The effect of HIV infection on phagocytosis and killing of Staphylococcus aureus by human pulmonary alveolar macrophages.

Pulmonary alveolar macrophages (PAM) play a central role in host defense against pulmonary infection. The authors studied the number, viability, and ultrastructure of PAM recovered by bronchoalveolar lavage from normal and HIV-infected subjects, and their ability to phagocytose and kill Staphylococcus aureus. PAM from HIV-infected subjects who did not have pneumonia were present in greater numbers and phagocytosed significantly more opsonized Staphylococcus aureus (32.5% and 27.3% for nonsmokers and smokers, respectively) than did PAM from healthy controls (19.5% and 18.2%). In 15 patients with AIDS and pneumonia (due to Pneumocystis carinii in 13/15), viability of PAM and their phagocytic capacity were significantly reduced; in smokers with AIDS and pneumonia, the PAM yield was also dramatically decreased. Killing of S. aureus was similar by PAM from all patient groups. HIV infection was associated with the electron microscopic finding in PAM of extensively ruffled PAM cell-surfaces and ingestion of lymphocytes. Thus, HIV infection stimulates the phagocytic capacity and produces morphologic changes consistent with the possibility that PAM are activated by this retroviral infection. In patients with AIDS who develop pneumonia, especially in smokers, the number, viability and phagocytic capacity of PAM are significantly decreased; our study could not determine whether this diminished activity reflects evolution of the HIV infection or a secondary effect of the pneumonia.

Vasodilators and primary pulmonary hypertension. Variability of long-term response.

Long-term response to vasodilator therapy was assessed in six patients with PPH. Following an acute trial, each patient was restudied after (1) two months of drug administration, (2) one month of abstinence from therapy, and (3) an additional two months of therapy. Three of six patients had no long-term reduction of PVR after treatment; one showed a progressive increase. Of the three patients whose PVR was still reduced at the end of the second therapy period none showed a return of PVR to baseline during the abstinence phase, which may suggest that long-term reduction of pulmonary vascular tone may modify the vasoconstrictive component of this disease. The heterogeneous response of this small number of patients to sequential drug administration and withdrawal demonstrates the difficulty of interpreting previously reported clinical trials and underscores the need for a well-designed controlled study of vasodilator administration in these patients.

Endotracheal mass resulting from a transtracheal oxygen catheter.

A 50 percent or greater savings in oxygen usage and aesthetic benefits leading to increased compliance are reasons for increasing use of the transtracheal catheter for administration of home supplemental oxygen. Minor complications of the procedure are common and include catheter dislodgement, bronchospasm, subcutaneous emphysema, bleeding at the catheter site, as well as hemoptysis and wound infections. Rare complications include retroflexion of the catheter into the upper trachea from coughing, and fracture of the catheter with loss in the trachea. New, improved catheters and detailed descriptions for operator use may reduce the frequency of these complications. This report describes a potentially serious complication of a transtracheal catheter system which resulted despite appropriate use and care of the catheter.

Acute oxygen in patients with sleep apnea and COPD.

Nocturnal oxygen administered to patients with disordered breathing ameliorates hypoxemia. As a result, an important chemical stimulus to arousal is diminished. This could cause prolongation of disordered breathing events, worsen respiratory acidosis, and induce potentially harmful cardiac arrhythmias. The presence of chronic obstructive pulmonary disease (COPD) could further aggravate the situation since such patients may have depressed hypercarbic responses. To test this hypothesis, 20 obese men with sleep apnea and COPD were studied polysomnographically on two nights receiving air on one or oxygen at 4 L/min on the other. Supplemental oxygen increased mean DOB event duration from 25.7 to 31.4 seconds (p less than 0.001), increased end apneic PCO2 from 52.8 to 62.3 mm Hg (p less than 0.025), and decreased mean end apneic pH from 7.34 to 7.28 (p less than 0.001). At the same time, it improved mean sleeping and end-apneic oxygen saturation. The number of ventricular extra-systoles (PVCs) per minute of sleep showed small increases in three subjects while breathing oxygen. Complex ventricular arrhythmias were unaffected by oxygen in five subjects. Oxygen eliminated atrioventricular block in two subjects. We conclude that nocturnal supplemental oxygen does not increase ventricular arrhythmias in the majority of patients with COPD and coexisting disordered breathing events. While the clinical significance of an oxygen associated increase in ventricular extrasystoles in three subjects is unclear, nocturnal monitoring by telemetry or ambulatory recorder should be sufficient to detect such patients.

Amebiasis presenting as pleuropulmonary disease.

Seven patients with amebic liver abscess presenting as pleuropulmonary disease were admitted to hospital initially because of pulmonary symptoms and were found to have amebic liver disease. Three categories of pleuropulmonary involvement included reactive inflammation of the pleura or lung, rupture of a hepatic abscess into the pleural space and rupture of a hepatic abscess into the bronchial airways. The preferred medical treatment is with metronidazole, but rupture of hepatic amebic abscess into the pleural space requires drainage in addition to medical therapy. In contrast, rupture into the bronchus may provide spontaneous drainage so that only medical therapy is needed. Recovery from amebiasis in all three categories is generally complete. Morbidity and mortality increase with failure to correctly identify amebic infection of the liver as the underlying cause. Because, in new cases, no findings specifically suggest that pleuropulmonary disease is a complication of hepatic amebic abscess, this possibility needs to be considered, especially in persons who are at risk of having been infected with amebae.