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Communications to the Editor |

Surgical Stress in ARDS Open-Lung Biopsy FREE TO VIEW

Ken-ichiro Inoue, MD; Hirohisa Takano, MD, PhD; Rie Yanagisawa, PhD; Miho Sakurai; Toshikazu Yoshikawa, MD, PhD
Author and Funding Information

Affiliations: National Institute for Environmental Studies, Tsukuba, Japan,  Kyoto Prefectural University of Medicine, Kyoto, Japan,  Harvard Medical School, Boston, MA

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: inoue.kenichirou@nies.go.jp



Chest. 2004;126(4):1383-1384. doi:10.1378/chest.126.4.1383
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To the Editor:

We read with great interest the recent case series by Patel and colleagues (January 2004).1In their discussion about complications 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.23 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 al4demonstrated 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.57 Therefore, surgery itself may aggravate ARDS. As Patel and colleagues1 concluded, clinicians should give careful consideration to the selection of patients with ARDS.

Patel, SR, Karmpaliotis, D, Ayas, NT, et al (2004) The role of open-lung biopsy in ARDS.Chest125,197-202. [CrossRef] [PubMed]
 
Takezawa, J Surgical stress and acute lung injury [in Japanese].Nippon Geka Gakkai Zasshi1996;97,739-744. [PubMed]
 
Endo, S, Inada, K, Sato, N, et al Cytokines in surgical stress [in Japanese].Nippon Geka Gakkai Zasshi1996;97,708-715. [PubMed]
 
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 Med1995;151,698-705. [PubMed]
 
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 Med2002;165,1329-1335. [CrossRef] [PubMed]
 
Yanagisawa, R, Takano, H, Inoue, K, et al Enhancement of acute lung injury related to bacterial endotoxin by components of diesel exhaust particles.Thorax2003;58,605-612. [CrossRef] [PubMed]
 
Inoue, K, Takano, H, Yanagisawa, R, et al Effect of 15-deoxy-delta 12,14-prostaglandin J2on acute lung injury induced by lipopolysaccharide in mice.Eur J Pharmacol2003;481,261-269. [CrossRef] [PubMed]
 
To the Editor:

We appreciate the interest of Inoue et al in our recent article (January 2004).1Although we acknowledge the role of cytokines in the pathogenesis of ARDS,2we would question the relevance of some of the citations in their letter. Specifically, we fail to see how aortic cross-clamping causing “ischemia/reperfusion of the lower body” and/or the inhalational exposure to diesel exhaust particles have relevance to the performance of open lung biopsy in ARDS patients, because our patients’ lung injuries did not have these etiologies. However, we do acknowledge that an inflammatory response to thoracic surgery could be one mechanism underlying the deterioration in gas exchange that we occasionally observed in our ARDS patients. Of note, some data suggest that limited surgery using a thoracoscopic approach can attenuate the cytokine response compared with that with open thoracotomy.34 However, thoracoscopy generally requires single-lung ventilation and therefore is not usually feasible in ARDS patients. We would also caution against the use of cytokines as an end point per se without corroborative physiologic and/or clinical outcome data.

References
Patel, SR, Karmpaliotis, D, Ayas, NT, et al The role of open-lung biopsy in ARDS.Chest2004;125,197-202. [CrossRef] [PubMed]
 
Ware, LB, Matthay, MA The acute respiratory distress syndrome.N Engl J Med2000;342,1334-1349. [CrossRef] [PubMed]
 
Yim, AP, Wan, S, Lee, TW, et al VATS lobectomy reduces cytokine responses compared with conventional surgery.Ann Thorac Surg2000;70,243-247. [CrossRef] [PubMed]
 
Sugi, K, Kaneda, Y, Esato, K Video-assisted thoracoscopic lobectomy reduces cytokine production more than conventional open lobectomy.Jpn J Thorac Cardiovasc Surg2000;48,161-165. [PubMed]
 

Figures

Tables

References

Patel, SR, Karmpaliotis, D, Ayas, NT, et al (2004) The role of open-lung biopsy in ARDS.Chest125,197-202. [CrossRef] [PubMed]
 
Takezawa, J Surgical stress and acute lung injury [in Japanese].Nippon Geka Gakkai Zasshi1996;97,739-744. [PubMed]
 
Endo, S, Inada, K, Sato, N, et al Cytokines in surgical stress [in Japanese].Nippon Geka Gakkai Zasshi1996;97,708-715. [PubMed]
 
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 Med1995;151,698-705. [PubMed]
 
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 Med2002;165,1329-1335. [CrossRef] [PubMed]
 
Yanagisawa, R, Takano, H, Inoue, K, et al Enhancement of acute lung injury related to bacterial endotoxin by components of diesel exhaust particles.Thorax2003;58,605-612. [CrossRef] [PubMed]
 
Inoue, K, Takano, H, Yanagisawa, R, et al Effect of 15-deoxy-delta 12,14-prostaglandin J2on acute lung injury induced by lipopolysaccharide in mice.Eur J Pharmacol2003;481,261-269. [CrossRef] [PubMed]
 
Patel, SR, Karmpaliotis, D, Ayas, NT, et al The role of open-lung biopsy in ARDS.Chest2004;125,197-202. [CrossRef] [PubMed]
 
Ware, LB, Matthay, MA The acute respiratory distress syndrome.N Engl J Med2000;342,1334-1349. [CrossRef] [PubMed]
 
Yim, AP, Wan, S, Lee, TW, et al VATS lobectomy reduces cytokine responses compared with conventional surgery.Ann Thorac Surg2000;70,243-247. [CrossRef] [PubMed]
 
Sugi, K, Kaneda, Y, Esato, K Video-assisted thoracoscopic lobectomy reduces cytokine production more than conventional open lobectomy.Jpn J Thorac Cardiovasc Surg2000;48,161-165. [PubMed]
 
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