usual method of giving the length, thickness, etc. The objection raised to this method is that the heart becomes completely ruined for pathologic collections.

The numerous vegetations in the pulmonary artery, both in Willigk's case and in this, plainly indicate the close relation between its intima and the neighboring endocardium.

Dilatation of the stem of the pulmonary artery, as well as of its left branch, is, strange to say, not infrequent in a stenosis of this type. Thus Frerichs found dilated sinus valsalvæ; Mannkopff, Bernard, dilatation of the entire stem; Benedict, both of the stem and the left branch; and Whitley and Philhouze, of the stem and both the branches way up into the lungs. Just how this dilatation comes about is hard to say. In case of aortic insufficiency there is nearly always a more or less pronounced degree of dilatation of the aortic arch. This is explained by the fact that a larger amount of blood is driven with an unusual amount of force into the aorta from the hypertrophied left ventricle. However, when there is stenosis, Friedreich has shown conclusively that the aorta is narrowed, and he does not mention any dilatation. It is, therefore, a peculiar circumstance that stenosis of the pulmonary orifice should be accompanied with dilatation. Cruveilhier remarks concerning Philhouze's case that he has no explanation to offer.

It might be supposed that the stenosis developed on an already existing insufficiency, and that, at an early stage of the trouble, the insufficiency had the upper hand and produced the dilatation. This, however, could not have been the case in Bernard's case of stenosis of the right conus arteriosus, in which the pulmonary segments were perfectly normal, and yet dilatation of the pulmonary artery was present.

Furthermore, one might suppose that the explanation might be that it was caused by an inflammatory change in the arterial wall lessening its strength; but this cannot be the case, since the arterial wall has been found normal in many cases of dilatation.

Since an explanation to account for this condition must necessarily be a theoretic one, I shall not attempt any speculations, but merely suggest a way in which this dilatation might come about.

It is possible for the concentric hypertrophy, which often is marked, to develop beyond what is actually called for by the degree of stenosis, perhaps as a result of a coexisting myocarditis; in that case a small stream of blood is driven with great force into the pulmonary artery, and the blood in it is then moved forward with greater difficulty than by a stream that does pass through a stenosis; a marked side pressure results, which may lead to dilatation of the thin wall of the pulmonary artery. Whether in the present case disease of the wall of the pulmonary artery played any rôle is hard to say. I do not believe it did, because both the external and the middle layers were healthy. The intima was, of course, swollen and infiltrated with numerous round-cells between the vegetations. But this coat is too thin and weak to play any rôle in the support of the wall of a large artery.

I believe the stenosis produced a stasis in the lesser circulation be

cause of the reduced vis a tergo, and Friedreich is hardly right to conclude, on the basis of Speer's case, in which the lungs were anemic, that the dyspnea was caused by anemia due to lack of blood in the lungs, for it is hardly conceivable that symptoms like hemoptysis (Whilly, Frerichs), bronchitis (Frerichs, Bernard), or edema of the lungs (Benedict) could occur with bloodless lungs. Besides this, Speer describes the lungs in his case as being infiltrated with a serous fluid. And even if this edema originated during the death agony, a stasis must have been present or the edema could not have occurred.

As a characteristic objective cardiac symptom there is, in addition to the remarkable hypertrophy of the right ventricle, a systolic murmur, heard best in the second left intercostal space, at the margin of the sternum. This murmur is transplanted either toward the apex, where it may be heard very distinctly, or it may extend a short distance up the left sternal border, but it cannot be heard in the neck. A weak arterial pulse would support the diagnosis of uncomplicated stenoses (Friedreich), but it has never been observed.

In the case under consideration the recognition of the condition during life was impossible, since the most characteristic differential symptom, viz., the limitation of the murmur to the right heart and pulmonary artery, was lacking. In both records the murmur is described as being heard in the arteries of the greater circulation. This strange fact may be explained by remembering that the cause of the murmur must have been the vegetations in the dilated, uneven pulmonary artery, which, by lying close up to the wall of the aorta, transmitted the sound to it.

The hard strong pulse too had a tendency to lead the attention of the examiner away from the right heart, while perhaps the smallness of the arterial pulse, given by most writers as a symptom, has been derived largely from theoretic reasoning (With).

Only one of the symptoms suggested to Professor Aarestrup involvement of the right heart, namely, the fact that the murmur was heard plainly on the right margin of the sternum, toward the base of the ensiform process. But it was, of course, impossible to base a diagnosis on this symptom alone, especially as the many other signs pointed away from valvular disturbances in the right heart.

Strangely enough no signs of passive hyperemia were present. Cyanosis of the lips was present in pneumonia, but in this case the splanchnic organs, not even the liver, contained as much blood as is usually found when the left heart is diseased.

There is no special causal connection between the condition found in the heart and the other pathologic conditions, the renal and pelvic inflammation, the pneumonia, and the meningitis, hence nothing need be said about them.

It is quite evident that the case which I have described does not present anything really new, especially so far as differential diagnosis is concerned, which is the objective point of our studies of diseases in the right heart at present. When a sufficient number of cases are reported, sufficient basis will be furnished for differential diagnosis, and to this end I have reported this case.

ON PARTIAL HYDRONEPHROSIS

ILLUSTRATED BY A CASE*

ANY obstruction whatsoever to the outflow of urine situated anywhere between the urethra and the renal pelves causes, as is well known, accumulation of the urine and dilatation of the urinary passages above the obstruction. Dilatation of the renal pelves and calices, with consecutive atrophy of the surrounding renal tissue, is designated "hydronephrosis," as suggested by Rayer.† Its form and extent depends essentially on the seat of the obstruction. Three forms of hydronephrosis are recognized: the bilateral, the total unilateral, and the partial or local.

1. Bilateral Hydronephrosis.—In this case the obstruction is situated below the ureters, either in the urethra, where there may be a stricture, or in the bladder, where hypertrophy of the prostate, calculus, and tumors may hinder the outflow. The dilatation of both ureters and the kidneys caused thereby rarely reaches any considerable extent, because the patient soon perishes eventually on account of cystitis, pyelitis, or suppurative nephritis, more rarely as a consequence of uremia, when the evacuation of the urine has been rendered wholly impossible. Only in extremely rare cases does the dilatation reach such a degree as to produce so much atrophy that too little renal tissue remains to carry on the excretion.

2. Unilateral Total Hydronephrosis.-Here the obstruction is situated in one of the ureters. The conditions in this form are somewhat different than in the preceding, inasmuch as only one kidney is placed out of action, while the other not only is undisturbed in its function, but even assumes the whole excretion. As life is not threatened directly during the development of the hydronephrosis, the dilatation may have time. enough to reach its highest degree. Thus one finds not infrequently that the hydronephrosis has developed to form a large sac filled with serous or mucoid fluid, filling the lower part of the abdomen, and occasionally this has been mistaken for ovarian cysts. In this case the obstruction lies either in the course of the ureter, or at one of its two openings, assuming different forms. Most often it is a stone from the pelvis, or rather from a calyx, which has been arrested either at the upper end of the ureter or in its course, or more often just above its opening into the bladder; as we know, the ureter becomes a little narrower in its course through the wall of the bladder than it is higher up. Or strictures are found which probably oftenest result from wounds caused by calculi,

Nord. med. Arkiv, 1873, vol. v.

†Traité des Maladies des Reins, 1841, vol. iii, p. 476.

which often are rough and angular, or covered with sharp points, as is the case with oxalate of calcium stones.

Occasionally hydronephrosis results from a defective development of one of the ureters, which is patent to a certain point in its course only, a solid string of connective tissue extending from this point to the bladder. The obstruction may not occur in the lumen of the canal only. Frequently the ureter is compressed from without by tumors, as, for instance, cancer of the uterus and its adnexa, ovarian cysts, cancer of the pelvis, or abscesses in this region and the lower part of the abdomen. One of the most frequent of the latter, namely, phlegmon in the connective tissue around the cecum and the lower part of the ascending colon is likely, on account of the anatomic conditions, to compress the right ureter, which runs in the connective tissue behind the bowel. Further, disturbances in the position of the neighboring organs, as, for instance, prolapse of the uterus, may place the ureter in such a position that it is difficult for the urine to pass through. Curiously enough, occasional instances of hydronephrosis have been found in which the ureter was patent and occupied its usual position, not being exposed to pressure from without. We owe to Virchow* the explanation of this peculiar condition. He found in all instances of this kind which he had opportunity to examine that the obstruction depended upon a valve formed by a fold of the wall of the ureter, and blocking the passage in the same way as the semilunar valves in veins. He believes that the valve or fold is formed on account of the oblique emergence of the ureter from the pelvis; consequently he must have found that in all cases the valve was situated just at the entrance into the ureter. I have not had opportunity to observe any instance of this kind.

3. Partial or Local Hydronephrosis. In this form only a part of the kidney is the seat of dilatation, the remainder being normal. It is found extremely rarely, and is dependent upon one of two conditions. Either the kidney has double ureters, one being impervious, or there is an obstruction above the ureter.

With respect to double ureter, let me recall briefly the anatomic conditions. Normally, we find that the ureter is a cylindric muscular canal, 1 to 3 mm. wide when filled, and extending from the trigonum Lieutaudii of the bladder to the hilus of the kidney, where it dilates very rapidly, or more gradually to a short canal, 15 mm. wide-the so-called renal pelvis. This divides into two short canals 10 mm. wide, one for the upper and one for the lower part of the kidney. These two principal branches, which are subject to some variation with respect to length and to lumen, divide again, giving off branches to the sides of the individual renal calices. When the two principal branches, instead of uniting in the hilus and of emptying into the pelvis, continue separately for a shorter or a longer distance toward the bladder, or, which is more frequent, empty, each by itself, into the bladder, then we have two ureters, one for each part of the kidney. In this case there is no renal pelvis in the usual meaning of the word, but rather two such pelves. This anomaly * Die krankhaften Geschwülste, vol. i, p. 268.

is not extremely rare: I have seen it twice in 500 bodies. In both cases the ureter from the upper half of the kidney entered the bladder about 1 cm. below and to the inside of the opening of the ureter from the lower half, which was situated at the usual point in the upper corner of the trigone. This, however, is not always the case, as one of the two ureters has been found to enter the bladder in the middle of the posterior wall.

It is to be expected that, in the same proportion as double ureters are less frequent than single, so also partial hydronephrosis dependent on occlusion or defective development of one of the ureters must be less frequent than the total.

An instance of partial hydronephrosis in a kidney with double ureters, of which one was defectively developed, is described by Heller.* In the body of a woman, seventy-nine years old, who was supposed to have a large ovarian cyst, and who died of croupous pneumonia, he found a large sac with thin walls which filled nearly the whole abdomen, and contained 3400 c.c. of a light brown, somewhat turbid, watery fluid, in which were albumin, urates, and urea. From the lowest part of the sac extended a tortuous dilated ureter, which terminated blindly at the lower part of the bladder, just behind the point where the ureter arises. On the anterior surface of the lower part of the sac, near the cecum, was found the lower half of the right kidney, somewhat flattened, with a slightly dilated pelvis from which arose a ureter which opened in the urinary bladder at the usual point. The left kidney was of usual size, but it also had two ureters which united immediately before their entrance into the bladder. Although there was no history in this case, so that it was impossible to learn how long the tumor had existed, Heller believes that in the absence of indications of inflammation in the region of the closed ureter the occlusion and hydronephrosis in this case were of fetal origin.

Heller† has also observed a case in which one of the two ureters had been closed by a stricture following a lesion caused by the passage of a stone. This occurred in an insane man, sixty-nine years old, who died of pulmonary gangrene; the upper half of the right kidney was changed into a sac as large as a fist, and filled with a clear serous fluid. On the inside was a layer of renal tissue 4 mm. in thickness, the sac passing downward into a finger-like projection from the end of which a solid string of connective tissue, about 1 cm. long, passed to the upper end of the open ureter, in the lower end of which was an oval calculus as large as a pea. The lower half of the kidney was normal in appearance, and provided with its own ureter, which was patent. The left kidney was healthy and had only one ureter.

The literature contains as yet only one case of local hydronephrosis with double ureter. This was observed by Valter (quoted by Heller) in a man thirty years old, in whom there were double ureters on both sides, the upper half of the right kidney being changed into a fairly large. sac, the corresponding ureter being dilated. How the obstruction arose in this case is unknown.

* Deut. Arch. f. klin. Med., 1869, vol. v, p. 267.

† Ibid., 1870, vol. vi, p. 276.