INDICATIONS/CONTRAINDICATIONS

Malignant Pleural Effusion

Many malignancies have been associated with pleural effusion, the most common being lung and breast cancer. In a prospective study by Villena et al., neoplasm was the most common cause (36%) of pleural effusion in 1,000 consecutive patients who underwent diagnostic thoracentesis. The most common place of origin of the tumor was the lung, followed by pleural mesothelioma. Rodriguez-Panadero et al. found pleural metastases in 29% of 191 patients with one or more malignant tumor elsewhere in the body; pleural effusion was present in 55% of the patients with pleural involvement. A prospective study of 278 consecutive patients with malignant pleural effusion showed a median survival of 211 days. Three factors predicted worse survival—leucocytosis, hypoxemia, and hypoalbuminemia. Patients with pleural effusion from breast carcinoma have better survival.

Malignancy can cause pleural effusion by one or a combination of the following mechanisms: Direct involvement of the pleura (breast, lung), seeding of the tumor to the pleural space via lymphatic and hematogenous routes, involvement of the mediastinal lymph nodes and lymphatic vessel embolization, involvement of the superior vena cava or the pericardium, and obstruction of the ipsilateral mainstem bronchus.

Pleural effusion associated with malignancy may be transudate or exudate. Low glucose (less than 60 mg/dL [3.33 mmol/L]) and low pH (less than 7.3) are associated with increased tumor burden, higher yield of pleural cytology, poorer response to pleurodesis, and shorter survival. The type and the mechanism of the pleural effusion are important for the management of the pleural effusion and the outcome of the procedure. Pleurodesis is less likely to be successful in the presence of bronchial obstruction or extensive tumor infiltration of the ipsilateral lung or pleura in which cases reexpansion of the lung after effusion drainage is unlikely. Other important factors to consider before making a decision regarding the best therapeutic option for pleural effusion are presence of treatment options for the malignancy, presence of symptoms and response to therapeutic thoracentesis, speed of reaccumulation of the effusion, size of the effusion, expected survival, the performance status, the social milieu of the patient, personal preference of the patient, clinician experience, and local availability. Based on these factors there are different clinical scenarios. If the effusion is small and the diagnosis points to a tumor sensitive to chemotherapy (breast, ovary, small-cell lung cancer, lymphoma, etc.) the best choice would be to administer systemic chemotherapy. Mediastinal radiation may be helpful in lymphoma and lymphomatous chylothorax. Further therapy may not be necessary if the effusion disappears or remains stable and well tolerated.

When there is no response to systemic therapy, the effusion is progressing or recurring, when the initial effusion is large and there is amelioration of the clinical signs and reexpansion of the lung after therapeutic thoracentesis, the patient should be considered for pleurodesis or indwelling pleural catheter (IPC). Exception of this rule is slowly (more than 1 month) recurring and short (less than 3 months) expected survival where the effusion can be managed with repeat thoracentesis. Diagnostic and possibly therapeutic bronchoscopy is mandatory before an attempt at pleurodesis when malignant airway obstruction is suspected. If pleurodesis or IPC are considered they should be carried out as early as possible before the development of trapped lung.

Benign Pleural Effusion—Congestive Heart Failure, Hepatic Hydrothorax, and Chylothorax

Cardiac disease is a common cause for recurrent pleural effusion. Specific etiologies include congestive heart failure, and acute and chronic pericarditis. The effusion in congestive heart failure is more often bilateral and of transudative type (diuresis may change the appearance of the fluid to exudative), whereas the effusion related to pericardial disease is more often left-sided and more likely to be an exudate.

Increased left atrial pressure and pulmonary capillary wedge pressure are essential for the development of pleural effusion associated with congestive heart failure. The mechanisms responsible for pleural effusion associated with pericarditis include simultaneous involvement of the pleura from the same process causing the pericarditis, contiguous inflammation, and involvement of the mediastinal lymphatics.

The treatment for pleural effusion due to cardiac disease is the treatment of the underlying cardiac problem itself combined with diuretic therapy in the case of congestive heart failure or anti-inflammatory agents in the case of pericarditis. In a case of a refractory symptomatic effusion, pleurodesis with talc or doxycycline may be considered. Unilateral pleurodesis may worsen the effusion on the opposite side. Placement of indwelling pleural catheter or pleuroperitoneal shunt can be considered as alternatives to pleurodesis.

Pleural effusion due to hepatic cirrhosis with portal hypertension in the absence of primary pulmonary, pleural, or cardiac disease is called hepatic hydrothorax. The incidence of hepatic hydrothorax is less than 5% of all cirrhotic patients. It usually appears in the presence of ascites, which is believed to cross the diaphragm via diaphragmatic defects. Huang et al. classified the defects to four types: type I, no obvious defect; type II, blebs lying on the diaphragm; type III, broken defects (fenestrations); and type IV, multiple gaps in the diaphragm. In as many as 20% of the patients with hepatic hydrothorax ascites cannot be identified even with ultrasound, hence the presence of ascites is not required for the diagnosis. The effusion is transudative in nature. In most of the cases, the hepatic hydrothorax is right-sided, followed by left-sided, and bilateral.

Treatment of hepatic hydrothorax is similar to treatment of ascites. Sodium restriction and diuretics may be effective. Patients who are compliant with the low sodium diet and have recurrent effusion are considered to have refractory hydrothorax. Treatment options for this group include repeated thoracentesis, peritoneovenous shunt, pleurodesis, video-assisted thoracoscopic surgery (VATS) repair of diaphragmatic defects, transjugular intrahepatic portosystemic shunt, and liver transplantation. Chest tube placement as a sole treatment may cause massive fluid shifts with electrolyte and protein depletion, bleeding, renal failure, and death and is not recommended. Huang et al. described 10 patients who underwent thoracoscopic pleura or mesh onlay repair of diaphragmatic defects with no postoperative recurrence of the effusion and improved pulmonary function. Pleurodesis in hepatic hydrothorax is complicated by the rapid passage of fluid between the abdomen and the chest, which does not allow for close contact between the parietal and visceral layers of the pleura. Nevertheless, successful pleurodesis with tetracycline and thoracoscopic talc pleurodesis have been described. Milanez de Campos et al. described 18 patients who underwent 21 VATS talc pleurodesis procedures with immediate success in 48% of the procedures. The success rate of the procedure increased to 60% when it was combined with suture of the diaphragmatic defect. High morbidity (57.1%) and mortality (38.9%) in the 3-month follow-up period were described. Ferrante et al. attempted VATS talc pleurodesis in 15 patients with successful control of hepatic hydrothorax in 53% after a single procedure and in 73% after two procedures.

In conclusion, VATS talc pleurodesis for hepatic hydrothorax is effective in 40% to 75% but may result in significant morbidity and mortality. Better results are seen in patients who undergo closure of the diaphragmatic defect than in patients without demonstrable defect. Some reports suggest CPAP may be helpful with chemical pleurodesis or alone by decreasing the pressure gradient between the chest and the abdomen and thereby decreasing the transfer of ascites.

Chylothorax is the presence of chyle in the pleural space due to leakage from the thoracic duct or its tributaries. The diagnosis is supported by triglyceride concentration greater than 110 mg/dL; an intermediate level between 50 and 110 mg/dL should be followed by lipoprotein electrophoresis of the pleural fluid—chylothorax contains chylomicrons; levels less than 50 mg/dL excludes the diagnosis of chylothorax. Pseudochylothorax is a chyliform effusion with high concentration of cholesterol that occurs in the setting of chronic pleural inflammation.

The thoracic duct ascends from the cisterna chyli at the level of first or second lumbar vertebra in a rightward position. It enters the thoracic cavity from the abdomen through the aortic hiatus and then ascends between the thoracic aorta and the azygos vein until it reaches the fifth thoracic vertebra where it crosses the midline and continues in the left posterior mediastinum to reach the left jugular or subclavian vein. Occasionally, there are two thoracic ducts in the mediastinum or a single thoracic duct empties in the right-sided veins. The level of the injury to the thoracic duct determines the side of the chylothorax.

The etiology of the chylothorax could be traumatic (surgical or nonsurgical) or nontraumatic. The nontraumatic chylothorax may be further separated into malignant (lymphomatous and nonlymphomatous) and nonmalignant. Exudative effusion is the most common finding but transudative chylothorax has been reported.

Computed tomography of the thorax and abdomen and pleural fluid analysis are the initial tests for evaluation of patients with chylothorax. Lymphangiography or lymphoscintigraphy may be utilized in patients with uncertain diagnosis, recurrent chylothorax after thoracic duct ligation, and suspected anomalous thoracic duct anatomy.

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