Thoracic empyemas

Thoracic empyemaEmpyemas are divided into three phases based on their natural history: acute exudative, fibrinopurulent, and chronic organizing. The acute exudative phase is characterized by the outpouring of pleural fluid (incited by pleural inflammation), which has a low viscosity, white blood cell count, LDH concentration as well as normal glucose level, normal pH. The pleura remains mobile during this phase.

A transitional or fibrinopurulent phase develops subsequently, marked by an increase in the turbidity, white content, and LDH levels of the fluid. In addition, the glucose levels and pH of the fluid decrease progressively and fibrin is deposited on both pleural surfaces, thereby limiting the empyema but also fixing (trapping) the lung. The chronic organizing phase begins 7–28 days after the onset of the disease, it is characterized by a pleural fluid glucose level < 40 mg/dL, a pH < 7.0. The pleural exudate becomes quite thick and the pleural fibrin deposits thicken and begin to organize, further immobilizing the lung. In patients with inadequately treated chronic empyema, erosion through the chest wall (empyema necessitatis), chondritis, osteomyelitis of the ribs or vertebral bodies, pericarditis, and mediastinal abscesses may occur.

The bacteriology of thoracic empyema has evolved. Prior to the discovery of penicillin, most empyemas were caused by pneumococci and streptococci. With modern antibiotics and improved anaerobic culture techniques, however, the most common isolates from adult empyemas are now anaerobic bacteria, particularly bacteroides species as well as fusobacterium and peptococcus species.

Staphylococcus is the most common organism causing empyema, and staphylococcal empyema is one of the most common complications of staphylococcal pneumonias in both adults and children. Gram-negative bacteria also continue to be significant pathogens, particularly in parapneumonic empyemas. Escherichia coli and pseudomonas species account for 66% of gram-negative thoracic empyemas, and other organisms include Klebsiella pneumoniae, proteus species, Enterobacter aerogenes, and salmonella. Rarely, fungi (aspergillus, Coccidioides immitis, blastomyces, and Histoplasma capsulatum) and parasites such as Entamoeba histolytica can cause thoracic empyemas. In a recent review, empyemas were found to contain anaerobic bacteria in only 35% of cases, aerobic bacteria in only 24%, and a combination in 41%. In addition, the average number of bacterial species isolated was 3.2 per patient. Aspiration of oropharygeal flora may represent a source of polymicrobial infection.

Incidence of Various Complications of Staphylococcal Pneumonia (in %).

Adults/Children

  • Abscess 25/50
  • Empyema 15/15
  • Pneumatocele 1/35
  • Effusion 30/55
  • Bronchopleural fistula 2/5

Although patients may rarely be completely asymptomatic, most patients with thoracic empyemas present with symptoms depending on the underlying disease, the extent of the pleural involvement, and the immunologic state of the patient. Patients typically complain of fever, pleuritic chest pain or a sense of chest heaviness, dyspnea, hemoptysis, and a cough usually productive of purulent sputum. Signs of thoracic empyema include anemia, tachycardia, diminished breath sounds with dullness to percussion on the involved side, clubbing of fingertips, and occasionally pulmonary osteoarthropathy.

Although the medical history, physical examination often suggest the presence of thoracic empyema, the plain chest radiograph is the most important noninvasive diagnostic test. Empyemas can have almost any appearance, may be associated with an underlying pneumonia, lung abscess, pleural effusion, but most commonly they appear as posterolateral D-shaped densities on x-ray. In large empyemas the mediastinum may be shifted away from the affected side. Bronchoscopy should be performed on all patients to exclude the presence of endobronchial obstruction. CT scanning provides critical anatomic detail regarding loculations and can assist in differentiation of empyema from lung abscess. Thoracentesis, however, is the procedure of choice for the diagnosis of thoracic empyema.

Treatment of thoracic empyemas

Goals for the treatment of thoracic empyemas include:

  1. control of the infection;
  2. removal of the purulent material
  3. elimination of the underlying disease.

Options for treatment include repeated thoracentesis, closed tube thoracostomy, open drainage, decortication, thoracoplasty, and muscle flap closure. Adjunctive maneuvers reported to aid in the disruption and drainage of loculated empyemas include instillation of fibrinolytic enzymes, placement of high (–100 cm H2O) suction, video-assisted thoracoscopic debridement. Initially, an intercostal catheter of adequate size is carefully inserted into the most dependent portion of the empyema cavity. If after 24–72 hours sepsis persists— or if there is any question as to the adequacy of drainage — a CT scan should be obtained. If complete drainage and reexpansion of the lung are achieved, no further drainage procedures are necessary.

Patients with residual spaces that are inadequately drained, patients with continued sepsis, and patients thought to require prolonged tube drainage are candidates for open drainage procedures. These can usually be safely performed 10 days after closed-tube drainage since the pleurae fuse by that time and the risk of lung collapse is eliminated. Simple rib resection involves the removal of short segments (3–6 cm) of one, two, or three ribs at the most dependent portion of the empyema cavity (at or anterior to the posterior axillary line). A tube can be placed through this opening and effective drainage established. A second approach involves the creation of a U-shaped flap of chest wall that is sewn to the parietal pleura after resection of short segments (3–6 cm) of one, two, or three ribs. This creates an epithelialized tract for long-term tubeless drainage of empyema cavities. The flap also acts as a one-way valve allowing fluid and air to escape during exhalation but sealing during inspiration to prevent the ingress of air. Symbas later modified the original Eloesser procedure by changing the flap to an inverted U-shaped flap with the base of the flap placed parallel to and at the level of the inferiormost aspect of the empyema cavity. This type of open drainage allows the empyema cavity to drain reliably and to be easily debrided, irrigated, and cleaned. Ultimately, through lung reexpansion, wound contraction, and granulation, the cavity often completely disappears.

Another option is early decortication and empyemectomy. This has been increasingly advocated in good-risk patients with early loculated empyemas and inadequate tube drainage or lung expansion. Furthermore, if performed early in the course of the process, resection of both pleural peels (decortication) can be performed via minimally invasive technique without the need for rib spreading. More advanced or chronic disease involves a thoracotomy with decortication with resection of the intact empyema itself (empyemectomy), if possible. The best results with this approach are obtained when the underlying lung is entirely normal and reexpands fully. Posttraumatic empyema, in particular, has been amenable to this treatment.

Empyemas that occur following pulmonary resection often are more difficult to manage. If residual lung is present, the general principles outlined above still apply, although a complicating bronchopleural fistula is often present. Simple tube drainage is instituted initially followed by open drainage if necessary. Empyemas following pneumonectomy, however, pose a special problem since there is no longer any lung to obliterate the infected space. In addition, postpneumonectomy empyemas frequently are associated with bronchopleural fistulas. In these patients, specific surgical procedures designed to obliterate residual intrathoracic spaces and in many cases close remaining bronchopleural fistulas may be required. In the absence of a fistula, sterilization and closure of a postpneumonectomy space (without obliteration) may be attempted using an irrigation catheter inserted into the apex of the chest cavity. An antibiotic solution specific for the organisms present is then infused into the chest. The solution is allowed to drain through a dependent tube or opening created by simple rib resection. After 2–8 weeks, the catheters are removed and the cavity is closed. The success rate with this technique is quite variable and is reported to be 20–88%. For patients who fail this approach and for those patients with bronchopleural fistulas, the main goal of therapy is to obliterate the residual space and close any bronchopleural fistulas. This is most readily accomplished by the transposition of muscle with or without omentum into the empyema cavity. Multiple muscles may be required, including pectoralis major, latissimus dorsi, serratus anterior, intercostal muscle, and rectus abdominis. Use of these muscles is highly successful in closing any remaining bronchopleural fistulas and in completely obliterating the remaining intrathoracic space. The success of muscle flap closure of empyema spaces has made thoracoplasty (once a common procedure for reducing empyema spaces) a rare operation.

Antibiotics are an important adjunct in the treatment of empyemas, but it must be emphasized that drainage is the primary treatment modality. Although antibiotic therapy is always instituted early in the course of therapy when signs of systemic infection generally are present, they need not be continued once effective drainage is established. In fact, overuse of antibiotics may lead to the generation of resistant bacteria and therefore compromise the success of any subsequent procedures designed to obliterate residual intrathoracic space.

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