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National Institute for Environmental Studies, Tsukuba, Japan Kyoto Prefectural University of Medicine, Kyoto, Japan
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{at}nies.go.jp
To the Editor:
We read with great interest the recent case series by Patel and colleagues (January 2004).1 In 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 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.567 Therefore, surgery itself may aggravate ARDS. As Patel and colleagues1 concluded, clinicians should give careful consideration to the selection of patients with ARDS.
References
Harvard Medical School, Boston, MA
Correspondence to: Sanjay Patel, MD, Department of Pulmonary and Critical Care Medicine, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115; e-mail: spatel{at}partners.org
To the Editor:
We appreciate the interest of Inoue et al in our recent article (January 2004).1 Although we acknowledge the role of cytokines in the pathogenesis of ARDS,2 we 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
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