03. Purulent-inflammatory diseases of lungs and pleura

TOPIC No.3 Purulent-inflammatory diseases of lungs and pleura.

 

Plan:

1.                Purulent-inflammatory diseases of lungs and pleura:

1.1.                 Bullous Lung Disease.

1.2.                 Lung Abscess.

1.3.                 Pneumothorax.

1.4.                 Pyopneumothorax.

1.5.                 Empyema.

 

1. Purulent-inflammatory diseases of lungs and pleura:

1.1. Bullous Lung Disease.

Bullae or blebs are saccular areas of subpleural air within the lung that are believed to result from an air leak from an adjacent alveolus. Generally, the term bleb refers to a smaller air collection and bulla to a larger one. although there are no specific numeric thresholds to distinguish between the use of the two terms. The important functional distinction is that the grossly apparent lesions (bullae) are associated with the loss of adjacent lung parenchyma, whereas this is not true of blebs. Blebs and bullae are not associated with normal alveoli or capillaries; hence, no gas exchange occurs within them, although they do communicate with the tracheobronchial tree (53).

 

Bullae and blebs are either congenital or acquired. Acquired lesions are usually a consequence of chronic infection related to a problem such as CF, 0±,-antitrypsin deficiency, or anothersimilar condition. Bullous emphysema is a common form of acquired chronic obstructive pulmonary disease in adults, but this is rarely seen in children. Congenital bullae and blebs apparently result from disordered development of alveoli and terminal airways during organogenesis. The discussion that follows deals principally with blebs and bullae rather than the underlying pulmonary diseases.

Figure : Chest x-ray of a large bulla with true infection; after the appropriate medical treatment fever, hemptysis and fluid level persisted and the bulla was resected.

The clinical symptoms of blebs and bullae are generally the result of either spontaneous pneumothorax from rupture into the pleural space or exercise intolerance because of diminished lung volumes and inadequate respiratory reserve. The latter problem is generally associated with underlying diffuse lung disease. Plain chest radiographs and CT are usually adequate for definitive imaging. Apical disease is most common, and bilateral disease is frequent. 0±.-Antitrypsin deficiency is unique in its propensity to form basal blebs (54).

Figure . A, Chest radiograph demonstrating the classic appearance of bronchiectasis in a pediatric patient with cystic fibrosis. B, Magnified view of patient in A demonstrating honeycombed appearance.

Figure : Chest x-ray showing a giant bulla occupying more than two thirds of the right hemithorax and compressing the underlying lung upward and towards the mediastinum.

 

Figure : Computed tomography showing the presence of a large bulla compressing and dislocating the underlying lung towards the mediastinum and posteriorly.

 

Figure : Perfusion scan showing an area with no uptake in the right upper field.

 

Figure: Pulmonary angiography showing an area with no vessels in the inferior two thirds of the left hemithorax. The vessels are compressed and dislocated upward.

The management of blebs and bullae is dependent on the degree of symptomatology and the underlying lung problem. Treatment of smaller lesions is usually limited to problems that result from air leak, specifically pneumothorax. Generally, tube thoracostomy is the appropriate treatment for the first spontaneous pneumothorax. Recurrent pneumothorax occurs in 20% to 50% of patients with congenital bullous disease, and this incidence increases significantly with each additional pneumothorax (55). It is therefore appropriate to consider definitive operative treatment after a first recurrent pneumothorax associated with congenital bullous disease.

The principles for operative management of lung bullae are to remove the area of involvement, to conserve all possible normal lung tissue, and to obtain a secure, airtight closure of the lung. The resections, therefore, generally are not segmental or lobar, but rather nonanatomic iature (55,56). Resection of bullae with or without pleurodesis is highly effective. Closure of the bleb margin can present problems, but modern stapling devices confer more security and efficiency to this procedure than do traditional suture closure techniques. Therefore, stapled resections are considered routine for this problem. Resection of bullae can be done through either a thoracoscopic approach or an open thoracotomy, with limited morbidity and mortality (55,56,57). The thoracoscopic approach appears to be highly effective, rapid, and less morbid than open thoracotomy. Potential problems with air leak are best prevented by concurrent pleurodesis or pleurectomy.

Figure : Operative view at thoracotomy of a single bulla with normal underlying lung.

Operative Steps

Surgical treatment of bullous emphysema is technically not difficult when the correct indications, technique and postoperative management are respected. However, it can lead to serious complications when performed inappropriately.

Surgical bullectomy is usually performed with videothoracoscopic techniques ⁴. This approach is ideal both for unilateral and bilateral bullectomy. When a bilateral approach is required, median sternotomy and simultaneous bilateral anterior thoracotomy also could be considered⁵. In this latter group of patients staged procedures also could be performed. Video assisted thoracoscopy can be immediately converted to open thoracotomy when intraoperative findings require it.

VATS bullectomy is performed under general anesthesia with double lumen endotracheal intubation. After discontinuing ventilation to the operated side, the first incision is usually made at the level of the 6th or 7th intercostal space in the midaxillary line. Careful inspection of the bulla and underlying lung parenchyma may be difficult since large bullae are usually under tension and obliterate the pleural space. The other two incisions are performed to achieve a “triangulation approach” and are used to place graspers and staplers. Pleural adhesions are coagulated and divided to completely mobilize the lung and bulla/bullae. The use of a thoracoscope with a working channel may further help to have an additional port available for instruments. The bulla can be incised and deflated to facilitate gentle manipulation of the lung; it is usually squeezed and twisted (“spaghetti procedure”) to identify the base. Traction on the surrounding parenchyma must be carefully performed to avoid injuring the lung surface with consequent prolonged air leaks during the postoperative period. Pedunculated bullae are easily excised with endostapling devices. Broad-based bullae can be removed with multiple applications of endoscopic staplers (Figures 10-12). The bulla is usually excised with a rim of “normal” lung parenchyma to avoid leaving open bronchioles. When removing bullae with underlying emphysematous lung, the stapler line is usually reinforced with commercially available strips⁶. Additional small bullae and blebs in the residual lung are either excised or coagulated.

Figure : The thoracoscopic resection of the bulla begins with use of a stapler and a reinforcing strip to buttress the staple line.

Figure : Thoracoscopic view after placement of the staple line. The bulla is gently retracted upward to provide space for the second stapler.

At the end of the procedure particular attention is paid to the presence of air leaks. If they are observed, surgical sealants may be applied to cover the holes and reduce or eliminate this complication. Gentle re-expansion of the residual lung is achieved to check how it fills the pleural cavity. If a residual space is anticipated, a pleural tent can be designed thoracoscopically to reduce it⁷. The pleural cavity is usually drained with two multifenestrated chest tubes in the costovertebral groove and behind the anterior chest wall. Postoperative pain control is usually obtained with intravenous continuous analgesia; epidural analgesia can be considered for bilateral bullectomy.

Other techniques have been described to treat bullous emphysema. Instead of resecting the bulla, it can be rolled or folded and plicated over itself placing a stapler at the base. This technique is better performed through an open approach and has the potential advantage of allowing reinforcement of the staple line with the bulla itself. However, our feeling is that bullae should always be completely resected since the risk of cancer is 36 times higher than in the normal lung parenchyma⁸. We routinely send the bulla for histology and random routine sampling has demonstrated the potential development of cancer⁹.

In a selected group of patients a modification of the Monaldi procedure has been proposed by Goldstraw¹⁰. CT scanning is used to select the optimal site for surgical incision. A portion of the underlying rib is resected and the pleura is opened to reveal the lateral wall of the dominant bulla. Two concentric purse-string sutures are placed and the bulla is incised. Talc is insufflated to elicit a fibrous reaction and promote a rapid and permanent contraction of the cavity. A 32 Foley catheter is inserted into the cavity and led out thorough the incision. The balloon of the catheter is inflated with 30 – 40 ml of air and the pursue-string sutures are tied around it. Suction is applied to the catheter with the resultant collapse of the bulla. Talc is insufflated around the free pleural space to induce pleurodesis and an intrapleural drainage catheter is placed thorough a basal stab incision. The wound is closed around the Foley catheter, which is secured under traction, apposing the wall of the bulla to the chest wall. The pleural drainage catheter is usually removed within 48 hours and the Foley catheter within 8 days.

 

The outcome after bleb resection is dependent on the amount of remaining lung and the extent of underlying disease. For congenital blebs with a large portion of the normal lung retained, the outcome is predictably excellent. For extensive local disease or for blebs acquired as a consequence of systemic disease, this is more problematic. Specifically, if preoperative evaluation shows that the bullae occupy more than one-third of the ipsilateral thorax, if ventilationBTb’perfusion scan shows little or no function in the area of the bullae, and if pulmonary function studies indicate tolerance for thoracotomy and lung resection, the outcome is much more favorable (55).

 

1.2. Lung Abscess.

Generally, a lung abscess develops when at least one of two fundamental problems exist: (1) a primary failure of host defenses is present, or (2) repeated aspiration of oral or intestinal bacteria into the tracheobronchial tree occurs. Some of the relevant deficiencies are provided in Table 61-1. As elsewhere, the abscess results from tissue necrosis related to pyogenic, toxin-producing bacterial organisms and to phagocytic cells that generate cytotoxic oxidants and proteases. Both cellular lung elements and the extracellular lung matrix are destroyed; tissue necrosis and cavitation within the lung parenchyma follow. The involved area is surrounded by atelectasis and pneumonia. A chronic lung abscess develops with varying degrees of circumferential fibrosis and may involve substantial destruction of parenchyma, usually in a lobar distribution. Typically, the abscess cavity communicates with the normal tracheobronchial tree, and this relation has important diagnostic and treatment implications.

 

FIGURE. Photomicrographs of lung after experimental microvascular injury. (A) Normal lung histology with normal alveoli [asterisk). (B) Neutrophil infiltration, alveolar edema (asterisk), intraalveolar hemorrhage [arrow), and acute lung injury. (From Turnage RH, Guice KS. Oldham KT. Pulmonary microvascular injury following intestinal reperfusion. New Horizons 1994:2:463, with permission.)

 

Lung abscesses that form without underlying structural abnormalities are now uncommon in infants and children, although they are still potentially serious. Cowles et al. from Michigan found that 71% of children with lung abscesses had an accompanying anatomic or physiologic comorbidity, and more than 90% had been treated for prior pneumonia (36). In the modern medical environment, infants and children at particular risk are those who are immunocompromised.

Although aspiration is a common event in infants and children, lung abscesses do not ordinarily follow. Certain groups of children, however, appear to be at particular risk. Among these are children with cerebral palsy or other causes of neurologic dysfunction who may be unable to protect the airway adequately. Repetitive, incompletely cleared aspiration events result. Institutionalized children with periodontal and dental disease and patients who have been treated with antibiotics for some other reason may also be at high risk, presumably because of the presence of a larger thaormal proximal reservoir of potentially pathogenic bacteria.

Lung abscesses are typically polymicrobial, with both anaerobic and aerobic bacteria. Since the 1970s, when anaerobic cultures became routine, oral anaerobic organisms have predominated in epidemiologic reviews of causative organisms. Bacteroides sp. group B Ol-hemolytic streptococci. Streptococcus pneumoniae, Escherichia coli, Pseudomonas sp. Proteus sp. and Aerobacter aerogenes ate all important and relatively frequent pathogens in this setting (37,38). This is in contrast to Staphylococcus aureus and Klebsiella pneumoniae, which were the most common and important causes of lung abscesses in Western countries in the 1980s. It remains important, however, to recognize that the latter organisms are both associated with substantial parenchymal lung destruction and are still important pathogens. Both require long-term and aggressive antibiotic treatment.

Secondary and even primary pulmonary infection with a variety of fungal and other organisms may also lead to the development of a lung abscess. Aspergillus, Actinomyces, and Nocardia spp are among these pathogenic organisms. Cavitary tuberculosis was once an important risk factor for the development of secondary pyogenic lung abscesses in adults. Given the worldwide resurgence of tuberculosis, including among children in the United States, it may be worthwhile to recall this experience in coming years.

The clinical presentation of a patient with a lung abscess commonly includes systemic complaints, such as fever, chills, night sweats, anorexia, and weight loss. Nonspecific respiratory symptoms, such as coughing and wheezing, are also frequent. More specific and alarming symptoms, such as a productive cough, fetid sputum, or hemoptysis, are later events associated with suppurative disease and cavitation. These latter findings in particular should lead to a prompt laboratory and imaging evaluation because the physical examination generally yields only nonspecific signs of pulmonary consolidation. The most important examination is generally a plain chest radiograph. A single cavity in a dependent location with an aireTb^fluid level is classic (Fig. 61-13). Predictably, lung abscesses occur in areas of the lung that are dependent. Two-thirds are found in the right lung; the superior segment of the lower lobe and the posterior segment of the upper lobe are most common (37,38). An ambulatory patient is more likely to have involvement of basal segments of the lower lobes because these are dependent on the upright position. Areas of surrounding consolidation, pneumonia, and a thick fibrous wall are all typical, but variable in appearance. It may be impossible to differentiate a lung abscess from an infected cystic lung lesion on radiographs obtained at a single point in time. Generally, sequential films demonstrate resolution of pneumonia or an abscess, whereas congenital cystic lesions remain and become conspicuous. A pneumatocele may develop after treatment of necrotizing pneumonia or a lung abscess and may have a residual cystic appearance; however, these airB”B*filled cavities typically do not have airB”b”fluid levels. In addition, patients generally improve clinically or have no symptoms after treatment when the typical air-filled cavity becomes apparent. CT and MR imaging are both excellent techniques for evaluating intrathoracic mass lesions such as a lung abscess; however, their routine use is not required, and their expense can be substantial.

FIGURE 61-13. Plain chest radiograph showing the classic appearance of a thick-walled pulmonary parenchymal abscess with an obvious airB”B*fluid level (arrow).

 (Courtesy of Don Frush. MD. Duke University Medical Center, Durham, NC.)

A lung abscess, like any other abscess, requires prompt drainage and treatment with appropriate antibiotics. Drainage may occur spontaneously into the tracheobronchial tree, and this is a time at which large amounts of purulent, malodorous sputum may be expectorated. Postural drainage and appropriate suctioning are simple yet fundamental aspects of care at this time. Infants, small children, and others who cannot eliminate sputum effectively may require more aggressive endoscopic or transpleural surgical drainage.

Endoscopic drainage of a lung abscess into the tracheobronchial tree can be achieved with a variety of needles, catheters, or other instruments passed through rigid or flexible instruments. If possible, this is preferred to other methods of surgical drainage. Intraoperative control of the airway is essential when endoscopic drainage of a lung abscess is performed because the decompression of purulent material into an adjacent bronchus or the contralateral lung may be life threatening if the abscess is sizable. The contralateral lung is best protected either by positioning the involved lung dependently or by selective intubation and balloon exclusion of the normal mainstem bronchus. A flexible endoscope has the advantage of better access to the peripheral airways, whereas a rigid bronchoscope allows the use of larger instruments and provides better visualization and control of the trachea and primary bronchi. The choice is best individualized. Most infants and children require general anesthesia for the initial endobronchial drainage procedure because of the absolute need for control of the airway. Fluoroscopy or ultrasound may provide valuable guidance in localizing the lesion intraoperatively, if necessary. Subsequent drainage or aspiration procedures may be needed, depending on the clinical response.

Transpleural diagnostic aspiration and both open and closed external drainage are all described and appropriate for selected patients. The risks of pleural contamination, empyema, and bronchopleural fistula, however, make these approaches desirable only in circumstances in which the abscess is peripheral in location and chronic enough that the visceral and parietal pleura are adherent. These approaches are best reserved for specific indications in complex abscesses after failure of initial drainage and antibiotics. Regardless of the drainage technique selected, the abscess contents require microbiologic evaluation to identify the organisms involved and to direct subsequent antibiotic therapy. Empiric initial therapy should cover anaerobic organisms, as well as gram-negative organisms and S. aureus. Clindamycin rather than penicillin G is recommended because increasing numbers of resistant oral anaerobes and resistant S. aureus organisms make penicillin therapy prone to failure. Antibiotic therapy is generally required for 6 to 12 weeks, although this depends on the patient’s response and the rate at which the chest radiograph clears (37.38). Most patients with lung abscesses are successfully treated with drainage and antibiotics alone. Patients with underlying immunodeficiencies that can be corrected or modified should have this done. Modulation of immunosuppression drugs in transplant recipients, delay in chemotherapy for oncology patients, treatment with granulocyte colony-stimulating factor, and other similar approaches are appropriate when possible.

Operative management of a lung abscess is reserved for patients with specific related complications. Failure to control the initial infection or recurrent infection, massive or recurrent hemoptysis, bronchopleural fistula, and a persistent cavitary lesion are indications for operative resection of the affected lung. Immunosuppressed patients are at particular risk for these complications. Although a trial of medical therapy is appropriate in immunosuppressed patients, failure is much more probable, and prompt parenchymal resection is often required. The surgical principle that governs management of the complicated lung abscess is that resection of the involved parenchyma is required. This generally takes the form of a formal lobectomy; if done in the face of acute inflammation, this can be a formidable technical challenge. In this circumstance, the bronchial stump closure requires particular care to avoid an air leak and a bronchopleural fistula.

 

 

1.3. Pneumothorax.

A pneumothorax is an accumulation of air within the pleural space. It may occur spontaneously or as the result of trauma, surgery, or a therapeutic intervention. If the air accumulates under pressure, a tension pneumothorax ensues. A pneumothorax decreases pulmonary volume, compliance, and diffusing capacity. If the pneumothorax is greater than 50% of chest volume, hypoxia may result secondary to ventilationB”B*perfusion mismatch. A normal lung can often compensate this for. Children with underlying chronic pulmonary disease may develop significant relatively smaller pneumothoraces secondary to diminished elastic recoil of their lungs, but the symptomatic consequences may be more significant because of their small margin of pulmonary reserve (60.61.62). Spontaneous pneumothorax may occur in children with no known underlying disease or may result from or. in fact, reveal an underlying condition, such as a congenital bleb, pneumonia with pneumatocele or abscess, tuberculosis, or cystic adenomatoid malformation. Traumatic pneumothorax may result from a tear in the pleura, esophagus, trachea, or bronchi. Iatrogenic causes include mechanical ventilation, thoracentesis or central venous catheter insertion, bronchoscopy, or cardiopulmonary resuscitation (60,63,64,65).

The most common presenting symptoms of pneumothorax are ipsilateral chest pain and dyspnea (60.64). Severe dyspnea should alert the surgeon to the presence of a tension pneumothorax. Physical examination may reveal diminished breath sounds on one side of the chest or a shift of the trachea from the suprasternal notch. A pneumothorax is usually detectable on a chest radiograph and is enhanced if the radiograph is taken at end expiration. It is common practice for the size of a pneumothorax to be described as a proportion of the chest field on an upright radiograph. The actual volume loss of the lung is greater than such a description because pulmonary volume is lost in three dimensions. The following formula is used to more accurately estimate this loss:

A number of factors determine the proper management of a pneumothorax. These include the initial size, symptomatology, ongoing expansion, presence of tension, and any contributing underlying condition. A spontaneous unilateral pneumothorax that is asymptomatic and less than 15% to 20% of the chest volume can usually be followed by observation alone (61,65). Pleural air reabsorbs at a rate of 1,25% per day. but this can be hastened by breathing supplemental oxygen (61.67). Classically, such a pneumothorax occurs in an ectomorphic. adolescent male. If there is no known underlying pathology, the chances are that such an episode represents the rupture of a subpleural bleb or cyst, the manifestation of a familial tendency, or perhaps even the presence of undetected tuberculosis (68). Pneumothorax recurs with a frequency of 50% after the first episode. 62% after the second, and 83% after the third (61,69).

Symptomatic or large pneumothoraces usually require intervention. Options for treatment of a small pneumothorax include thoracentesis, placement of a unidirectional (Heimlich-type) valve, or placement of a small pigtail catheter (70,71,72). However, if air is continuously aspirated or if the pneumothorax recurs, a standard chest tube should be inserted. A tension pneumothorax poses a surgical emergency and a chest tube should be placed immediately. If a chest tube is not immediately available or if the patient’s condition deteriorates during preparation for placement, a large-bore (14-gauge) needle should be placed in the second intercostal space anteriorly to relieve the tension. If the pneumothorax recurs after tube thoracostomy, or if the air leak persists, further intervention is necessary. The choice of intervention is determined by the cause of the condition. In a posttraumatic pneumothorax, large or persistent air leaks may indicate damage to the airway or the esophagus. Appropriate diagnostic studies using esophagograms. bronchoscopy, esophagoscopy. thoracoscopy, or thoracotomy should be undertaken and direct repair of the injury, if present, performed. If the air leak is due to lung parenchymal injury, chest tube drainage is usually adequate. In a nontraumatic pneumothorax, the persistence of an air leak may accompany a chronic underlying condition, such as cystic fibrosis, bronchopulmonary dysplasia, lung cysts, or blebs. Treatment of these patients usually requires resection of the local pathology or pleurodesis.

Pleurodesis can be undertaken by instilling chemical agents into the pleural space through a chest tube, by thoracoscopy, or by thoracotomy. In the past, agents such as silver nitrate, quinacrine, iodized oil. and hypertonic glucose have been used, but currently, talc or tetracycline derivatives, such as doxycycline or fibrin sealant, are more commonly used (47,73,74,75,76,77). Talc is less painful and more uniformly successful than doxycycline. Treatment with talc has been shown to be particularly effective in treating pneumothoraces in children with cystic fibrosis (47). A more recent study in adults does suggest that talc may have systemic distribution and may rarely produce adult respiratory distress syndrome (78). Autologous blood patching may be useful in preventing pneumothorax after lung biopsy (79).

Traditionally, thoracotomy has been used for more aggressive interventions such as mechanical pleurodesis. pleurectomy. or resection of lung blebs or cysts. However, thoracoscopy has emerged as a preferred technique by many for all these interventions (80.81.82.83). It allows excellent visualization of the entire pleural space with a low surgical morbidity. It also allows use of a wider range of anesthetic techniques because older children can often undergo thoracoscopic pleurodesis under sedation with intercostal nerve block. The results of thoracoscopic pleurodesis for pneumothorax have been excellent, and complications of the technique are very uncommon (80.84).

 

1.4. Pyopneumothorax.

Background: Pleural effusion is defined as the collection of at least 10-20 mL of fluid in the pleural space. Pleural effusion develops because of excessive filtration or defective absorption of accumulated fluid. The presence of pleural effusion may be a primary manifestation or a secondary complication of many disorders.

Pathophysiology: The inner surface of the chest wall and the surface of the lungs are covered by the parietal and visceral pleural, respectively, with a potential space of 10-24 µm between the 2 pleural surfaces. Normally, this space is filled with a very small amount of fluid. However, large amounts of fluid can accumulate in the pleural space under pathological conditions. The parietal pleura have sensory innervation and small apertures that aid in the absorption of particles and fluid. Both pleural surfaces mainly are supplied by systemic arterial vessels. Lymphatic vessels from the parietal pleura drain to lymph nodes along the anterior and posterior chest wall, while lymphatics from the visceral surface drain to the mediastinal lymph nodes. Normally, the pleural space contains a small amount of a colorless alkaline fluid (0.1-0.2 mL/kg), which has a low amount of protein (<1.5 g/dL). Approximately 90% of accumulated fluid in the pleural space is drained by the venous side, while the other 10% is absorbed by the
lymphatics.

A delicate balance between the oncotic and hydrostatic pressures of the pleural space and the capillary intravascular compartments regulates filtration and drainage of pleural fluid. Hydrostatic and oncotic pressures are many-fold higher in the plasma than in the pleural space, but the net absorption of pleural fluid is slightly higher than the net filtration forces. In addition, the lymphatic drainage from the parietal pleura can surpass the rate of fluid filtration in the pleural space by several fold.

Chest wall and diaphragmatic movements enhance absorption of pleural fluid by the vascular and lymphatic vessels. Excessive filtration of fluid can overwhelm these efficient absorptive mechanisms and lead to the formation of pleural effusion.

Pleural effusions usually are classified as transudates and exudates. Diseases that affect the filtration of pleural fluid result in transudate formation, such as in congestive heart failure and nephritis. Transudates usually occur bilaterally because of the systemic nature of the causative disorders. Inflammation or injury increases pleural membrane permeability to proteins and various types of cells and leads to the formation of exudative effusion.

Frequency:

·                    In the US: US and international frequency are similar.

·                    Internationally: Nonbacterial infectious agents, such as viruses and Mycoplasma pneumoniae, cause more pleural effusion in children than do bacterial organisms. Although bacteria are more likely than viruses to cause effusion, the frequency of viral infection in children is much higher than bacterial infection, explaining the above. As many as 20% of these infections can cause small and transient effusion that resolves spontaneously.

Several decades ago, pleural effusion complicated 70% of Staphylococcus aureus pneumonia cases, with a positive culture in 80% of the pleural fluid specimens. In the late 1970s, pleural effusion occurred in 75% of cases of pneumonia secondary to Haemophilus influenzae type b. In a report by Murphy et al, empyema complicated the course of pneumonia in 9 out of 21 patients with Streptococcus pneumoniae. A report by Chartrand indicated that empyema complicated the course of pneumonia in 57 out of 79 patients with S aureus infections.

Pleural effusion occurs in 6-12% of cases of pulmonary tuberculosis in children. More recently, of 175 children with pulmonary tuberculosis from Spain, 39 patients (22.1%) had pleural effusion.

Congenital effusions, including chylothorax, occur in 1 per 10,000-15,000 live births annually. In a recent review of 74 patients with intrathoracic lymphomas, Chaignaud found pleural effusions in 71% (10 out of 14) of children with lymphoblastic lymphoma and in 11.7% (7 out of 60) of children with non-Hodgkin lymphoma.

Mortality/Morbidity: Most effusions caused by viral and mycoplasmal infections resolve spontaneously. Empyema has a more complicated course if not treated early, especially in children younger than 2 years. Thirty years ago, the mortality rate from empyema was 100%. Currently, the mortality rate from empyema is 6-12% in infants younger than 1 year. Malignant effusion carries a much worse prognosis depending on the underlying tumor.

History: The clinical picture and presenting symptoms depend on the underlying disease and size of the effusion.

·                    Often, in parapneumonic effusion or empyema, history of a recent upper respiratory tract infection, bronchitis, or pneumonia exists.

·                    Commonly, an initial improvement associated with antibiotics occurs, and then fever and onset of chest pain recurs.

·                    Pleurisy causes chest pain, tightness, and shortness of breath. Pain can be referred to the shoulder.

·                    Subpulmonic fluid collection can be associated with vomiting, abdominal pain, or abdominal distension caused by partial paralytic ileus.

·                    Parapneumonic effusion and empyema usually present with chills, fever, anorexia, tachypnea, and sweating.

·                    Accumulation of a small amount of fluid may be asymptomatic.

·                    A large collection of fluid leads to dyspnea, respiratory distress, dull pain, and coughing, which may vary with alteration in body position.

·                    Malignancy-related effusion often occurs after the diagnosis is established and can be associated with significant and rapid weight loss.

·                    Although effusion occurs in association with systemic lupus erythematosus, it is rarely the initial manifestation. Inquiry should be made into exposure to tuberculosis (TB), recent trauma, surgery, and central line placement.

Physical:

·                    The patient may look tachypneic and anxious because of pain, discomfort, or hypoxemia.

·                    A pleural rub may be the only initial manifestation during the early stage of pleurisy. The rub disappears as more fluid accumulates between the 2 pleural surfaces.

·                    Dullness to percussion, decreased air entry, decreased tactile and vocal fremitus, and voice egophony over the effusion all may be present, although difficult to detect in younger children.

·                    Large fluid collection causes fullness of the intercostal spaces and diminished chest excursion on the affected side.

·                    Excessive unilateral fluid accumulation shifts the mediastinum and displaces the trachea and cardiac apex to the contralateral side.

Causes: In children, infection is the most common cause of pleural effusion. Congenital heart disease (CHD) constitutes the second most common etiology, followed by malignancy.

·                    In 1968, Wolf reported 60 cases of empyema in 98 cases of pleural effusion. Of the remaining 38 children in the same series, 34% had nonempyemic parapneumonic effusion, 26% had malignant effusion, and 16% had effusion caused by TB.

·                    In a recent Canadian study of 127 children with pleural effusion, Alkrinawi reported the frequency of several types of effusions. Fifty percent of effusions were parapneumonic, 17% were caused by CHD, 10% by malignancy, 9% by renal disease, 7% by trauma, and 6% were associated with other causes.

·                    In another North American report of 210 children admitted with pleural effusion, Hardie showed that 68% of the effusions were parapneumonic (50 out of 143 had empyema), 11% were caused by CHD, 5% were caused by malignancy, and 3% were associated with other causes.

·                    The types of bacteria causing pleural effusions and their sensitivities to different antibiotics have changed over the years.

o        In Freij’s 1984 review of 227 cases of pediatric parapneumonic effusion and empyema, 76% had positive cultures; S aureus accounted for 29% of cases, S pneumoniae accounted for 22% of cases, and Haemophilus accounted for 18% of cases. Most of the cases of Haemophilus were type B.

o        In Brook’s 1990 series of 72 patients with gross pus and positive cultures from empyema, careful anaerobic cultures were included. A total of 93 organisms were isolated—60 aerobic and 33 anaerobic. H influenzae, S pneumoniae, and S aureus were the predominant aerobic organisms found in association with pneumonia. Anaerobes, including Bacteroides and Fusobacterium, were found frequently, particularly in empyema associated with aspiration pneumonia. Anaerobes also were found in empyema associated with intraoral and subdiaphragmatic abscesses.

o        In Hardie’s more recent 1998 series of 64 children with complicated parapneumonic effusions, 26 had positive cultures (88% were S pneumoniae). It was found that 26% of the S pneumoniae were penicillin-resistant. The decrease in complicated parapneumonic effusion caused by H influenzae is attributed to immunization. The authors speculate that the availability of broad-spectrum antibiotics effective against S aureus may account for the decrease in complicated parapneumonic effusion caused by this organism.

·                    Pleural effusion occurs in 8-22% of pulmonary tuberculosis in children. Tuberculous pleural effusion usually is unilateral and associated with an underlying parenchymal disease in almost 60% of the cases.

·                    Malignancy-related effusion is associated more often with lymphoblastic lymphoma than with Hodgkin disease.

·                    Congenital effusions, including chylothorax, occur in 1 per 10,000-15,000 births (see Image 9).

o        Congenital effusion can be associated with Down syndrome, diaphragmatic hernia, hydrops fetalis, polyhydramnios, and pulmonary hypoplasia.

o        Chylothorax may be congenital or acquired.

§     Acquired chylothorax usually follows surgical trauma to the thoracic duct.

§     Obstruction, thrombosis, or high pressure in the superior vena cava caused by cardiac malformation or Fontan repair of various cardiac anomalies also can cause chylothorax.

·                    Unusual intrapleural fluid collections include fluids given via a central venous catheter, which inadvertently has been placed or migrated to an intrathoracic location, and inadequate absorption of cerebrospinal fluid from a ventriculopleural shunt.

·                    Other rare causes of pediatric pleural effusion are rupture of a pulmonary hydatid cyst into the pleural space, in association with Lemierre syndrome (postpharyngitis anaerobic sepsis with internal jugular vein thrombophlebitis).

·                    Hemothorax can occur as a result of trauma, malignancy, pulmonary infarction, and postpericardiotomy syndrome. Hemothorax has been reported from puncture of the pleura by a costal exostosis. Hemothorax should be suspected if pleural fluid hematocrit is more than 50% of peripheral blood hematocrit.

Lab Studies:

·                    Obtain a complete blood count, differential white count, and blood culture initially in a patient suspected of having a pleural effusion.

·                    Although nonspecific, the erythrocyte sedimentation rate often is very elevated in children with empyema and may be useful for comparison in the follow-up period.

·                    Studies helpful in interpretation of pleural fluid analysis include serum glucose, lactate dehydrogenase (LDH), protein, triglycerides, and electrolytes or pH.

·                    Serologic studies may be helpful if specific organisms, such as Mycoplasma, Legionella, or adenovirus, are suspected.

·                    Pleural fluid analysis

o        Unless frank pus is obtained, fluid should be sent for Gram stain and culture, acid-fast stain and culture, cell counts, pH, protein, glucose, LDH, triglycerides, and cytology. Stains and cultures may be adequate studies if frank pus is collected.

o        Obtain pleural fluid hematocrit if hemothorax is suspected.

o        Counterimmunoelectrophoresis of urine and pleural fluid can be helpful in identifying some of the common bacterial organisms wheo pathogens are isolated.

o        Measurement of adenosine deaminase activity in the pleural fluid can be helpful if TB is suspected.

o        Pleural effusions usually are classified as transudates or exudates. Examination of the pleural fluid facilitates diagnosis, although criteria for distinguishing transudates and exudates, often called Light criteria, are based on studies in adults. The usefulness of these criteria in children has been challenged by Alkrinawi’s study, which found that 4-12 of 26 children with parapneumonic effusion had transudative instead of exudative biochemistries.

§     An exudate has 1 or more of the following characteristics: Pleural protein–systemic protein ratio higher than 0.5, pleural LDH–systemic LDH ratio higher than 0.6, and pleural LDH higher than two thirds of the upper limit of the normal serum LDH value.

§     In general, exudates generally have protein concentration higher than 3 g/dL or a specific gravity of 1.020 on a refractometer.

§     In exudative effusion, the pleural glucose level usually is less than 60 mg/dL. A pleural glucose–serum glucose ratio less than 0.5 can be seen in several conditions, such as parapneumonic effusion, TB, malignancy, esophageal rupture, or rheumatoid effusions.

§     The pleural pH is affected by the arterial pH values. Measuring the arterial pH simultaneously may be needed to ensure that the low pleural pH is not caused by systemic acidosis. In measuring the pleural pH, the fluid should be collected anaerobically in a heparinized syringe and transported on ice (which may keep the pH constant for 12 h if the temperature is kept at 0°C). Low fluid pH is usually associated with low glucose and high LDH levels, and any discrepancy in these measures may indicate a laboratory error. Pleural fluid pH less than 7.2 is observed mostly in exudative effusions, urinothorax, and systemic acidosis. A complicated parapneumonic effusion with a pH less than 7 would be most likely to require chest tube drainage, while an effusion with a pH value of 7-7.2 may or may not need drainage. Production of ammonia by urea-splitting bacteria (eg, Proteus species) may increase pleural fluid pH instead of diminishing it.

§     Exudates are caused by infection, pancreatitis (left-sided), systemic lupus erythematosus and other rheumatologic diseases, chylothorax, malignancy, and trauma. In chylothorax, the lipid level typically is 1-4 g/dL but may be lower in the unfed patient, particularly the newborn. Lymphocytes are the predominant cell.

§     Hemorrhagic effusion can be caused by malignancy, trauma, vascular erosion, and coagulopathy. In malignancy, cytologic studies may be diagnostic if positive, but negative cytologic examination does not rule out the possibility of malignancy. In a recent retrospective study, Chaignaud found that cytologic examination and immunotyping of the cells in the pleural fluid were diagnostic in 71% of children with lymphoblastic lymphoma, obviating the need for general anesthesia and open biopsy of the mediastinal masses.

§     A transudate has none of the chemical characteristics of an exudate. Usually, the protein concentration is less than 3 g/dL, pleural LDH is less than two thirds of the upper level of normal serum LDH, pleural protein and LDH concentration/serum levels are less than 0.5 and less than 0.6, respectively. A pH of 7.45 or a pH higher than the patient’s blood pH is consistent with transudative effusion.

§     Transudates are caused by congestive heart failure, hypoalbuminemia, nephrosis, hepatic cirrhosis, and iatrogenic causes (eg, misplaced central line, complication of ventriculopleural shunt).

Imaging Studies:

·                    Chest x-ray

o        A chest x-ray may show underlying pneumonia before pleural fluid starts accumulating. Most effusions are found on the anteroposterior (AP) and lateral chest radiograph. On an upright film, and even in lateral decubitus films, loss of the costophrenic angle is seen.

o        With increasing size of pleural effusion, the hemidiaphragm is obscured, and a mass effect with shift of the mediastinum away from the affected side is seen (see. If a film is taken with the patient supine, one may see only a nonspecific haze over the affected hemithorax, as the fluid layers in the posterior area. To confirm that the fluid is free flowing, posteroanterior and lateral decubitus films with the affected side down often are obtained. Conventional wisdom holds that, if a 10-mm layer of fluid is visible, sufficient fluid is present for thoracentesis to be successful. In very large effusions, the affected side is opacified, and the decubitus film is not helpful .

o        In adults, the minimum amount of fluid required before observed in an upright x-ray film is approximately 400 mL, whereas lateral decubitus films (with the affected side down) may detect as little as 50 mL of fluid accumulation.

o        A lateral decubitus film with the affected side being upwards may facilitate the evaluation of the underlying lung for the presence of atelectasis or infiltrates.

·                    Ultrasound

o        Ultrasound is effective for visualizing an effusion and determining if fluid is free flowing or loculated. It also may be used to guide thoracentesis. Ultrasound also may help distinguish a large solid chest mass from an effusion.

o        In a recent retrospective study, Ramnath suggested a beneficial role for early use of ultrasound to identify effusions with evidence of organization. Patients with complicated effusions had significantly shorter hospital stays when treated aggressively with decortication rather than tube thoracostomy. The same study showed that children who had no evidence of organization in their chest ultrasound studies and who were treated with intravenous antibiotics and thoracentesis or chest tube had a similar hospitalization course to those who had similar ultrasound findings but were treated aggressively with thoracoscopy or decortication.

·                    CT scan

o        CT scan can show an effusion.

o        In adults, the presence of parietal pleural thickening on contrast-enhanced CT scan is a specific but nonsensitive indicator of an exudate.

o        Unless an underlying mass is a concern, a CT scan rarely is needed to diagnose a pleural effusion.

o        Chest CT scan is helpful in identifying underlying lung parenchymal conditions .

o        Chest CT scan also is likely to be valuable for management decisions in complicated effusions and in patients not responding to therapy.

Other Tests:

·                    A purified protein derivative (PPD) test should be performed, particularly if risk factors for TB are present. A recent study by Merino reported a sensitivity of 97.4% for more than 5-mm PPD skin test induration in 39 children with tuberculous pleural effusion.

Procedures:

·                    Thoracentesis

o        Thoracentesis is recommended for diagnosis of most pleural effusions of sufficient size; however, prospective studies in children are lacking.

o        Thoracentesis often is not performed if the diagnosis is thought to be certain, and the likelihood of empyema or malignancy is low. Such circumstances include small bilateral infiltrates in congestive heart failure or nephrosis or a small parapneumonic effusion in an afebrile child recovering from pneumonia.

o        Thoracentesis should be performed when pleural effusion compromises respiratory status, with empyema or malignancy, or iewborns.

·                    Pleural biopsy may be needed in cases of unexplained inflammatory effusion, suspected tuberculosis, or malignancy.

Histologic Findings: N/A

Medical Care: Treatment of the underlying disorder generally is all that is required for effusions caused by renal, cardiac, or rheumatologic diseases.

·                    Parapneumonic effusion usually progresses through 3 stages (exudative, fibrinopurulent, organizational). The exudative stage is associated with capillary leak during the first 3 days, the fibrinopurulent stage is associated with bacterial invasion of the pleura from 3-7 days, and the organizational stage is characterized by fibroblast growth occurring from 2-3 weeks if the effusion is not treated properly.

·                    Parapneumonic effusion and empyema are treated initially with empiric antibiotics based on the patient’s age and the organisms and sensitivities commonly present in the community. As stated above, the most common cause is S pneumoniae.

o        Antibiotics can be changed if a positive culture is obtained.

o        In a hospitalized patient with complicated parapneumonic effusion, antibiotics are administered intravenously while a thoracostomy tube is present until the patient is afebrile and clearly improving clinically. Oral antibiotics frequently are continued for weeks following these procedures.

Surgical Care: Prospective studies in pediatric parapneumonic effusion and empyema are lacking; much of practice is based on studies in adults and retrospective analysis of series of children. Technologic and pharmacologic advances have provided options and changes in approach. In the early exudative stage, thoracentesis and antibiotics may be effective.

·                    Chest tube placement is necessary to drain fluid causing respiratory distress.

o        Some clinicians believe that unorganized parapneumonic effusion or empyema can be treated with antibiotics alone, without the need for chest tube placement.

o        In the late 1960s, Walter et al reviewed their experience of treating 38 children with pleural effusion and 60 with empyema over a period of 15 years. All the patients who had nonempyemic effusions did not require chest tube drainage, and 13 of the 60 patients with empyema needed thoracentesis only, without placement of a chest tube.

o        Murphy et al described 9 children with empyema secondary to S pneumoniae, and 3 of these patients had thoracentesis but did not require chest tubes.

o        Redding et al treated 8 of 15 children with empyema without chest tube drainage. The 7 patients who had chest tube drainage had longer hospital stays and longer durations of parental antibiotics therapy than those who did not have the chest tube.

o        Ginsburg et al reported that 49 of 65 children with H influenza pneumonia had pleural effusion; only 20 of these 49 children required chest tube placement, one required open chest drainage, and the rest did not need chest tube drainage.

o        Recently, Chan et al reviewed their experience of treating 47 children with empyema over 26 years in a Canadian institution. The empyema was divided into acute, fibropurulent, and chronic effusions. Of the patients who had acute empyema, 3 out of 7 did well without chest tube placement. Most of the 39 children with fibropurulent effusions were treated successfully with chest tube, and only 7 of them required decortication for persistent loculation.

o        Criteria for chest tube placement based on pleural fluid characteristics derive mainly from experience in adults and include the following:

§     Frank pus on thoracentesis

§     Organisms seen on Gram stain

§     Pleural fluid pH less than 7 or glucose less than 40

o        As the effusion becomes fibrinopurulent and subsequently organizes, chest tubes often become ineffective because fibrinous strands and loculations divide the pleural space into compartments. Chest ultrasound and CT scan may demonstrate this process. To avoid or treat this condition, fibrinolytic agents have been instilled via the thoracostomy tube. Although streptokinase and urokinase have been used safely in children, concerns about these agents (allergy, in the case of streptokinase, and the possibility of transmission of viral agents from the humaeonatal kidney cells used to produce urokinase) have dampened the enthusiasm for the use of these drugs. Recombinant tissue plasminogen activator may prove useful, but studies are lacking.

·                    Open thoracotomy with lysis of adhesions generally has been reserved for cases in which fevers and illness have failed to respond to antibiotics and chest tube drainage, or if drainage of loculated fluid by thoracostomy tubes has not been successful.

·                    The advent of video-assisted thoracoscopic surgery (VATS), which allows visualization of the pleural space but is less invasive than open thoracotomy, has made early surgical intervention more attractive. A recent retrospective analysis of early VATS in children compared with the previous practice of thoracentesis, fibrinolytic therapy, and treatment failures (either thoracotomy or VATS) showed that early VATS decreased the number of procedures and hospital days when compared to earlier approaches.

·                    Pleural biopsy may be needed in cases of unexplained inflammatory effusion, suspected tuberculosis, or malignancy.

Consultations:

·                    Pediatric surgeon

·                    Pediatric pulmonologist

·                    Pediatric infectious disease specialist

Diet: Dietary consultation should be obtained early in chylothorax and in complicated pleural effusion and empyema in which the course may be prolonged.

·                    Chylothorax may respond to a diet with fat supplied as medium chain triglycerides (MCT) with a resolution of the chylous effusion at the end of 2 weeks. MCT oil is absorbed directly into the portal circulation and does not contribute to chylomicron formation. Its use may decrease lymph flow as much as 10-fold.

·                    If chylothorax persists, a trial of intravenous alimentation for a longer period of 4-5 weeks may be considered.

·                    Children with complicated pleural effusion and empyema may have significant anorexia and increased needs. High-calorie high-protein foods that appeal to the child should be provided early, and nasogastric feeds should be considered early, particularly in younger children.

Activity:

·                    Pain and chest tube placement may limit motility.

·                    Analgesia can facilitate cough and airway clearance, especially in the presence of an underlying pneumonic process.

Antibiotics are administered for parapneumonic effusions caused by aerobic and anaerobic organisms. Specific agents should be used based on the patient’s age and types of organisms and sensitivities commonly seen in the community; therefore, the list of antibiotics below only should be used as a guide. More than 1 agent may be used for synergy and polymicrobial infections. The antibiotics may be changed if the organisms and their sensitivities are identified. Initially, administer antibiotics intravenously while a thoracostomy tube is present and until some arbitrary time after the child is afebrile and improving clinically; then, the patient can be switched to oral medications for 1-3 weeks.

Empyema usually requires a longer duration of antimicrobial therapy.

Antituberculous drugs for TB-associated effusion should be administered for 6-9 months. Chemotherapeutic agents are used for malignancy. Steroids are indicated for connective tissue disorders and may be useful for tuberculous effusion.

Drug Category: Antibiotics — Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

 

 

 

 

 

 

Drug Category: Antituberculous drugs — For treatment of drug-susceptible TB infection. Recent recommendations include 6-9 months duration of therapy. The 6-month regimen includes 2 months of isoniazid (INH), rifampin, and pyrazinamide once per day, followed by 4 months of INH and rifampin daily or 2 months of INH, rifampin, and pyrazinamide daily, followed with 4 months of INH and rifampin twice a week under directly observed therapy (DOT). For drug resistant TB, initial treatment should include 4 drugs until susceptibility is determined. Therapy should last 12-18 months.

 

 

 

Drug Category: Corticosteroids — May increase absorption of pleural effusion.

Further Inpatient Care:

·                    Follow-up may be required in complicated cases for evidence or progression of pleural fibrosis

Further Outpatient Care:

·                    Some experts recommend serial chest radiographs to ensure clearing. Some perform a CT scan after the plain x-ray films clear.

Complications:

·                    Complications are uncommon in properly treated parapneumonic effusions.

·                    Possible complications include respiratory failure caused by massive fluid accumulation, septicemia, bronchopleural fistula, pneumothorax, or pleural thickening.

Prognosis:

·                    Most viral and mycoplasmal effusions resolve spontaneously.

·                    Empyema has a more complicated course if not treated and drained early, especially in children younger than 2 years. Thirty years ago, the mortality rate from empyema was 100%. Currently, the mortality rate from empyema is 6-12% in infants younger than 1 year.

·                    Most tuberculous effusions resolve completely with the use of proper antituberculous agents.

·                    Malignant effusion carries a much worse prognosis depending on the underlying tumor.

·                    Most patients recover well after parapneumonic effusion or empyema if appropriately treated. Follow-up studies of children who have recovered from empyema are sparse but encouraging. Most children had complete clinical recovery with no residual radiologic or lung function changes.

·                    McLaughlin et al evaluated the outcome of 16 children with pleural effusion over an 11-year period. Fourteen of these patients had chest-tube drainage, and limited thoracotomy was performed in 5 of the 16 patients. Thirteen children were monitored for a mean duration of 66 months after discharge from the hospital (range, 5-150 mo), and the other 3 children had chest radiographs at 1, 2, and 3 months after discharge. Eight children had normal chest x-ray findings at follow-up visits, 7 had slight pleural thickening, and one had moderate pleural thickening 7 months after discharge from the hospital. No correlation between lung volumes and chest radiograph changes were observed in 5 patients who had total lung capacity less than 89% predicted value.

·                    Murphy et al reported the results of follow-up chest radiographs taken 1 month to 7 years after discharge in 8 of the 9 children diagnosed with pneumococcal empyema. Radiologic improvement usually was not apparent for 1-2 weeks after initiation of treatment. However, 6 patients had normal follow-up x-ray films, and only 2 had mild pleural thickening. Pulmonary function testing performed several months to years after the resolution of infectious effusions showed that most patients have either normal or low-normal lung volumes and airway flows.

·                    According to a study by McLaughlin et al, children discharged from Children’s Hospital of Boston in 1969-1980 with a diagnosis of empyema were seen 5-140 months after discharge. Thirteen of 16 patients were evaluated and had, at most, mild restriction on pulmonary function testing and pleural thickening on chest radiograph. One child who had thoracotomy with rib resection had a second case of pneumonia and scoliosis less than 10 degrees.

·                    In Redding et al’s report of 15 children who had pulmonary function testing 2 years after developing empyema, no evidence of restriction was found, and only 7 of the children had mild obstruction. Most importantly, none reported reduced exercise tolerance. They showed no difference between children treated with and without surgery.

·                    Murphy et al reported the results of follow-up pulmonary function tests performed in 5 of the 9 patients who had pneumococcal empyema. Four of the 5 patients had some increase in their residual volume with no other evidence of obstructive lung disease or impaired long-term performance.

 

1.5. Empyema.

Empyema refers to the accumulation of infected fluid in the pleural space. In children, this is usually the result of severe pneumonia (97). However, empyema may also result from infection of the retropharyngeal, mediastinal, or paravertebral spaces, thoracic trauma, or an immunocompromised state (97,98). In 1962. the American Thoracic Society described what are now the three classic stages of empyema (99). The first stage, or  the exudative stage, is characterized by an accumulation of thin pleural fluid with few cells. The pleura and lung are mobile, and the fluid is amenable to drainage by thoracentesis. This stage may last only 24 to 72 hours. The second stage is the fibrinopurulent stage. Consolidation of infected pleural fluid results in an accumulation of fibrinous material, formation of loculations. and loss of lung mobility. This stage lasts 7 to 10 days. The third stage is the organizing stage. A pleural peel forms secondary to fibroblast proliferation and resorption of fibrin. The lung becomes entrapped, and capillary proliferation extends from the fibrinous peel into the visceral pleura itself. This usually occurs 2 to 4 weeks after the initial development of the empyema.

The causes of ET in children include (see Figure 46.1):

1. Pneumonia (usually caused by Staphylococcus aureus, S. pneumoniae, group A streptococci or Haemophilus influenza). There may be anaerobic infections, infections secondary to aspiration, or infections with Mycoplasma pneumoniae and viruses.

2. Mycobacterial infections (especially in immunosuppressed patients) and fungal infections.

3. Ruptured lung abscess (usually caused by S. aureus).

4. Trauma (e.g., penetrating trauma to the lungs, fracture of ribs, or perforated oesophagus).

5. Amoebiasis (from amoebic abscess).

6. Contiguous infections of the oesophagus, mediastinum, or subdiaphragmatic region.

7. Spread of infections of the retropharyngeal, retroperitoneal, paravertebral, or subphrenic spaces.

8. Malignancy, including Kaposi sarcoma in children with human immunodeficiency virus (HIV) infection.

Host factors that contribute to alterations in pleural permeability, such as noninfectious inflammatory diseases, infection, trauma, or malignancy, may allow accumulation of a thin serous fluid (pleural effusion or parapneumonic effusion) in the pleural space, which may become secondarily infected. As the body attempts to fight off infection, the cavity starts filling up with pleural fluid, pus, and dead pleura cells.

The development of parapneumonic pleural effusions is gradual, and progression to empyema occurs in three phases:

1. Exudative stage, or acute phase: This stage is characterised by increased permeability and a small serous fluid collection. At this stage, the pleural cavity fills with an abnormal amount of pleural fluid containing some pus from the infectious condition, contains mostly neutrophils, and is often sterile.

2. Fibrinopurulent stage: This second phase is marked by a thickening of the fluid, the accumulation of fibrin—a fibrous, protein-based coagulant—in the cavity, and the formation of fibrin membrane deposition, which forms partitions or loculations within the pleural space.

3. Organising stage, or chronic phase: If left untreated, the chronic phase begins, during which a pleural peel is created by the resorption of fluid, forming a thick fibrous material that can entrap the lung parenchyma.

Left untreated, the ET burrows through the parietal pleura, usually into the chest wall, to form a subcutaneous abscess that eventually may rupture through the skin and discharge spontaneously, forming an empyema necessitans18 (Figure 46.2).

Before the widespread use of antibiotics, empyema was caused principally by infections of Streptococcus pneumoniae, Streptococcus pyogenes. Staphylococcus aureus, and Haemophilus influenzae. The introduction of sulfapyridine and penicillin decreased the overall incidence of empyema, but S. aureus emerged as the primary offending pathogen. Since the mid-1980s, effective therapy for S. aureus has allowed the emergence of a variety of bacterial organisms, including anaerobic bacteria, as common causes of empyema in children (100):

Contemporary series report a preponderance of H. influenza and Streptococcal species in children (101.102.103.104). However, some series still report S. aureus as the most common pathogen (100,105.106.107,108). Interestingly, a number of these latter series are from developing countries (105.106.107.108). Children with empyema generally present with fever, cough, respiratory insufficiency, and chest pain (100,105,109). Physical signs may include dullness on chest percussion, tactile and vocal fremitus, decreased breath sounds, rales, and a pleural friction rub (100,109). A chest radiograph reveals a thickened pleura in addition to the primary pneumonic process and pleural fluid. Transthoracic ultrasound or chest CT scan are beneficial in assessing the degree of pleural thickening, fluid loculation, and lung consolidation (100.102,110). The diagnosis of empyema is confirmed by thoracentesis. The fluid is characteristically turbid and may be thick during the later stages of the infection. Laboratory analysis reveals a specific gravity greater than 1.016. protein greater than 3 g per dL, lactate dehydrogenase (LDH) greater than 200 U per L. pleural fluid protein/serum protein ratio greater than 0.5, pleural fluid LDH/serum LDH ratio greater than 0.6. and white blood cell count higher than 15.000 per mm³. Fibrin clots may also be present (109). Once the diagnosis of empyema is made, appropriate antibiotics should be administered based on Gram’s stain and culture of the pleural fluid or sputum. Frequently, however, antibiotics have already been started prior to drainage and the fluid is unrevealing. Complete drainage of the empyema should be accomplished either by thoracentesis or tube thoracostomy (111). Some children present with such advanced disease that the pleural involvement has passed the exudative stage. In these patients, thoracentesis or even tube drainage may not be adequate to obtain a clinical response. In general, the longer the prehospital or pretreatment illness has persisted, the more likely further interventions will be needed (112.113).

Investigations

Imaging

• Plain chest radiography (upright views) should show obliteration of the diaphragmatic margins (costophrenic angles) with pleural fluid collections (Figure 46.3). Because up to 400 ml may be required before these costophrenic angles are obscured in older children and adolescents, further diagnostic imaging may be needed.

• The erect chest x-ray may show an air fluid level (Figure 46.4) if there is lung collapse, an associated pneumothorax, and/or infection with anaerobic bacteria.

• Indistinct diaphragmatic contours merit lateral decubitus views of the chest. This may show layering of fluid. The absence of free layering on the decubitus films does not exclude the possibility of a loculated pleural effusion.

Figure 46.3: Empyema with lung entrapment.

Figure 46.4: Empyema with air fluid levels.

• In moderate effusion, the radiograph may demonstrate displacement of the mediastinum to the contralateral hemithorax, as well as scoliosis.

Figure. Anteroposterior (A) and lateral (B) chest radiographs show a large right thoracic empyema. The decubitus radiograph did not show any layering of the pleural fluid.

• Free-flowing pleural effusions suggest less complicated parapneumonic processes, which may not require extensive diagnostic and therapeutic interventions.

• An ultrasound scan is a sensitive test and can also be used to localise loculated effusions and to guide targeted drainage.

• C omputed tomography (CT) may identify the presence of consolidated lung or fibrinous septations. In situations of complex fluid collections, chest CT imaging is the study of choice because it can detect and define pleural fluid and image the airways, guide interventional procedures, and discriminate between pleural fluid and chest consolidation.

Figure. Ultrasonography and/or CT of the chest are helpful during the initial evaluation of children with a pleural effusion and possible empyema. A, In the ultrasound study, note the loculations identified in the pleural fluid. B, On the CT scan, a large pleural effusion (asterisk) is noted. Also there is collapse of the underlying lung parenchyma as well as septations (arrow).

• Viewing the pleural space by using a thoracoscope to examine its characteristics may also help the diagnosis in complex cases.

Other Investigations

• Thoracocentesis is the standard diagnostic test. Aspirated pus or fluid should always be cultured; in a febrile patient, blood cultures should be done also. Where the cause of the pleural effusion is not clear or if the fluid is bloodstained, cytological investigation should also be done.

• Blood culture is obtained to assist in the identification of the offending organism. In paediatric patients, where sputum production is uncommon, identifying the cause of the pulmonary symptoms early in the course of a pulmonary infection is difficult. However, with parapneumonic effusions, the patient may become bactaeremic as the organism invades the pleural space, and a blood culture may reveal the organism.

• Total serum protein.

• Total white cell blood count.

• Culture and serologic studies of the aspirated pleural fluid, which may reveal bacterial, mycobacterial, and fungal isolates.

• Cell count and differential of aspirated pleural fluid are taken. Although the pleural fluid obtained at thoracentesis is typically purulent, with an elevated white blood count (WBC) count and a predominance of leucocytes, an effusion evaluated early in the infectious process may well be more transudative, with a less cellular WBC and a differential that has fewer leucocytes predominant. Regardless of the cell count and differential, the treatment should be based on clinical course, pending the culture results. Cytokine analyses of pleural fluid have been performed in experi-mental settings and may prove to add prognostic value on the degree of inflammation present; these may be beneficial in determining treatment course in the near future.

• Where malignant effusion is suspected, cytological investigation is mandatory. Rarely, a pleural biopsy may be indicated.

• Pleural fluid latex agglutination (or counterimmunoelectrophoresis (CIE) for specific bacteria) may be helpful if the cause of the infection cannot be ascertained from the usual culture results.

A suboptimal clinical response of the patient to antibiotics and drainage determines the need for additional intervention. Most patients are free of fever and residual pleural fluid within 3 to 5 days following institution of therapy. Persistence of fever or loculation of the pleural fluid requires the surgeon to consider further intervention (101.111.112.113).

Figure . This schematic shows management of empyema depends on the stage. Simple drainage is usually possible for stage I disease. However, most patients present to the surgical service with stage II disease. Fortunately, stage III disease is not frequent today but was quite prevalent 30 years ago.

The nature and timing of this intervention has remained a subject of debate. The primary surgical objective must be to remove all the residual infected pleural fluid, to break up any loculations, and to free the lung to expand and fill the pleural space. The lung expansion allows better clearance of infection from the lung parenchyma itself. Many pediatric surgical series have discussed decortication for this objective. Properly used, the term decortication refers to the removal of a thick, fibrotic visceral peel that is restricting the underlying lung (114). In fact, the procedure actually described in most series is better termed pleural debridement because fluid and fibrinous peel from the visceral and parietal pleural surfaces are removed to extract truly infected material. This can be accomplished without the trauma and blood loss usually associated with true decortication procedures, and pleural debridement should be considered earlier in the course of the empyema. Although some more recent reports still advocate formal thoracotomy or minithoracotomy to accomplish this. (103,107,115) thoracoscopic debridement has clearly become a mainstream therapy (Fig. 60-9).

Figure . Over the past decade, most surgeons have utilized thoracoscopy for surgical management of empyema. A, Often, sponge forceps can be placed directly through the incisions to extract the inflammatory debris. B, In the postoperative photograph, three 8- to 10-mm incisions have been used for the thoracoscopic debridement. The chest tube is exteriorized through the most inferior incision. A small Penrose drain has been placed in one of the incisions because this was the site of a catheter that had been placed by the pediatric service for drainage of the empyema.

However, despite optimism that early thoracoscopic intervention may hasten recovery from empyema, no prospective studies have confirmed this. Pleural loculations in some patients can be lysed by instilling urokinase or streptokinase through existing chest tubes before resorting to surgical intervention.

Figure . This thoracoscopic view shows the inflammatory septations that can develop after the development of an empyema. These septations often result in loculations of the fluid, which makes chest tube drainage alone ineffective. Note the collapsed lung (asterisk) as a result of this inflammatory material.

In the event that a lung abscess develops, treatment may require pneumonostomy. wedge resection, or lobar resection. Radiographic findings often lag behind clinical response; therefore, they should not be used alone as indications for further intervention. With prompt and adequate treatment, the overall outcome for children with empyema is excellent. Pulmonary function after recovery is usually clinically normal, although some investigators have found mild restrictive or obstructive disease on follow-up spirometry.