Emergency Medicine

Recognizing and Managing Thoracic Empyema

How does empyema develop and who is most at risk for it? When should a pleural effusion be considered an empyema? When is thoracentesis safe? How do treatment considerations differ in the exudative and fibropurulent stages of the condition? The author reviews what clinicians should know.

By Michael J. Bono, MD, FACEP

Thoracic empyema, the accumulation of pus in the pleural cavity, has long been recognized as a significant disease entity. Hippocrates described empyema 2400 years ago, and his technique of open drainage with rib resection was practiced until 1918, when the Empyema Commission Report questioned the procedure. Before antibiotics, empyema was a complication in 10% of patients who survived a bout of pneumonia. The antibiotic era brought about a drastic reduction in the incidence of fulminant pneumonia, and consequently the occurrence of pneumonia complicated by empyema plummeted. Penetrating thoracic trauma and complications of thoracic surgery have since emerged as the most common etiologies of empyema.

CONTIGUOUS SPREAD OF ORGANISMS

The most common cause of empyema is the direct contiguous spread of organisms from a focus of infection. As in the pre-antibiotic era, bacterial pneumonia remains the most likely source of infection. Empyema secondary to underlying bacterial pneumonia is called postpneumonic or parapneumonic empyema. Subdiaphragmatic abscess, lung abscess, esophageal perforation, vertebral osteomyelitis, and retropharyngeal abscess may all cause empyema from the direct contiguous spread of organisms.

Up to 20% of empyemas are associated with instrumentation of the pleural space, such as in thoracentesis, tube thoracostomy, or violation of the thoracic cavity during placement of a subclavian central line. In rare instances, empyema will result from lymphatic or hematogenous spread from a distant infection that does not involve the lung. This is more common in children than adults and probably represents a subclinical pneumonic process.

In 1962, the American Thoracic Society categorized parapneumonic empyema into three stages according to the natural progression of the disease. The first stage is the exudative stage, which is very similar to the formation of a parapneumonic effusion. A focus of infection near the pleura causes a small sterile pleural effusion. In this stage, the fluid is characterized by a low cell content of predominately polymorphonuclear leukocytes and normal pH and glucose levels. The lung remains fully expandable in this stage.

The fibropurulent or transitional stage is the beginning of the true infection. Bacteria invade the previously sterile pleural fluid, and there is an increase in both the number of polymorphonuclear leukocytes and the amount of pleural fluid. Fibrin is deposited on both the parietal and visceral pleura as a continuous sheet or membrane, which prevents extension of the empyema. The membrane tends to trap and fix the lung, preventing full expansion.

During this second stage there is a tendency toward loculation, making tube thoracostomy drainage difficult. Pleural pH and glucose levels fall and lactate dehydrogenase levels increase.

The third stage, called the organization or chronic stage, is characterized by the ingrowth of fibroblasts and capillaries from both the parietal and visceral pleural surfaces. This produces an inelastic membrane called the pleural peel, which severely limits lung expansion.

Before the advent of antibiotic therapy, Streptococcus pneumoniae was the most frequent cause of thoracic empyema. Today, Staphylococcus aureus has emerged as the most common causative organism in patients of all ages, particularly in children under age two. Other bacteria implicated in the etiology of empyema, besides S. pneumoniae, are Pseudomonas aeruginosa, Klebsiella pneumoniae, Escherichia coli, and anaerobic organisms.

NONSPECIFIC SIGNS AND SYMPTOMS

Signs and symptoms of empyema are nonspecific. Patients will frequently present with pleuritic chest pain, fever, chills, cough, and shortness of breath. Night sweats, weight loss, and fatigue are also common complaints. Some patients may only complain of a vague heavy sensation in the involved hemithorax. If an empyema develops during a course of antibiotic therapy for bacterial pneumonia, clinical symptoms may be absent.

Tachypnea, tachycardia, and splinting of the affected side are classic physical signs. Further physical examination may reveal limited respiratory excursions, dullness on percussion, and decreased breath sounds on the affected side. Pain on percussion as well as a friction rub over the involved chest wall may be evident. The gingiva and teeth should be examined because gingivitis is a common risk factor for empyema, and the absence of teeth practically excludes the diagnosis of anaerobic pneumonia. Organisms implicated in anaerobic pneumonia are Porphyromonas gingivalis, Prevotella melaninogenica, Fusobacterium nucleatum, Actinomyces species, spirochetes, and anaerobic streptococci.

Aspiration is another risk factor for thoracic empyema. It is estimated that 50% of healthy adults aspirate oropharyngeal contents into their lungs during sleep. The aspirated material is usually cleared by alveolar macrophages and normal mucociliary action, preventing disease. Alcoholics, drug abusers, stroke patients, and post-ictal seizure patients may aspirate oropharyngeal contents more frequently and in greater volumes, putting them at risk for anaerobic pneumonia and subsequent empyema. Other patients at risk for aspiration pneumonia are those with swallowing disorders, nasogastric or endotracheal tubes, or neurologic dysfunction of the oropharynx.

Alcoholic patients may present with few clinical signs of infection, such as fever, due to their immunocompromised state. Any immunocompromised patient with cough, dyspnea, fever, or just general malaise should be aggressively evaluated for pneumonia and empyema.

Posteroanterior and lateral chest X-rays may demonstrate pleural fluid and underlying parenchymal lung disease. In rare instances, an air fluid level in the pleural space or signs of loculated fluid may be found. In patients with suspected pleural effusion or empyema, a lateral decubitus chest X-ray is particularly important for several reasons. If the fluid has progressed to the fibropurulent stage or the organizational stage and becomes loculated, it will not layer out along the chest wall.

Thoracentesis, the mainstay of the diagnostic process, may be safely performed if the height of the pleural fluid layer is at least 10 mm along the lateral chest wall in the decubitus position. Because distinguishing between empyema and other parenchymal processes clinically and radiographically is often difficult, further imaging studies such as computed tomography or ultrasound of the thoracic cavity may be necessary.

OVERLAP WITH PLEURAL EFFUSIONS

Empyema can be considered an exudative pleural effusion complicated by infection. Therefore, the differential diagnosis is identical to that of the patient presenting with an exudative pleural effusion. The most common exudative pleural effusion is a parapneumonic effusion, which is any effusion associated with a bacterial pneumonia or lung abscess. An estimated 40% of patients with bacterial pneumonia will have an accompanying pleural effusion. If these parapneumonic effusions grow bacteria on culture, then they represent true infections of the pleural space and are termed empyemas.

There is a great deal of overlap between parapneumonic pleural effusions and empyemas, and it is difficult to discuss one without the other. Organisms that cause bacterial pneumonias associated with parapneumonic effusions are S. pneumoniae, S. aureus, Streptococcus pyogenes, and anaerobes and gram-negative species such as E. coli, P. aeruginosa, Klebsiella, and Haemophilus influenzae. Many of these parapneumonic effusions will be culture-positive and should be considered empyemas.

Most clinicians will diagnose empyema on the basis of clinical and radiographic findings (see X-ray example below). As noted, the diagnosis is guided by thoracentesis, which may yield thick purulent material (frank pus) or a thin serous liquid. Although pleural fluid becomes opaque with a white blood cell (WBC) count of 10,000/mm³, the absolute number of WBCs in the pleural fluid needed to differentiate exudative pleural effusion and empyema is subject to debate, ranging from greater than 5000/mm³ to 100,000/mm³.

Confirmation of empyema. This 44-year-old man, who complained of shortness of breath of two weeks' duration and dyspnea on exertion, had a thoracic empyema with more than 2000 ml of frank pus.

A rational approach is to designate empyema as any pleural effusion with positive bacterial cultures. However, a wide variation exists, particularly in the surgical literature. Polymorphonuclear leukocytes are the predominating cell form; the fluid has a high protein content (more than 3 g/dl), and low glucose concentration (less than 20 mg/dl). Gram's stain may be helpful in identifying the organism.

Fluid obtained from thoracentesis should be sent for red blood cell count, WBC count and differential, protein, glucose, amylase, lactate dehydrogenase, and pH. The pH determination is particularly important, because if it is less than 7.0 (or less than 7.2, some authors say), prompt tube thoracostomy is recommended to prevent loculation and further progression of the infection. Fluid is also evaluated for odor, color, and turbidity. Gram's stain, acid-fast bacilli (AFB) stain, cytology, and aerobic, anaerobic, fungal, and AFB cultures should all be submitted for testing. Sputum stains and culture are usually equivocal, but they may be helpful in some cases.

GOALS OF TREATMENT

All patients diagnosed with empyema will require hospitalization. Treatment is hotly debated, but the goals are adequate drainage of the pleural space to allow full lung expansion and control of local and systemic infection. If the empyema is thin, as in the exudative stage, repeated thoracentesis may provide complete drainage. Coupled with appropriate antibiotic therapy, this may be the only treatment required, especially in children.

Most authors agree that if the pleural fluid has entered the fibropurulent stage, where bacteria and a large number of polymorphonuclear cells predominate, thoracostomy tube drainage is required. In fact, closed thoracostomy tube drainage is recommended for any pleural fluid that is either Gram's-stain positive or has a pH less than 7.0 (or, again, less than 7.2, others would say) or a glucose less than 40 mg/dl.

Once the pleural fluid has entered the fibropurulent stage, varying success rates with thoracostomy tube drainage have been reported. Despite attempts at drainage and appropriate antibiotics, some patients will continue with a febrile and toxic course. These patients will require videothoracoscopy or a limited thoracotomy with or without rib resection for drainage, with manual disruption of loculations and adhesions. Rarely will limited thoracotomy be unsuccessful.

The development of minimally invasive video- assisted thoracic surgery has greatly aided thoracic surgeons in the diagnosis and treatment of intrathoracic diseases. It allows the surgeon to identify and drain loculated fluid, remove adhesions, and perform decortication without the trauma of an open thoracotomy.

Intrapleural administration of fibrinolytics has been used with variable success for 50 years in patients with empyema. Fibrinolytics dissolve fibrinous clots and membranes, preventing loculation and fluid sequestration, and enhancing chest tube drainage. Early results were hampered by impurities in the fibrinolytic agents. A recent study prospectively compared intrapleural fibrinolytics and chest tube drainage with intrapleural saline and chest tube drainage in empyema patients. The study found a higher success rate and fewer referrals to surgery in the fibrinolytic group. A Cochrane review of intrapleural fibrinolytic therapy versus conservative management in the treatment of parapneumonic effusions and empyema could not recommend routine use of fibrinolytics because of the small number of randomized controlled trials.

PROGRESSION TO THE CHRONIC STAGE

In a few instances, the empyema will have progressed to the chronic stage as a result of delays in seeking medical attention, inappropriate antibiotics during the earlier stages, or inadequate initial drainage. The thick fibrous pleural peel that develops during this stage must be removed by decortication, which requires extensive thoracotomy.

Empyema necessitans is a very rare condition in which an empyema goes undetected over a long period of time and progresses to the chronic stage. Eventually the empyema erodes through the chest wall and spontaneously drains onto the surface of the body. Empyema necessitans has been reported as a complication of thoracic actinomycosis.

Unrecognized empyema may also erode internally into a bronchus, forming a bronchopleural fistula. Characterized by an unrelenting cough that produces foul-smelling sputum, a bronchopleural fistula can cause asphyxia by draining into the contralateral bronchial tree. Patients with empyema necessitans or bronchopleural fistula will require admission and urgent thoracic surgical consultation.