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1 Departments of Thoracic Surgery, Mount Zion Hospital and University of California School of Medicine
Totally absent evidence of lobar bronchial obstruction in our own cases of middle lobe atelectasis has made us question the hitherto accepted concept of primary nodal bronchial compression and secondary distal atelectasis. For the reasons noted in the body of the paper, we feel the evidence for this mechanism quoted in the many papers on the subject to be unsubstantiated, except in rare instances.
There is undoubtedly a selectively increased incidence of middle lobe atelectasis complicating even minor inflammatory proceses here. Our concept is that the basic pathogenetic factor for atelectasis lies in the isolation of this small lobe from the right upper and lower lobes, and thus from the aerating effects of collateral ventilation. Secondary infection superimposed upon repeated or protracted middle lobe atelectasis enhances the development of the chronically shrunken middle lobe with occasional prominence of the regional peribronchial nodes, as a consequence, not a cause.
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