Adult Chest Surgery

Chapter 126. Surgical Treatment for Chest Wall Infections 

Soft tissue infections of the chest wall often present in physically debilitated immunocompromised individuals either de novo or after surgical or other trauma. These infections can manifest in various ways, including a discrete mass that may be confused with other chest wall tumors, a diffuse superficial spreading infection, or a draining sinus tract. A number of organisms are involved from common bacterial species such asStaphylococcus aureus to more exotic organisms such as the larvae of the Tumbu fly (Cordylobia anthropophaga), which causes cutaneous myiasis.1 This chapter reviews the various pathogens of chest wall infections and discusses their treatment.

CLINICAL PRESENTATION

Patients afflicted with chest wall infections typically are immunocompromised. Many have been actively immunosuppressed for organ or bone marrow transplantation, or they are being treated with immunomodulating agents for chronic inflammatory disease such as rheumatoid arthritis. Steroid drugs are the most common anti-inflammatory agents used in this setting. Other individuals are immunocompromised as a result of physical debilitation from chronic illness, alcoholism, or poor nutrition. Still others may start out as healthy but become predisposed to infection or inoculated after trauma or surgery.

Infections can seed the chest wall by one of three mechanisms: (1) direct extension from an underlying pulmonary infection/empyema (empyema necessitans), (2) inoculation of the chest wall, and (3) hematogenous spread, with each organ exhibiting a distinct pathway. Manifestations of chest wall infection vary with the pathogen itself and range from discrete masses to draining sinuses to superficial spreading necrotizing infections. Systemic signs of infection vary with the underlying pathogen. Some are asymptomatic, whereas others cause low-grade temperatures and malaise. Yet others lead to septic shock physiology. Diagnosis can be obvious but often is difficult owing to the unusual presentations and rarity of some pathogenic organisms involved. Clinical suspicion is confirmed and complemented by culture data. Treatment rests on symptomatic support as well as antibiotics alone or combined with surgical debridement.

PATHOGENS

Bacterial: Necrotizing Infections

Necrotizing infections of the chest wall are characterized by extensive tissue necrosis with the production of gas elsewhere in the body. Typically, these infections are associated with mild trauma or are seen postoperatively. Multiple aerobic and anaerobic organisms have been isolated, including anaerobes such as Bacteroides spp., Peptostreptococcus spp., and Clostridium spp., as well as aerobes such as Streptococcus pyogenes, S. aureus, and members of the Enterobacteriaceae family. Fungal species have been isolated as well and are reviewed in Chap. 109.2–6 These infections violate tissue planes and are not contained by typical host immune defenses. They can develop quickly in both immunocompromised and immunocompetent individuals and lead rapidly to death if not expectantly diagnosed and treated with extensive surgical debridement and systemic antibiotic therapy.

Although necrotizing infections involve a spectrum of disease, they can be loosely classified as follows: (1) crepitant anaerobic cellulitis, (2) necrotizing fasciitis, and (3) nonclostridial and clostridial myonecrosis.

Nonclostridial and clostridial myonecrosis typically affects the perirectal and lower extremities and rarely affects the chest wall and hence will not be discussed.2–6 All these infections have an anaerobic component and typically are mixed aerobic-anaerobic infections. Clinical signs of these infections include marked tissue destruction with an associated putrid gaseous discharge.

Crepitant anaerobic cellulitis involves both aerobic and anaerobic organisms such as Bacteroides spp. and Peptostreptococcus spp., have the characteristics of a necrotic soft tissue infection, and typically there is abundant gas in the patient's poorly vascularized tissues. Systemic toxicity, severe pain, and marked tissue destruction are limited, which distinguishes this type of infection from necrotizing fasciitis. Treatment involves the selection of appropriate antibiotics and, occasionally, tissue debridement.

Necrotizing fasciitis is an infrequent infection with an exceptionally high mortality ranging from 40% to 70% in most series. Streptococcal species, especially S. pyogenes, are typically implicated. Other organisms, including anaerobes such as Peptostreptococcus, Bacteroides, and Fusobacterium spp., are frequently coisolated. In addition to S. pyogenes, other aerobic organisms also have been isolated, including S. aureus and members of the Enterobacteriaceae family.2–6 Clinically affected tissues have extensive involvement, with necrosis of the superficial and often the deep fascia, along with thrombosis in the associated blood vessels. Systemic toxicity is often evident. Rapid diagnosis and treatment with appropriate antibiotics and surgery are the only way to reduce the prohibitively high mortality associated with this disease.

Bacterial: Nonnecrotizing Infections

Actinomyces spp. are members of a large group of pleomorphic gram-positive bacteria, which, in turn, are members of the oral flora of both humans and animals. Actinomyces spp. in particular are major components of dental plaque. A. israelii, A. gerencseriae, and Propionibacterium propionicus cause actinomycosis in humans as well as animals.7–13 Other species of Actinomyces can be involved in mixed anaerobic and other infections, where they may not always play an obviously pathogenic role. Actinomycosis is a chronic disease that is characterized by the production of abscesses or granulomas that eventually develop draining sinuses often containing sulfur granules. The disease occurs in the thoracic as well as in other regions of the body. Cervicofascial involvement is most common, with over 50% of patients presenting with cervical or jaw masses, which, left untreated, develop into draining sinsuses.7–13 The organism spreads by direct extension and does not respect any anatomic barriers. Hematogenous spread of the organisms is rare and only typically occurs from thoracic disease.

Thoracic actinomycosis represents approximately 10–30% of cases. Afflicted individuals typically are males with poor dental hygiene and nutritional status. Thoracic actinomycosis results from aspiration of the organism from plaque on the teeth and may involve the chest wall, the lungs, or both.7–13 Rarely, the disease may be caused by direct extension from the abdomen or from the cervical area. Symptoms are similar to those of other chronic pulmonary diseases (e.g., chronic cough and shortness of breath) and hence are difficult to diagnose. Thoracic disease may spread extensively to adjacent tissues or organs and often disseminates through the bloodstream, resulting in abscesses in distant sites such as the brain. Chest wall infection results either from hematogenous spread or from direct extension of the disease from the pulmonary parenchyma, as often occurs with untreated bacterial empyema. This is termed empyema necessitans.14,15 Treatment of actinomycosis is chiefly medical with IV and oral penicillin. Surgery is often needed to debride the chest wall in cases of extensive chest wall involvement or chest wall extension from the pulmonary parenchyma.

Primary infection of the chest wall by Mycobacterium tuberculosis is rare. Clinically, chest wall infections usually manifest as an abscess or tumor.7,16 Affected individuals typically are inoculated directly by the organisms. The disease is not limited to immunocompromised individuals because it can occur in immunocompetent individuals. However, the disease, as expected, is more extensive in the immunocompromised. Diagnosis is difficult and requires bacteriologic culture for definitive diagnosis. Treatment involves antituberculous chemotherapy and adequate surgical therapy. Other Mycobacterium spp. that rarely involve the chest wall include M. marinumand M. ulcerans.7,16 However, the extremities are more typically involved, and hence they are not discussed further.

Chest wall infection also can occur from direct spread of bacterial organisms from underlying untreated empyema, termed empyema necessitans, as mentioned earlier. The involved organisms usually are polymicrobial. Affected individuals typically are elderly or immunocompromised. Treatment involves antibiotics with surgical debridement of the affected chest wall as well as lung parenchyma, which often requires a Clagett procedure.

Fungal Infections

Phycomyces and Aspergillus spp. also can cause a necrotizing chest wall cellulitis in immunocompromised hosts. These infections are characterized by their invasion of blood vessels with subsequent vessel thrombosis. ThePhycomyces spp. are characterized by broad-based nonseptate hyphae; organisms include Rhizopus, Mucor, and Absidia spp. Aspergillus spp. histologically are characterized by branching septate hyphae.16–18 Aspergilluschest wall infections may be primary or from a disseminated infection. Affected individuals usually are immunocompromised. Children with chronic granulomatous disease are often affected by chest wall Aspergillus.17,18 The dermal lesion presents an indurate plaque that leads to a necrotic ulcer. Treatment includes antifungal agents along with surgical debridement.

Miscellaneous

A number of parasitic organisms can manifest as chest wall infections if the chest wall is inoculated. These include organisms such as the larvae of Tumbu fly (Cordylobia anthropophaga), which causes cutaneous myiasis, and leishmaniases which is caused by a different protozoan Leishmania species.1 These diseases are difficult to diagnose, and in patients who travel out of their endemic regions, a high degree of suspicion is required. Other organisms that can have cutaneous manifestations include Bacillus anthracis, streptococcal species (impetigo), or Staphyloccocus spp. (furnucle or carbuncle).19 However, these organisms typically are not restricted to chest wall disease and hence are not discussed further.

PRINCIPLES OF TREATMENT

Surgical treatment of chest wall infection requires expedient diagnosis and extensive debridement of infected tissue to normal regions. Appropriate extended courses of antimicrobials are required as well. Important considerations for operative debridement include the use of frozen sections to obtain disease-free margins and the lack of hesitance to debride widely to achieve disease-free tissues. Adjunctive measures such as use of hyperbaric oxygen for necrotizing infections has been described but never have been proved to be of benefit.20

Reconstruction after extensive debridement has been greatly facilitated in recent years by negative-pressure wound therapy using a vacuum-assisted closure (VAC) device (Fig. 126-1). This involves the placement of a foam sponge over the wound and the application of regulated suction to clear the wound of exudates. The sponge is changed every 3–4 days. VAC devices promote wound healing and granulation tissue formation by still unclear mechanisms; although some have postulated the regulation of various cytokines.21 VAC sponges provide coverage for large wounds, eliminate the need for frequent and often painful dressing changes, and contract the wound over time, thereby minimizing the remaining area to be covered by future skin grafts or pedicled flaps.

Figure 126-1.

 

Negative-pressure wound therapy with a vacuum-assisted closure device promotes formation of granulation tissue and wound healing.

Tissue coverage of these wounds is provided after all areas of active infection have been debrided, healthy granulation tissue is observed, and the patient has recovered sufficiently to tolerate further surgery. Coverage schemes vary depending on the size and depth of the wound to be covered and can range from split-thickness skin grafts to the need for pedicled omental and local muscle flaps fashioned often with the help of a plastic surgeon (see also Chap. 117). However, the wound must be clean with an adequate granulation tissue bed to accept the graft and, as stated before, a patient well enough with adequate nutritional status to engraft the flap.

Newer techniques are currently being developed that incorporate biologic graft substitutes such as treated human cadaver skin (AlloDerm, LifeCell, Branchburg, NJ) and treated porcine submucosa (Surgisis, Cook, Bloomington, IN).22–24 These biologic substitutes can be used to cover the wound and serve as a matrix for tissue ingrowth as well as provide a barrier to superinfection. Long-term results and efficacy of these substitutes have yet to be determined.

SUMMARY

Chest wall infections present in physically debilitated, immunocompromised individuals. These infections have various manifestations from discrete masses to extensive cellulitic infections. A number of organisms are involved. Treatment rests on tissue culture data for appropriate antibiotic selection as well as surgical debridement for extensive necrotic disease.

CASE PRESENTATION

A 65-year-old man with a past medical history significant for chronic alcoholism with recurrent pneumonias presented with a chronic cough, hemoptysis, and a draining chest wall mass. The patient stated that the mass had been present for the past 6 months and now was draining yellow fluid. Gram stain of the fluid showed no hyphae.

1.     What is your diagnosis?

  a. 

Actinomycosis

  b. 

Aspergillosis

  c. 

Nocardiosis

  d. 

Candidiasis

5.     What is the medical treatment for this condition?

  a. 

Penicillin

  b. 

Ceftriaxone

  c. 

Tetracycline

  d. 

Fluconazole

9.     What is present in the fluid that gives it its yellow color?

  a. 

Sulfur

  b. 

Neutrophils

  c. 

Macrophages

  d. 

Mucus

EDITOR'S COMMENT

Much like resections for malignancies, surgical chest wall infections require a multidisciplinary approach. The presence of infection forbids the use of nonbiologic materials to cover the defects created by the aggressive debridements that may be required. Plastic surgery input becomes even more crucial. The use of the VAC sponge has been a major improvement, drastically reducing the time to heal as well as reducing the size of the defect that has to be addressed.

–LZ

REFERENCES

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14. Stallworth J, Mack E, Ozimek C: Methicillin-resistant Staphylococcus aureus empyema necessitatis in an eight-month-old child. South Med J 98:1130–1, 2005.[PubMed: 16351034]

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16. Marik PE: Fungal infections in solid organ transplantation. Expert Opin Pharmacother 7:297–305, 2006.[PubMed: 16448324]

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18. Smolinski KN, Shah SS, Honig PJ, Yan AC: Neonatal cutaneous fungal infections. Curr Opin Pediatr 17:486–93, 2005.[PubMed: 16012261]

19. Wenner KA, Kenner JR: Anthrax. Dermatol Clin 22:247–56, 2004.[PubMed: 15207306]

20. Jallali N, Withey S, Butler PE: Hyperbaric oxygen as adjuvant therapy in the management of necrotizing fasciitis. Am J Surg 189:462–6, 2005.[PubMed: 15820462]

21. Venturi ML, Attinger CE, Mesbahi AN, et al: Mechanisms and clinical applications of the vacuum-assisted closure (VAC) device: A review. Am J Clin Dermatol 6:185–94, 2005.[PubMed: 15943495]

22. Pu LL: Small intestinal submucosa (Surgisis) as a bioactive prosthetic material for repair of abdominal wall fascial defect. Plast Reconstr Surg 115:2127–31, 2005.[PubMed: 15923867]

23. Abenavoli FM: Usefulness of AlloDerm. Plast Reconstr Surg 116:677, 2005.[PubMed: 16079721]

24. Butler CE, Langstein HN, Kronowitz SJ: Pelvic, abdominal, and chest wall reconstruction with AlloDerm in patients at increased risk for mesh-related complications. Plast Reconstr Surg 116:1263–75; discussion 76–7, 2005. 

  

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