What are the valuable and helpful diagnostic testing modalities available in the evaluation of a pleural effusion?
How is empyema diagnosed and managed?
When does a malignant pleural effusion deserve serial drainage versus an indwelling drainage catheter versus pleurodesis?
What are the indications for chest tube placement (tube thoracostomy) in patients with a small pneumothorax?
When can a chest tube be removed, and how is that done?
Pleural effusion complicates many different diseases making its precise incidence difficult to determine. The rate is estimated at 3.2 patients per 1000 population. The causes of effusions are varied (Table 243-1), with heart failure as the most common etiology. No data on hospital admission rate due to pleural effusions exists. Morbidity and mortality from pleural effusions correlates with the underlying etiology rather than the pleural effusion itself. Patients with pleural effusions secondary to malignancy or cirrhosis tend to have a poor prognosis while pleural effusions secondary to treatable or ameliorable conditions such as pulmonary emboli or surgery tend to have much better prognoses.
Table 243-1 Differential Diagnosis of Pleural Effusions |Favorite Table|Download (.pdf)
Table 243-1 Differential Diagnosis of Pleural Effusions
- Heart failure
- Postcoronary artery bypass graft
- Postcardiac injury syndrome
- Pneumonia: parapneumonic effusion or empyema
- Pulmonary embolism
- Trapped lung
- Acute or chronic atelectasis
|Gastrointestinal||Cirrhosis or other causes of portal hypertension|
|Gynecologic||Ovarian hyperstimulation syndrome|
- Primary lung cancer
- Metastatic disease to the lung
- Meig syndrome
|Rheumatologic/collagen vascular diseases|
- Systemic lupus erythematosis
- Rheumatoid arthritis
- Drug induced
- Radiation therapy
|Idiopathic||Yellow nail syndrome|
Normally, only a small 0.1 to 0.2 mL/kg or approximately 6 to 12 cc occupies the space between the visceral pleura lining the lung and the parietal pleura lining the chest wall and diaphragm. Fluid due to filtration from microvessels and stoma in the parietal pleura moves out of the pleural space by connecting to lymphatic channels. In the normal physiologic state the rate of pleural fluid turnover is 0.15 mL/hr, and in disease states this can be increased to approximately 30 ml/hr. A pleural effusion may collect in the pleural space due to increased production or decreased reabsorption of this fluid. Potential mechanisms of abnormal fluid accumulation include increased capillary permeability of the microvessels primarily in the parietal pleura, stoma obstruction, and decreased plasma oncotic pressures (Figure 243-1). In addition to serous fluid (hydrothorax), blood (hemothorax), lipid (chylothorax), and pus (empyema) may occupy the pleural space. Symptoms likely result from decreased chest wall compliance and stimulation of neurogenic receptors rather than direct compression of lung tissue.
Pathophysiology of pleural effusion genesis. (Reproduced, with permission, from Doherty GM. Current Diagnosis & Treatment: ...