Computed tomography in a patient with a peripheral lung cancer in the right upper lobe revealed obliteration of the extrapleural fat and direct connection of the tumor with an intercostal soft tissue mass of similar density. The findings were suggestive of chest wall invasion by the cancer which was, however, proven to be false after en bloc resection of the tumor and the contiguous chest wall. Such a diagnostic pitfall could be avoided if special attention were paid to the asymmetry of the CT image at the level of upper thoracic outlet due to improper positioning of the patient.

Adenocarcinoma↗

PubMedDate not supplied

Exercise-induced asthma: a difference in opinion regarding the stimulus.

There has been some controversy regarding the mechanism whereby exercise can provoke an attack of asthma. It is generally agreed that heat and water are lost from the respiratory tract in bringing the air inspired to body conditions. During strenuous exercise, there is a marked increase in ventilation rate and some of the burden to heat and humidify the inspired air is transferred to the intrathoracic airways. The net effect of the air conditioning process is to cool and dehydrate these airways. There have been two hypotheses put forward to account for the mechanism whereby these events lead to exercise-induced asthma (EIA). One hypothesis proposes that cooling of the airways followed by rapid rewarming, at the end of exercise, leads to a reactive hyperemia and edema of the bronchial vascular bed "which if sufficiently severe results in the airway obstruction of EIA." The other hypothesis proposes that the rate of loss of water from the periciliary fluid during exercise exceeds the rate of return and, as a result, there is an increase in ion concentration and subsequent hyperosmolarity of the periciliary fluid. Thus the events related to drying rather than cooling are the stimulus to EIA. This paper presents the case against rapid rewarming of the bronchial vasculature as the stimulus to EIA and puts forward an argument and data in support of the case for airway drying and an increase in osmolarity being the critical event which determines the presence and severity of EIA.

Asthma↗

PubMedDate not supplied

Non-isotonic aerosol challenge in the evaluation of bronchial hyperresponsiveness.

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Aerosols↗

PubMedDate not supplied

Airway responsiveness in asthma: bronchial challenge with histamine and 4.5% sodium chloride before and after budesonide.

Inhalation of histamine is commonly used to assess the severity of and to monitor treatment of asthma. Histamine causes airways to narrow by acting directly on specific receptors. Hyperosmolar saline causes airways of asthmatics to narrow indirectly by endogenously mediated events that are potentially modified by drugs used to treat asthma. We wished to determine if hyperosmolar saline (S) is a useful challenge for assessing the airway responsiveness of asthmatic subjects being treated with steroids and to compare changes in airway responses to those changes observed with histamine (H). The airway responses to S and H were assessed by the dose of aerosol provoking a 20% fall in FEV1 and the percent fall in FEV1 per unit dose of aerosol inhaled-the dose response slope (DRS). We studied asthmatic subjects before and during treatment with budesonide-1000 micrograms per day. There was a significant correlation (Spearman's) between PD20 to H and S and DRS to H and S after budesonide (P < 0.05). After 2 months of treatment; the mean PD20 (95% CI) was increased 4.6 (2.5, 8.6) fold to H, and 9.7 (4.2, 22) fold to S, (P = NS) the DRS reduced 7.0 (4.3, 11.5) fold to H and 16.6 (8.4, 33) fold to S (P = NS). Responsiveness to H, measured by PD20 remained throughout the treatment, whereas five subjects did not record a 20% fall after S and the DRS decreased to values close to those we measured in healthy subjects. In conclusion, challenge with 4.5% sodium chloride can be used to assess the early benefits of treatment with aerosol steroids.

Adolescent↗