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This retrospective study of elective pneumonectomy for complicated inflammatory lung disease was done to define modern-day mortality and morbidity. One hundred twenty-four patients received elective pneumonectomy. Patient ages ranged from 6 months to 71 years. Past, recurrent, or new pulmonary tuberculosis was present in 107 patients (86.3%). Clinical presentation involved recurrent infections or severe suppurative sequelae (abscess, empyema). Forty-seven patients had chronic hemoptysis and 25 patients had past or recent massive hemoptysis (> 600 ml of hemoptysis fluid within 24 hours). Nutritional deficiencies were common. One hundred six patients (85.5%) had end-stage destroyed lungs. Evaluative bronchoscopy showed inflammatory endobronchial changes in 106 patients (85.5%), bronchial strictures in 4, and indolent endobronchial tumor in 2. Lung separation was by double-lumen tube in 96 patients, single lung-single tube in 6, bronchus blocker in 6, and prone posture in 9. Extrapleural pneumonectomy was done in 83 patients (66.9%). Fifty-seven of these procedures were left sided and 26 were right sided. Standard transpleural pneumonectomy was done in 41 patients (33.1%): 30 left sided and 11 right sided. Nine pneumonectomies were conducted with the patient in the prone position. Four patients had completion pneumonectomy. Hospital mortality was three deaths (2.4%). Morbidity included postpneumonectomy empyema in 19 patients (15.3%). Seven postoperative bronchopleural fistulas occurred. Empyema in most patients was managed by open pleural drainage (thoracostoma) and later space closure. Pneumonectomy proved effective therapy with low mortality but postpneumonectomy empyema posed serious morbidity.

Twelve successive patients with massive haemoptysis were treated by emergency rigid bronchoscopy and lavage of the bleeding lung with cold saline. All patients stopped bleeding during the procedure and all blood and clot was evacuated from the accessible airways. The bleeding source was localised to a lobe in seven cases, and lateralised in the remaining five patients. Two patients had a second haemorrhage during that hospital stay and cold saline lavage again terminated it. Further therapy, either surgical or medical was based on information obtained during the respite from haemorrhage achieved with this technique. There was no hospital mortality in the series.The conservative management of haemoptysis is generally successful, but 10-15% of all patients with rhaemoptysis may bleed to a life-threatening extent.1 2 This figure includes patients with limited pulmonary reserve in whom the spillage of moderate amounts of blood into the tracheobronchial tree causes critical deterioration in lung function, and those in danger of asphyxiation from the sheer volume of blood aspirated. The various methods of management of lifethreatening haemoptysis include drug therapy endoscopic control measures (endobronchial balloon tamponade, topical adrenalin application, and lung isolation with double lumen endotracheal tubes), bronchial artery embolisation techniques, and lung resection. The performance of a pulmonary resection on a patient who is actively bleeding and whose respiratory reserve is unknown is necessarily hazardous. The occurrence of massive haemoptysis in poor risk patients has encouraged the development of nonsurgical methods of management. Our experience with emergency rigid bronchoscopy and cold saline lavage in 12 patients with massive haemoptysis forms the basis of this report. No similar experience has been reported.

In addition to being a potent hepatocarcinogen, aflatoxin B1 (AFB1) is a pulmonary carcinogen in experimental animals, and epidemiological studies have shown an association between AFB1 exposure and lung cancer in humans. This study investigated AFB1 bioactivation and detoxification in human lung tissue obtained from patients undergoing clinically indicated lobectomy. [3H]AFB1 was bioactivated to a DNA binding metabolite by human whole lung cytosols in a time-, protein concentration-, and AFB1 concentration-dependent manner. Cytosolic activation of [3H]AFB1 correlated with lipoxygenase (LOX) activity and was inhibited by the LOX inhibitor nordihydroguaiaretic acid (NDGA; 100 microM), indicating that LOXs were largely responsible for the observed cytosolic activation of AFB1. In whole lung microsomes, low levels of indomethacin inhibitable prostaglandin H synthase (PHS)-mediated [3H]AFB1-DNA binding and cytochrome P-450 (P450)-mediated [3H]AFB1-DNA binding were observed. Cytosolic glutathione S-transferase (GST)-catalyzed detoxification of AFB1-8,9-epoxide, produced by rabbit liver microsomes, was minimal at 1 and 10 microM [3H]AFB1. With 100 microM [3H]AFB1, [3H]AFB1-8,9-epoxide conjugation with reduced glutathione was 0.34 +/- 0.26 pmol/mg/h (n = 10). In intact, isolated human lung cells, [3H]AFB1 binding to cellular DNA was higher in cell fractions enriched in macrophages than in either type II cell-enriched fractions or fractions containing unseparated cell types. Indomethacin produced a 63-100% decrease in [3H]AFB1-DNA binding in macrophages from five of seven patients, while NDGA inhibited [3H]AFB1-DNA adduct formation by 19, 40 and 56% in macrophages from three of seven patients. In alveolar type II cells, NDGA decreased [3H]AFB1-DNA binding by 30-100% in cells from three patients and indomethacin had little effect. SKF525A, an isozyme non-selective P450 inhibitor, enhanced [3H]AFB1 binding to cellular DNA in unseparated cells, macrophages, and type II cells, suggesting that P450-mediated bioactivation of AFB1 is not a major pathway by which AFB1-8,9-epoxide is formed in human lung cells. Overall, these studies suggest that P450 has a minor role in the bioactivation of AFB1 in human lung. Rather, LOXs and PHS appear to be important bioactivation enzymes. Co-oxidative bioactivation of AFB1, in combination with the low conjugating activity displayed by human lung cytosolic GSTs, likely contributes to human pulmonary susceptibility to AFB1.