General Thoracic Surgery (General Thoracic Surgery (Shields)) [2 VOLUME SET]

Editors: Shields, Thomas W.; LoCicero, Joseph; Ponn, Ronald B.; Rusch, Valerie W.

Title: General Thoracic Surgery, 6th Edition

Copyright 2005 Lippincott Williams & Wilkins

> Table of Contents > Volume I - The Lung, Pleura, Diaphragm, and Chest Wall > Section IX - The Chest Wall > Chapter 42 - Infections of the Chest Wall

Chapter 42

Infections of the Chest Wall

Joseph LoCicero III

Chest wall infections can be categorized either as primary problems arising spontaneously or as secondary infections caused by previous procedures or preexisting disease states. The result is the same, with equally devastating potential complications. Management of such infections may be as simple as administering routine antibiotic therapy or may require multiple and prolonged drainage procedures and complex reconstructive operations. Prompt intervention is essential to minimize serious morbidity.

SKIN AND SOFT TISSUE INFECTIONS

The thorax accounts for one fifth of the total body surface area and thus can be afflicted with many common, nonspecific soft tissue infections. Furuncles and boils common to any hair-bearing surface frequently occur. Superficial infections often develop in minor injuries and burns of the chest, as they do elsewhere in the body.

Abscesses

Soft tissue abscesses may occur anywhere on the chest wall. They are characterized by the usual signs and symptoms of an abscess anywhere on the body and are rarely associated with an abnormal chest radiograph. Two potentially serious infections specific to the chest wall and involving large potential spaces are subpectoral and subscapular abscesses. These occasionally present as primary infections but more often are secondary to a chronically infected thoracotomy incision. They are characterized by local pain, with or without swelling, combined with fever and leukocytosis. Computed tomography (CT) easily identifies and localizes the problem. Prompt drainage and appropriate antibiotic therapy usually lead to successful resolution. Suction catheters are rarely required because these spaces are obliterated once drained. Occasionally when the abscess is large, several counterincisions are made to d bride and pack the space more completely.

With the worldwide increase in tuberculosis and immigration of people from the Third World to North America, pulmonary tuberculosis may be seen in any thoracic surgical practice. Like scrofula, mycobacteria can cause a soft tissue infection of the chest wall. Hsu and colleagues reviewed its management in 1995. Patients present with a slowly enlarging painless mass on the chest wall. A CT scan is helpful to rule out the possibility of pulmonary involvement. Diagnosis can be made with a diagnostic aspiration of the abscess. Treatment should be combination antituberculous therapy for 6 to 9 months. Surgical d bridement is reserved for failures. If the diagnosis is not made before d bridement, a broad-spectrum antibiotic should be added. Fungal infections of the chest wall should also receive long-term antibiotic therapy, but radical d bridement is a mandatory part of the therapy.

Gangrene

Necrotizing soft tissue infections may occur as a complication of empyema or trauma. These infections frequently begin when the pleural material is drained through the soft tissues either by chest tube or thoracotomy. Pingleton and Jeter (1983) reported extensive synergistic gangrene of the chest wall with Bacteroides melaninogenicus and Streptococcus viridans after tube thoracostomy for empyema. Delay in recognition led to the patient's demise. This author and Vanecko (1985) reported destruction of the pectoralis major and serratus muscles that was caused by clostridial myonecrosis at the site of a tube thoracostomy in a patient with Boerhaave's syndrome. Radical d bridement and daily dressing changes under general anesthesia eventually led to a successful outcome. Viste and colleagues (1997) reported a case of necrotizing infection caused by gastric herniation after laparoscopic fundoplication. Urschel and associates (1997) reviewed the world literature and found a 90% mortality rate for this devastating problem. A more recent review by Losanoff and colleagues (2002) found that the mortality rate had decreased to 60%.

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Infections of the head and neck as well as dental manipulation have been identified as sources of necrotizing fasciitis of the chest. Steel (1987) described a case of necrotizing ulceration of the chest wall after dental manipulation; it was successfully treated by surgical d bridement and chemotherapy. He noted that the primary suspect organisms were Streptococcus milleri and Bacteroides species. Nallathambi and colleagues (1987) reviewed the current literature and discovered 28 chest wall and mediastinal infections related to dental manipulation or pharyngeal abscesses. These rapidly progressive, mixed aerobic and anaerobic infections have been associated with a 32% mortality rate. Antibiotic prophylaxis for deep dental manipulations and careful follow-up for any early signs of sepsis are essential.

Early recognition, radical d bridement of all involved necrotic tissue, high-dose antibiotic therapy, prolonged ventilatory support, and delayed closure with biologic tissue represent the only salvation for these patients. The antibiotic of choice used to be single-drug treatment with high-dose penicillin, but many organisms of the normal flora above the diaphragm have become resistant to penicillin. Therapy should begin presumptively with a combination that includes penicillin or ampicillin, an aminoglycoside, and clindamycin or metronidazole. Once cultures and susceptibilities are available, the antibiotic regimen should be tailored accordingly.

INFECTIOUS CHEST WALL INVASION

With drug resistance and superinfection during antibiotic therapy, virulent organisms occasionally cause pneumonia that has the capability of direct chest wall invasion. Suchyta and associates (1987) reported a community-acquired chronic Acinetobacter calcoaceticus pneumonia with direct chest wall involvement discovered only at autopsy. Yuan and associates (1992) successfully treated a patient with pneumonia and extensive chest wall involvement attributed to Actinobacillus actinomycetemcomitans. This patient required high-dose penicillin therapy for 3 months. However, as Hseih and colleagues (1993) point out, Actinomyces species (i.e., israelii, naeslundii, and odontolyticus) infections usually respond to antibiotic (penicillin) therapy, and surgical intervention may not be necessary if pretherapeutic diagnosis can be made.

EMPYEMA NECESSITATIS

Infrequently seen today, the soft tissue infection called empyema necessitatis is caused by an undrained underlying pleural infection. An untreated empyema may eventually burrow through the chest wall and into the subcutaneous tissue of the chest. Suspicion of this entity should be raised by the patient's history and confirmed by physical and radiographic examination of the chest. The soft tissue component may require separate drainage but often resolves with appropriate drainage of the empyema.

MONDOR'S DISEASE

Mondor's disease is a benign condition consisting of localized thrombophlebitis occurring in the superficial veins of the breast and anterior chest wall. The true incidence of this entity is unknown. Reports have been infrequent. Because the condition produces few symptoms and signs, most examples are probably not referred to informed examiners for study.

The earliest description was by Fagge (1869). Williams (1931) attributed the disease to thrombophlebitis, as did Mondor (1939), for whom the condition is named. Most cases occur in women, and frequently no antecedent cause can be found. Radical mastectomy may predispose to the development of this disease, as Herrman (1966) proposed, whereas benign conditions, such as fibrocystic disease, have no association with this entity. In a few instances in which a biopsy was performed, Farrow (1955) described a sclerosing endophlebitis with complete or partial obliteration of the lumen.

Clinically, the disease presents as a cordlike structure in the subcutaneous tissue of the axilla, chest, or abdomen. Its greatest significance may be the possible confusion with inflammatory carcinoma of the breast. It does not tend to recur or lead to thromboembolism. In most subjects, no specific therapy is indicated because it regresses spontaneously.

MISCELLANEOUS INFECTIONS

Several other conditions may manifest as infections of the chest wall. Golladay and associates (1985) noted three benign conditions in 24 children who presented with chest wall masses. These included trichinosis, nodular fasciitis, and myositis ossificans, all confirmed by excisional biopsy. The latter two were almost certainly secondary to localized trauma.

Cartilage and Bony Structures

Tietze's Syndrome

Painful, nonsuppurative swelling of the costal cartilages without abnormal histologic change is referred to as Tietze's syndrome. This condition, which is not a disease, was described in two patients by Tietze (1921), who attributed the changes to tuberculosis. This has never been confirmed. Since Tietze's publication, case reports have been sporadic. Kayser (1956), who reviewed the world literature, could find only 156 cases.

The true frequency of this condition is not known, but the symptom complex appears to be common. Peyton (1983)

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Rarely are further tests necessary to confirm this diagnosis, but Edelstein and colleagues (1985) pointed out that CT scan of the chest is helpful to exclude chest wall masses in these patients.

As might be expected for a condition as vague as this, several invasive treatments have been advocated, from hydrocortisone infiltration to surgical removal of the involved area. The latter hardly seems justified. In most patients, reassurance and symptomatic treatment with compounds containing ibuprofen are sufficient.

Costochondritis

Infections of the costal cartilage cause great debility. They are chronic beyond all expectation and thus demoralizing to the patient and the surgeon alike. When recognized and treated properly, response is rapid, but the required treatment is exceedingly radical for what appears to be such a minor problem. This often leads to delay in appropriate management. Recognizing the basic problem, Moschowitz (1918) pointed out that chronicity resulted less from the type of infecting organism than from the avascular nature of the cartilage. He correctly urged removal of the cartilage for cure.

Before 1940, most chondritis was spontaneous, usually caused by tuberculosis. Some cases were caused by typhoid or paratyphoid fever. Today most infections are surgical complications. Most follow median sternotomy performed for cardiac procedures; some follow thoracotomy, tube thoracostomy, or chest wall trauma. Occasionally, fungal infections may burrow through the chest wall to cause chondritis.

Because the fifth to ninth costal cartilages are contiguous or fused, infections involving any one of these segments dictate a major resection for cure. The xiphoid is partially a cartilaginous structure and thus may promote bilateral spread of the infection. This avascular hyaline cartilage behaves like a foreign body, once infected. When free of perichondrium, it begins to take on a moth-eaten appearance in the depths of a draining wound. The disintegration of the cartilage occurs slowly, but the cartilage is never completely reabsorbed. Sequestra that are characteristic of chronic osteomyelitis do not classically form in chondritis. The cartilage remains exposed and unmoved in the depths of the narrow, granulating wound.

Many organisms have been cultured from costochondritis. The primary infecting organisms include Escherichia coli, Streptococcus pneumoniae, Pseudomonas aeruginosa, Mycobacterium tuberculosis, staphylococci, streptococci, and Nocardia. Once the wound is opened and drained, subsequent cultures may grow a variety of organisms, depending on the environment and the antibiotic regimen the patient is receiving.

Usually, the disease manifests as a draining sinus in the region of the cartilages. Local pain and tenderness are present. As with any other chronic infection, general debility and, perhaps, low-grade fever accompany an elevated white cell count. In most patients, the diagnosis is confirmed by tenderness over the cartilages and infection in the vicinity.

The preferred therapy is radical excision, as Murphy (1916) and Moschowitz (1918) advocated. Any involved cartilage should be removed completely (Fig. 42-1). If the lower ribs are involved, all fused segments must be excised. No bare cartilage should remain in the infected wound. The more conservative approach is to pack the wound and reconstruct it later, as Lewis (1967) and Talucci and Webb (1983) advocated. Others, such as Hines and Lee (1983) and Arnold and Pairolero (1984), have shown that the defect may be closed in one stage with minimal morbidity. Techniques of reconstruction are discussed later in the chapter.

Osteomyelitis

Sternal Osteomyelitis

Although spontaneously appearing osteomyelitis of the sternum or ribs did occur when tuberculosis was prevalent, it is rare today. Even when tuberculosis was more common, osteomyelitis of the sternum was uncommon. In a series of more than 1,000 patients with bone and joint tuberculosis reported by Wassersug (1941), the sternum was involved in only 1.1%. Today, primary sternal osteomyelitis occurs in heroin addicts.

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The factors implicated in the development of postoperative sternal infections, enumerated by Talamonti and associates (1987), include diabetes, low cardiac output, use of bilateral internal thoracic artery grafts, and, most significantly, reoperation for excessive postoperative bleeding.

Manifestations of this condition are similar to those of chondritis. When osteomyelitis involves the sternum, an associated chondritis may occur, which can be mistaken for the principal cause of chronicity. The first sign of postoperative sternal osteomyelitis may be an unstable sternum or serosanguineous discharge. Novick and Fishman (2003) pointed out several findings on spiral CT that can be beneficial in determining if a patient has associated mediastinitis with a sternal infection. The most common findings were fat hyperdensity and stranding, fluid collections and mass effect at the level of the great vessel origin from the aortic arch.

In chronic sternal osteomyelitis, the most successful results have been achieved by extensive sternal and chondral removal followed by myocutaneous reconstruction. The most commonly used reconstruction is bilateral pectoralis major flap advancement, as described by Johnson and associates (1985). A modified H incision is used to mobilize the pectoralis major muscles, with the blood supply based on the thoracoacromial artery (Fig. 42-2A). This also allows adequate exposure of the sternum, which is then excised (Fig. 42-2B). If possible, the upper manubrium with the clavicular attachments is left intact. This prevents skeletal problems as the shoulders rotate anteriorly and inferiorly. Next, the humeral heads of the pectoralis major muscles are transected, and the flaps are advanced over drains to close the defect (Fig. 42-2C). This gives a good cosmetic result with preservation of pulmonary function.

Rib Osteomyelitis

Diagnosis of osteomyelitis of the ribs is usually made because of local inflammatory signs and symptoms or because of a persistently draining sinus. When the infection is secondary to open drainage of an empyema, it can be one cause of a slowly healing wound. Sequestration from ribs affected by osteomyelitis has been reported. The sequestrum may even pass into the lungs, as Roe and Benioff (1955) noted. Recently, Chang and colleagues (1999) reported on a series of 12 patients with tuberculous rib osteomyelitis.

Confirmation is usually made by chest radiography. Although CT scanning of the chest is usually not necessary for confirmation of the diagnosis, it may help in evaluating possible underlying associated intrathoracic pathology, as suggested by Wechsler and Steiner (1989).

Excision of all diseased bone usually provides adequate treatment for osteomyelitis of the ribs. To prevent the problem after empyema drainage, Churchill (1929) recommended a

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Sternoclavicular Osteomyelitis

Sternoclavicular osteomyelitis is a relatively new problem that occurs not only in addicts but also in individuals who have had subclavian catheters, as well as in patients with no known antecedent interventions. However, as Haddad and colleagues (2002) report, the latter group is usually ill, either with a chronic debilitating illness such as diabetes mellitus or liver failure or an overwhelming acute illness such as sepsis from a remote site.

The inciting organisms vary widely, depending on the etiology. In my experience, both gram-positive organisms, such as Staphylococcus and group B Streptococcus, and gram-negative organisms cause these infections. Buescher and colleagues (1994) recorded a case of Aspergillus infection in a patient undergoing chemotherapy for acute myelogenous leukemia. An interesting report by Berrocal and associates (1993) from Peru found 7 cases of brucellar sternoclavicular arthritis among 1,729 cases of primary brucellosis.

These patients present with fever and severe unremitting pain in the joint. Some patients even demonstrate instability of the joint and have difficulty lifting objects and even writing in severe cases. Routine radiographs are not helpful. Even CT scans may be of little help. These scans may not show much bony destruction because the damage begins in the joint (Fig. 42-3A). The condition must be inferred from the surrounding soft tissue involvement. Magnetic resonance (MR) imaging is a much more sensitive tool than CT for detecting joint disease and therefore presents a more dramatic image (Fig. 42-3B). The joint as well as the soft tissue swelling is more clearly defined.

Treatment requires the same radical d bridement as other cases reported here. To remove the joint completely and any possibility of recurrence, one must bear in mind that the sternoclavicular joint is contiguous with the clavicle, sternum, and first rib. This area should be removed en bloc. To create the best closure, removal of a portion of the second rib is helpful, whether it is involved or not. A trapdoor incision is made beginning above the clavicle, extending to the midline, down the midline, and across the anterior chest below the disease, usually the third rib. A flap is made, including the pectoralis muscle. Sometimes, it is involved in the infection and a portion must be sacrificed, but every effort should be made to salvage as much of it as possible. The internal thoracic artery and vein are ligated above the third rib. The platysma and scalene muscles are divided above and the sternum is bisected to the third rib. The second and third ribs are divided beyond the infection, and the clavicle is cut in half or more. The first rib is cleared at this point and divided. The specimen is removed and cultures taken before sending the specimen to the pathology laboratory. Closed suction drains are placed, and the flap is advanced into place with interrupted sutures. Foreign material or mesh should be avoided. The long-term result is excellent for both infection control and chest wall function (Fig. 42-4). Burkhart and associates (2003) reported on 26 patients with a complication rate of 7.7% and a mortality rate of 3.8%.

Osteoradionecrosis

One of the most difficult problems encountered by the thoracic surgeon is a large necrotic ulcer of the chest wall after radiation therapy for carcinoma of the breast or other condition. Often, more infection and necrosis exist than are visible externally. Prosthetic materials usually cannot be used in the infected field. With radiation becoming a standard in the minimal surgical techniques of breast cancer, and despite all the precautions taken by radiation therapists, these problems are on the rise. Treatment requires close cooperation between the thoracic surgeon and the plastic and reconstructive surgeon.

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The foremost principle in the treatment of a radionecrotic ulcer is wide surgical excision and primary coverage of the defect, as Arnold and Pairolero (1984, 1989) described. Tissue of the affected area should be sent for pathologic analysis when radiation was performed for a local malignancy to ensure that no residual tumor is present.

Provisions for covering the expected defect with viable tissue must be carefully considered before the surgical procedure. Understanding and use of myocutaneous flaps have advanced. Jurkiewicz and colleagues (1980) described a variety of flaps, including pectoralis major, rectus abdominis, and latissimus dorsi flaps (Fig. 42-5). Other innovative flaps include segmentally split pectoral girdle flaps [proposed by Tobin (1990)] and free extended forearm flaps [suggested by Schmidt and colleagues (1987)].

The latissimus flap was first described by Tansini (1906) but was rediscovered by McCraw and colleagues (1978). Hines and Lee (1983) used this flap in five patients and noted that even if the primary blood supply the thoracodorsal artery was cut at the time of initial mastectomy, collateral blood supply appeared adequate. They also pointed out that the muscle, albeit smaller and thinner when the thoracodorsal nerve has been resected, remains usable. Within the past few years, plastic and reconstructive surgeons have applied microvascular techniques to this flap. Free flaps have been used with great success, with and without the associated skin as well as inside the chest, as reported by Hammond and associates (1993) and outside the chest as described by Hidalgo and colleagues (1993).

In most instances, foreign material should be avoided when infection is present. Usually, the resulting paradoxic movement of the chest wall in these patients is minimally debilitating and not worth the risk for secondary infection. Myocutaneous flaps have been beneficial when a large portion of the chest wall or sternum must be removed (see Chapter 47).

IMMUNOCOMPROMISED PATIENTS

Patients who are immunocompromised because of malignancy, malnutrition, or human immunodeficiency virus infection present special problems. In granulocytopenic patients, findings of severe chest wall infections may be subtle. Aranha and co-workers (1988) recommend antibiotic therapy and surgical d bridement with the early findings of erythema, localized tenderness, and temperature elevation. Golladay and Baker (1987) note that in immunocompromised children, invasive aspergillosis is the offending infection one third of the time, with high mortality rates even with early aggressive intervention.

In patients infected with human immunodeficiency virus, common organisms often cause serious chest wall infection. Martos and colleagues (1989) reported two cases of tuberculosis of the chest wall. Rodriguez-Barradas and associates (1992) found chest wall infections related to pneumococcal pneumonia. Asai and colleagues (2003) reported on a patient with mucormycosis during antileukemia therapy.

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Reading References

Arnold PG, Pairolero PC: Chest wall reconstruction: experience with 100 consecutive patients. Ann Surg 199:725, 1984.

Culliford AT, et al: Sternal and costochondral infections following open heart surgery. J Thorac Cardiovasc Surg 72:714, 1976.