The essential abnormality in bronchiectasis, according to Kline,1 is the absence, atrophy, damage or destruction of elastic and muscular tissues of the bronchial wall. Usually severe inflammation of the various coats occurs first with damage or destruction of the elastic and muscular tissues. Finally there is complete destruction of a portion or all of the bronchial wall, associated with inflammatory and chronic changes of the regional pulmonary parenchyma. In children staphylococci, in adults the Miller-Vincent micro-organisms are frequently the causative agents responsible for the necrotizing changes. Cylindric, fusiform or saccular bronchiectasis develops, depending on the location, extent and severity of the process.
Bloch and Francis2 differentiate primary or predisposing factors in the etiology and secondary or immediate agents. The primary factors consist largely of acute infectious diseases involving the upper respiratory tract. Among the secondary causes involvement of the nasal sinuses, chiefly the maxillary, is increasingly recognized as