To determine if screening by specialists could reduce unnecessary test ordering and reduce costs related to diagnostic workup in patients undergoing evaluation for tuberculosis.

In recent years, considerable advances have been made in treating primary pulmonary hypertension (PPH). These have provided a series of therapeutic options, ranging from the oral administration of calcium channel blockers to the continuous infusion of prostacyclin and/or lung transplantation. These therapeutic advances have highlighted the need for the better understanding of etiology and pathogenesis. Among the key uncertainties, the following are defined as leading uncertainties: (1) the nature of the initiating lesion; (2) the shared pathogenetic mechanisms that culminate in the pathologic lesions of PPH; (3) the molecular genetic bases for familial PPH and for susceptibility to PPH; (4) understanding of the obliterative-proliferative occlusive process in the small muscular pulmonary arteries; and (5) redefinition of "primary" and "secondary," ie, a revised nomenclature of pulmonary hypertension. A revised classification based on etiology is presented.

Primary cardiac sarcomas carry a dismal prognosis with no known curative therapy using standard treatment approaches. By its very location, the possibility of a radical complete resection--the underlying principle in the management of any soft-tissue sarcoma--is precluded. While literally in a continuous "blood bath," cardiac sarcomas are associated with a very high rate of hematogenous metastases. This report describes the management of a case in a 51-year-old white man with a high-grade unresectable cardiac sarcoma who was treated with hyperfractionated (twice daily) radiotherapy to a total dose of 7,050 cGy along with a radiosensitizer, (5'-iododeoxyuridine. The patient currently is disease-free and functioning well more than 5 years following this novel treatment approach.

Evaluate the use of mediastinoscopy in the surgical diagnosis and treatment of mediastinal cystic masses in adults.

To examine the incidence and consequences of atrial arrhythmias in surgical ICU patients following major noncardiac, nonthoracic surgery.

Nine cases of symptomatic bradycardia are presented in which treatment with intravenous glucagon was administered when atropine failed to improve the patient's condition significantly. Although the cause often was not obvious at presentation, all nine subjects took oral medications that could have contributed to the development of symptomatic bradycardia. Eight of nine patients demonstrated clinical improvement 5 to 10 min after glucagon administration, which was consistent with its peak clinical action. Beta-blockers, calcium channel blockers, and digoxin were ultimately thought to have contributed to the majority of these presentations. This report suggests that glucagon may have a role in the treatment of symptomatic bradycardia, particularly in the presence of beta-adrenergic blockade and perhaps calcium channel blockade. Furthermore, the results in these cases suggest that future clinical trials should not be limited to drug-induced symptomatic bradycardia.

Asymptomatic HIV-infected individuals are increasingly recruited for studies involving invasive procedures such as bronchoscopy. We sought to determine the response to and outcome of a request for a research bronchoscopy in HIV-positive individuals with no respiratory disease, and whether this would adversely affect future decisions to have a medically indicated bronchoscopy.

To evaluate the incidence and risk factors for catheter-related central vein thrombosis in ICU patients.

To determine the incidence of primary graft failure (PGF) following lung transplantation, assess possible risk factors, and characterize its effect on outcomes.

To assess the effect of nitric oxide inhalation on pulmonary hemodynamics and oxygenation in patients with COPD receiving long-term oxygen therapy (LTOT).

Tropical pulmonary eosinophilia (TPE) usually affects people living in the tropics, especially those in Southeast Asia, India, and certain parts of China and Africa. However, owing to the rising frequency of world-wide travel and the migration between continents, this disease is increasingly seen in the West, where the diagnosis can be easily missed since it is rarely encountered and can mimic many other conditions. Cases of TPE have typically been reported to masquerade as acute or refractory bronchial asthma. TPE results from a hypersensitivity reaction to lymphatic filarial parasites found in endemic regions. There is evidence that it is more likely to occur in nonimmune individuals, ie, visitors to endemic regions, than in individuals of endemic populations who have developed immunity to filarial infections. Clinical features include paroxysmal cough, wheezing and dyspnea, and systemic manifestations such as fever and weight loss. A history of residence in a filarial endemic region and a finding of peripheral eosinophilia >3,000/mm3 should initiate a consideration of this disease. Other criteria for the diagnosis of TPE include absence of microfilariae in the blood, high titers of antifilarial antibodies, raised serum total IgE >1,000 U/mL, and a favorable response to the antifilarial, diethylcarbamazine, which is the recommended treatment. This disease, if left untreated or treated late, may lead to long-term sequelae of pulmonary fibrosis or chronic bronchitis with chronic respiratory failure. Herein lies the importance of early diagnosis and treatment of TPE.