Contributions to the pathology and therapeutics of typhus fever / by Joseph Bell.

  • Joseph Bell
Date:
[1860]
Catalogue details

Licence: Public Domain Mark

Credit: Contributions to the pathology and therapeutics of typhus fever / by Joseph Bell. Source: Wellcome Collection.

    13/100 (page 397)
    results are confirmatory of those of Louis; and it would be a strange sort of putrefaction which would stop short at the left and not affect the right ventricle. But further, in many of our cases dissection was performed before putrefaction of the body had commenced, and, as we have before remarked, the voluntary muscles were unaltered. Again, we often observed that the change of the muscular structure only penetrated to a certain depth, and was found to termi¬ nate by a well-defined line. Thus, we could see the external portion of the ventricle affected to the depth of from one-eighth to the fifth of a line, and in such cases the musculi pectinati and column® carnese remain unaffected. But the great argument against this argument [of putrefaction] is the fact of our having been able to connect the important physical phenomena during life with the softened condition as observed after death. We have traced the rise, pro¬ gress, and retrocession of the weakened condition during life, in cases which, from their close similarity with those that have presented this special alteration of the heart after death, furnish the strongest possible proof that the patients had laboured under, and afterwards recovered from, this peculiar alteration of the heart.”—Disease of the Heart, p. 371. Such facts prove most satisfactorily that the softening of the heart is not the result of putrefactive decomposition. (b) Inflammation.—Both Louis and Stokes regard the disease as a secondary effect of typhus poison, but contend that the change is of a wcm-inflammatory nature. Whilst the first part of this proposition may be readily admitted, yet the correctness of the last clause may be questioned. Let us examine the grounds upon which Louis and Stokes have founded their conclusions. Louis states that he found “in nearly all the cases of softening, the walls of the ventricles were evidently much less thick than usual, those of the left especially, which were often only three lines thick.* He also informs us that he found the parts diseased, of a pale colour, and devoid of moisture, and without either puru¬ lent secretion, or effusion into pericardium :—• “ If these facts,” he observes “ are insufficient to enable us to discover the cause of the softening of the heart, at least they exclude the idea of one of those affections which usually induce a great number of diseases, viz., inflammation. For how can we allow that inflammation is the cause of an acute softening, accompanied by a diminution of thickness, paleness of colour, and a kind of dry¬ ness of texture which is the seat of it? . . . If we knew any cause of disease exactly the reverse of inflammation, it would be proper to refer this softening to it. . . . The walls of the heart, although more or less softened, showed no purulent secretion, nor was there any inflammation of the pericardium, which would have been the case had this softening been caused by inflammation.j- * Un autre fait qu’il importe de signaler, c’est que dans presque tous les cas de ramollissement dont il s’agit, les parois des ventricules, celles du gauche sur- tout, etaient manifestement moins epaisses, et debeaucoup, que dans l’etait naturel (souvent trois lignes pour le ventricule aortique). Et comme cette diminution d’epaisseur etait bornee aux cas de ramollissement, il faut la considerer ce me semble, comme une disposition morbide.— (Op. cit., tom. i. p. 531.) fSi ces faits sont encore insuffisants pour decouvrir la cause du ramollissement du coeur, au moins sont-ils exclusifs de l’une de celles qui president a un grand nombre des lesions, je veux dire l’inflammation. Car comment l’admettre dans un ramollisement aigu, accompagne de l’amincissement, de la decoloration et d’une