Ann Thorac Surg 2005;79:1730-1731
© 2005 The Society of Thoracic Surgeons
Original articles: General thoracic: Invited commentary
INVITED COMMENTARY
Marisa De Feo, MD, PhD
Department of Cardiothoracic and Respiratory Sciences, Second University of Naples-A. O. Monaldi Hospital, Via Posillipo, 9, 80123 Naples, Italy
(E-mail: marisa.defeo{at}tin.it).
Vacuum-assisted wound infection management represents a relatively novel strategy [1] that is gaining worldwide acceptance and is yielding encouraging results for postoperative mediastinitis, as the authors of this article previously reported [2]. The mechanisms underlying the effectiveness of this method have been partially identified (ie, the application of negative pressure to healing wound tissue is expected to prevent local ischemia by increasing microvascular blood flow to eventually accelerate the process of wound closure [3]). Wackenfors and colleagues have tried to verify this hypothesis of pathophysiologic mechanism in an animal model. The study identifies a correlation between microvascular flow and applied pressure, distance from the wound edge and tissue density. The finding that both O2 and lactate increase in the wound during VAC therapy is also of great interest because it supports the hypothesis of enhanced migration and proliferation in granulation tissue cells. Nevertheless, the present study does not provide direct demonstration (ie, evidence of the biomolecular mechanisms involved in this theory).
Animal models, although widely validated in previous experiments, have the obvious limitation of differing from the human setting. In the clinical situation, postoperative mediastinitis is a multifarious entity, representing a more or less challenging complication because of the coexistence of several patient-related factors related to the perioperative course [4]. Both systemic and local conditions may affect the mechanisms of wound healing. In this perspective, a major limitation of this study is the use of noninfected animals that lack the systemic and local conditions associated with active sternal wound infection. How would changes in local oxygenation, microcirculation, and metabolism occurring with bacterial infection interact with the mechanism of vacuum? How would these factors have influenced the results of such experiments? One wonders whether the pressure-dependence of the VAC effect would maintain the same dynamics in infected wounds as shown by the authors. Even tissue density itself, which influences the effect of VAC on the wound by modulating negative pressure transduction to the wound tissue is greatly altered in case of infection. Further studies are needed to generate data that are more applicable to clinical practice; animals with reproduced clinical sternal wounds and greater negative pressures, similar to those used in clinical wound treatment are needed for this objective. Such studies, along with the present one, are of utmost importance, because the VAC method is new, and detailed explanation of its mechanisms of action will enable tailoring methods for different patients and clinical situations.
 |
References
|
|---|
- Catarino PA, Chamberlain MH, Wright NC, et al. High-pressure suction drainage via a polyurethane foam in the management of poststernotomy mediastinitis Ann Thorac Surg 2000;70:1891-1895.[Abstract/Free Full Text]
- Gustafsson RI, Sjogren J, Ingemansson R. Deep sternal wound infection: a sternal-sparing technique with vacuum-assisted closure therapy Ann Thorac Surg 2003;76:2048-2053.[Abstract/Free Full Text]
- Morykwas MJ, Argenta LC, Shelton-Brown EI, McGuirt W. Vacuum-assisted closure: a new method for wound control and treatment: animal studies and basic foundation Ann Plast Surg 1997;38:553-562.[Medline]
- De Feo M, Renzulli A, Ismeno G, et al. Variables predicting adverse outcome in patients with deep sternal wound infection Ann Thorac Surg 2001;71:324-331.[Abstract/Free Full Text]
Top
References