Two cases of acute haemorrhagic pancreatitis / by J.H. Bryant.

  • Bryant, John Henry.
Date:
[1900]
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Licence: In copyright

Credit: Two cases of acute haemorrhagic pancreatitis / by J.H. Bryant. Source: Wellcome Collection.

Provider: This material has been provided by The Royal College of Surgeons of England. The original may be consulted at The Royal College of Surgeons of England.

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    necrosis, but I have not been able to find any note of it as having occurred outside the peritoneal cavity. Flexner2 and Williams3 4 have published the results of their work on the pathology of this curious change in the fat and they both give important summaries of the work of other patho- logists. The first pathologist who directed attention to fat necrosis was Balseri in 1882; he found it either within the inter-acinous tissues of the pancreas or in the adjacent and distant fat. Langerhans5 injected the sterilised pulp of fresh pancreas into the peritoneal tissues of rabbits and inflammation resulted with evidence of fat necrosis. He, however, only had one successful experiment out of 12. He satisfied himself that a decomposition of the fat molecule occurred with liberation of the fatty acids and considered that it was due to the action of the fat-splitting ferment. Dettner6 experimented with pure trypsin which produced a sero-hsemorrhagic effusion in the peritoneal cavity but no fat necrosis. Hildebrand7 suggested that the hemorrhage in acute hemorrhagic pancreatitis was due to trypsin and that the fat necrosis was caused by the action of the fat- splitting ferment. Hlava8 produced hemorrhagic pancrea- titis and fat necrosis by injecting Klebs-Loffier bacilli into the pancreas after a laparotomy. Kosenbach and Jung9 experimented with trypsin and with portions of pancreas which they introduced into the abdominal cavities of rabbits. They obtained fat necrosis with pieces of pancreas once out of four times. Flexner’s conclusions are as follows:— 1. In peritoneal fat necrosis the fat-splitting ferment is demonstrable at certain stages of the pathological process. 2. It is present in greatest amount in the early stages and may disappear in the later ones when the healing is well advanced. 3. Although it cannot be affirmed that steapsin is the direct cause of the necrosis of tissue such an assumption is rendered highly probable by its constant occurrence in the diseased areas, its absence from the healthy fat, and the 3 Journal of Experimental Medicine, 1897, vol. xi., pp. 413 to 425. 3 Boston Medical and Surgical Journal, 1897, vol. i., pp. 345 to 348, and 1898, vol. i., 342. 4 Virchow's Archiv, 1882, Band xc., p. 520. 5 Experimenteller Beitrag zur Fettgewebsnekrose, Virchow’s Fortschrift. 6 Inaugural Dissertation, Gottingen, 1895. 7 Centralblatt fiir Chirurgie, 1895, Band xxii., p. 297. 8 Centralblatt filr Pathologie, 1897, Band viii., p. 792. 8 Inaugural Dissertation, GBttingen, 1895.