BIRMINGHAM EYE INFIRMARY

J. V. Solomon
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Abstract

the endocardium was so extensively affected, there had been at some period of their history pericardial inflammation; though it was subordinate to the other affection, and much of the effusion into the serous sac was the result of post mortem change. The state in which the heart was found had either been brought about by intense inflammation with an injected condition of the cellular substances, followed by serous infiltration pressing on the muscular fibres, and thus directly weakening them, or diminishing their consistence. Or, this weakness might have been secondary, there being first the common condition of inflammation of a tissue in close connexion with muscle; viz., excitement, followed to undue extent in these cases by depressed vitality of the contiguous muscular fibre, which persisted. The weakened contractile force of the heart would cause smallness, irregularity, and feebleness of the pulse; but not necessarily slowness. This might or might not depend wholly upon "nervous paralysis of the heart's cavities," from the morbid changes extending to the cardiac ganglia; but I think a mechanical reason may be given to account in some measure for it. From the congested state of every organ after death, we may infer that the same condition was present to a great extent during life; and the heart must have partaken in this repletion. With weakened, atrophied muscular fibre, and inelastic lining membrane, the organ refused to be stimulated by the normal influx of blood into the systemic ventricle; but a gorged condition arising, the blood slowly oozed into the aorta, and was conveyed at a sluggish pace over the body. We may explain the changes in the nutrition of the muscle and its atrophy, by adopting Dr. Hodgkin's idea of defective nourishment, from partial blocking up of the coronary arteries by this fibroid deposit. Unfortunately, these vessels were not examined. I regret, also, that percussion was not employed for the purpose of testing the undue sonorousness of the chest, by which, according to M. lavirotte (Rev. Med. Chir., tom. xviii, p. 229), we may diagnose fibrinous concretions of the heart. If polypus obstructs the circulation, causing the lungs to receive less blood, and thus rendering them less dense, thickened endocardium, bulging into and diminishing the calibre of the ventricles, would act in the same manner. We may have hyperemis and anmmia each producing cerebral symptoms, such as were witnessed in these cases ; but there can be little doubt that here a defective supply of blood to the brain was the cause of them. Yet there probably was at times a state of passive congestion, causing hebetude and headache; and the second patient told me that he had been much troubled with epistaxis for a week or two before admission.
伯明翰眼科医院
心内膜广泛受累,病史上曾有心包炎症;虽然它是从属于另一种感情的,浆液囊里的大部分积液是死后变化的结果。心脏所处的状态,要么是由于注射了细胞物质的强烈炎症引起的,接着是浆液浸润压迫肌肉纤维,从而直接削弱了它们,或者减少了它们的一致性。或者,这种虚弱可能是继发性的,首先是与肌肉密切联系的组织发炎的常见情况;也就是说,在这种情况下,伴随兴奋而来的是相邻肌肉纤维的活力下降,这种情况持续存在。心脏收缩力的减弱会导致脉搏变小、不规则和无力;但不一定是慢。这可能取决于也可能不完全取决于“心脏腔的神经性麻痹”,从病态的变化延伸到心脏神经节;但我认为,在某种程度上,可以用机械上的原因来解释。从死后每个器官的充血状态来看,我们可以推断,在很大程度上,生命中也存在着同样的情况;心脏一定也参与了这种充盈。由于肌纤维减弱、萎缩,内膜缺乏弹性,器官拒绝接受正常流入全身心室的血液的刺激;但是由于出现了充血的情况,血液慢慢地渗进主动脉,以缓慢的速度在全身输送。我们可以通过采用霍奇金博士的营养缺陷的观点来解释肌肉营养的变化及其萎缩,这种营养缺陷是由肌瘤沉积物部分阻塞冠状动脉引起的。不幸的是,这些容器没有被检查。我还感到遗憾的是,没有使用叩击法来检验胸部是否有不适当的声音,根据拉维罗特先生(dr . Med. Chir.)的说法。,汤姆。Xviii,第229页),我们可以诊断心脏纤维性结块。如果息肉阻碍循环,导致肺部接受的血液减少,从而使其密度降低,心内膜增厚,向心室膨胀并缩小心室的直径,也会以同样的方式起作用。我们可能有充血症和贫血症,每一种都会产生大脑症状,如在这些病例中所见;但毫无疑问,这是由于脑部供血不足造成的。然而,有时可能会有一种被动充血的状态,引起疼痛和头痛;第二个病人告诉我,在入院前的一两个星期里,他一直被鼻出血困扰着。
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