fully with the subject. One paper, however, is worthy of note, as forming an exception to this statement. Rokitansky, in 1838, reported eight cases of this lesion and discussed at length its etiology and pathology. He laid especial stress upon the association of spontaneous rupture with atheromatous degeneration of the artery wall and expressed the belief that this or some other form of degeneration or faulty development would be found in every case to account for the accident and that it never occurred in individuals with healthy vessels. In seven of his eight cases atheroma was the direct cause and in the eighth there was congenital defect in the development of the aorta, its walls being very thin and non-resisting. He also described at some length those cases in which the rupture led to the formation of a dissecting aneurism. Since 1850 the contributions to this subject have been trebled, 96 papers in all having been published and more than that number of cases recorded. Of these papers two are of especial note; one by Broca in 1852 (Bull. Soc. Anat. de Paris, Vol. xxvii, 275) and the other by Bostroem in 1888 (Deutsch. Archiv.). Broca, in addition to reporting a very interesting case in a man 29 years old, analyzed twenty-eight other cases which he had been able to collect from the literature up to his time. Like Rokitansky, Broca called attention to the frequent association of this lesion with atheroma, which is undoubtedly the most important factor in its etiology, and, in addition, emphasized a further fact of importance in the same connection, also mentioned by Rokitansky, by ascribing a certain percentage of cases directly to hypertrophy of the left ventricle associated with atheromatous degeneration of the aorta. According to Broca the increased force of ventricular contraction in these cases produces a more powerful recoil of the column of aortic blood following systole than the weakened vessel can stand, especially if there are protruding edges of calcareous plates offering additional resistance to the flow of blood. The result of such a condition of affairs as this is a tearing up of the intima, and in some cases also of the media with it, the rupture of the outer coat occurring some time later as a rule, either with or without an infiltration of blood between the two outer coats. For ruptures to occur in this way it is necessary that the aortic valves be healthy and allow no regurgitation of blood, and for this reason aortic valvular disease is but rarely noted in these cases. It was present in only two of the 50 cases that we have collected. The paper by Bostroem mentioned as the second of importance since 1850 is probably the most exhaustive treatise on the subject of dissecting aneurisms. that has been published. He does not deal with cases of simple rupture, but confines himself strictly to that form of rupture which leads to the infiltration of blood between the various coats of the vessel, and which we will speak of later on. In Woodward of Washington, D. C., contributed a short paper on this subject in 1875 (Transactions Medical Society, Washington, D. C., 1875), in which he upholds the view that rupture may occur in a perfectly healthy aorta. this he stands at variance with the best authorities as already stated. Unfortunately in the case that he cites as illustrating his view the aorta, though not extensively diseased, was by his own account of it not normal, showing evi- ' dently areas of fatty change, which though they did but little damage, must have rendered the vessel less resistant than normal. It is safe to assume that Woodward's view is not a correct one and that underlying every case of rupture there is some alteration, some reduction in the strength of the aortic walls. Age and Sex.-It would most naturally be supposed that the largest number of cases of spontaneous rupture of the aorta or of any other vessel, or of the heart itself, would occur in men, since they are more exposed to hardships and to enduring heavy strains than are the gentler sex. Moreover, alcoholism and syphilis, which play such an important part in the causation of atheromatous degeneration, though not uncommon among women, are far more frequent among men, and the results of our analysis of 50 cases taken from the literature of the past century, at random, from which all the figures subsequently to be given are taken, shows that this accident occurs in men in the proportion of 68 per cent. to 28 per cent. in women, there being 34 males, 14 females, and 2 cases in which the sex was not mentioned. With respect to age, one would expect to find the number of cases increase as life advances, the greater number being among the aged. Broca showed that of his 28 cases the majority occurred between the ages of 30 and 60. Among our own cases this is also true, for between these ages there were 27 cases, while previous to 30 only 6, and after 60 but 11, making 17 in all, with 6 others the ages of which are not given. In other words, 54 per cent. of all cases occurred between 30 and 60, and but 34 per cent. at all other ages. How to explain the fact that the greater number of cases does not occur later in life than 60 is difficult, unless we take into consideration the fact that as a rule after the age of 60 less heavy work is done, and consequently less strain endured, and also that atheroma, when due to alcoholism and syphilis, as it most frequently is, developes comparatively early in life. Immediate Cause of Rupture.-While underlying the rupture of the vessel and being its determining cause is some defect in the walls of the vessel itself, some condition that causes a lessened resisting power to the force of the contained blood current, in the majority of cases one can find, in addition, some immediate cause for the fatal accident. In the case that we report there being unfortunately no history obtainable, we can not say with absolute certainty what the rupture was to be attributed to, but from the histories of other similar cases, and from the fact that the man died while at work, and further, that he was accustomed to heavy labor, we are jus tified, as already stated, in assuming that the strain of some unusual effort probably determined the accident. In reviewing our collected cases on this point it is interesting to note to what immediate cause the breakage of the vessel was attributed by the various recorders. Thus for example out of the 50 cases the recorders neglected to mention whether or not any cause was apparent in 21 cases, leaving 29 in which this point was discussed. Out of this number in only 5 cases, or in 17.25 per cent., it was stated that no cause whatever could be discovered, the patients dying while perfectly quiet, either in bed or sitting still, and apparently in perfect health. For the remaining 24 cases the following causes were given: Unclassified strains, 6, or 20.71 per cent.; strain of vomiting, 3, or 10.34 per cent.; strain of convulsions, 5, or 17.25 per cent., leaving 10 cases in which the apparent determining cause was a greatly heightened blood pressure in 8, as mentioned and described both by Rokitansky and Broca, brought about by hypertrophy of the left ventricle in 5, or 12.25 per cent.; and by passions (anger, etc.) in 3, or 6.89 per cent., the remaining 2 cases being caused by some accident, as a fall, etc. From these figures it will be seen that practically all cases of rupture, barring those due to accident, are due to heightened blood pressure brought about in some way. It is easily seen how an hypertrophied heart can bring about this result, or how the passions can reflexly produce the same thing. Strains of one kind or another heighten the arterial pressure in a double manner, as pointed out by Broca (loc. cit.) in 1852. In the first place, contraction of the abdominal muscles compresses the abdominal aorta to a certain extent, in this way increasing the tension in the thoracic portion of the vessel; this in turn still further increases the blood pressure by reflexly causing the heart to act more vigorously against the unusual resistance thus produced. Under the double strain the walls give way. BIBLIOGRAPHY. 1 Breithaupt, C. W., "De Ruptura Aortae," 8vo. Berolini, 1836. 2 Von Heider, T., "Ueber Spontane Ruptur der Aorta Ascendens, 8vo. Bitterach, 1857, 3 Kreisler, O., De Spontanea Aortae Ruptura," 8vo. Halis Saxonum, 1854. 4 Langerbach, C. J. A., Ueber Aorten Rupturen mit Bezug auf Einen Fall von Totalen Quer-Ruptur der Aorta in Folge einwerkung indirecter Gewalt," 40, Kiel, 1869. 5 Rehm, H.," Ueber die Ruptur der Aorta," 8vo. Erlangen, 1852. 6 Rupprecht, B., "De Ruptura Aortae Spontanea," Berolini, 1839. 7 Vehling, C., Perforation der Aorta in, dem Digestionstractus," 8vo. Buckeburg, 1878. 8 Wollner, W., Ueber die Spontane Ruptur der Aorta und das Verhältniss der Arterienerkrankung ueberhaupt," 8vo. Erlangen, 1856. 9 Agnew, E. J., "A Case of Rupture of the Aorta," Tr. M. and Phys. Soc., Calcutta, 1829, IV., 439. 10 Armitage, “Rupture of the Abdominal Aorta in a Child," Tr. Path. Soc., Lond. 1857-58, IV, 85. 11 Bennett, J. R. A Case. Med.-Chir. Tr. Lond. 1849, XXXII, 157-165. 1 Pl. 12 Beyer. A Case. Gen. Ber. d. k. Rhein, Med.Coll. Koblenz, 1816, 72. 13 Bishop, C. S., A Case Communicating with the Oesophagus. Proc. Path. Soc. Philad. 1860, II, 58-60. 14 Bonnemaison, Rev-Med-de Toulouse, 1878, XII, 273-282 15 Bracey, A. British M. J. Lond. 1866, II, 38. 16 Bristow, Tr. Path. Soc. Lond. 1863, XIV, 86. 17 Broca, Bull. Soc. Anat. de Paris, 1850, XXV, 246-255. Also another Case, Ibid, 1852, XXVII, 273. 18 Browning, B., British Med. Journ. 1871, II, 661. 19 Chamberlain, W. H., N. Y. Med. Journ. 1874, XX, 401-412. 20 Crisp, Treatise on Stricture, Diseases and Injuries of Blood Vessels, London, 1874, 290. 21 Champernois, "Observations du Rupture Violent des Membranes Internes de L'Aorte," J. de la Sect. de Med. de la Soc. Acad. Loire-Inf. Nantes, 1854, n. s. XXX, 207-214. 22 Chauvel, J.," Note Sur les Ruptures de L'Aorta," Gaz. Med. de Par. 1865, 3, s. XX, 409-429. Alos another Case. Ibid 1866, 3. s. XXI, 271-276. 23 Cowdell, C., "Two Cases due to Ulceration of the Aorta," Assos. M. J. Lond. 1853, 539-541. 24 Bruberger, Berl. Klin. Woch. 1870, VII, 360–362. 25 Buck, N. Y. M. J. 1867, IV, 375. 26 Burge, J. H. H. Proc. Med. Soc. Kings Co., Brooklyn, 1876, I, 19. 27 Collender, G. W. Tr. Path. Soc. Lond. 1856-7, VIII, 164-166. 28 Anon, Med. Times and Gaz. Lond. 1857, XIV, 376. [Case of Dr. Ball.] Lancet, Lond. 1839, II, 833. 29 Allg. Wien Med. Ztg. 1869, XIV, 370. Med. Times and Gaz. Lond. 1870, I, 95. Rep. Com. Pub. Charat. and Corrections, N. Y. 1871, XII, 47. 33 Anon, Ber. d. k. k. Krankenanst Rudolph-Stiftung in Wien, 1868-69, 122. Lancet, 1832-33, p. 129. 66 34 37 Dickenson, Tr. Path. Soc. Lond. 1866, XVII, 84. 38 Duffey, G. H., Med. Times and Gaz. Lond. 1865, II, 680. Also another case. Doublin, Q. J. M. Sc. 1866, X LI, 202. 39 Elliotson, J. Lancet, Lond. 1832. I, 129–132. 40 Ellis, C. Boston M. and S. J. 1855, LII, 418. Also another case, Ibid, 1861, LXV, 371. Two other cases, Ibid, 1865, LXXII, 80. 41 Emmert, E. F. Schweiz. Ztschr. f. Nat. u. Hielk. Heilb. 1838, III, 125-129. 42 Fauvelle, Bull. Med. du Nord. Lille, 1864, 2, s. v. 182, 183. 43 Foot, A. W. Doub. Q. J. M. Sc. 1873, LVI, 427. 44 Forster, J. C. Tr. Path. Soc. Lond. 1848-50, I, 243. Also a case due to accident, Ibid, 1856-57, VIII, 163. 45 Morgagni, De Ledibus et Causis Morborum, Epist. XXV1 § 15, 17, 21, Epist. XXVII and XXVIII. 46 Fox, A. W. Lancet, Lond. 1879, I, 511. 47 Gaskoin, Tr. Path. Soc. Lond. 1863, XIV, 84. 48 Giegel, A. Wurzb. Med. Ztschr. 1861, II, 107-112. 49 Gibert, Bull. Soc. Anat de Paris, 1858, XXXIII, 434. 50 Gordon, S. Med. Press and Circ. Lond. 1874, n. s. XVII, 243. 51 Green, Prov. M. and S. J. Lond. 1850, 608. 52 Hanot, Bull. Soc. Anat de Paris, 1870, XLV, 408. 53 De La Harpe, P. Bull. Soc. Med. de la Suisse Rom. Lausanne, 1877, XI, 97-9. 51 Harrington, H. L. Chicago M. J. and Exam, 1879, XXXVIII, 362. 55 Harris, Boston, M. and S. J. 1867, LXXVI, 63. 56 Hartigan, J. F. Tr. M. Soc. Dist. Col. Wash. 1874, I, 53-57. 57 Harvey, Doub. Q. J. M. Sc. 1857, XXIII, 223. 58 Hawkes, J. Tr. Path. Soc. Lond. 1871, XXII, 115-117. 59 Herr, Aerztl. Mitth. a. Baden, Karlsruhe, 1863, XVII, 161-163. A case with hemoptysis. 60 Hill, G. Med. Times and Gaz. Lond. 1863, n. s. I, 30. In a woman of 20. 61 Hume, J. Glascow M. J. 1831, IV, 140. 62 Humpage, E. Lond. M. Gaz., 1833, XII, 531. 63 Jackson, J. B. S. A. J. M. S. 1848, n. s. XVI, 300. Another case, Ibid, 1848, n. s. XVI, 301. 64 Johnson, G. Tr. Path. Soc. Lond. 1848-50, I, 244. 65 Kelly, C. Tr. Path. Soc. Lond. 1868, XIX, 185. Another case, Ibid, 1869, X X, 148. 66 Kolb, Ztschr. d. k. k. Gesellsch. d. Aertzte zu Wien. 1858, XIV, 595. 67 Laborde, Compt Rend. Soc. de biol., 1859, Par. 1860, 3, s. I, 30. 68 Lynn, Med. Rec. and Researches, Private Med. Assn. Lond. 1798, 71-82, 1 pl. 69 M'Dowall, J. W. Edinb. M. J. 1876, XXII, 318321. 70 Magnan, Bull. Soc. Anat de Paris, 1864, XXXIX, 512. 71 Laennec; Tract de L'auscultation Medicale, Etc., Paris, 1831, Vol. III, p. 295. (CONCLUDED NEXT WEEK.) THE STRUGGLES OF SIR JAMES Y. SIMPSON.-A life of the late Sir James Simpson has just been published, written by his daughter, in which are many interesting facts connected with his life not generally known before, and of these the Medical Record makes the following notes: James Simpson was the son of the village baker at Bathgate in Linlithgowshire. At the age of fourteen he went to the University of Edinburgh, and was one of the hard-working, frugal race of Scotch scholars. He lived on $50 a year, his only extravagances being books. A significant entry is quoted from his diary; it is as follows: "Finnan haddies, 2d. (4 cents); bones of the leg, 10s. ($7.50)." In 1838, when he was twenty-seven years old, he became lecturer in obstetric medicine in the Extra-Mural School. Two years after he was appointed professor of obstetrics at the University. In 1847 he discovered chloroform. At the early age of fifty-eight he died, his end hastened by overwork. THE PREVENTIVE TREATMENT OF RABIES. By John Ruhräh, M. D., Physician in Charge of the Pasteur Institute of the City Hospital of Baltimore. NINETY-NINTH ANNUAL MEETING OF THE MEDICAL AND CHIRURGICAL FACULTY OF THE preventive treatment of rabies by the Pasteur method should be particularly interesting to the society at this time owing to the fact that the College of Physicians and Surgeons has established a Pasteur department at the City Hospital. Although the department has been open for the reception of patients only two weeks, there are already six patients under treatment. In calling your attention to this subject there are a number of points to be considered. In the first place, it is well to note the prevalence of rabies in the various countries. It is a disease widely distributed and more common than generally supposed. In Russia and France it is quite common and deaths from the disease by no means rare. In Germany and Sweden, owing to the high dog tax and the better police supervision of all animals, the disease is comparatively rare. In the United States the disease is far more common than is generally supposed. There have been a great many animals examined by competent veterinarians, or by inoculation experiments in the various laboratories, and if I am correctly informed, in almost all cases where the disease was suspected it proved to be true rabies. In man, too, there have been numerous cases both here in Maryland and in the other States. The disease is most common in children, and more common in adult males than females. It is more apt to follow bites on exposed portions of the body, than elsewhere. Another important point is that of cauterization of the wound. When this has been done, the danger of infection is very much lessened. In the uncauterized cases about 83 per cent. of the people bitten by animals known to be rabid develop the disease, while in cauterized cases under the same conditions only 33 per cent. are affected. Another point of importance in thus. briefly considering the preventive treatment is the period of incubation. The average case develops in from six to ten weeks, but cases have occurred as early as the twelfth day, and as late as eighteen months after infection. The action of the attenuated virus used in the treatment is not instantaneous, but it requires somewhere in the neighborhood of fifteen days after the injection has been given to establish an immunity. It is manifest, therefore, that cases developing before that period are unaffected by the treatment. Fortunately, these cases are rare and we do not often see failure from this cause. The technique of the method is quite simple. The virus used is obtained from the spinal cord of a rabbit that has died of rabies, after having been inoculated subdurally with the "laboratory" or "fixed" virus. This cord is removed as soon after the death of the rabbit as practicable, and is divided into three inch lengths and suspended in drying bottles over caustic potash. These bottles are then placed in a dark room, free from dust and draughts. This room is kept at a temperature of twentythree degrees centigrade the whole year round. When a case is to be treated, a cord that has been drying for fourteen days is selected and under the strictest aseptic precautions a half centimeter is cut off and rubbed up into a perfectly smooth emulsion with three cubic centimeters of sterilized water. On the first day of the treatment the emulsions of the fourteenth and thirteenth day cords are used. The three cubic centimeters of fluid are injected into the subcutaneous tissue of the abdomen. Af |