Intrathoracic aneurysm / by F. de Havilland Hall.

  • Hall, Francis de Havilland.
Date:
1913
Catalogue details

Licence: In copyright

Credit: Intrathoracic aneurysm / by F. de Havilland Hall. Source: Wellcome Collection.

Provider: This material has been provided by The University of Leeds Library. The original may be consulted at The University of Leeds Library.

    19/98 page 15
    and a gradually increasing difficulty of breathing. The former is probably due to implication of the vagi or recurrent laryngeal nerves, or to compression of the small branches of the pneumogastric forming one of the pulmonary plexuses ; and the latter to direct pressure upon the trachea or bronchial tubes. Reflex irritation of the vagi will cause most alarming and paroxysmal attacks of dyspnoea due to spasm of the adductors of the vocal cords, precisely resembling attacks of laryngismus stridulus occurring in childhood. As Gairdner long ago pointed out, pressure of an aneurysm upon the pulmonary plexus of nerves may give rise to symptoms very closely resembling those met with in spasmodic asthma. The possibility of the presence of an aneurysm should therefore be borne in mind, in the event of the sudden occurrence of an asthmatic paroxysm in a previously healthy man. Occasionally pressure upon the trachea will give rise to dyspncea with paroxysmal exacer- bations resembling asthma. This is probably due to varia- tions in the fulness of the aneurysmal sac. Dyspnoea may also result from congestion of the lungs, from pressure on the vessels in the root of the lung, or from a dilated con- dition of the bronchi. Inflammatory changes in the pleura may occur by extension from the aneurysmal sac, and a plem-al effusion may be the result, giving rise to persistent dyspncea. Secondary changes in the heart, as a result of aortic regurgitation, may also cause dyspnoea. The sudden onset of dyspnoea in a patient in whom an aneurysm may or may not have been suspected may be due to the rapid dilatation of some portion of the aneurysmal sac already in contact with the trachea; this may bulge into the air- passage, and may even be recognised by the aid of the laryngoscope.The character of the stridor may be of assistance in deciding as to the cause of the dyspnoea. If stridor be heard only with inspiration, the difficulty of breathing arises from paralytic stenosis of the glottis, whereas if the obstruction be seated in the trachea there will be stridor with both inspiration and expiration. In November, 1900, I opened a discussion on Aneurysm at the Medical Society of London by reading notes on a case which had been under my observation for nearly five years^
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