Main causes of hydrothorax are cancer, cardiovascular diseases, renal diseases, acute pancreatitis, hepatic cirrhosis and thromboembolism.
Malignancy as a cause of hydrothorax
More than 25% cases of hydrothorax are secondary to cancer, and 35% of patients with lung cancer, 23% with breast cancer (12% with adenocarcinomas of unknown primary site), and 10% of patients with lymphoma develop malignant pleural effusions during the course of disease. Approximately 10% of effusions are secondary to primary pleural tumors (mostly mesotheliomas). The mechanism (as noted above) is primarily through lymphatic obstruction in either the peripheral lung or central lymph node channels of the mediastinum. Malignant hydrothorax can be serous, serosanguineous, or frankly bloody and are diagnosed primarily by demonstrating malignant cells in the fluid. Cytologic confirmation is successful 50%, 65%, and 70% of the time after one, two, three thoracenteses, respectively. Closed pleural biopsy alone is successful in only 50% of cases, but coupled with thoracentesis it can increase the diagnostic yield to 80%. Thoracoscopy with direct pleural biopsy, however, is successful in 97% of patients and should be considered with a suspicious effusion after two negative thoracenteses.
Treatment of malignant hydrothorax is strictly palliative since most patients die within 3–6 months of developing a malignant hydrothorax. Prompt diagnosis and therapy are essential. The goals of treatment are lung reexpansion and pleural symphysis. This is most readily accomplished with placement of a chest tube (20–28F) and closed tube drainage for 24–48 hours. Generally, no more than 1 L is allowed to drain initially. Subsequently, 200–500 mL is allowed to drain every 1–2 hours until the effusion is fully drained. This controlled draining avoids the rare complication of reexpansion pulmonary edema. Once full lung expansion is obtained (regardless of the ongoing drainage), pleurodesis should be performed with an appropriate agent before loculations have formed. Different chemical, radioactive, and infectious agents have been used in the past with varying success rates, including mechlorethamine (success rate 48–57%), thiotepa (nil to 63%), fluorouracil (66%), bleomycin (50–100%), quinacrine (50–83%), tetracycline (83–100%), doxorubicin (80%), mitoxantrone (76%), talc (87–100% insufflation; 83–100% slurry), radioactive colloidal gold and chromium phosphate (50%), and Corynebacterium parvum (81%). Finally, mechanical pleurectomy without chemical instillation can control pleural effusions in over 99% of patients, but this requires an operative procedure (although usually only thoracoscopy). Previously, tetracycline was the most popular agent, but this option is no longer available. Doxycycline, bleomycin, and talc are now the most frequently used. Talc is inexpensive, highly effective, and easily administered either as a powder insufflated into the open chest or as a slurry instilled through a chest tube. The other two agents are less successful and are expensive (bleomycin costs $1000 per 30-unit vial). In addition, two randomized trials have proved talc to be superior to both bleomycin and tetracycline. Some hesitancy to use talc has been expressed because of the associated patient discomfort, but there have been no reports of unmanageable pain similar to that seen previously with tetracycline instillation. Furthermore, talc no longer contains asbestos, and the induction of fibrothorax, which is a long-term theoretical concern, is not a problem in these short-lived patients. Talc is a foreign body, however, and use of antibiotics during pleurodesis for empyema prophylaxis may be prudent.
Complications following pleurodesis include pneumothorax, loculated hydrothorax, fever, infection (empyema), respiratory distress syndrome (particularly following bilateral simultaneous pleurodeses, which for this reason alone are contraindicated), and recurrence. Fortunately, problems are uncommon, and most patients can have their chest tubes removed within 48–72 hours following talc pleurodesis.
Hydrothorax are common findings in patients with moderate to severe heart failure. The heart failure may be secondary to ischemia, valvular heart disease (mitral stenosis, mitral regurgitation, etc), viral myocarditis, congenital heart disease, and other less common lesions. The effusion may be bilateral or unilateral. When unilateral, the right hemithorax is most often affected. Fluid frequently involves the interlobar fissures (most commonly the minor fissure on the right) and can form localized collections simulating mass lesions known as “pseudotumors.” Other cardiovascular causes of pleural effusions include constrictive pericarditis and pulmonary venous obstruction.
Hydronephrosis, nephrotic syndrome, and acute glomerulonephritis are on occasion associated with hydrothorax. Rupture of the collecting system into the pleural space can also produce a hydrothorax. In this latter case, the pleural fluid creatinine will be elevated (fluid:serum creatinine ratio significantly > 1.0).
Moderate to severe pancreatitis is associated with a pleural effusion that characteristically occurs on the left, contains fluid with an amylase concentration substantially higher than that in the serum. Rarely pseudocysts of the capsule of the pancreas may communicate with the pleural space, resulting in high-volume pleural effusions.
Approximately 5% of patients with cirrhosis and ascites will develop a hydrothorax. In contrast to pancreatitis, nearly all of these effusions occur on the right side.
Pulmonary thromboembolism are sometimes accompanied by a hydrothorax. These effusions are typically serosanguineous and small, but they may be frankly bloody and massive. Characteristic x-ray findings are almost always present in the lung. Since the fluid is usually reabsorbed in a short period of time, drainage is seldom necessary.