impregnated sponges and less frequent dressing changes for prevention of catheter-related infections in critically ill adults: A randomized controlled trial. JAMA 2009; 301:1231–1241 7. Timsit JF, Mimoz O, Mourvillier B, et al: Randomized controlled trial of chlorhexidine dressing and highly adhesive dressing for preventing catheter-related infections in critically ill adults. Am J Respir Crit Care Med 2012; 186:1272–1278 8. Maki D, Mermel L, Kluger D, et al: The Efficacy of a Chlorhexidine Impregnated Sponge (Biopatch) for the Prevention of Intravascular Catheter-Related Infection—A Prospective Randomized Controlled Multicenter Study [abstract 1430]. Programs and Abstracts of the Fortieth Interscience Conference on Antimicrobial Agents and Chemotherapy, Toronto. Washington, DC, American Society for Microbiology, 2000, p 422 DOI: 10.1097/CCM.0000000000000739
Critical Care Medicine
The authors reply:
D
r. Lorente (1) correctly observes that our meta-analysis did not differentiate the effect of chlorhexidineimpregnated dressings on different types of access. The small number of studies precluded meaningful sensitivity analyses, although the three studies which included arterial catheters all noted that a benefit was seen in this subgroup. As we noted in a previous meta-analysis, arterial catheter infections may be an underrecognized source of infection (2), and finding effective prevention measures, such as chlorhexidineimpregnated dressing, is critical. Likewise, a differential effect of chlorhexidine on different sites would not be unexpected, as higher risk sites (e.g., arguably [3] femoral sites) should see a more drastic reduction than lower risk sites. However, as we are now in the era where zero central catheter infections is not just a goal but an expectation by payers (4), even moderate-risk reductions of lower risk sites are clinically relevant. We agree with Dr. Lorente (1) that further research on the effectiveness of these dressings across different patient care settings and types of devices is needed. The authors have disclosed that they do not have any potential conflicts of interest. Nasia Safdar, MD, Infectious Disease, University of Wisconsin Hospital and Clinics, Madison, WI, and William S. Middleton Memorial Veterans Hospital, Madison, WI; John C. O’Horo, MD, MPH, Department of Medicine, Division of Infectious Diseases, Mayo Clinic, Rochester, MN
REFERENCES
1. Lorente L: Does Chlorhexidine-Impregnated Dressing Reduce the Risk of Catheter-Related Bloodstream Infection in All Vascular Access? Crit Care Med 2015; 43:e50–e51 2. O’Horo JC, Maki DG, Krupp AE, et al: Arterial catheters as a source of bloodstream infection: A systematic review and meta-analysis. Crit Care Med 2014; 42:1334–1339 3. Marik PE, Flemmer M, Harrison W: The risk of catheter-related bloodstream infection with femoral venous catheters as compared to subclavian and internal jugular venous catheters: A systematic review of the literature and meta-analysis. Crit Care Med 2012; 40:2479–2485 4. Medicaid program; Payment adjustment for provider-preventable conditions including health care-acquired conditions; final rule. In: Centers for Medicare and Medicaid Services. Washington, DC, Federal Register, 2011, pp 32816–32838 DOI: 10.1097/CCM.0000000000000831
The authors reply:
W
e read with peculiar interest the letter by Dr. Lorente (1) regarding our editorial (2) about the meta-analysis published by Safdar and Maki (3). In the letter, the author pointed out two main limitation of the meta-analysis. First, among the randomized controlled trials included in the meta-analysis, at least three of them mix central venous catheters (CVC) and arterial catheters (AC). Second, the insertion site is variable (jugular, femoral, or subclavian). As shown in some studies, catheter-related bloodstream infection rate www.ccmjournal.org
e51
Online Letters to the Editor
varies with catheter type (arterial vs venous) and catheter site (jugular, femoral, or subclavian for CVC; arterial and femoral for ACs). Thus, the heterogeneity in catheter type and site precludes the conclusion of Safdar and Maki (3): chlorhexidineimpregnated dressing may not have the same efficiency in all situations. We already discussed these limitations in our editorial (2). Furthermore, we have suggested that a subgroup analysis would be useful to tackle this issue. In our opinion, these limitations do not diminish the value of the meta-analysis by Safdar and Maki (3). Use of chlorhexidine-impregnated dressing decreases the absolute risk of catheter-related bloodstream infection (CRBSI) by 1.7%. The use of these devices may be considered as an additional strategy to reduce CRBSI. If the risk of CRBSI is very low, as for arterial radial catheters (4), this kind of dressing may not be as effective as expected for others intravascular catheters. However, in a culture of safety, no strategy should be discarded too quickly. A cost analysis for a universal use of this dressing for all CVCs may help to make a decision. The authors have disclosed that they do not have any potential conflicts of interest. Yazine Mahjoub, MD, Hervé Dupont, MD, PhD, Medical and Surgical Intensive Care Unit, Department of Anesthesia and Intensive Care, Amiens University Medical Center, Amiens, France, and INSERM U-1088, Jules Verne University of Picardie, Amiens, France
REFERENCES
1. Lorente L: Does Chlorhexidine-Impregnated Dressing Reduce the Risk of Catheter-Related Bloodstream Infection in All Vascular Access? Crit Care Med 2015; 43:e50–e51 2. Mahjoub Y, Dupont H: Chlorhexidine-impregnated dressing: An efficient weapon against catheter-related bloodstream infection? Crit Care Med 2014; 42:1742–1743 3. Safdar N, Maki DG: The pathogenesis of catheter-related bloodstream infection with noncuffed short-term central venous catheters. Intensive Care Med 2004; 30:62–67 4. Lorente L, Santacreu R, Martín MM, et al: Arterial catheter-related infection of 2,949 catheters. Crit Care 2006; 10:R83 DOI: 10.1097/CCM.0000000000000810
Heart-Lung Interactions: Have a Look on the Superior Vena Cava and on the Changes in Right Ventricular Afterload To the Editor:
W
e would like to congratulate Lansdorp et al (1) for the beautiful physiological study that they recently published in Critical Care Medicine regarding mechanical ventilation–induced intrathoracic pressure distribution and heart-lung interactions. We would like to make three comments. First, and most importantly, Lansdorp et al (1) have very well demonstrated invasively what we suggested noninvasively 10 years ago using transesophageal echocardiography regarding the potential collapse of the superior vena cava (SVC) related to tidal ventilation (2). If we look at the transmural
e52
www.ccmjournal.org
pressure of the SVC (PtmSVC), the authors report a significant decrease during tidal ventilation. If we calculate, using the data provided in Table 2 in (1), mean changes in PtmSVC during tidal ventilation at 8 mL/kg at two different parts of the SVC, one just at the entry into the right atrium (where the surrounding pressure is the pericardial pressure) and the other above (where the surrounding pressure is actually the pleural pressure), they found a mean decrease of 2.2 mm Hg for the latter and a 0.5 mm Hg increase for the former, just reflecting that the SVC actually acts as a Starling resistor and may collapse at the junction between the pleural and pericardial pressure (3). Second, we are puzzled by the absence of change in the transmural right atrial pressure (PtmRA) during tidal ventilation. The reason for this is not so obvious. As noted by the authors, it could reflect the absence of change in the pressure gradient for systemic venous return (SVR), as previously suggested by Fessler et al (4), although we do not have the mean systemic pressure, that is, the inflow pressure for SVR, and the outflow pressure for SVR is not the PtmRA but the intravascular right atrial pressure. However, it could also reflect the fact that the afterload effect of mechanical ventilation on the right ventricle plays a large role in some patients. Presentation of the data in two groups of patients according to the change (increase or decrease) in PtmRA would help us to analyze the results. Unfortunately, the authors did the analysis according to pulse pressure variation (PPV, low or high), which, to our knowledge, are not relevant since the afterload effect of mechanical ventilation has also been reported to induce significant PPV. Finally, we disagree somewhat with the authors’ interpretation that a decrease in chest wall compliance may increase the transmission of pressure from the airways to the pleural space. This is an “unsuitable” wording. In fact, it just reflects the fact that since chest wall compliance (CCW) is decreased, the pleural pressure (Ppl) is increased for the same delivered tidal volume (TV), as indicated by the equation CCW = TV changes/Ppl changes. The authors have disclosed that they do not have any potential conflicts of interest. Antoine Vieillard-Baron, MD, PhD, Xavier Repessé, MD, Cyril Charron, MD, University Hospital Ambroise Paré, Assistance Publique des Hôpitaux de Paris, Université Versailles Saint Quentin en Yvelines, Boulogne, France
REFERENCES
1. Lansdorp B, Hofhuizen C, van Lavieren M, et al: Mechanical Ventilation–Induced Intrathoracic Pressure Distribution and HeartLung Interactions. Crit Care Med 2014; 42:1983–1990 2. Vieillard-Baron A, Chergui K, Rabiller A, et al: Superior vena caval collapsibility as a gauge of volume status in ventilated septic patients. Intensive Care Med 2004; 30:1734–1739 3. Jardin F, Vieillard-Baron A: Ultrasonographic examination of the venae cavae. Intensive Care Med 2006; 32:203–206 4. Fessler HE, Brower RG, Wise RA, et al: Effects of positive end-expiratory pressure on the gradient for venous return. Am Rev Respir Dis 1991; 143:19–24 DOI: 10.1097/CCM.0000000000000740 February 2015 • Volume 43 • Number 2
Copyright of Critical Care Medicine is the property of Lippincott Williams & Wilkins and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
ACs was 59% radial and 41% femoral. In the RCT by Timsit et al (7) published in 2012 were included 1,879 patients and 4,163 IVC, 1,962 CVC (47%), and 2,201 AC (53%). The distribution per site between CVCs was 37% jugular, 29% subclavian, and 34% femoral. The distribution per vascular access between ACs was 65% radial and 35% femoral. In the RCT by Maki et al (8) were included 1,401 IVC; however, the distribution of vascular access was not reported in this RCT published as abstract in a congress. Thus, the number of AC is important to exclude them from the conclusion and to say that the use of chlorhexidine-impregnated dressing could reduce the risk of CVC colonization and CVC-bloodstream infection. However, the conclusion of the meta-analysis saying that the use of chlorhexidine-impregnated dressing could reduce the risk of IVC colonization and IVC-bloodstream infection suggests that this effect is in all IVC accessed. In my opinion, the findings of the meta-analysis by Safdar et al (1) suggest that chlorhexidine-impregnated dressing may be another measure to prevent IVC-bloodstream infection. However, it could be interesting to analyze if the preventive effect of chlorhexidine-impregnated dressing to reduce the risk of IVCbloodstream infection is present in all IVC accesses; this would help us in taking decision and to optimize the distribution of healthcare cost. The author has disclosed that he does not have any potential conflicts of interest. Leonardo Lorente, MD, PhD, Intensive Care Unit, Hospital Universitario de Canarias, La Laguna, Santa Cruz de Tenerife, Spain
REFERENCES
1. Safdar N, O’Horo JC, Ghufran A, et al: Chlorhexidine-Impregnated Dressing for Prevention of Catheter-Related Bloodstream Infection: A Meta-Analysis. Crit Care Med 2014; 42:1703–1713 2. Mahjoub Y, Dupont H: Chlorhexidine-impregnated dressing: An efficient weapon against catheter-related bloodstream infection? Crit Care Med 2014; 42:1742–1743 3. Lorente L, Jiménez A, Martín MM, et al: Lower catheter-related bloodstream infection in arterial than in venous femoral catheter. Eur J Clin Microbiol Infect Dis 2012; 31:487–490 4. Lorente L, Santacreu R, Martín MM, et al: Arterial catheter-related infection of 2,949 catheters. Crit Care 2006; 10:R83 5. Lorente L, Henry C, Martín MM, et al: Central venous catheter-related infection in a prospective and observational study of 2,595 catheters. Crit Care 2005; 9:R631–R635 6. Timsit JF, Schwebel C, Bouadma L, et al; Dressing Study Group: Chlorhexidine-impregnated sponges and less frequent dressing changes for prevention of catheter-related infections in critically ill adults: A randomized controlled trial. JAMA 2009; 301:1231–1241 7. Timsit JF, Mimoz O, Mourvillier B, et al: Randomized controlled trial of chlorhexidine dressing and highly adhesive dressing for preventing catheter-related infections in critically ill adults. Am J Respir Crit Care Med 2012; 186:1272–1278 8. Maki D, Mermel L, Kluger D, et al: The Efficacy of a Chlorhexidine Impregnated Sponge (Biopatch) for the Prevention of Intravascular Catheter-Related Infection—A Prospective Randomized Controlled Multicenter Study [abstract 1430]. Programs and Abstracts of the Fortieth Interscience Conference on Antimicrobial Agents and Chemotherapy, Toronto. Washington, DC, American Society for Microbiology, 2000, p 422 DOI: 10.1097/CCM.0000000000000739
Critical Care Medicine
The authors reply:
D
r. Lorente (1) correctly observes that our meta-analysis did not differentiate the effect of chlorhexidineimpregnated dressings on different types of access. The small number of studies precluded meaningful sensitivity analyses, although the three studies which included arterial catheters all noted that a benefit was seen in this subgroup. As we noted in a previous meta-analysis, arterial catheter infections may be an underrecognized source of infection (2), and finding effective prevention measures, such as chlorhexidineimpregnated dressing, is critical. Likewise, a differential effect of chlorhexidine on different sites would not be unexpected, as higher risk sites (e.g., arguably [3] femoral sites) should see a more drastic reduction than lower risk sites. However, as we are now in the era where zero central catheter infections is not just a goal but an expectation by payers (4), even moderate-risk reductions of lower risk sites are clinically relevant. We agree with Dr. Lorente (1) that further research on the effectiveness of these dressings across different patient care settings and types of devices is needed. The authors have disclosed that they do not have any potential conflicts of interest. Nasia Safdar, MD, Infectious Disease, University of Wisconsin Hospital and Clinics, Madison, WI, and William S. Middleton Memorial Veterans Hospital, Madison, WI; John C. O’Horo, MD, MPH, Department of Medicine, Division of Infectious Diseases, Mayo Clinic, Rochester, MN
REFERENCES
1. Lorente L: Does Chlorhexidine-Impregnated Dressing Reduce the Risk of Catheter-Related Bloodstream Infection in All Vascular Access? Crit Care Med 2015; 43:e50–e51 2. O’Horo JC, Maki DG, Krupp AE, et al: Arterial catheters as a source of bloodstream infection: A systematic review and meta-analysis. Crit Care Med 2014; 42:1334–1339 3. Marik PE, Flemmer M, Harrison W: The risk of catheter-related bloodstream infection with femoral venous catheters as compared to subclavian and internal jugular venous catheters: A systematic review of the literature and meta-analysis. Crit Care Med 2012; 40:2479–2485 4. Medicaid program; Payment adjustment for provider-preventable conditions including health care-acquired conditions; final rule. In: Centers for Medicare and Medicaid Services. Washington, DC, Federal Register, 2011, pp 32816–32838 DOI: 10.1097/CCM.0000000000000831
The authors reply:
W
e read with peculiar interest the letter by Dr. Lorente (1) regarding our editorial (2) about the meta-analysis published by Safdar and Maki (3). In the letter, the author pointed out two main limitation of the meta-analysis. First, among the randomized controlled trials included in the meta-analysis, at least three of them mix central venous catheters (CVC) and arterial catheters (AC). Second, the insertion site is variable (jugular, femoral, or subclavian). As shown in some studies, catheter-related bloodstream infection rate www.ccmjournal.org
e51
Online Letters to the Editor
varies with catheter type (arterial vs venous) and catheter site (jugular, femoral, or subclavian for CVC; arterial and femoral for ACs). Thus, the heterogeneity in catheter type and site precludes the conclusion of Safdar and Maki (3): chlorhexidineimpregnated dressing may not have the same efficiency in all situations. We already discussed these limitations in our editorial (2). Furthermore, we have suggested that a subgroup analysis would be useful to tackle this issue. In our opinion, these limitations do not diminish the value of the meta-analysis by Safdar and Maki (3). Use of chlorhexidine-impregnated dressing decreases the absolute risk of catheter-related bloodstream infection (CRBSI) by 1.7%. The use of these devices may be considered as an additional strategy to reduce CRBSI. If the risk of CRBSI is very low, as for arterial radial catheters (4), this kind of dressing may not be as effective as expected for others intravascular catheters. However, in a culture of safety, no strategy should be discarded too quickly. A cost analysis for a universal use of this dressing for all CVCs may help to make a decision. The authors have disclosed that they do not have any potential conflicts of interest. Yazine Mahjoub, MD, Hervé Dupont, MD, PhD, Medical and Surgical Intensive Care Unit, Department of Anesthesia and Intensive Care, Amiens University Medical Center, Amiens, France, and INSERM U-1088, Jules Verne University of Picardie, Amiens, France
REFERENCES
1. Lorente L: Does Chlorhexidine-Impregnated Dressing Reduce the Risk of Catheter-Related Bloodstream Infection in All Vascular Access? Crit Care Med 2015; 43:e50–e51 2. Mahjoub Y, Dupont H: Chlorhexidine-impregnated dressing: An efficient weapon against catheter-related bloodstream infection? Crit Care Med 2014; 42:1742–1743 3. Safdar N, Maki DG: The pathogenesis of catheter-related bloodstream infection with noncuffed short-term central venous catheters. Intensive Care Med 2004; 30:62–67 4. Lorente L, Santacreu R, Martín MM, et al: Arterial catheter-related infection of 2,949 catheters. Crit Care 2006; 10:R83 DOI: 10.1097/CCM.0000000000000810
Heart-Lung Interactions: Have a Look on the Superior Vena Cava and on the Changes in Right Ventricular Afterload To the Editor:
W
e would like to congratulate Lansdorp et al (1) for the beautiful physiological study that they recently published in Critical Care Medicine regarding mechanical ventilation–induced intrathoracic pressure distribution and heart-lung interactions. We would like to make three comments. First, and most importantly, Lansdorp et al (1) have very well demonstrated invasively what we suggested noninvasively 10 years ago using transesophageal echocardiography regarding the potential collapse of the superior vena cava (SVC) related to tidal ventilation (2). If we look at the transmural
e52
www.ccmjournal.org
pressure of the SVC (PtmSVC), the authors report a significant decrease during tidal ventilation. If we calculate, using the data provided in Table 2 in (1), mean changes in PtmSVC during tidal ventilation at 8 mL/kg at two different parts of the SVC, one just at the entry into the right atrium (where the surrounding pressure is the pericardial pressure) and the other above (where the surrounding pressure is actually the pleural pressure), they found a mean decrease of 2.2 mm Hg for the latter and a 0.5 mm Hg increase for the former, just reflecting that the SVC actually acts as a Starling resistor and may collapse at the junction between the pleural and pericardial pressure (3). Second, we are puzzled by the absence of change in the transmural right atrial pressure (PtmRA) during tidal ventilation. The reason for this is not so obvious. As noted by the authors, it could reflect the absence of change in the pressure gradient for systemic venous return (SVR), as previously suggested by Fessler et al (4), although we do not have the mean systemic pressure, that is, the inflow pressure for SVR, and the outflow pressure for SVR is not the PtmRA but the intravascular right atrial pressure. However, it could also reflect the fact that the afterload effect of mechanical ventilation on the right ventricle plays a large role in some patients. Presentation of the data in two groups of patients according to the change (increase or decrease) in PtmRA would help us to analyze the results. Unfortunately, the authors did the analysis according to pulse pressure variation (PPV, low or high), which, to our knowledge, are not relevant since the afterload effect of mechanical ventilation has also been reported to induce significant PPV. Finally, we disagree somewhat with the authors’ interpretation that a decrease in chest wall compliance may increase the transmission of pressure from the airways to the pleural space. This is an “unsuitable” wording. In fact, it just reflects the fact that since chest wall compliance (CCW) is decreased, the pleural pressure (Ppl) is increased for the same delivered tidal volume (TV), as indicated by the equation CCW = TV changes/Ppl changes. The authors have disclosed that they do not have any potential conflicts of interest. Antoine Vieillard-Baron, MD, PhD, Xavier Repessé, MD, Cyril Charron, MD, University Hospital Ambroise Paré, Assistance Publique des Hôpitaux de Paris, Université Versailles Saint Quentin en Yvelines, Boulogne, France
REFERENCES
1. Lansdorp B, Hofhuizen C, van Lavieren M, et al: Mechanical Ventilation–Induced Intrathoracic Pressure Distribution and HeartLung Interactions. Crit Care Med 2014; 42:1983–1990 2. Vieillard-Baron A, Chergui K, Rabiller A, et al: Superior vena caval collapsibility as a gauge of volume status in ventilated septic patients. Intensive Care Med 2004; 30:1734–1739 3. Jardin F, Vieillard-Baron A: Ultrasonographic examination of the venae cavae. Intensive Care Med 2006; 32:203–206 4. Fessler HE, Brower RG, Wise RA, et al: Effects of positive end-expiratory pressure on the gradient for venous return. Am Rev Respir Dis 1991; 143:19–24 DOI: 10.1097/CCM.0000000000000740 February 2015 • Volume 43 • Number 2
Copyright of Critical Care Medicine is the property of Lippincott Williams & Wilkins and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
