We read with interest the recent case report and review of post- obstructive pulmonary edema by Willms and Shure. A recent case at our hospital prompted a review of the anesthesia-related litera­ture.

We note that these authors implicate post-anesthesia laryngo- spasm as the most common cause of this syndrome in adults. Although they reported that the majority of patients were free of diseases predisposing to pulmonary edema, they did not comment on the presence of factors which might increase the risk of airway obstruction in the anesthesia-related subgroup.

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We read with great interest the study by Jackson et al on the trends in asthma mortality in 14 different countries. As stated by these authors, “it is clearly of considerable importance to ascertain in countries with increasing reported asthma mortality rates, whether these trends are real or due to changes in accuracy of certification or in diagnosis fashions”. We wish to add some comments about the accuracy of methodology used in these epidemiologic studies reporting asthma mortality data, ie, the accuracy of death certificates. We wish to report a discrepancy between the French statistics concerning asthma deaths and our own experience, which was previously reported in this journal.

We compared the age distribution of asthmatic patients who died from asthma during the same period (1983 to 1984) as reported in the two following studies: 1) the report of asthma mortality in France given by Bousquet et al using the data of the Institut National de la Sante et de la Recherche Mёdicale (data also used by Jackson et al) and 2) the report of asthmatic deaths observed in a prehospital mobile emergency care unit in Paris, France.

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We have read with interest the retrospective study by Leslie et al (Chest 1988; 94:603-08) on the clinical features of patients with undiagnosed pleural effusions subjected to repeat pleural biopsies with the purpose of distinguishing those patients with nonspecific pleuritis (NPE) from malignant (MPE) or tuberculous pleural eflusions (TPE). According to their analysis, all patients having two or more of the following factors should undergo an aggressive diagnostic approach given the likelihood of underlying malignant or granulomatous disease: weight loss, fever >38°C, positive PPD, pleural fluid lymphocytosis greater than 95 percent, and a large efiusion.

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Collapsed lung is one of the important problems in critically ill patients, and the clinical condition may worsen rapidly. Treatment with a therapeutic fiber­optic bronchoscopic procedure at the bedside was introduced and good results were reported in many studies. This therapeutic procedure includes repet­itive sputum suctioning and bronchial washing with normal saline solution; complete or partial re-expan­sion of atelectasis was attained in 60 to 90 percent of the cases.

When the lung volume decreases, the alveolar radius will decrease and the alveolar pressure rise according to Laplace relationship: Рт = 2 T/r (Рт-alveolar pres­sure, T-alveolar surface tension, r-alveolar radius). In these conditions, the surfactant will work to lower the alveolar surface tension; this reduction in surface tension offsets the reduction in alveolar radius and prevents alveolar pressure from rising. But if the atelectasis is profound, the reduction in surface ten­sion can not overcome the reduction in alveolar radius, and the alveolar pressure will rise and create a higher critical opening pressure in the atelectatic alveoli and lower lung compliance. The above findings are espe­cially common in cases with a small area of collapse. In these cases, the transpulmonary pressure of the atelectatic alveoli is often too low to overcome the critical pressure. These refractory atelectasis do not easily re-expand even after the above broncho­scopic procedures. It would be useful if we could introduce positive pressure ventilation directly into the collapsed area to overcome the critical opening pressure. But if we can not sufflate the air directly into the atelectatic alveoli, the insufflated air will tend to be distributed into the noncollapsed areas because of lower airway resistance and higher lung compliance. This will result in a hyperinflated normal lung area which in turn will compress the collapsed area.

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After 12 of the 14 procedures, the chest x-ray film showed complete reexpansion; in the remaining two, case 5 and the secondary procedure in case 12, the x-ray film showed partial re-expansion. In case 5 the collapsed lung reexpanded completely after six days of continuous, intensive, pulmonary care. In case 12, a third bronchoscopic procedure was performed with immediate full re-expansion (Table 1).

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Twelve patients were admitted to the medical or surgical ICU for the different critical conditions (Table 1). The duration of lung collapse ranged from 24 to 120 hours. All had received intensive respiratory care since admission to prevent atelectasis. When the lung collapsed, another 24 hours of respiratory therapy was per­formed before the fiberoptic bronchoscope procedure.

A fiberoptic bronchoscope was used. A three-way adaptor was connected to the suction channel of the bronchoscope. One port was used to introduce room air by Ambu bag, the other port was connected to a pressure gauge to monitor the peripheral airway pressure during air insufflation (Fig 1).

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