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In a retrospective survey of lower limb amputations (diabetic major amputations n=34, minor n=33; non-diabetic major 28, minor 27), pressure sores developed following 55% of major and 20% of minor amputations (p<0.001). Sores developed after major amputations in 68% of diabetic but in only 39% of non-diabetic patients (p=0.018). The incidence of sores after minor operations did not differ between the two groups. After major amputations sacral sores were more common in diabetic than in non-diabetic patients (59 versus 36%, p=0.041), but the incidence of heel ulcers was similar. The mean age of patients developing sores was greater than in those who did not, in both diabetic (p<0.025) and non-diabetic patients (p<0.01). Peripheral vascular disease appeared to be a more important risk factor than neuropathy for pressure sore development. Sores were no more common after epidural or spinal than after general anaesthesia. The Waterlow score was a poor predictor of the risk of developing a sore. The incidence of sores was not related to pre-operative creatinine or albumin concentrations, but was greater in those whose haemoglobin concentration on the first or second post-operative day was <10 g/dL (p=0.015). In conclusion, pressure sores are very common following amputation and especially so after major amputations in diabetic patients. All potential amputees should be managed as being at high risk of developing sores. Copyright © 2001 John Wiley & Sons, Ltd.

In a retrospective survey of lower limb amputations (diabetic major amputations n=34, minor n=33; non‐diabetic major 28, minor 27), pressure sores developed following 55% of major and 20% of minor amputations (p<0.001). Sores developed after major amputations in 68% of diabetic but in only 39% of non‐diabetic patients (p=0.018). The incidence of sores after minor operations did not differ between the two groups. After major amputations sacral sores were more common in diabetic than in non‐diabetic patients (59 versus 36%, p=0.041), but the incidence of heel ulcers was similar. The mean age of patients developing sores was greater than in those who did not, in both diabetic (p<0.025) and non‐diabetic patients (p<0.01). Peripheral vascular disease appeared to be a more important risk factor than neuropathy for pressure sore development. Sores were no more common after epidural or spinal than after general anaesthesia. The Waterlow score was a poor predictor of the risk of developing a sore. The incidence of sores was not related to pre‐operative creatinine or albumin concentrations, but was greater in those whose haemoglobin concentration on the first or second post‐operative day was <10 g/dL (p=0.015). In conclusion, pressure sores are very common following amputation and especially so after major amputations in diabetic patients. All potential amputees should be managed as being at high risk of developing sores. Copyright © 2001 John Wiley & Sons, Ltd.

According to chemical data, methanol raises the shrinkage temperature of collagen significantly more than ethanol (86° C versus 70° C). Since increase of shrinkage temperature appears desirable in tissues to be embedded in paraffin, methanol was substituted for ethanol in Carnoy's fluid. This methanol-Carnoy mixture is referred to as methacarn solution. The fixation-embedding procedure was similar to that described in the study of Carnoy fixation. Methacarn-fixed sections showed little or no shrinkage and compared well with material fixed in Carnoy's or Zenker's fluid. Myofibrils, especially in endothelial and epithelial cells, were more prominent in methacarn- than in Carnoy-fixed tissues.

The Carnoy-fixation, paraffin-embedding procedure was modified to minimize shrinkage and to suit the schedule of general histology laboratories. Blocks of tissues were fixed in Carnoy's fluid overnight, transferred to absolute alcohol in the morning and washed in three changes of alcohol for a total of 6–8 hours. Tissues were then left in methyl benzoate overnight, transferred to an Autotechnicon in the morning, cleared in xylene and xylene-paraffin 1 hour each and infiltrated in 2–3 changes of paraffin for a total of 4–5 hours. This procedure has worked well in our hands for nine years.

The functional and digestive activities of the bovine alimentary tract, particularly the rumen, have been extensively studied during the past decade. Much of this research has been greatly facilitated by the use of the rumen fistula. Because certain limitations and disadvantages exist in present rumenal techniques the evolution of new techniques or the improvement of existing techniques as a means of gaining insight into digestive tract problems is important. The development of methods (a) for quantitatively sampling a continuously moving system without perceptibly upsetting normal physiologic relationships, (b) for sampling ingesta so that the exact source and identification of the sample is known and (c) for obtaining more information with regard to the digestive processes in other parts of the alimentary tract requires further attention.Young (1951) describes a technique for establishing a simple duodenal fistula in a 700 Ib. steer in which the eleventh rib is resected and the periosteum is used for subsequent osseous deposition thus strengthening the fistula area. McDonald (1953) modified Young’s technique and successfully established duodenal fistulas in sheep. The operation is illustratively presented by Dougherty (1955).Dougherty and Cello (1949), in studying absorptive processes in the digestive tract of sheep, employed an abomasal-duodenal-shunt fistula which was patterned, for the most part, after the technique described by Markowitz (Crocker-Markowitz fistula) (1954). Similar preparations for measuring the passage and composition of digesta from the abomasum of sheep were used by Phillipson (1952) and Masson and Phillipson (1952).Available literature does not describe an abomasal-duodenal-shunt fistula or

Castle and Locke1 fed muscle meat to normal persons, recovered the meat by causing vomiting, and refed it to patients who had pernicious anemia, thus causing a response of reticulated erythrocytes, an increase in the number of erythrocytes, and clinical improvement similar to that found when liver or its extract was used.This work led Sturgis and Isaacs,2 in collaboration with Sharp,3 to try the effect of feeding desiccated gastric tissue to patients who had pernicious anemia, with results similar to those obtained with liver or its extract. Likewise, Castle and Locke's work led me to feed raw gastric tissue to patients who had the disease, with results which already have been reported in six cases,4 and which were similar to those obtained with liver and liver extract. Another fact which suggested the use of gastric tissue was that I5 had found that in approximately

The demonstration by Minot and Murphy1 that the feeding of liver brings about complete remission in pernicious anemia led to the development of liver extracts of various types, of which that of Cohn and his associates2 is most generally used. A search for the effective substance in liver led to partial purification of the material, but these more or less purified substances developed by Cohn and his associates3 and by West and his associates4 have proved too expensive to be practical in the treatment of pernicious anemia.To Gänsslen5 belongs the credit of having first prepared at moderate expense an extract of liver suitable for injection intramuscularly. He injected daily into the gluteal muscles 2 cc., equal in effect to from 200 to 400 Gm. of liver.Castle and Taylor6 obtained a maximal response in reticulocytes from a single intravenous injection of the extract

Fenwick,1 in 1877, was the first to discover gastric atrophy in association with severe anemia. Cahn and von Mering,2 in 1886, were the first to notice the absence of free hydrochloric acid in pernicious anemia. Since that time much has been written regarding the occurrence of achlorhydria in pernicious anemia. The statistics of various authors differ considerably as to the incidence of free hydrochloric acid in this disease. It is now the consensus that practically all cases of pernicious anemia are accompanied by achlorhydria, The statistics of Levine and Ladd3 on 143 cases probably represent the present opinion as clearly as possible. They found achlorhydria in all except three of their 143 cases of pernicious anemia, and, in two of these three, the diagnosis of pernicious anemia was somewhat doubtful. This leaves only one of the 141 definite cases in which there was free hydrochloric acid. The

Functional disturbances affect practically every organ in the human body, including the esophagus. They may manifest themselves in various forms, such as globus hystericus, and the symptoms may be multitudinous, but there is one type that stands separate from the other, to which H. S. Plummer, in 1914, gave the name of hysterical dysphagia. Hysterical dysphagia is characterized by a sense of obstruction at or about the esophageal introitus, is practically always associated with pallor and secondary anemia, and frequently with enlargement of the spleen. It must be remembered, however, that the line of demarcation between hysterical dysphagia and other types of functional dysphagia is not always clear or definite, although as a whole it represents a very definite clinical entity.Vinson,1 in 1922, published the first paper on the diagnosis and treatment of this disease. Since that time many more cases of dysphagia of a functional

We have applied the term agranulocytosis to the condition in which there is complete or almost complete absence of granular leukocytes, accompanied by leukopenia and relative increase but, in most instances, absolute decrease of lymphocytes. The term hypogranulocytosis, which was first suggested by Weiss,1 we have applied to that condition in which there is less marked reduction in the number of granular leukocytes and well marked leukopenia, without absolute increase in the number of lymphocytes but with relative lymphocytosis. These terms are not applied to such distinct clinical entities as acute aplastic anemia, acute leukemia with normal or reduced total leukocyte count and agranulocytosis produced by known poisons such as benzene and roentgen rays; for the purposes of this discussion, however, they are applied to the peculiar blood picture associated with various types of infection. Brown2 seems to have been the first to report a case of pharyngeal

The use of liver and extract of liver has served to keep alive and relatively well most patients who have thus been treated regularly. In 1926, Minot and Murphy,1 in an epochal report, showed the value of feeding mammalian liver to patients with pernicious anemia. Whipple, Robscheit-Robbins and Hooper,2 in 1920, and Robscheit-Robbins and Whipple,3 in 1925, showed its value in anemia produced by repeated bleeding of animals. In 1927, Minot4 reported on the treatment of patients with an effective fraction of liver produced by Cohn. This substance brought about characteristic improvement in the condition of the blood and in the general symptoms. Minot, Cohn, Murphy and Lawson,5 in the following year, reported further on the results of treatment with extract of liver.Porter, Williams, Forbes and Irving,6 in 1929, reported on the production of a stable, aqueous extract of liver. Sixteen of the forty-five cases reported by them were

The recent experiments of Mann, Bollman and Magath1 have shown that a dog will become jaundiced after the complete extirpation of the liver and that the injection of hemoglobin increases the rapidity with which the icterus develops. These observations indicate that the liver must be considered, at least to some extent, as an excretory organ for the bile pigments. The physiologic possibility of a true hemolytic jaundice of extrahepatic origin, a point that heretofore has not met with universal acceptance, must be recognized. The observations of van den Bergh,2 Lepehne,3 McNee,4 Feigl and Querner5 and others on the changes in the van den Bergh reaction in cases of hemolytic jaundice have further served to emphasize the importance of a more accurate knowledge of the activity of the liver.Jaundice may be produced by three separate pathologic processes: (1) by a mechanical obstruction to the extrahepatic biliary passages with resultant resorption

Phenylhydrazine hydrochloride has come into general use as a therapeutic agent in the treatment of polycythemia vera. It was employed experimentally in animals in 1885 by Hoppe-Seyler.1 Morawitz and Pratt2 in 1908 used it for the purpose of producing experimental anemia in animals, and Eppinger and Kloss3 in 1918 were the first to apply it clinically in cases of polycythemia vera. The reports that have appeared in the literature since that time concerning the treatment of polycythemia vera by means of phenylhydrazine have, in the main, been very favorable. Good results have been reported by Eppinger and Kloss,3 Taschenberg,4 Levi,5 Owen,6 Brown and Giffin,7 Altnow and Carey,8 Stealy9 and Cabot.10 Bryan11 alone called attention to possible serious unfavorable effects of phenylhydrazine. In the early cases an unnecessarily severe anemia was produced and the occurrence of thrombosis was noted. The

Castle and Locke 1 have demonstrated that meat fed to normal persons and recovered by vomiting, and then fed to patients with pernicious anemia, contains some material that produces the same effect on the blood of patients with pernicious anemia as that which was shown by Minot and Murphy to result from the administration of liver. Practically all cases of pernicious anemia are accompanied by achylia, and I2 have shown that approximately 26 per cent of a large series of relatives of patients suffering from pernicious anemia have achlorhydria.Because of these facts, I decided to try the effect of feeding the raw and cooked stomach of a meat-producing animal to patients with pernicious anemia. By consultation with Mann and Feldman3 of the Mayo Foundation, it was found that the stomach of swine resembles the stomach of human beings much more closely than does that of bovine animals