The presence of lymphatic fluid within the pleural space is termed chylothorax. Because of the high concentration of fat, protein, lymphocytes, and antibodies in the thoracic duct lymph, continuous loss of this fluid can produce serious nutritional and immunological deficiencies. Its accumulation within the pleural and pericardial spaces may encroach upon the lung and heart and seriously compromise the functions of these organs.

The lymph originating in the intestine (chyle) contains 0.4 to 5 g per cent total fat, 65 to 220 mg per cent total cholesterol, 1.2 to 4.1 g per cent albumin, 1.1 to 3.6 g per cent globulin, and electrolytes in similar concentrations to plasma. It also contains 400 to 6800 lymphocytes and 50 to 600 erythrocytes per mm³.

Of the thoracic lymph 95 per cent originates in the liver and intestinal tract. Some 60 to 70 per cent of ingested fat is transported to the bloodstream by the thoracic duct: only fatty acids with less than 10 carbon atoms in the chain are absorbed directly into the portal venous system.

The thoracic duct (Fig. 1) 1977 is a muscular tube that communicates with an extensive collateral circulation. Its multiple unidirectional valves conduct lymph in a cephalad direction. The thoracic duct usually originates from the cisterna chyli on the anterior surface of the vertebral column at about the level of L2 and ascends through the diaphragmatic aortic hiatus behind the oesophagus and between the aorta and the azygous vein on the surface of the right anterior vertebral column to about the level of T5. There the duct crosses behind the aorta and aortic arch, ascending through the left posterior mediastinum along the oesophagus into the base of the left neck, and emptying into the venous system in the area of the confluence of the left jugular and subclavian veins.

After the ingestion of a fatty meal the volume of intestinal lymph may increase by 10 times over its basal flow rate; starvation and rest markedly diminish the volume.

Congenital chylothorax is rare, and due to birth trauma or congenital defects or malformations. External trauma, usually hyperextension of the spine and rarely penetrating missile injuries, and intraoperative trauma cause approximately 50 per cent of cases of chylothorax. Malignant neoplasms, usually lymphoma, bronchogenic carcinoma, or other metastatic mediastinal malignancies also cause approximately 50 per cent of cases. Other rare causes include tuberculosis, aortic aneurysm, filariasis, and pulmonary lymphangiomatosis.

The rapidity with which a chylous pleural effusion accumulates is reflected in the symptoms associated with it. Gradual chylothorax is associated with the insidious onset of dyspnoea; rapid accumulation causes marked respiratory distress and shock. The clinical context, such as a postoperative or post-traumatic state or the presence of an antecedent malignancy, may suggest the diagnosis.

The chest radiograph demonstrates an opacified hemithorax or suggests the presence of a pleural effusion. Computerized tomography of the chest confirms the presence of a pleural effusion, and may reveal the underlying cause of the effusion, if an abnormality is identifiable within the chest.

The recovery of non-clotting milky fluid from the pleural space, with analysis revealing free microscopic fat and a fat content higher than that of plasma, is strongly suggestive of chylothorax. Other causes of milky pleural fluid are pseudochyle (present with malignant tumours or infection), which contains only a trace of fat, and cholesterol pleural effusions (associated with tuberculosis or rheumatoid arthritis), which contain a high concentration of cholesterol crystals. If the milky pleural fluid has a triglyceride level more than 110 mg/100 ml, there is a 99 per cent likelihood that the fluid is chyle. If the triglyceride level is less than 50 mg/100 ml, there is only a 5 per cent likelihood of the fluid being chyle.

The management of chylothorax depends upon the underlying cause and the extent of nutritional depletion. Lampson and associates in 1948 applied ligation of the thoracic duct in the management of chylothorax and decreased the mortality rate from 50 per cent to 15 per cent. Surgical treatments include supradiaphragmatic ligation of the thoracic duct, shunting into the peritoneal cavity or into one hemithorax or the other, and pleurectomy.

Conservative management includes control of the encroachment upon the lung by the chylous pleural effusion using intercostal catheter closed drainage. Total parenteral nutrition is required, with medium chain triglycerides being administered orally.

Radiation therapy is occasionally successful in patients with mediastinal lymphoma and carcinoma.

In the neonate idiopathic chylothorax generally responds to thoracentesis. Traumatic chylothorax may initially be treated conservatively as outlined above. However, if pleural fluid losses exceed 1500 ml/day for 1 week, or 500 ml/day for 2 weeks, operative management should be employed. If conservative management is unsuccessful after 2 weeks in those patients with underlying malignancy, irradiation to the tumour bed may be useful.

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