Disclosure
Because of the broad nature of this subject, this article is organized into 3 major categories. In the first section, infections of the lung are discussed, with a focus on bronchiectasis, lung abscess, and pneumatocele. Next, infection of the pleural space (empyema) is presented. In the last section, mediastinitis is covered. This review focuses on the surgical management of these infections. The interested reader is referred to the following articles for particular information beyond the scope of this article: Actinomycosis
Background
Bronchiectasis, defined as irreversibly dilated and damaged bronchi associated with chronic suppuration, was first described in 1819 by Roennec. In 1892, Sir William Osler recognized the role of bronchial obstruction and inflammation in the pathophysiology of bronchiectasis. Little changed for many years until the emergence of effective antibiotics and widespread immunization. For the past several decades, the incidence of bronchiectasis has been low.
Lung abscess results from a serious suppurative infection of the pulmonary parenchyma. Its description was initially attributed to Bomnet in the 17th century. As with bronchiectasis, the development of modern antibiotics has markedly reduced the incidence of lung abscess.
Pneumatoceles are air-filled cysts that develop in the pulmonary parenchyma, usually during the resolving phase of pneumonia. The thin-walled cysts may be single, but they are most often multiple. The incidence of a pneumatocele after pneumonia is about 2%. Overdistention of air spaces distal to a bronchiolar obstruction can result in a localized air collection termed a pneumatocele.
The mechanism of pneumatocele formation is bronchiolar inflammation and edema, which usually develop during the resolving phase of a pneumonia. This condition may produce a ball-valve phenomenon that leads to overdistention of the distal portion of the lung. Pneumatoceles are seen as well-defined, thin-walled radiolucencies on the chest radiograph. The most common complication of pneumatocele formation is pneumothorax secondary to rupture through the visceral pleura. A tension pneumatocele can occur if the lesion is unusually large; the cause of large lesions is often positive pressure ventilation. Secondary infection may also occur.
Etiology
Bronchiectasis is caused by repeated damage to the distal bronchi from inflammation or infection. Although the initial event rarely results in irreversible damage, repeated subsequent insults destroy the bronchial epithelium and peribronchial tissues.
Bronchiectasis can be congenital or acquired. Congenital bronchiectasis is most commonly due to the impaired mucociliary clearance seen in children with Kartagener syndrome or alpha1-antitrypsin deficiency. Other causes include Marfan syndrome, absence of bronchial cartilage (ie, Williams-Campbell syndrome), bronchopulmonary sequestration, and asthma. The most common genetic cause of bronchiectasis is cystic fibrosis (CF). This autosomal recessive disorder affects the body's exocrine gland function and results in the production of thick inspissated mucus (ie, mucoviscidosis).
The exact pathogenesis of bronchiectasis in CF patients is unclear. Some believe it is related to impaired ciliary function resulting in reduced mucus transport. Others
suggest it is due to impaired intraluminal bacterial destruction and increased bacterial epithelial binding, especially of Pseudomonas aeruginosa. This concept is counterintuitive because patients with CF typically have neutrophil-predominant inflammation in the bronchi.
Acquired bronchiectasis is usually the result of repeated infection, though any cause of chronic airway obstruction can lead to bronchiectasis. Causative agents include the common pathogens associated with pneumonia such as Streptococcus, Haemophilus, and Staphylococcus species; Mycoplasma and Chlamydia species are less frequently seen. Viruses, Histoplasma or Aspergillus organisms, and tuberculosis have also been recovered from children with bronchiectasis.
In children, lung abscess results from an infection of the lung parenchyma that was not or could not be effectively treated with systemic antibiotics, though necrotizing pneumonia (particularly Staphylococcus bacteria) may result in lung abscess formation. Causes include inadequate clearance mechanisms and inadequate host defenses. Reduced cellular defenses are seen in children immunocompromised because of transplantation, chemotherapy, and chronic granulomatous disease. Impaired humoral defenses occur in children with agammaglobulinemia, immunoglobulin A deficiency, and complement deficiencies.
Aspiration is the leading cause of lung abscess in children, particularly in those who have neurologic impairment. Relatively infrequent etiologies are clinically significant periodontal and dental disease and prolonged antibiotic therapy. Lung abscesses are typically polymicrobial. Causative organisms include both aerobic and anaerobic organisms, but oral anaerobic flora are most common. Important aerobic or facultative organisms include Streptococcus pyogenes, Staphylococcus aureus, P aeruginosa, Escherichia coli, and Klebsiella pneumoniae. These bacteria are frequently cultured in patients with pneumonia and are responsible for considerable tissue destruction and morbidity, which explains their role in lung abscess formation. Other pathogens include enteric gram-negative bacilli; Aspergillus, Nocardia, or Actinomyces species; and Mycobacterium tuberculosis.
No specific genetic factor is known to predispose individuals to pneumatocele formation. However, pneumatoceles are associated with hyper-IgE syndrome (Buckley-Job syndrome), which predisposes the patient to staphylococcal pneumonia, the organism most commonly responsible for the formation of pneumatoceles. Other organisms that may lead to this condition include Streptococcus pneumoniae, Haemophilus influenzae, E coli, S pyogenes, Serratia marcescens, K pneumoniae, adenovirus, M tuberculosis, and Pneumocystis jiroveci. Trauma and hydrocarbon ingestion may also play a role.
Pathophysiology
The pathogenesis of bronchiectasis begins with a functional obstruction of the bronchial lumen. This obstruction causes inflammation and infection, leading to destruction of the bronchial epithelial lining, damage to the peribronchial connective tissue, and eventual dilatation and dysfunction of the airway. At first, the ciliary epithelium is destroyed and replaced by cuboidal squamous tissue. Cylindrical bronchiectasis occurs when inflammation and infection destroy the peribronchial elastic tissue, causing regular bronchial dilation. When the damage extends to the cartilaginous and muscular layers, aneurysmal dilation occurs and leads to saccular bronchiectasis. This process occurs predominantly in the distal bronchi and periphery, where cartilaginous support is decreased.
Lung abscesses occur when a bronchial or parenchymal infection is untreated or when it progresses, causing local tissue necrosis and cavitation. As previously stated, aspiration in neurologically impaired children causes local bronchial necrosis, which frequently affects the posterior segment of the right upper lobe or the superior segments of the lower or middle lobe. In these patients, immobility, impaired pulmonary toilet, and weakness all contribute to abscess formation.
Pneumatoceles form when inflammatory changes or peribronchial abscess formation causes proximal narrowing of the bronchus. This narrowing then leads to distal dilatation of the bronchi and alveoli due to a ball-valve effect. Another proposed mechanism is that the inflammation ruptures the bronchiolar walls and causes air corridors that allow air to dissect down to the visceral pleura. Blunt thoracic trauma is thought to cause pneumatoceles by external compression of the lung followed by rapid decompression from increased negative intrathoracic pressure. This process leads to what is known as a bursting lesion, the precursor of a traumatic pneumatocele.
Clinical presentation
Children with bronchiectasis usually have chronic cough and foul-smelling sputum that contains mucoid plugs. They are often toddlers with fever, wheezing, and chest pain. Many have hemoptysis, which can range from blood-tinged sputum to life-threatening hemorrhage.
Children with lung abscess may initially present like those with bronchiectasis, with a chronic productive cough, chest pain, and hemoptysis. As with bronchiectasis, purulent sputum is common in older children, whereas younger children are most likely to swallow sputum than to expectorate. Children with lung abscess also commonly develop systemic signs and symptoms, including fever, night sweats, chills, weight loss, and malaise. If the abscess cavity communicates with the bronchial tree, collapse of the abscess, with eventual resolution during systemic antibiotic therapy, is possible. If no communication develops, a capsule surrounding the necrotic lung becomes thick and fibrotic. This capsule may eventually rupture, causing pyopneumothorax and septic shock.
Because infants and young children account for most cases of staphylococcal pneumonia, pneumatoceles are most frequently found in this age group. The typical presentation of a patient with a pneumatocele includes fever, cough, and respiratory distress.
Evaluation
Children with bronchiectasis and lung abscess are likely to have decreased breath sounds, tachypnea, and wheezing. Findings on plain chest radiography are often not diagnostic of bronchiectasis, but they may reveal increased bronchial markings and possibly atelectasis adjacent to areas of overinflation. Bronchography was historically used to confirm bronchiectasis.
Today, high-resolution CT scanning is the modality of choice for diagnosing these infections. CT scanning allows for detailed delineation of the lung parenchyma and small airways. It shows dilatation of the small airways accompanied by adjacent atelectasis and mucus-filled cysts containing air-fluid levels. Bronchial walls may also be thickened.
Bronchoscopy is useful for obtaining cultures to guide medical treatment and to determine if extensive compression, a foreign body, a tumor, or abnormal airway anatomy is present.
The initial radiographic appearance of lung abscess is similar to that of pneumonia. Frontal and lateral plain chest radiography shows consolidation, usually in a dependent area. This finding usually involves the superior segment of the right lower lobe or the posterior segment of the right upper lobe. As the lung tissue becomes necrotic, partial clearing may be observed on plain radiography. As the lung abscess develops, a cavity with an air-fluid level can be seen. This must be distinguished from the air-fluid levels found in empyema (see Infections of the Pleura) and pneumatocele, a noninfectious collection of air surrounded by lung parenchyma that does not contain mucus or pus. In most cases, plain radiography in conjunction with the history and physical findings are sufficient to establish the diagnosis. When uncertainty exists, chest CT or thoracic ultrasonography may be helpful in delineating details not well visualized on plain radiography.
In children with pneumonia and a developing pneumatocele, breath sounds may be diminished focally or bilaterally. Inspiratory crackles and expiratory wheezes are common. Over time, after the pneumonia resolves, the patient may have diminished breath sounds over the area of the pneumatocele. On average, pneumatoceles are seen on chest radiography about 5-7 days after a patient is admitted for pneumonia. Chest CT is occasionally performed to improve characterization of the lesion.
Medical treatment
The primary treatment for bronchiectasis is medical and consists of a prolonged course of appropriate antibiotics, vigorous chest physiotherapy, and postural drainage. Children with CF and bronchiectasis require aggressive medical treatment, including careful nutritional monitoring, home physiotherapy, and, frequently, the use of inhaled aminoglycoside antibiotics, N-acetylcysteine, or dornase alpha (occasionally in combination).
Effective treatment for children with lung abscess begins with obtaining appropriate cultures so that effective antibiotic therapy can be initiated. Bronchoscopy is useful when a child cannot produce an adequate sputum sample and to ensure that no foreign body is present.
In the absence of cultured organisms, empiric intravenous (IV) therapy consisting of clindamycin or ampicillin-sulbactam is appropriate. If the child is toxic, empiric vancomycin and/or broadened gram-negative coverage may be required. When risk factors such as CF or immunocompromise are present, the addition of an aminoglycoside is warranted. As with any abscess, adequate drainage is essential to cure. Bronchoscopy is often used to open a bronchus occluded with mucus or sputum, allowing chest physiotherapy to provide the necessary drainage.
In general, medical care of a pneumatocele is aimed at treating the underlying pneumonia. Treatment consists of antibiotics directed against the most common pathogens: S aureus and S pneumoniae. Positive-pressure ventilation should be avoided if possible because it can increase the size of a pneumatocele, a tension pneumatocele, or a tension pneumothorax. Selective bronchus intubation to aerate the good lung may be necessary to prevent these complications.
Surgical treatment
Surgical intervention for bronchiectasis is reserved for children with localized disease and indolent, recurring infections; hemoptysis; persistent chest pain; and other indicators suggesting the failure of medical treatment. For children with CF, Schuster and Schwartz (1979) suggest the following guidelines for surgical intervention: (1) a localized segment with disease advanced beyond that of the rest of the lung; (2) a bronchiectatic segment that is clearly irreversible; and (3) a patient who can tolerate thoracotomy and partial lung resection. The guiding principle for bronchiectasis surgery is to preserve as much of the lung parenchyma as possible.
Preoperative evaluation commonly includes pulmonary function testing, nutritional assessment, and ventilation-perfusion scanning to determine if the affected area is contributing to gas exchange. This information allows the surgeon to remove the affected area by performing segmentectomy or lobectomy. Aggressive preoperative nutrition and respiratory therapy combined with early postoperative extubation and careful pain control all contribute to successful outcomes.
In children with lung abscess, surgery is reserved for those in whom medical treatment fails. As previously stated, adequate drainage of the abscess cavity is an important factor in successful treatment. If bronchoscopy is performed, care must be taken to protect the unaffected lung and segments from spillover aspiration and contamination. In abscesses that are relatively peripheral and well circumscribed, percutaneous needle aspiration and catheter placement under CT or ultrasonographic guidance is appropriate. Surgical resection is indicated in children who do not respond to extensive antibiotic therapy and drainage, those with severe hemoptysis, and those with chronic abscess lasting longer than 3 months. Other indications include fungal infection, multiple abscesses, and centrally located abscess cavities. Every effort is made to limit tissue loss by performing wedge resection, segmentectomy, and, occasionally, lobectomy.
Complications after surgical resection for both bronchiectasis and lung abscess are infrequent and include atelectasis, bronchopleural fistula, and wound infection. Follow-up care after hospital discharge consists of 4-6 weeks of antibiotic therapy, if the process is resolving, as shown on chest radiographs. Outcomes are generally good, and recurrences are rare.
Pneumatoceles are essentially a nonsurgical disease. Most spontaneously resolve in weeks to months. In rare cases, a life-threatening lesion, such as a tension pneumatocele or pneumothorax, prompts emergency percutaneous drainage. A secondarily infected pneumatocele occasionally requires drainage. These procedures are associated with the complication of bronchopleural fistula. Rarely is aggressive surgical resection of the affected lobe indicated.
Background
Empyema is an infected effusion in the pleural cavity. The name comes from the Greek word empyein, which means pus producing. As early as 300 BC, Aristotle described draining pus from a chest incision with a metal tube. In 1876, Hewitt introduced the idea of closed drainage by using rubber tubing that emptied into a column of water. Over the next 100 years, surgical therapies, such as thoracoplasty and open decortication, were performed. Since the 1970s, thoracoscopy has been performed in children, and, at present, thoracoscopic drainage with decortication is widely considered the standard of care in the management of empyema.
Although pleural effusions most frequently occur in children with pneumonia, empyema is a rare complication, occurring about 5% of the time. Boys and girls are affected with equal frequency, with a median age of 7 years. The disease most often occurs in the winter and spring.
Etiology
The most common cause of empyema is pneumonia with an exudative parapneumonic effusion, which may or may not be overtly infected. Other causes include esophageal perforation, trauma, operations involving the pleural space, and septicemia. As in pneumonia, aerobic organisms play a greater role than anaerobes in the pathogenesis of empyema. Gram-positive organisms are about twice as common as gram-negative organisms, and S aureus, S pneumoniae, and S pyogenes predominate. The most common gram-negative organisms are Klebsiella, Pseudomonas, and Haemophilus species, whereas the most common anaerobes are Bacteroides and Peptostreptococcus. Of interest, rare children with pneumonia in whom both aerobic and anaerobic species are isolated are more likely to develop an empyema than are those with an infection due to a single organism.
Pathophysiology
The potential space between the parietal and visceral pleura normally contains a small amount of fluid that helps facilitate lung movement. Many conditions lead increase the volume of pleural fluid because of altered fluid dynamics. Examples include congestive heart failure (increased capillary hydrostatic pressure), nephrotic syndrome (decreased plasma oncotic pressure), thoracentesis (decreased pleural cavity hydrostatic pressure), and malignancy (decreased lymphatic drainage). The pleural effusion can predispose a patient to empyema formation because it serves as a substrate for organisms and impairs leukocyte function. The fluid may become infected from an adjacent pneumonia, pleural surgery, or trauma, or infection may spread hematogenously from a distant site.
Three stages in the development of empyema are described. During the exudative phase, pleural fluid increases in volume. This fluid is characterized by a low WBC count and lactate dehydrogenase (LDH) level. The second stage is the fibrinopurulent phase in which fibrin, bacteria, leukocytes, and cellular debris accumulate. This is the stage in which loculation of fluid may occur. The fluid is more acidotic than before, with lowered levels of glucose and an increased level of LDH. The organizing stage follows and is characterized by fibroblast proliferation. A pleural peel forms and often leads to lung entrapment. This explains the high incidence of restrictive lung patterns in children who have had empyema. This pattern of lung function substantially improves over time with appropriate therapy.
Clinical presentation
Patients typically have a complicated pneumonia with fever, productive cough, and occasionally, chest pain. Patients with anaerobic infections tend to have a course more indolent than that of patients with aerobic infections. Weight loss is also most commonly seen with anaerobic infections. On physical examination, the typical patient is febrile, tachycardic, and tachypneic, with pulse-oximetry readings in the high 80s or low 90s. They may appear to be in respiratory distress, with nasal flaring and accessory muscle use. The affected side has decreased chest wall motion, diminished breath sounds, and dullness to percussion. Splinting to the involved side and associated curvature of the spine is often observed.
The diagnosis of empyema must be entertained early in such a patient. The index of suspicion for pleural effusion should increase if fever persists 48 hours after antibiotics are started.
Evaluation
Patients with empyema typically have leukocytosis with a left shift. Metabolic acidosis may also be present. In general, markers of inflammation are markedly elevated. Imaging should begin with plain radiography of the chest (upright if possible). This may show blunting of the costophrenic angle or absence of the diaphragm in its entirety, suggesting a large amount of fluid in the chest. This may also be associated with a pulmonary infiltrate. If suggestive of an effusion, decubitus radiography with the affected side down should be performed next to help quantitate the amount of fluid and determine its mobility. Ultrasonography of the chest can help in distinguishing an infiltrate from a loculated fluid collection, which appears as echogenic stripes amid the fluid.
Some believe that ultrasonography is a better modality for evaluating loculations than CT scanning, but both are excellent. Unlike CT scanning, ultrasonography requires neither IV administration of contrast material nor radiation. CT scanning, on the contrary, is not operator dependent, as is ultrasonography, and CT may be especially important if airway obstruction or a foreign body is suspected. It is also useful for distinguishing between intrapleural and intraparenchymal lesions. This distinction is important because each requires a different treatment strategy.
Thoracentesis is commonly recommended as part of the evaluation of a pleural effusion. When thoracentesis is performed, LDH levels exceeding 7500 mg/dL are associated with a need for surgical intervention. However, thoracentesis is unnecessary when a complex effusion is evident. Rather, the authors recommend that patients with loculated effusions be brought to the operating room for video-assisted thoracic surgery (VATS) (when available) with removal of the fluid and decortication if needed. If loculations are not found intraoperatively, a chest tube is placed. In institutions and/or circumstances in which VATS is not readily available or immediately appropriate, immediate chest-tube drainage is preferred to thoracentesis, followed by chest-tube insertion at a later time.
Medical treatment
Broad-spectrum antibiotic therapy should be started empirically and then refined when either sputum or pleural-fluid cultures are obtained. In addition, inhaled beta-agonists should be administered as needed. Chest percussion therapy and postural drainage also play important roles. Intrapleural thrombolytic therapy with streptokinase, urokinase, or alteplase has been successful in draining complex effusions in about 70-90% of patients. Similar to VATS, this therapy requires the placement of a chest tube. This treatment can be painful and often requires several applications. Therefore, the authors prefer to consider medical management only in patients for whom surgery or a general anesthetic is contraindicated.
Surgical treatment
The mainstay of surgical therapy for empyema is drainage of intrapleural pus and decortication by means of a VATS procedure. The procedure is indicated in patients in whom an empyema is clinically diagnosed and in whom CT scanning or ultrasonography show a loculated fluid collection.
The boundaries of the pleural space are the visceral pleura, which envelopes the lungs, and the parietal pleura, which is the inner lining of the thoracic cavity. When performing a VATS procedure, one must be aware of the surrounding structures to avoid injuring them. In the superior aspect, the subclavian vessels lie just deep to the pleura. Medially located are the mediastinal structures, including (from anterior to posterior) the thymus and trachea, heart, phrenic nerve, aorta (on right), vena cava (on left), and the esophagus. Situated posteriorly and laterally are the ribs with their intercostal vessels and nerves. Also situated posteriorly is the sympathetic chain, and azygous vein is to the left. Inferiorly lies the diaphragm.
No absolute contraindications are specific to VATS decortication. VATS can be performed in patients with previous thoracotomies or extensive intrathoracic adhesions; however, treatment of these patients should be reserved for surgeons with advanced thoracoscopic skills.
Over the last few decades, the care of children with empyemas has been controversial. However, most agree, that patients with clinically significant pleural effusions require early drainage. If an empyema appears complex on CT or ultrasonography, the authors advocate drainage with a chest tube rather than starting with thoracentesis. Because appropriate sedation is required to place a chest tube in children, the authors prefer to do this in the operating room, starting with VATS. This step adds little time to the procedure and is an outstanding diagnostic tool. If an empyema is found, the adhesions are lysed, the collection is drained, and decortication is performed. Thoracotomy is rarely indicated. This management plan is supported in the literature and decreases the duration of antibiotic therapy, the duration of chest-tube placement, the number of invasive interventions per patient, and the total length of hospitalization.
The process of obtaining informed consent should always include a discussion about the possibility of thoracotomy. Blood should be sent for typing and crossmatching. The patient is intubated, and a bronchial blocker is placed on the surgical side. As an alternative, the endotracheal tube is positioned in the mainstem bronchus of the contralateral lung. The patient is then positioned in the lateral decubitus position with the affected side up. An axillary roll is essential, and a sandbag may be used for support. Great care should be taken to pad all pressure points. The patient's chest is prepared with 10% povidone-iodine (Betadine) and draped. This should be done widely enough that a thoracotomy can be performed if necessary.
Local anesthetic is injected subcutaneously about 2 cm inferior to the scapular apex. A 5-mm transverse incision is made, a Veress needle is placed, and a pneumothorax is achieved to 8 Torr by using carbon dioxide gas. A 5-mm trocar is then placed, and the thoracoscope is placed into the pleural space. A second 5-mm trocar is placed in similar fashion under direct thoracoscopic guidance in the anterior aspect of the chest at about the same level. A third trocar is usually unnecessary. The lung is gently compressed to achieve the best visualization and working environment. A suction-irrigator device is used to evacuate pus, and a specimen is sent for culture and sensitivity testing. The pleural space is then irrigated.
The fibrin peel is removed in piecemeal fashion from the parietal pleura. Removing peel from the visceral pleura risks injury to the lung and is unnecessary. Throughout the procedure, the scope can be moved between the trocars as necessary for adequate visualization and decortication of the entire pleural cavity. The anterior trocar is removed, and a chest tube is placed through this wound and guided posterior to the lung to the apex under direct visualization. The lateral trocar is then removed, and the lung is re-expanded with positive pressure ventilation. The fascia and skin are closed with absorbable suture. The patient is typically extubated postoperatively, and the chest tube is placed to suction with 10-20 cm H2O pressure depending on the size of the child. Chest radiography is obtained postoperatively.
IV antibiotics, chest percussion therapy, and postural drainage are the mainstays of treatment after the procedure. The chest tube can usually be placed with a water seal on the first or second postoperative day if no air leak is present. The tube is then removed if the lung remains inflated 4 hours after water-seal placement. In general, findings on chest radiography lag behind the clinical picture; therefore, radiography is not meaningful in the short term, except to exclude a pneumothorax.
When VATS decortication is performed, the major complication to avoid is lung injury. Lung injury can lead to a persistent air leak, which can substantially lengthen the patient's postoperative course. Other possible complications include injury to the thoracic duct, intercostal vessels, subclavian artery, and mediastinal structures. The best way to prevent these complications is the use of meticulous and careful operative technique. The prognosis of children undergoing VATS decortication for empyema is excellent. Most patients are ready for discharge within 7 days. |
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Background The mediastinum is defined as the space from the thoracic inlet to the diaphragm situated between the pleural sacs of the lungs. The superior mediastinum lies above a line from the lower manubrium to the fourth thoracic vertebrae and contains the thymus, trachea, upper esophagus, and aortic arch. The inferior mediastinum may be subdivided into anterior, middle, and posterior sections. The anterior mediastinum contains fat and lymphoid tissue. The middle mediastinum comprises the heart, pericardium, aorta, carina, mainstem bronchi, and lymph nodes. The posterior mediastinum includes the esophagus, descending aorta, vagus nerve, and thoracic duct. Infection of the mediastinum (ie, mediastinitis) may result from adjacent disease with direct extension, hematogenous spread, or direct introduction into the mediastinal space. The organs and tissues involved determine the manifestations and approach to treatment of these infections. In the preantibiotic era, most cases of mediastinitis resulted from extension of infections from adjacent structures, (primarily head and neck infections), though they were occasionally due to extension of pulmonary and pleural infections. Most recently, direct invasion of the mediastinum after surgical intervention has become the most common cause of mediastinitis. Mediastinitis can be divided into acute and chronic infection. Three broad categories of acute mediastinitis are described: postoperative sternotomy infection, mediastinitis secondary to perforation of the esophagus or penetrating trauma, and extension from an adjacent infection or by means of hematogenous spread. Chronic mediastinitis has been arbitrarily subdivided into granulomatous and fibrosing or sclerosing mediastinitis, though these likely represent a continuum of chronic infection. Etiology The microbiology of mediastinitis depends on whether it is acute or chronic and the source of the infection. Poststernotomy mediastinitis most frequently results from infection with S aureus and coagulase-negative staphylococci, though enteric gram-negative bacilli, P aeruginosa, Candida albicans, corynebacteria, and others have been reported. The flora implicated in infection following esophageal perforation have been rarely described but likely include polymicrobial infections with oral flora (eg, S aureus, S pyogenes, a variety of anaerobes). Organisms described in descending necrotizing mediastinitis include oral flora, S pyogenes and Peptostreptococcus, Prevotella, and Fusobacterium species. Chronic mediastinitis seems to be a granulomatous complication of infection with tuberculosis and histoplasmosis. Pathophysiology Since the advent of modern-day pediatric cardiothoracic surgery, the most common cause of mediastinitis is direct invasion of the anterior (and potentially deeper) mediastinum after sternotomy. This mediastinitis occurs in 0.15-5% of pediatric sternotomy procedures and is associated with an 8% mortality rate. The next most frequent cause of mediastinitis is perforation of the esophagus or penetrating trauma. Esophageal perforation may occur spontaneously (typically near the gastroesophageal junction secondary to high air pressure or blunt trauma), after emesis (Boerhaave perforation), secondary to the acute penetration or subacute erosion of an esophageal foreign body, during instrumentation (typically at the narrow proximal end), or after a surgical procedure. Finally, the least common antecedent to mediastinitis is an adjacent or distant infection that spreads directly or metastasizes to the mediastinum hematogenously. Descending necrotizing mediastinitis is a serious complication of head and neck infection. In the preantibiotic era, it was much more common than it is now, and it could be secondary to peritonsillar abscess, Ludwig angina, mastoiditis, retropharyngeal abscess, epiglottitis, sinusitis, parotitis, and lymphadenitis. At present, this dreaded infection most often results from spread from dental or pharyngeal infections. Such extension may follow anatomic pathways, such as the visceral division of the deep cervical fascia enveloping the esophagus, trachea, larynx, and thyroid or by means of the carotid sheath. Other foci of contiguous spread include the lungs, pleura, pulmonary lymph nodes, pericardium, tracheostomy sites, subphrenic structures, and vertebral osteomyelitis. Clinical presentation Symptoms of acute mediastinitis generally include fever, substernal chest pain, and systemic manifestations of severe infection such as hypotension. Poststernotomy infection often manifests with local erythema, tenderness, and drainage. Dehiscence and an unstable sternum may also be present. Other symptoms include neck pain, dysphagia, and symptoms consistent with pleural effusion (which is frequently present). Infants may be fussy or have spasmodic or irregular respirations. Most patients with chronic mediastinitis have no symptoms for extended periods then develop symptoms due to compression of mediastinal structures, which cause them to seek medical attention. Some may also have low-grade fever, weight loss, or symptoms suggestive of anemia. Evaluation Diagnostic studies often demonstrate leukocytosis with a left shift and elevated levels of inflammatory markers (eg, erythrocyte sedimentation rate, C-reactive protein concentration). Blood cultures and local cultures should be obtained and may help direct antimicrobial therapy. Chest radiography may show a widened mediastinum, mediastinal emphysema, pneumothorax, pneumo/hemothorax, foreign body, and/or pleural effusions. CT scanning is more sensitive than radiography and improves the anatomic detail. If CT scanning is not possible, MRI may be useful. If esophageal perforation is suspected, barium swallow study is indicated. Analysis of the pleural fluid may reveal elevated amylase levels after the first day or two, in addition to findings typical of empyema. Pericardiocentesis may provide material for culture in cases arising from or involving the pericardium. Tissue biopsy may be required as well. Esophagoscopy should be reserved for removal of esophageal foreign bodies and has a minimal role in the diagnosis of mediastinitis. In patients with suspected chronic mediastinitis, the workup consists of a purified protein derivative of tuberculin (PPD) skin test, chest radiography, urine testing for Histoplasma antigen, and Histoplasma serologic testing. Tissue biopsy is occasionally necessary. Medical and surgical treatment The cornerstones of treatment of mediastinitis are surgical drainage, broad-spectrum antibiotic therapy, and supportive care. Superficial median sternotomy infections with a stable sternum may be managed with local drainage and appropriate antimicrobial and supportive care. When deep mediastinal structures are involved, a variety of treatment options are possible after debridement and drainage are accomplished and antibiotics begun. These options include simple closure, closure over drains, vacuum-assisted closure, bilateral pectoralis myocutaneous flap closure, other muscle-flap closure, and open management with delayed closure, among others. Sternal osteomyelitis is generally treated with antibiotics for 4-6 weeks. A flexible approach is required to manage mediastinitis associated with esophageal perforation or penetrating trauma. In general, the perforation should be drained, and gastrostomy and feeding jejunostomy should be accomplished. Mainstays of surgical management again include debridement, drainage, and irrigation. Drainage of the pretracheal space and superior mediastinum can be accomplished with a low cervical incision. A transthoracic approach is required to manage involvement of the inferior mediastinum (caudal to the fourth thoracic vertebrae). Perforation or laceration of the distal esophagus may be managed with transthoracic debridement, drainage, irrigation, and primary closure if it is attempted in the first 12-24 hours. Delay beyond this time usually precludes primary closure, resulting in the need for debridement and closure over drainage tubes. The approach to the patient with descending necrotizing mediastinitis should include wide local mediastinal debridement, drainage, and irrigation in addition to the use of broad-spectrum antibiotics. Tracheostomy to protect the airway is generally also required. Thoracoscopy also has a role in the management of mediastinitis, but only in the hands of an advanced thoracoscopic surgeon. Its use may hasten recovery and diminish postoperative pain and morbidity. The treatment of chronic mediastinitis is relatively troublesome. Antimicrobial therapy alone is seldom successful. Excision of involved tissues is often necessary to alleviate symptoms of compression. However, surgical intervention is seldom more than palliative, especially late in the course of the disease.
Infections of the Lung, Pleura and Mediastinum: Surgical Perspective excerpt | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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