Pleural Disease in the Critically III Patient
Andres F. Sosa
Crescens Pellecchia
Mark M. Wilson
I. PLEURAL EFFUSIONS
A. General principles.
1. Pleural disease itself is an unusual cause for admission to the intensive care unit (ICU).
2. Exceptions are a large hemothorax for monitoring the rate of bleeding and hemodynamic status, an unstable pneumothorax (PTX), and a massive unilateral or bilateral pleural effusion causing acute respiratory failure.
3. Early recognition of an empyema is crucial.
B. Etiology.
1. Pleural effusions may be due to an imbalance of hydrostatic and oncotic pressures, capillary permeability changes, impaired lymphatic drainage, loss of lung volume (atelectasis), or combinations of these.
2. Congestive heart failure (CHF) is the most common cause of all pleural effusions, most of which are bilateral.
3. Hepatic hydrothorax occurs in 6% of patients with liver cirrhosis and clinical ascites.
4. Parapneumonic effusions due to community-acquired and nosocomial pneumonia are common in critically ill patients.
5. If pus is aspirated at thoracentesis or the Gram stain shows bacteria, the diagnosis of empyema is established, and immediate drainage is needed.
6. Other frequent causes of pleural effusion in the ICU include pancreatitis, pulmonary embolism, hypoalbuminemia, hemothorax, and postsurgical (cardiothoracic or abdominal) effusions. Esophageal rupture (elevated salivary amylase in pleural fluid) is an unusual but potentially life-threatening event requiring immediate diagnosis and therapy.
C. Pathophysiology.
1. Atelectasis causes pleural fluid by decreasing local pleural pressure; this creates a vacuum in the pleural space leading to extravasation of transudative fluid.
2. Hepatic hydrothorax results from movement of ascitic fluid through congenital or acquired diaphragmatic defects.
3. Pleural effusions from pancreatitis result from direct irritation of the diaphragm, extravasation of enzymes into the pleural space (pancreatic duct leaks), or fistulous tracts.
4. Effusions from pulmonary emboli result from increased capillary permeability, imbalance in microvascular and pleural hydrostatic pressures, and pleuropulmonary hemorrhage.
5. Pleural effusion, with or without PTX, occurs in 75% of cases of esophageal rupture.
6. Hemothoraces (fluid with a pleural fluid-to-blood hematocrit ratio >50%) warrant complete drainage.
D. Diagnosis.
1. Pleural effusions appear on supine CXR as increased homogeneous densities over the lower lung fields compared with the upper lung fields.
2. With hepatic hydrothorax, the CXR usually reveals a normal cardiac silhouette and a right-sided pleural effusion in 70% of patients. The fluid is transudative.
3. Parapneumonic effusions are commonly ipsilateral to a new infiltrate or consolidated lobe.
4. Effusions from pancreatitis are usually small and left sided (60%) but may be isolated to the right (30%) or bilateral (10%). The fluid is an exudate with amylase values greater than that of serum.
5. Pulmonary emboli usually produce exudative effusions; however, 20% are transudates.
6. A presumptive diagnosis of esophageal rupture requires immediate confirmation with contrast esophagrams. Amylase of salivary origin appears in pleural fluid in high concentration. The pH falls rapidly and progressively approaches 6.00.
E. Treatment.
