The management of tuberculous empyema.

Tuberculous empyema is usually caused by rupture of a subpleural parenchymal focus through the visceral pleura. The immediate result of such a rupture is the occurrence of hydrothorax, the so-called idiopathic pleural effusion. In most instances, particularly with adequate drug treatment, the site of rupture seals. The fluid is then absorbed or removed by thoracentesis and the lung re-expanded, usually with little residual evidence of parenchymal disease. Too often, however, the bronchopleural fistula remains open and the hydrothorax converts into pyothorax, either pure tuberculous or mixed. The scene is then set for the tragic course which in 1915 caused Robinson to designate tubercubous empyema as the “Patriarch of the Surgical Scrap Heap.” The occasional demonstration of acid-fast organisms in the bone marrow, or of miliary tubercles in the liver, of patients with tuberculous empyema has been cited by some as evidence that the initial pleural effusion is only one phase of a tuberculous bacteremia which results from a lymphohematogenous progression of a primary pulmonary focus. These bone marrow and liver signs may be explained on a purely arithmetical basis. As long as the lesion is confined to the pulmonary parenchyma the lymphatic drainage is restricted to the hilar nodes and the chance of progression to the thoracic duct and the systemic circulation is small (Fig. 1). When, however, the lesion ruptures into the pleural space the possibility of lympho-hematogenous extension is increased (Fig. 2). In addition to the hilar nodes, the pleural lymphatics also drain through the paravertebral, the paraaortic and parasternal lymph plexuses. There are thus four times as many opportunities for pleural infection to reach the systemic circulation as when the infection remains restricted to the parenchyma.1 It is not surprising, therefore, that one is occasionally able to find lesions in the bone marrow, spleen, liver or kidneys in patients with tubercubous empyema. Auerbach’s 2 demonstration of a bronchopleurab fistula in 49 per cent of 311 autopsies done in patients who died with tubercubous empyema would seem to be conclusive evidence as to its pathogenesis. Once empyema is established, a serious threat to the patient’s life is presented. We are all too familiar with the chain of events; sepsis, amyboidosis, progressive tubercubous pulmonary fibrosis and insufficiency, which exacted such a toll in pre-chemotherapy days. Physicians often differed as to the best method of treatment of this serious condition but there was little difference of opinion as to the high morbidity and mortality rates that were encountered. The mortality rate for pure tubercubous empyema ranged from 70 to