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DOC 0000017443

419 pages · May 08, 2026 · Broad topic: General · Topic: 800 00 Wom · 305 pages OCR'd
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£<f • on the subject believe that the cerebral effects of uremia are the result of retention of ph*nn?io compounds, A smaller number believe that retained nitrogenous substances such as Indican and unidentified products of intermediary protein metabolism are the responsible agents. The only sphere of agreement is the well-established fact that injection of normal urine into labors- / _ I' , _ , tory animals in adequate doses will produce coma and death, whereas the urine from patients in uremia is relatively non-toxic, the toxic substances remaining in the bloodstream of the affected individuals. It is interesting to note in tbe transactions of the Macey Foundation on Renal Function from 1949 to 1953 that a conference has not been devoted to the subject of uremia, 2 - Hepatic Coma. The cerebral effects of hepatic failure consisting of high fever and progressively deepening coma have been stressed by Heyd, and are often known as the Heyd syndrome; The cause of the coma is generally attributed to the retention of or ammonium carbonate. However, with the introduction of the artificial kidney the removal of ammonia by dialysis, which is readily accomplished, has been shown to have no influence on the comatose condition of the patient. Some investigators have postulated the retention of bile acids as the cause of the coma. There is even less information available on hepatic coma than on uremia. , 3 - Eclampsia. Eclampsia remains "a disease of theory". The convulsions and coma that occur in these patients are of unexplained origin. The concensus of opinion to date is that the effects are brought about by spasm of the smaller blood vessels but the cause of the vascular spasm remains undetermined. 4 - Cachexia. The disorientation and coma of patients with cachexia resulting from malignant disease have provoked remarkably little attention in recent years. Willis believes that the cachectic state is an expression of malnutrition with the retention of acetone bodies and is therefore related to diabetic coma. However, there are no adequate studies to substantiate this theory and the treatment of such patients with intravenous glucose and injections of insulin jhas not been carried out to my knowledge. ^
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