|
|
||||||||
Ann Thorac Surg 1997;64:276-279
© 1997 The Society of Thoracic Surgeons
Department of Thoracic Surgery, Roswell Park Cancer Institute, Buffalo, New York
| Abstract |
|---|
|
|
|---|
Methods. We performed a collective review of the literature to summarize information on etiology, prevention, treatment, complications, and outcome of chest wall necrotizing soft tissue infections. Manual, Medline, and Current Contents searches of the English-language medical literature were done.
Results. There were 9 reported cases of necrotizing soft tissue infection of the chest wall. Eight were complications of invasive procedures and operations. Tube thoracostomy for empyema (4 patients) was the most common antecedent procedure. Excessive soft tissue dissection during chest tube insertion was implicated in the genesis of these infections. Necrotizing infections complicated esophageal operations in 2 patients. Overall mortality was 89%. Only 3 of the 9 patients underwent early and adequate debridement. Chest wall stability and wound reconstruction were problematic in patients who survived the initial septic illness.
Conclusions. Necrotizing soft tissue infections of the chest wall are highly lethal infections that require urgent and aggressive debridement. Diagnostic delay and inadequate debridement are common reasons for treatment failure. Repetitive surgical debridement is often needed to control sepsis. Wound closure is challenging in patients who survive the initial septic phase of their illness.
| Introduction |
|---|
|
|
|---|
| Material and Methods |
|---|
|
|
|---|
We excluded reports of infection originating in the neck or abdomen that secondarily extended into the chest wall. Articles that briefly alluded to cases of thoracic involvement but did not give specifics were also excluded. Nine cases of necrotizing soft tissue infection of the chest wall were found, and form the basis of this review [17].
| Results |
|---|
|
|
|---|
|
|
| Comment |
|---|
|
|
|---|
Clinical features of necrotizing soft tissue infections include wound pain; crepitus; foul, watery wound discharge; skin blistering; and rapid progression to septic shock [911, 13]. The external appearance of the skin wound may initially betray the magnitude of the necrotizing infection beneath it; this contributes to diagnostic delay. Soft tissue gas, detected clinically or radiologically, is a classic sign, but its absence does not exclude the presence of a necrotizing infection [13]. The common misconception that soft tissue gas is always present in a necrotizing infection is responsible for delayed diagnosis in some cases. The infection spreads rapidly through the soft tissue planes and produces severe systemic sepsis. Progression to septic shock, multiple organ failure, and death ensues if aggressive treatment is not instituted immediately. Even with timely and skilled treatment, mortality for nonthoracic necrotizing soft tissue infections ranges from 15% to 50% [9, 10, 13].
Some necrotizing infections are caused by single organisms. Myonecrosis (gas gangrene) from Clostridium perfringens infection and necrotizing fasciitis due to Streptococcus pyogenes are two classic examples of single-organism necrotizing infection. However, most necrotizing soft tissue infections are caused by a mixture of aerobic and anaerobic bacteria, which act synergistically to cause fulminant infection [14, 15]. Organisms commonly identified include aerobic and anaerobic streptococci, coagulase-negative and coagulase-positive staphylococci, facultative and aerobic gram-negative rods, Bacteroides species, and Clostridium species [13, 14]. Facultative organisms lower the oxidation-reduction potential of the wound microenvironment and promote favorable conditions for the growth of anaerobes. Anaerobes interfere with host phagocyte function, and thereby facilitate the proliferation of aerobic bacteria [16]. Several bacteria, such as Bacteroides fragilis, produce ß-lactamase enzymes that interfere with antibiotic activity against itself and other components of the polymicrobial infection.
Bacterial necrotoxins, such as those produced by Clostridium perfringens and Streptococcus pyogenes, cause tissue necrosis. In addition, the infectious process activates the coagulation system, which in turn produces local vascular thrombosis and infarction. Bacterial heparinase production contributes to this process. As the infection progresses, pressure increases within the soft tissues and further impairment of blood supply results [15].
Treatment of necrotizing soft tissue infections entails early surgical debridement, fluid resuscitation, antibiotics, and general cardiorespiratory supportive care to maintain vital organ function [1113, 17]. The most common pitfall in treatment is delay or inadequacy of surgical debridement. Debridement should be early and aggressive; all necrotic tissue must be excised. "Incision and drainage" approaches are not appropriate. These infections are characterized by necrotic tissue and watery drainage, as opposed to the viable tissue and pus that are typical of bacterial abscesses. Repeat debridement, sometimes on a daily basis, should be done until the local infectious process has been arrested [5, 13, 18, 19]. After sepsis is controlled, coverage of the wound is usually obtained by skin grafting.
Intravenous fluid resuscitation, mechanical ventilation, and inotropic support follow well-established principles for managing septic shock. These principles are reviewed elsewhere [2022]. Nutritional support is started after urgent resuscitation and debridement have been done. Antibiotic coverage should be broad spectrum, and anaerobic coverage is essential. Many antibiotic combinations are acceptable; initial empiric therapy of surgical infections has recently been reviewed in detail [15, 23, 24]. Enterococci are the most common organisms not covered by "standard" broad-spectrum combinations [13].
Topical wound agents may be beneficial, but their therapeutic role is much less important than aggressive debridement and systemic antibiotics [12, 18, 19]. Topical antibiotic therapy for necrotizing infections is based on extensive experience with these agents in burn therapy. Assessment of tissue viability may be difficult if tissues are covered by antimicrobial creams, so some authors do not use them in the early stages of the illness [12]. Other agents, such as hydrogen peroxide and sodium hypochlorite, have been used but their true value is not known [18].
Hyperbaric oxygen therapy has an uncertain role in the management of necrotizing soft tissue infections. Some studies suggest a survival benefit [17, 25], but others do not [18, 26]. Survival from clostridial myonecrosis is probably improved by hyperbaric oxygen therapy [26, 27]. For other types of necrotizing soft tissue infection, hyperbaric oxygen therapy may hasten local wound healing and closure [13, 25]. Most investigators agree on one point: hyperbaric oxygen therapy is not as important as urgent surgical intervention. Debridement should take priority over patient transfer to a hyperbaric oxygen facility.
Despite aggressive therapy, mortality caused by necrotizing soft tissue infections is high. Factors associated with increased mortality include delay in debridement, extent of soft tissue involvement, and advanced age [13, 19]. This review shows that involvement of the chest wall is also associated with a very high mortality (89%).
| Necrotizing Soft Tissue Infections: Chest Wall |
|---|
|
|
|---|
Necrotizing soft tissue infections of the chest wall are probably not as rare as this review would suggest. Because they typically complicate surgical procedures, many cases are undoubtedly not reported. The 89% mortality in this collective review is approximately twice that reported for other anatomic sites. Delay or inadequacy of debridement, and severity of the underlying thoracic condition, are responsible for this high mortality. The importance of early, aggressive, and often repetitive surgical debridement cannot be overemphasized.
Adequate debridement of chest wall necrotizing infections usually entails removal of one or more ribs, in addition to infected soft tissue and skin. The resultant defect is not merely a problem of wound care and coverage, as in other anatomic areas; loss of chest wall stability poses additional physiologic problems. Prolonged mechanical ventilation is required until pleural symphysis is obtained. The only survivor in this collective series was ventilated for approximately 2 months [5]. Survivors of necrotizing soft tissue infections are very debilitated; aggressive weaning is not advisable [6].
After the initial septic phase of necrotizing chest wall infection, wound reconstruction and closure are required. Hard tissue reconstruction, with mesh or other prosthetic material, is not advisable because of the risk of subsequent infection [28]. Soft tissue reconstruction and skin coverage can pose tremendous problems. Some of the muscles normally used for chest wall reconstruction are sacrificed during debridement [6]. Simply allowing the wound to granulate may suffice [5], but second-line soft tissue coverage options, such as omentum [28], should be considered. Skin grafts are usually required for final skin coverage [5, 6]. Graft take is usually acceptable if a suitable soft tissue bed is available, but grafting over exposed ribs leads to poor graft take and poor-quality skin coverage [6].
| Footnotes |
|---|
|
|
|---|
| References |
|---|
|
|
|---|
This article has been cited by other articles:
![]() |
M. D. Tata, K. C. Kwan, M. R. Abdul-Razak, S. Paramalingam, and W. C. Yeen Adjunctive use of superoxidized solution in chest wall necrotizing soft tissue infection. Ann. Thorac. Surg., May 1, 2009; 87(5): 1613 - 1614. [Abstract] [Full Text] [PDF] |
||||
![]() |
I. E. Konstantinov, P. Saxena, J. Shehatha, A. Mitchell, and S. Cherian Novel Aeration Technique for Necrotizing Fasciitis of the Chest Wall Ann. Thorac. Surg., December 1, 2008; 86(6): 1973 - 1974. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. O'Connor, A. Kells, S. Henry, and T. Scalea Vacuum-Assisted Closure for the Treatment of Complex Chest Wounds Ann. Thorac. Surg., April 1, 2005; 79(4): 1196 - 1200. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Amini, A. Gabrielli, L. J. Caruso, and A. J. Layon The Thoracic Surgical Patient: Initial Postoperative Care Seminars in Cardiothoracic and Vascular Anesthesia, September 1, 2002; 6(3): 169 - 188. [Abstract] [PDF] |
||||
![]() |
D. B. Safran and W. G. Sullivan Necrotizing fasciitis of the chest wall Ann. Thorac. Surg., October 1, 2001; 72(4): 1362 - 1364. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Freixinet, P. Rodriguez, N. Santana, M. Hussein, F. Cruz, and F. Rodriguez de Castro Necrotizing Fasciitis of Thoracic Wall Complicating Chest Tube Drainage Asian Cardiovasc Thorac Ann, March 1, 2001; 9(1): 76 - 77. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. D Urschel Classic diseases revisited: Necrotizing soft tissue infections Postgrad. Med. J., November 1, 1999; 75(889): 645 - 649. [Abstract] [Full Text] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |