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 XI - The Pleura > Chapter 58 - Parapneumonic Empyema

Chapter 58

Parapneumonic Empyema

Joseph S. McLaughlin

Mark J. Krasna

Pleural effusion is a common accompaniment of the inflammation of bacterial pneumonia. These uncomplicated effusions are nonpurulent, have a negative Gram's stain result for bacteria, have negative results by culture, and are generally free flowing. Light (1985, 1991, 2002) and associates (1972, 1980), using biochemical parameters, noted a pH greater than 7.30, a normal glucose level, and a lactic acid dehydrogenase (LDH) concentration less than 1,000 IU/L. Most parapneumonic effusions resolve with appropriate antibiotic treatment and resolution of the pulmonary infection.

Thoracic empyema occurs when bacteria invade the normally sterile pleural space. The process was described by Andrews and colleagues, reporting for the American Thoracic Society (ATS) in 1962, as a continuum of three stages (Table 58-1).

Stage 1 is characterized by the presence of an exudative effusion from increased permeability of the inflamed and swollen pleural surfaces. This stage corresponds to the uncomplicated parapneumonic effusion of Light and colleagues (1980) and is initially sterile. Fibrin is deposited and polymorphonuclear leukocytes are present in small numbers. With bacterial invasion, the process blends into the fibropurulent stage 2, true empyema or Light's complicated pleural effusion. Initially, the fluid is still relatively clear and yellow, but the white blood cell count is greater than 500 cells per microliter, the specific gravity is greater than 1.018, and the protein level is greater than 2.5 g/dL. The pH is less than 7.2 and the LDH levels reach 1,000 IU/L. Although fibrin deposits and early angioblastic and fibroblastic proliferation are seen in later phases of the exudative stage, these processes accelerate and heavy fibrin deposition takes place on both pleural surfaces, particularly the parietal pleura. The effusion becomes purulent, with a white cell count above 15,000 cells per L. Biochemically, the pH decreases to levels below 7.0, the glucose decreases to less than 50 mg/dL, and the LDH increases to greater than 1,000 IU/L. Stage 3 begins as early as 1 week after infection with collagen organization and deposition on both pleural surfaces and entrapment of the underlying lung. This process is mature in 3 to 4 weeks, and the organized collagen on the pleural surface is termed a peel. The effusion at this point is grossly purulent, and at least 75% of the volume is sediment on standing. Chronicity is characterized by dense fibrosis, contraction and trapping of the lung, atelectasis, and prolonged pulmonary infection and reduction of the size of the hemithorax. Fibrothorax with invasion of the chest wall and narrowing of the intercostal spaces may be thought of as the end stage of this process.

Complications of the empyema process may take place early or late. Necrosis of the visceral pleural surface, as noted by Hankins and associates (1978), may result in bronchopleural fistula heralded by sudden expectoration of, at times, copious amounts of purulent sputum. Marks and Eickhoff (1970) noted that the necrosis of the parietal pleura and the chest wall and skin results in empyema necessitatis. These conditions are usually seen in patients treated with antibiotics for pneumonia who have unrecognized empyema. Often, these patients have persistent, low-grade fever until the empyema drains through the chest wall or into the lung. Rarely, osteomyelitis of the ribs or spine may occur. Invasion of the mediastinum with pulmonary esophageal fistula and pericarditis have also been reported. Metastatic spread is unusual, but Scheld (1998) has suggested that up to 12% of brain abscesses are from pleuropulmonary disease, including empyema.

COMMUNITY-ACQUIRED PNEUMONIA

According to the American Thoracic Society (2001), community-acquired pneumonia (CAP) is the sixth most common cause of death in the United States and is the most common infectious cause of death. There are approximately 5.6 million cases of CAP in the United States each year, 1.1 million requiring hospitalization. The outpatient mortality rate ranges from 1% to 5%, and the overall mortality rate is 12%. Guidelines for the evaluation and treatment of CAP

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As noted by Bartlett and associates (2000), up to 50% of the pathogens responsible for CAP are never identified despite careful and extensive testing. There is no single test that can identify all potential pathogens, and all diagnostic tests have their limitations. Sputum Gram's stains and cultures are often unable to identify Streptococcus pneumoniae and frequently encountered pathogens such as Mycoplasma pneumoniae, Chlamydia pneumoniae, and Legionella species and respiratory viruses. These may be detected at a later time by serologic testing. Furthermore, atypical infections can occur and involve either more than one bacterial species or a bacterial pathogen and a virus. Thus, an empiric approach to the initial treatment of community-acquired infection is recommended, based on the patient's status as defined by Bartlett and Mundy (1995): (a) outpatients with no history of cardiopulmonary disease and no modifying factors; (b) outpatients with cardiopulmonary disease [congestive heart failure or chronic obstructive pulmonary disease (COPD)] or other modifying factors such as risk factors for drug-resistant Streptococcus pneumoniae (DRSP) or Gram-negative bacteria; (c) inpatients not admitted to the intensive care unit (ICU) who (i) have cardiopulmonary disease and/or other modifying factors (including residing in a nursing care facility) or who (ii) have no cardiopulmonary disease and no other modifying factors; and (d) ICU-admitted patients with either risk or no risk for Pseudomonas aeruginosa. Antibiotic therapy is based on the probable bacterial etiology of pneumonia in the four groups. Parenthetically, appropriate efforts should be made to identify the agent or agents involved and specific antibiotic therapy directed to their eradication.

Patients in group I (outpatients) are most commonly infected with Streptococcus pneumoniae, Mycoplasma pneumoniae, Chlamydia pneumoniae, and respiratory viruses. Less common are Legionella species and Haemophilus influenzae (in cigarette smokers). The mortality rate of this group is less than 1% to 5%. Roughly 50% to 90% of these patients have no identifiable etiologic agents. Patients in group II (outpatients with comorbidity) have congestive heart failure or COPD, but no risk factors for DRSP or Gram-negative bacteria (including residing in a nursing care facility). Streptococcus pneumoniae remains the most likely pathogen, but DRSP is a consideration in this group and modifies the antibiotic therapy. The mortality rate in group II is less than 5%, but according to Fine and associates (1996, 1997), as many as 20% of patients treated initially as outpatients will require hospitalization. Group III patients are admitted to the hospital due to severe pneumonia. They are divided into two groups: those with cardiopulmonary disease or modifying factors (including residing in a nursing care facility) and those with no cardiopulmonary disease and no modifying factors. Modifying factors and cardiopulmonary disease increase the mortality rate significantly. Group IIIA patients suffer mortality rates ranging from 5% to 25%. Group IV patients have severe pneumonia defined by the study group as those admitted to an ICU. They are divided further into patients with no risk for Pseudomonas aeruginosa infection and those with risk for Pseudomonas aeruginosa infection. Patients with severe CAP have a mortality rate of up to 50% (Tables 58-2 through 58-5).

HOSPITAL-ACQUIRED PNEUMONIA

The Official Statement of the American Thoracic Society (1995) noted that hospital-acquired pneumonia (HAP) is a major cause of death within the hospital setting. It is generally defined as pneumonia occurring 48 hours after admission and excludes pneumonia existing prior to hospital admission. It is thought to occur at a rate of 5 to 10 cases per 1,000 hospital admissions with increases of 6 to 20 times that rate among patients who are mechanically ventilated. Craven and Driks (1987), Craven and associates (1991),

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Craven (1991), Rouby (1992), Bartlett (1986), and Prod'hom (1994) and their associates as well as Schleupner and Cobb (1992) found that the bacteria most frequently associated with HAP are enteric Gram-negative bacteria and Staphylococcus aureus. Accumulated data suggest that the etiology is polymicrobial in up to half of mechanically ventilated patients. The role of viruses has yet to be defined. As with CAP, initial diagnosis and treatment of HAP is based on an empirically based review of numerous studies to determine the cause of the pneumonia and its treatment. It is recognized that these studies have the basic shortcoming of being unable to identify the etiologic agents initially in a significant number of patients. Accordingly, patients have been categorized by the ATS into mild-to-moderate pneumonia and severe pneumonia. These groups are further characterized based on the presence or absence of risk factors and the time [early (<5 days) or late (>5 days)] of onset of the pneumonia (Table 58-6). This cookbook approach to therapy must be supplemented by appropriate bacteriologic studies and directed treatment based on these studies.

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BACTERIOLOGY

The bacterial etiology of empyema has changed over the years. Before the development of antibiotics, 10% of patients who survived pneumonia developed empyema. According to Ehler (1941), Streptococcus and Pneumococcus were the most frequent organisms. After the introduction of antibiotics, the incidence of empyema from these organisms was markedly reduced, as was the mortality rate. Staphylococcus became much more prevalent, and in the 1950s and 1960s, Ravitch and Fein (1961) found that this organism produced 90% of empyema in children under 2 years of age. In more recent times, as pointed out by Varkey and associates (1981) and Bergeron (1990), penicillin-resistant Staphylococcus, Gram-negative bacteria, and anaerobic organisms have been the predominant microbes. Bartlett and colleagues (1974a) reported that 76% of empyema patients had positive culture results for either anaerobes exclusively (35%) or anaerobes in combination with aerobes (41%). Anaerobic bacteria are normal flora of the mouth, intestine, and female genital tract. They are difficult to culture, being extremely oxygen sensitive. Multiple organisms, 50 in the series of Sullivan and colleagues (1973), are frequently cultured, but the most common is Peptostreptococcus. Similar findings were recorded by Ali and Unruh (1990).

Brook and Frazier (1993) independently studied 197 patients with culture-positive empyema from two military hospitals. Aerobic organisms were isolated in 127 patients (64%), mixed aerobic and anaerobic organisms in 45 patients (23%), and anaerobic organisms in 25 patients (13%). The predominant aerobic or facultative bacterial isolates were Streptococcus pneumoniae (70), Staphylococcus aureus

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Lemense and associates (1995) at the Medical University of South Carolina studied, retrospectively, 43 patients with empyema. Twenty-four of the 43 patients (56%) had parapneumonic empyema, and 19 patients had empyema from a variety of causes including gunshot wounds, thoracotomy, and esophageal rupture. Most nonparapneumonic empyemas had positive cultures (84%), whereas only 11 of 24 patients with parapneumonic empyema (46%) had positive cultures on Gram's stain. Alfageme and associates (1993) noted increasing numbers of patients with Staphylococcus empyema, particularly in alcoholics.

The propensity for developing empyema varies considerably with the type of bacteria producing the primary pneumonia, the setting in which the infection is acquired, and the alteration in these produced by antibiotic therapy administered for primary pneumonia or for concurrent conditions. For example, as reported by Bartlett (1974a) and Fang (1990) and their colleagues, Light (1990), and Johnson and Finegold (1994), S. pneumoniae is responsible for 60% to 75% of CAPs, but only 2% of patients with pneumococcal pneumonia develop empyema (Tables 58-7 and 58-8). -hemolytic Streptococcus accounts for 1% to 2% of CAPs, but up to 10% of adults and 50% of children develop empyema. In hospital settings, Staphylococcus and aerobic, Gram-negative bacteria are the most common agents producing pneumonia. Both have significant potential to produce empyema.

CLINICAL FEATURES

Empyema may be heralded by an exacerbation or recurrence of the septic course of pneumonia or may present as a continuation of symptoms and manifestations of the primary pneumonic process. Antibiotics have blunted and changed the clinical picture, and there may be only subtle progression from the symptoms and signs of pneumonia to those of empyema. The most common presenting symptoms of empyema according to Varkey and associates (1981) are shortness of breath (82%), fever (81%), cough (70%), and chest pain (67%), all of which are common to pneumonia. The presentation of these symptoms in a patient with febrile respiratory illness or the accentuation or prolongation of these symptoms in a patient with pneumonia should alert the clinician to the possibility of empyema. The clinician should be aware that the incidence of pleuritic chest pain and leukocytosis are similar whether or not pleural effusion is present.

Empyema from aerobic bacterial pneumonia usually presents as an acute febrile illness with chest pain, sputum production, and leukocytosis. Anaerobic pleural infection is more indolent and, in Bartlett's (1974a) series, averaged 10 days before presentation. The majority of these patients have a history of alcoholism or unconsciousness, frequently have lost weight and have mild anemia. Hospital-acquired infection and immunosuppression may alter this course.

Physical examination reveals a toxic, anxious patient with tachycardia and tachypnea. Restricted and guarded chest wall excursion may be present. Percussion of the chest wall may elicit pain and dullness over the empyema

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DIAGNOSIS

Traditional Radiographic Evaluation

The presence of a significant pleural effusion in association with a lower respiratory illness is typical, but this clinical picture may also be seen with pulmonary embolism, acute pancreatitis, Dressler's syndrome, tuberculosis, and other conditions. Light and associates (1980) have suggested that bilateral decubitus chest radiographs be obtained. With the involved side down, the distance between the inside of the chest wall and the outside of the lung should not exceed 10 mm. If this distance exceeds 10 mm, thoracentesis should be performed.

When seen by the surgeon, many empyemas are advanced and empyemic collections are loculated. Because the posterior lateral diaphragmatic angle is the most dependent position of the thorax, most empyemas are found in this area. The inverted D or pregnant lady sign, as coined by LeRoux and Dodds (1964), on the lateral view is classic (Fig. 58-1). The differentiation of lung abscess with effusion from empyema and bronchopleural fistula may also be suggested by plain radiographic examination (Fig. 58-2). Friedman and Hellekant (1977) noted that the air fluid levels of lung abscess are usually of the same dimensions in posterior/anterior and lateral views, whereas empyema air fluid levels are rarely the same in these views.

Computed Tomography

Computed tomographic (CT) scanning is now used universally to identify underlying parenchymal disease and to distinguish empyema from lung abscess (Fig. 58-3). Fluid density and the presence of loculations can be determined, the latter being an important factor in treatment planning. CT-guided thoracocentesis is a highly accurate and safe technique that is used routinely.

Sonography

Alternately, sonography of the chest may be used. Sonography can demonstrate pleural fluid collections, loculations, and parenchyma involvement and may be used to guide thoracocentesis. The choice of this technique is institutionally dependent.

MANAGEMENT

Effective management of empyema requires (a) control of infection and sepsis by appropriate antibiotic therapy, (b) evacuation of pus from the pleural space, and (c) obliteration of the empyema cavity. Once the diagnosis is established, treatment must proceed with all possible haste. In Bartlett's (1974b) series of 43 patients with anaerobic empyemas, five patients (12%) died. He attributed all five deaths to a delay in appropriate drainage. In Ashbaugh's series (1991), delay in instituting drainage increased the mortality rate from 3.4% to 16%.

Colice and colleagues (2000) published the American College of Chest Physicians' Consensus Statement of the Treatment of Parapneumonic Effusions. The study group examined 789 citations from a Medline search. Twenty-four articles were identified for full review by the panel. Meta-analysis was performed and recommendations presented, primarily addressing techniques of drainage. However, it should be noted that, as with all meta-analyses, it has the significant shortcoming of incomplete comparative analysis despite extensive data. Drainage tube size could not be compared, and specific antibiotic therapy was not

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Antibiotic Therapy

Appropriate antibiotics should be administered promptly. Many patients, when first seen by the surgeon, will have already been treated with antibiotics and, according to LeMense and colleagues (1995), approximately 50% of cultures with parapneumonic empyema will be negative. The yield is higher with empyema secondary to HAP. Despite these facts, aerobic and anaerobic cultures of the blood and empyema fluid should be obtained. If the cultures become positive, antibiotic therapy should be guided by these results. Initial antibiotic therapy is usually based upon empiric guidelines for the treatment of CAP or HAP.

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Thoracentesis

The appearance of the fluid provides a first and major source of information concerning diagnosis and treatment. Straw-colored, clear, or slightly cloudy fluid is found in sterile parapneumonic effusions. This condition corresponds to early stage 1 of the ATS classification and the uncomplicated effusion of Light (1980), the benign effusion of Potts (1976), and the low pH pleural effusion of Van Way (1988) and their associates. Twenty to 70% of these will clear with appropriate treatment of the primary pneumonia. The problem and dilemma is that benign-appearing fluid may herald an impending frank empyema. Therefore, the fluid must be examined by Gram's stain, cultured for aerobic and anaerobic bacteria, and tested for antibiotic sensitivity. Biochemical changes (i.e., low pH, low glucose, and high LDH) indicate and precede positive culture and, according to Light (1991) and others, can serve as a guide to therapy. Cloudy or frankly purulent fluid is diagnostic. Aerobic pus has little or no offensive odor. Anaerobic pus is usually foul smelling.

Needle aspiration of the fluid collection should be performed with an 18-gauge needle under local anesthesia and radiographic or sonographic guidance. If the fluid appears benign, is not loculated, and can be removed totally or nearly so, thoracentesis may be all that is necessary to control the disease process. Traditionally, leukocyte counts, Gram's stains, cultures, and glucose and LDH determinations were recommended. Of these, only culture and pH determinations are of practical value. A pH of less than 7.1 indicates an empyema, and positive cultures may serve as a late guide for antibiotic therapy. Radiographic examination should be repeated in 24 hours to ascertain the status of the effusion. If the volume has increased or if the patient's status has not improved, a closed chest tube thoracostomy is indicated. If thoracentesis demonstrates cloudy or purulent fluid, or if the effusion is greater than one half of the hemithorax (even if free flowing), fibrin loculations are probably present and closed chest tube drainage is required. The presence of obvious pus also indicates the need for closed chest tube drainage. It is noted that, in meta-analysis, the mortality rate of patients treated primarily by thoracentesis is 10% and 46% of patients require additional procedures.

Chest Tube Drainage

Closed chest tube drainage is the usual first step in the treatment of acute empyema. However, this approach may take a number of forms. Traditionally, a No. 36F or larger tube was placed in the most dependent area of the empyema cavity as determined by previous thoracentesis and radiographic examination. Underwater seal drainage with moderate suction ( 20 cm H₂O) is applied to drain the purulent

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Bouros and associates (1997) compared streptokinase and urokinase in a double-blind study of 50 consecutive patients with either complicated pleural effusion or frank empyema who had inadequate drainage through the chest tube (<70 mL per 24 hours). Clinical and radiologic improvement was noted in all but two patients (8%) in each group who required surgical intervention. The mean volume of drainage was significantly increased (urokinase, 420 mL per 24 hours; streptokinase, 380 mL per 24 hours). The mean number of installations was six in both groups and the mean lengths of stay were approximately 11 days. Two patients in the streptokinase group suffered high fever. The total cost for drug therapy was approximately twice as much in the urokinase group. The researchers concluded that fibrinolytic therapy is a valuable adjunct to chest tube drainage and that, despite the cost, urokinase may be desirable because of local and systemic reactions to streptokinase. These reactions included fever, chills, and chest pain. In Laisaar and colleagues' (1996) series, enzymatic treatment was effective in 72% of patients, but 28% required

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The technique is simple. A 12 to 16 F chest tube is placed in the effusion guided by CT, ultrasonography, or fluoroscopy. For moderate-sized unilocular collections, a single drain is usually all that is necessary. If collections are large or if multiple loculations are present, more than one drain may be placed. Following drain placement, all fluid is aspirated. Follow-up imaging is then performed to determine the final position of the drains and the location and amount of any remaining pleural fluid. If significant loculations remain, additional drains should be placed. The drains are then attached to 20 cm water suction via a closed underwater seal system. The drains are irrigated daily with sterile saline to maintain patency. The decision to proceed with fibrinolytic agents is based primarily on the amount of fluid remaining after catheter placement. If all fluid was drained during the first 2 days following drain placement and the lung has expanded, no fibrinolytic agents are recommended. If significant amounts of fluid remain, fibrinolytics are injected through the drains into the pleural cavity (assuming that no bronchopleural fistula is present). Generally, 100,000 units of urokinase or 250,000 units of streptokinase are dissolved in 250 mL of normal saline solution. Following installation of 75 to 100 mL of the fibrinolytic solution, the catheters are clamped and the patient is instructed to intermittently change position from supine to each decubitus position in order to facilitate mixing of the solution with the pleural fluid. After 1 to 4 hours, the catheters are unclamped and as much fluid as possible aspirated. The net amount of fluid is recorded. The procedure should be repeated after 1 to 2 hours of suction drainage. Three separate irrigations daily are recommended. Three criteria are used to determine when to remove the chest tubes. Clinical improvement with resolution of fever and leukocytosis is desirable. However, if the pleural space is considered adequately drained and an alternate source of fever is apparent (i.e., persistent pneumonia), it is not considered absolutely necessary that the white blood cell count be normal and the patient afebrile. The second criterion is that almost all of the pleural fluid was drained as determined by radiographic evaluation. If any fluid remains and the clinical response is incomplete, the drainage process should be continued. The third criterion is that there should be no more than 20 mL of net drain output over a 24-hour period.

Open Drainage

Open drainage was the classic method of draining empyema cavities prior to the antibiotic era. Historically, Graham and Bell (1918), when reporting to the Empyema Commission, demonstrated that open drainage was an effective treatment for empyema. They demonstrated that open drainage must not be performed during the acute phase of the disease since an open pneumothorax was produced with reduced ventilation, hypoxia, and death. Once the lung is fixed to the chest wall and ventilation is assured, open drainage is safe. In times past, this was heralded by increased sediment in the fluid drained by thoracocentesis from the empyema cavity. When the sediment reached 75%, open drainage was said to be safe.

At the present time, open drainage through a thoracostomy tube may be performed in situations where the lung has not expanded completely, a space exists, and circumstances dictate that no further therapy is indicated. Once the space has become stable (usually 2 3 weeks following chest tube insertion), there are no gross up and down movements of the water column, and pneumothorax fails to occur when the chest is open to atmospheric pressure, the chest tube is cut off a few centimeters from the skin and anchored in place with a safety pin and tape. The tube may be withdrawn a few centimeters per week as space is obliterated and granulation tissue fills the tract and drainage decreases.

Eloesser (1935) was able to maintain patency of the open drainage tract achieved by rib resection with a modified skin flap technique. According to Ali and colleagues (1996), this is a useful procedure in those instances where a large space exists and prolonged drainage is anticipated.

Video-Assisted Thoracoscopic Decortication

As evidenced by Angelillo Mackinlay (1996) and Landreneau (1996) and their colleagues as well as one of us (M.K.) (1998) and both authors (1996) and their associates, video-assisted thoracic surgery (VATS) has become the primary modality for treating complicated empyema after initial therapy (with or without chest tube drainage) in many institutions. VATS allows adhesiolysis and d bridement with better exposure than minithoracotomy. Decortication for lung expansion prior to fibrosis can be accomplished with equal facility. Although chest tube drainage combined with enzymatic d bridement is effective, VATS therapy results in a higher (90%) success rate, shorter hospital stay, and less cost. Wait and co-workers (1997) concluded that it can routinely salvage patients in whom chest tube drainage with enzymatic d bridement was not successful.

The VATS procedure is described in Chapter 18. A dual-lumen endotracheal tube is inserted for single-lung ventilation. Its position is confirmed by bronchoscopy. Blood pressure, central venous pressure, arterial oxygen saturation (SaO₂), and end tidal CO₂ are monitored continuously. The patient is placed in the lateral decubitus position. A two- or three-port triangular approach is used with the ports later serving as chest tube drainage sites. The empyema cavity is entered, loculations broken up, adhesions lysed with endoshears and cautery, fibrin and purulent material removed

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VATS is highly effective in the treatment of parapneumonic empyema. The combined mortality rate in Angelillo Mackinlay's (1996) and Wait's (1997) and their associates' series is 4.8% and, most important, no additional procedures were necessary.

Thoracotomy, Minithoracotomy, and Decortication

Although VATS has the advantages of greater patient tolerance, open thoracotomy with d bridement and decortication is an effective means of dealing with empyema. Most studies of this technique predate the widespread use of VATS. Van Way and associates (1988) reported on 22 patients in which d bridement and decortication were performed and in which drainage was established through limited thoracotomy. The process resolved completely in all and there were no deaths in this series. Miller (1990) described 52 patients treated with open thoracotomy. Good results were obtained in 50 patients, and there were no operative deaths. Mandal and associates (1998) treated 179 consecutive adult patients with primary empyema. Ninety underwent closed thoracostomy, with a cure rate of 62% and a mortality rate of 11%. Twenty-four of these required a second procedure. Seventy-six patients underwent decortication as either a primary or secondary procedure, with a cure rate of 88% and a mortality rate of 1.3%. Thus, 42% of these patients required decortication. In a meta-analysis of 159 patients undergoing surgical procedures, the mortality rate was 1.9% and 11% of the patients required at least one additional intervention.

Empyemectomy

Empyectomy is rarely performed. It requires an extrapleural dissection of the parietal pleura and tedious dissection of the sac from the lung. Just as in decortication of a chronically collapsed and trapped lung, lung damage requiring undesirable and unnecessary resection is often the result.

CHRONIC EMPYEMA

Chronicity refers to a state of continued infection associated with both fibrosis and a pleural space that is often compromised by bronchopleural fistulae. Fortunately, this is an uncommon occurrence following appropriate treatment. In the past, such spaces were treated by some form of thoracoplasty. This generally took the form of a modified Shede procedure. Ribs were resected over the cavity, the parietal pleura was removed, and the muscle bundles were allowed to fall against the visceral pleura. The procedure was effective, but mutilating. Hankins and associates (1978) concluded that muscle translocation into the cavity with occasional rib resection is the more desirable and effective procedure.

TREATMENT OF EMPYEMA IN CHILDREN

Empyema in infants and children is usually associated with pneumonia. Its incidence has diminished greatly in response to the successful treatment of pneumonia with antibiotics. In addition, its bacterial etiology has changed concomitantly with the evolution of microbial resistance. Nearly two decades ago, Foglia and Randolph (1987) found that the most frequent causes of empyema were Haemophilus influenzae, -hemolytic streptococci, Streptococcus pneumoniae, and anaerobes. At present, Hardie and co-workers (1996) have found that Streptococcus pneumoniae, often penicillin and erythromycin resistant, is the most common organism. Gustafson and associates (1990) found that anaerobic bacteria produce effusions that loculate quickly and are difficult to drain, whereas staphylococcal effusions are most commonly unilocular and relatively easier to drain.

The clinical scenario has changed as well, with empyema seen more often in older children as opposed to infants. Hardie and colleagues' (1996) study of CAP complicated by empyema, revealed that 40% of empyemas were due to Streptococcus pneumoniae, 15% of which were resistant to penicillin, and 44% of cultures were negative. None of the empyemas were associated with Staphylococcus aureus or Haemophilus influenzae. Only one empyema was caused by group A Streptococcus. Miller (1990) noted that the culture-negative status of these children is now a common finding because of pretreatment with antibiotics in the community setting.

Campbell and Nataro (1999) noted that host defenses are weakened in the nutrient-rich purulent space due to (a) lack of phagocytic surface for optimal white cell function, (b) low levels of opsonins and complement, and (c) conditions of acidosis, hypoglycemia, and hypoxia. Furthermore, Bryant and Salmon (1996) found that many antibiotics do not work optimally in pleural empyema despite efficient penetration into the pleural space.

Fever is the most common presenting symptom in childhood empyema. Fever, cough, and dyspnea are present in 75% of children on admission. Decreased breath sounds, tactile and vocal fremitus, and tachypnea and tachycardia are often present according to Middlekamp (1964) and McLaughlin (1984) and their associates and Chonmaitree and Powell (1983). Other symptoms are grunting respiration,

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The treatment of empyema in children remains controversial, but the goals of therapy were clearly outlined by Mayo and associates (1982) (Table 58-11).

The possibility of empyema in children as heralded by clinical signs and symptoms and radiographic evidence of pleural involvement or infusion requires prompt attention. A CT scan should be performed if the presence of fluid is in question and thoracentesis should be performed for visual, biochemical, and cultural evidence of infection.

Antibiotics administered intravenously, according to Gram's stain, culture, and sensitivity studies, and pleural drainage are the mainstays of treatment. Foglia and Randolph (1987) demonstrated that most children treated with appropriate antibiotics and chest tube drainage recover. This course depends on the disease stage, type of bacteria, and degree of lung trapping. If rapid recovery does not occur, additional intervention is indicated. Raffensperger and colleagues (1982) recommended minithoracotomy or full thoracotomy. Gustafson and colleagues (1990) noted that aggressive care, including early thoracotomy, led to early recovery and excellent long-term results. Rizalar and associates (1997) reported on 32 patients treated by early decortication for postpneumonic empyema with no deaths and no recurrences. In older children, VATS deloculation, decortication, if necessary, and drainage were used by de Campos and associates (1997) with good results. Gandhi and Stringel (1997) performed VATS decortication in nine children (mean age 4, range 21 months to 13 years) with successful outcomes in all. One child required a blood transfusion because of bleeding following difficult and extensive decortication. Open drainage is never indicated in children because of late skeletal deformities. We do not believe that the use of enzymatic d bridement is indicated in infants and small children. However, Rosen and associates (1993) and Kornecki and Sivan (1997) reported success with adjuvant use of enzymatic d bridement. A controlled trail is needed to define the use of enzymatic d bridement in children.

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