Diffuse alveolar hemorrhage syndrome due to 'silent' mitral valve regurgitation.

A variety of clinical diseases are associated with diffuse alveolar hemorrhage. Although mitral valve disease can cause hemoptysis, it rarely is associated with diffuse alveolar hemorrhage at presentation. A 49-year-old woman was admitted to the hospital with the abrupt onset of fever, anemia, dyspnea, azotemia, and diffuse alveolar infiltrates. Two-dimensional echocardiography done several months earlier to evaluate atypical chest pain had been unremarkable. Fiberoptic bronchoscopy 2 days after admission to the hospital revealed fresh blood throughout the tracheobronchial tree. The infiltrates resolved rapidly and completely during systemic steroid therapy only to reappear as the steroids were tapered, suggesting a beneficial therapeutic response. Results of serologic evaluation were negative. Transbronchial biopsies showed inflammation and hemosiderin-laden macrophages; no specific diagnosis was established. The patient was scheduled for open lung biopsy. The surgeon was concerned about the history of chest pain and requested placement of a pulmonary artery catheter, which revealed severe pulmonary hypertension. Transesophageal echocardiography and subsequent cardiac catheterization showed severe mitral regurgitation. Mitral valve replacement resulted in complete elimination of symptoms.

Spontaneous resolution of a lung mass due to infection with Mycobacterium terrae.

A 61-year-old smoker had a large right lung mass suggestive of bronchogenic carcinoma. Bronchoscopy showed what appeared to be tumor occlusion of a right middle lobe subsegment. Biopsies were nondiagnostic for malignancy. A scheduled percutaneous needle aspiration biopsy 1 week later was canceled because of a significant reduction in size of the lung mass. Acid-fast bacilli were subsequently found in bronchoscopic specimens, and treatment was started with isoniazid, rifampin, pyrazinamide, and ethambutol. The organism was identified as Mycobacterium terrae. In vitro resistance was noted to isoniazid. The early reduction in size of the mass before antimycobacterial therapy suggested that spontaneous regression may be part of the natural history of pulmonary infection with Mycobacterium terrae.

Hemodynamic effects of amrinone in a canine model of massive pulmonary embolism.

Amrinone, an inotrope with vasodilating properties, is of potential use in managing the right ventricular failure and pulmonary vasoconstriction induced by massive pulmonary embolism (PE). Therefore, to determine the hemodynamic effects of amrinone in a canine model of massive PE, autologous blood clot was infused into ten dogs (eight treated and two control animals) in an amount sufficient to decrease mean systemic arterial pressure (MAP) by at least 25 percent. This resulted in an increase in mean pulmonary artery pressure (MPAP) from 13.4 +/- 3.7 mm Hg to 44.4 +/- 4.8 mm Hg (p less than 0.01), a decrease in MAP from 122 +/- 9.5 mm Hg to 35.6 +/- 9.8 mm Hg (p less than 0.01), and a decrease in cardiac output from 2.73 +/- 0.834 L/min to 1.22 +/- 0.61 L/min (p less than 0.01). Amrinone was administered in an initial bolus of 0.75 mg/kg followed by an infusion of 7.5 micrograms/kg/min, which resulted in significant hemodynamic improvement in all subjects, with a fall in MPAP to 35.3 +/- 5.1 mm Hg (p less than 0.01), an increase in MAP to 98.1 +/- 31.1 mm Hg (p less than 0.01), and an increase in cardiac output to 2.01 +/- 0.7 L/min (not significant) at 5 min. Cardiac output continued to increase to 2.56 +/- 0.16 L/min (p less than 0.01) at 35 min. We conclude that amrinone alleviated pulmonary hypertension, systemic hypotension, and low cardiac output in a canine model of massive PE.

Pulmonary embolism: improvement in hemodynamic function with amrinone therapy.

We have described a 57-year-old man who had had lower extremity vascular surgery complicated by PE. Dyspnea, hypotension, hypoxemia, and CHF developed, but thrombolytic therapy was not started because of the recent surgical procedure; instead, he had plication of the inferior vena cava. Because of persistent pulmonary artery hypertension and decreasing cardiac indices, amrinone therapy was begun, and resulted in marked hemodynamic improvement.

Rat lung glutathione release: response to oxidative stress and selenium deficiency.

We performed experiments to characterize the glutathione-dependent metabolism occurring during tert-butyl hydroperoxide infusion in isolated perfused rat lungs and to examine the effect of selenium deficiency on this metabolism. Selenium deficiency resulted in decreased lung glutathione peroxidase activity but normal glutathione reductase activity and glutathione content. Infusion of the hydroperoxide into control lungs caused a proportional increase in tissue glutathione disulfide (GSSG) concentration and release of GSSG into the perfusate up to an infusion rate of 250 nmol of tert-butyl hydroperoxide X min-1 X 100 g body wt-1. Infusion rates greater than this resulted in continued rise of tissue GSSG concentrations but GSSG release into the perfusate plateaued. Infusion of tert-butyl hydroperoxide into selenium-deficient rat lungs resulted in much lower concentrations of tissue GSSG and GSSG release into the perfusate; however, release in the selenium-deficient rat lung was also found to be saturable at infusion rates of 450 nmol of tert-butyl hydroperoxide X min-1 X 100 g of body wt-1. Selenium deficiency in the rat decreases the rate of reduction of infused tert-butyl hydroperoxide by glutathione and may predispose the lung to free radical damage.

Effects of bacterial endotoxin on protecting copper-deficient rats from hyperoxia.

The administration of very low doses of bacterial endotoxin protects rats during exposure to hyperoxia and is associated with the induction of lung antioxidant enzyme activities. Copper-deficient rats have increased susceptibility to O2 toxicity, which may be related to their decreased lung superoxide dismutase activity (SOD) or decreased plasma ceruloplasmin concentrations. To determine whether endotoxin can protect against hyperoxia in this susceptible model, we exposed copper-deficient and control rats to a fractional inspiratory concentration of O2 greater than 0.95 for 96 h after pretreatment with 500 micrograms/kg of bacterial endotoxin or phosphate-buffered saline (PBS). Mortality in the copper-deficient and control rats given PBS and exposed to O2 for 96 h was 100%. Copper-deficient rats died significantly earlier during the exposure than controls. No mortality occurred in either group treated with endotoxin and hyperoxia despite the decreased activity of copper-dependent enzymes in the copper-deficient rats. Copper-deficient rats treated with endotoxin and exposed to hyperoxia did increase lung Cu-Zn-SOD activity, but activity remained below levels found in air-exposed controls. Mn-SOD activity was found to be induced above air-exposed controls in the copper-deficient rats treated with endotoxin and exposed to hyperoxia. Hyperoxic exposure resulted in a marked increase in plasma ceruloplasmin concentrations in the control rats, but no increases in ceruloplasmin occurred in the copper-deficient animals. Endotoxin protects copper-deficient rats from hyperoxia despite their decreased lung Cu-Zn-SOD activity, and decreased plasma ceruloplasmin.

Transbronchial needle aspiration staging of bronchogenic carcinoma.

Transbronchial needle aspiration (TBNA) has been advocated as a reliable technique in the nonsurgical staging of patients with bronchogenic carcinoma. Some have questioned the reliability of TBNA, however. We used TBNA directed by computed tomography (CT) in 88 consecutive patients with bronchogenic carcinoma who had undergone chest CT. Chest CT was 94% sensitive, 79% specific, and 85% accurate in evaluating the mediastinum for malignant lymphadenopathy. There were 19 malignant aspirates in 44 patients with malignancy and apparent adenopathy evaluated by chest CT. No malignant carinal aspirates were obtained in any patient with a normal mediastinum evaluated by chest CT. There were 2 false positive needle aspirates. One patient with apparent right paratracheal adenopathy and malignant needle aspirate had no mediastinal neoplasm detected at surgery. The other false positive aspirate had been contaminated by tracheal debris. The overall sensitivity, specificity, and accuracy of TBNA mediastinal staging were 50, 96, and 78%, respectively. We conclude that CT scanning is a useful adjunct in the staging of patients with bronchogenic carcinoma, and that TBNA is a sensitive and highly specific staging technique that may negate the need for surgical staging in a large number of patients with bronchogenic carcinoma.

Tracheocarotid fistula secondary to laryngeal carcinoma presenting as massive hemoptysis.

Tracheovascular fistulas are not traditionally included in the differential diagnosis of massive hemoptysis. We report the first such case due to a tracheocarotid fistula produced by occult subglottic laryngeal cancer. Also described is the unusual role the cuffed endotracheal tube played in obscuring the diagnosis and palliating the hemorrhage.