Remarks on (i) chronic haemolytic (ii) pancreatic jaundice / by H.D. Rolleston.

  • Rolleston, Humphry Davy, Sir, 1862-1944.
Date:
[1912?]
Catalogue details

Licence: In copyright

Credit: Remarks on (i) chronic haemolytic (ii) pancreatic jaundice / by H.D. Rolleston. Source: Wellcome Collection.

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    contradistinction to obstructive or hepatogenous jaundice. The experimental investigations of Minkowski and Naunyn on geese (1886) and others showed that bile was manufactured only in the liver, and that jaundice could not occur when that organ was removed from the circulation. Stadelmann (1881-3) and, later, W. Hunter, proved that the jaundice caused by toluylenediamine was really due to inflammation and obstruc¬ tion by viscid bile of the small intrahepatic ducts, and it was concluded, partly from microscopic examination and partly from analogy, that the jaundice seen in various infective and toxic conditions—such as septicaemia, pneumonia, acute yellow atrophy, haemoglobinuria, snake-bite, and poisoning by drugs— in which no obstruction was visible, was also caused by intrahepatic cholangitis. Or, as Hunter summed up in “Allbutt’s System of Medicine” (1897, IV, 81): “Instead, then, of the two varieties of jaundice formerly described—one hepatogenous or obstructive, the other haematogenous or non¬ obstructive—it is necessary now to recognise one class only. All jaundice is hepatogenous, the result of absorption of bile formed and excreted by the liver.” The cases in which no gross obstruction was forthcoming were spoken of as toxaemic or haemohepatogenous. The view expressed by Hunter is that generally accepted at the present time, though, as will be shown later, the pendulum is beginning to swing back to the haematogenous origin as regards certain cases. Before going on to this question it may be mentioned that at different dates Frerichs, Liebermeister, Szubinski, Minkowski, Pick, and others suggested that in certain conditions, such as toxaemia, disturbance of the metabolism of the liver cells may lead to secretion of bile directly into the blood-vessels or lymphatics of the liver instead of into the bile capillaries (diffusion or acathetic jaundice, jaundice from parapedesis, paracholia). This hypothesis, which is obviously difficult or impossible to prove, was framed to explain cases of non¬ obstructive or toxaemic jaundice. The channel by which bile when dammed up in the liver reaches the circulation was shown by Saunders (1803), Fleischl (1874), and Vaughan