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Critical Study of Ureteral Calculi1: (Based on a Series of 758 Private Cases)
CRITICAL STUDY OF URETERAL CALCULP (BASED ON A SERIES OF 758 PRIVATE CASES) A. RAVICH
A stone of the urinary bladder having been discovered by Prof. Elliot Smith in the grave of a prehistoric Egyptian boy of about sixteen, computed to have lived about 7000 years ago makes calculous disease of the urinary tract one of the oldest ailments known to man (1). Stone specialists flourished long before the time of Hippocrates, yet in spite of such a hoary existence the etiology of urinary calculus is still controversial. Until the advent of the cystoscope some forty-five years ago, its prevention and cure had not been materially improved upon. With the combined use of the cystoscope and x-ray however, some of the predisposing causes have been ascertained and their correction facilitated. ETIOLOGY
The brilliant advances of physiological chemistry during the past two decades have added considerably to our knowledge of calculus deposition. It remains for the modern urologist however, to evaluate and correlate the physio-chemical factors with the clinical data to arrive at some definite conclusions about the etiology of calculous disease. Various theories have been advanced from time to time only to succumb under the onslaught of more advanced scientific researches. Thus, a theory which appears perfectly logical today may be disproved entirely tomorrow. Accordingly race, climate, geography, food, water, vitamines, etc., which at one time or another held sway as the most important causative factors in kidney stone formation have been dropped one by one into their proper places in the light of recent experimentation. 1 Read at the Twenty-ninth Annual l\Ieeting of the American Urological Association, Toronto, Canada, l\Iay 31, 1932.
171
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A. RAVICH
Many of the previously recognized etiological factors referred to bladder stones, to which rats, the most commonly used experimental animal, are particularly susceptible during captivity. It had been shown that vitamin deficient diets have a deleterious effect on the organism by making the individual less resistant to infection and more prone to stasis. Van Leersum (2) believes there is a connection between vitamin A deficiency and the formation of phosphatic calculi by keraOn the other hand, Rost tinization of the tubular epithelium. (3) substantiates the contention of Perlman and Weber that the formation of phosphatic stones should not be considered merely an avitaminosis but agrees with McCollum and Simmonds that they are due to some deficiency in diet. Ranganathan (4) thinks there is a close relationship between diet and the chemical composition of stones. Newcomb (5) seems to feel that the degree of acidity or alkalinity of the urine exerts some influence on the precipitation of stone-forming salts. Normal urine is a strongly supersaturated solution but in certain pathological conditions the concentration and saturation may be greatly increased. Urinary salts do not obey the ordinary laws of chemical solutions. If the total amount of salts found in normal urine were mixed with water, only a small percentage would be found in solution, the remainder being precipitated. Uric acid, for instance is ten to twenty times more soluble in urine than in pure water. The abnormal solubility of stoneforming salts seems to depend upon the protective action of certain colloids which in normal urine prevents their precipitation into calculi. In stagnant concentrated urine, there seems to be a disproportionate increase in the number of crystals with a relative diminution in the number of colloids necessary to keep all the salts in solution. The solubility of the stone-forming salts depends on the state of subdivision of the urinary colloids. During the process of "aging" the colloids coalesce and become larger and larger, thereby rapidly reducing their total surface area and with it diminishing their surface energy. The sparingly soluble salts not being retained in a state of adsorption in relation to the
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173
"aging" colloids, the watery parts of the urine become supersaturated and a crystalline precipitate forms. This seems to be the phenomenon that occurs when strongly uratic urine is permitted to stand in a test tube. After a time the macroscopic uric acid gravel which Beer calls uric acid showers adheres to the side walls or falls to the bottom. Lichtwitz claims that urinary stagnation may cause inflammatory changes which precipitate the colloids in the tubules in the form of a "gel" that acts as a nucleus for a stone. Crystalloid precipitation then occurs with incrustations around these precipitated colloids. This contention is borne out by the modern concept of the physiology of the kidney which recognizes that the filtrate found in Bowman's capsule by osmosis contains no colloids. During the passage of this fluid through the tubules however, colloids are added. Since urinary colloids are entirely different from those found in blood serum, it is reasonable to suppose that the former must be secreted by the secretory epithelial cells that line the tubules. The amount of colloid in the urine seems to depend upon the diet and is increased when this is rich in protein. With a deficient diet, the protective action of the colloids is diminished and the excess of free salts is precipitated with a resulting formation of urinary calculi. On the other hand, calculi have been produced in animals by greatly increasing the crystalline content of the urine thereby disturbing the quantitative crystalloid-colloid relationship (6). J. Meyer (7) considers urine as a simple aqueous supersaturated solution of various salts which follows the ordinary laws of ionization and concentration. The concentration of the salts in solutions varies with their hydrogen ion concentration (pH). As this swings from the alkaline to the acid side, the concentration of the phosphates, oxalates, urates and uric acid increases in the order named. As the concentration of the various salts in urine increases in the presence of stasis the tendency to precipitation around some nucleus is increased regardless of the chemical composition of the urine. Yagishita (8) in a recent article on his experimental investiga-
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A. RAVICH
tions of the ongm of kidney stones based on a series of 564 rabbits concludes that by far the most important element in their causation is a gradually increasing moderate urinary blockage without which stones practically never form. In the presence of blockage, however, the formation of calculi is assisted materially by other factors, the most important of which, he believes is the increased excretion of stone-forming salts in the urine. Squier (9) states that faulty drainage causes retention of crystals, a colloid crystalloid imbalance and precipitation and coalescence of the crystals. When Keyser and Braasch produced oxamide calculi in rabbits they were usually found in the tiny pocket behind the cusp of the free margin of the calices, where it is probable that the urinary stream exerts less force in washing the crystalline material forward. They also point out that the smaller concrements found in the human kidney generally lie in the minor calices. Mechanical interference with urinary drainage may be responsible for lowering the local resistance of the kidney to infection and may produce conditions favorable to the retention of crystals precipitated from the urinary solution. Infection, congenital malformations and anatomical abnormalities, trauma and prolonged confinement to bed following fractures are some of the contributing factors. The great majority of urinary calculi seem to arise in a clinically uninfected urine. In a fairly large clinical experience in his office and in hospitals the author can truthfully state that he has never seen a primary calculus in the kidney, ureter or bladder without more or less concomitant urinary stasis in these organs. The great majority of renal calculi are apparently passed out into the ureter before they attain a size sufficiently large to be retained within the kidney. Although the reproductive organs of males and females are entirely different, their relationship to the lower ends of the ureter is quite analogous. In both sexes the kidneys are alike, which seems to account for the fact that in my private series of 350 cases of renal calculus during the past ten years, 176 were in females and 174 in males. This corresponds more or less to the statistics presented by other writers. The increased tendency to
CRITICAL STUDY OF URETERAL CALCULI
175
nephroptosis and pyelitis in females may account for the relative increase in the number of renal calculi in this sex as compared with the preponderance of ureteral calculi in males. Thus, whereas there were only 55 infected urinef; in 174 renal calculi in males, there were 96 infected urines in the 176 females. Although the bladders of both sexes are intrinsically alike, physiologically, the influence exerted extrinsically by the collarlike prostate around the vesical neck with the tendency to incomplete emptying of the bladder, as contrasted with the relative freedom from obstruction in the female urethra, apparently accounts for the wide difference in the number of vesical calculi in males and females. The presence of stagnant urine in the bladder so common among male adults seems to produce an increasing concentration of the urine in which the urinary salts increase more rapidly than the colloids and are precipitated and welded into a stone. It seems that the lower calyx of the kidney does not drain off as readily as the middle or upper calyces unless these are obstructed by congenital or acquired infundibular constriction. Joly claims that the lower calyx is the most frequent site of stone formation in the kidney. Ureteral calculi usually originating in the lower calyx are either washed down or forcibly ejected from this pool by some sudden jolt or peristaltic contraction into the ureter. If the calculus is small enough and the ureteral lumen is sufficiently patent, the stone easily finds its way into the bladder and out through the urethra. All too often however the calculus becomes impacted and must be removed either by cystoscopic manipulation or operation. Since most ureteral obstructions occur in the pelvic portion of the ureter, calculi are most frequently impacted in this location as shown by the following table from the author's series of 758 cases of ureteral calculi treated during the past ten years. Location of calculus at first examination Kidney·......................................................... 19 Lumbar ureter down to synchondrosis. . . . . . . . . . . . . . . . . . . . . 148 Upper half of pelvic ureter. . . . . . . . . . . . ................ 130 Lower half of pelvic ureter....... . . . . . . . .................. 287
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At ureteric orifice . . . . ... In bladder . . . . . . . . . . . .. Position not stated .... Passed before examination. In urethra .............. .
. ................ .................
24 20
.... .....
81 44 5
In most of the statistical studies on this subject males are more frequently afflicted with ureteral calculi than females. In the above series, 529 or 69.8 per cent ·were in males and 229 or 30.2
FIG.
1.
ROENTGEN OGRAM SHOWING BILATERAL HYDROURETER CAUSED BY UTERINE FIBROID
per cent in females. Of 220 cases reported by Jeanbrau (10), 61 per cent were males and 39 per cent females. W. Grossman (11) in a study of 380 cases of ureteral calculi reported 242 or 63.7 per cent in males and 138 or 36.3 per cent in females. Bumpus and Scholl (12) reported 880 cases at the Mayo Clinic from 1901-1924 in which 68 per cent were males and 32 per cent females. Israel and others report about the same proportion.
y_
P. p, L
FIG.
2.
RELATION OF THE HYPERTROPHIED PROSTATE TO THE CAPSULE, POSTERIOR URETHRA, URETERS, SEMINAL VESICLES AND VAS DEFERENS
(From Tandler and Zuckerkandl)
Fm.
3.
PosTERIOR Vrnw OF BLADDER SHOWING LATERAL DISPLACEMENT OF VAs DEFERENS AND SEMINAL VESICLES WITH EFFECT ON URETERS CAUSED BY PROSTATIC HYPERTROPHY
(From Tandler and Zuckerkandl)
177
~~--··--·--~
178
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A. RAVICH
Bumpus and Thompson (13) reporting on 1001 cases of ureteral ,calculi at the Mayo Clinic in the ten years from 1919 to 1928 base their principal argument against ureteral obstruction as an
FIG. 4.
POSTERIOR Vrnw SHOWING TREMENDOUS HYPERTROPHY OF PROSTATE WITH !TS EFFECT ON VAS DEFERENS AND URETERS
(From Tandler and Zuckerkandl)
etiological factor in stone formation upon the fact that since pelvic inflammation in females is admittedly an important cause for ureteral obstruction which they claim is not present in males, they conclude that ureteral obstruction therefore cannot play much of a role in the causation of ureteral stone (fig. 1). The
179
CRITICAL STUDY OF URETERAL CALCULI
author however begs to take exception to this conclusion. Anatomically there is a very close relationship between the prostate and seminal vesicles and the lower end of the ureter (14) (figs. 2, 3, 4, and 5), and any pathology present in these organs will exert either a mechanical or inflammatory effect on the ureter .
.[
FIG. 5.
DILATATION OF THE URETERS DUE TO CHRONIC VESICAL NECK OBSTRUCTION
(From Tandler and Zuckerkandl)
The great bulk of ureteral calculi occur in adults between twentyone and fifty years of age, as shown by the following table: Age incidence 11-20 years....................................................... 16 21-30 years . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 190 31-40 years. . . . . ........... . . . . . . . . . . . . . . . . . . . . . . . . . . . . 260 41-50 years . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 177 51-60 years.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83 61-70 years................. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19 Over 70 years . . . . ............... ............................ 4 Not stated . . . . . . . ......... 9 Youngest 11 years; oldest 74 years.
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It is well known that the sexual life of the males in the above mentioned age group leads to engorgement and inflammation of the prostate and seminal vesicles. In this series the condition of the prostate and seminal vesicles was noted in 393 of the 529 male cases shown in the following table: Condition of prostate and seminal vesicles
N"ormal..... . . . . ................................... 82 Slightly enlarged. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 173 11oderately enlarged... . ................. 112 Very large..................... . . . . . . . . . . . . . . . . . 14 Median prostatic bars. . . .............................. 12
Whereas ureteral calculi when first seen are preponderately associated with clear uninfected urine and may accordingly be classed as primary calculi, renal and vesical calculi however being more frequently associated with pyuria and infection may be considered as secondary calculi. This secondary nature of stone formation being more frequent in the kidney than in the ureter may account for the fact that whereas of the 758 ureteral calculi in this series there were 685 single and 73 multiple stones, of the 350 renal calculi cited above 235 were single against 115 multiple. The causative agency was apparently equal on both sides as shown by the following: 342 ureteral calculi on right side 404 ureteral calculi on left side 12 ureteral calculi were bilateral SYMPTOMS
The following table is interesting: History of colic
78 gave no history of colic 157 came in for first attack 141 had two attacks 382 had multiple attacks
::\Iany of these patients complain of typical colic starting in the kidney and radiating downwards along the ureter and terminating in the iliac region, groin, scrotum, penis or vulva and occasionally along the inner side of the thigh and leg. At times when the
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181
pain radiates anteriorly and not downwards and is more or less continuous, one often finds the calculus impacted at the ureteropelvic junction. The colic seems to be initiated by the sudden over-distension of the renal pelvis with urine stretching the capsule and the nerves supplying it. Calculi impacted at the lower end of the ureter may simulate prostatitis. At times patients are erroneously treated for lumbago, sacro-iliac disease and subluxation. Some of these are actually put in plaster casts and sciatic nerves stretched and injected only to be relieved by the discovery and elimination of a ureteral calculus. Pain on the right side fairly typical of appendicitis is quite frequent as shown by appendectomies in 226 of the 1001 cases reported by Bumpus and Thompson and 30 reported by Cabot in his series of 143 ureteral calculi. W. Grossman reports 15 of his 380 cases treated for appendicitis of which 8 had appendectomies. In the author's series 36 had been treated for appendicitis of which 28 had appendectomies. This would seem to indicate that the careful surgeon of today requests a urological survey before operation in all doubtful cases of right-sided pain. Owing to the marked abdominal distension occasionally present with stones of the upper ureter, a number of patients were treated for acute intestinal obstruction, pancreatitis, gastric ulcer, gall bladder disease, etc. One hundred and thirty-five patients presented marked gastric distress over varying periods. One hundred and eighty-five had gross hematuria. DIAGNOSIS
Ureteral calculus although relatively simple to diagnose with the aid of the x-ray may at times necessitate a very extensive examination. In this series 684 cases gave positive evidence of stone on the x-ray film, whereas 74 were negative. Of those that were negative, 54 showed a scratch on the wax tip catheter. Of the remaining 20, 8 were found projecting from the ureter opening, 2 were diagnosed from the appearance of the orifice, 1 presented a filling defect in the urogram and 9 were free in the bladder. AL times the grating noted on withdrawal of the catheter assisted in making the diagnosis. In the author's
------- -
----~----------------
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A. RAVICH
practice the wax-tipped catheter was as important a diagnostic measure as x-ray and in uric acid stones was often the only means whereby a diagnosis could be made. RECURRENCE
The number of recurrences in this series amounted to 20 on the same side. 12 developed stones on the opposite side, and 6 on both sides. Most of these were in cases that failed to follow
FIG.
6.
AUTHOR'S
IRRIGATING URETERAL BOUGIES
up correction of the existing ureteral obstruction. Bumpus and Thompson report 3.2 per cent recurrence in their cases, whereas Bumpus and Scholl reported 10 per cent recurrences in their series. TREATMENT
Manipulative cystoscopic measures were necessary in most of the cases in this series. Included in these procedures were (a) simple passage of a ureteral catheter to dislodge the stone, (b)
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183
dilatation of the ureter by indwelling single or multiple catheters or by the author's irrigating ureteral bougies (fig. 6), (c) extraction of stones impacted within the ureteric orifice or intramural portion of the ureter by the Howard Spiral stone dislodger, (d) enlargement of the ureteric orifice by either an electric cutting current or scissors, and (e) lithotripsy of a growing bladder stone by the author's lithotriptoscope. In the remaining cases the stones were either passed spontaneously or required open operation. The accompanying table presents the end results of the cases studied: Results of treatment 48 456 37 20 9 8 3 3 38 40 3 17 68 5 3
passed calculus spontaneously. passed calculus after simpler cystoscopic manipulations. extracted from ureteric orifice. found in bladder and extracted. required cutting of orifice with cystoscopic scissors. required fulguration of orifice. brought out imbedded in wax bulb. required lithotripsy for stones passed and remaining in bladder. not heard from. still under treatment or observation. had multiple calculi in whom the smaller were removed cystoscopically followed by operative removal of the larger stones. were advised operation and wandered off. were operated by author. extracted from posterior urethra. died of other causes.
Combining the 17 who were advised operation with the 68 operated cases yields an operative incidence of 11.2 per cent as against 9.5 per cent reported by Claude B. Squires (15) of 606 cases reported from the Crowell Clinic from 1915-1930. Bumpus and Thompson report that 480 of their 1001 cases or 48 per cent were subjected to operation with a mortality of 0.2 per cent. Dourmashkin (16) reports 79 operative cases or 13.4 per cent in his series of 589. W. Grossman operated on 126 of his 380 cases with a mortality of 3 per cent. Jeanbrau had a mortality of 1.4 per cent in his operative cases and Barney and Richard Chute (17) reported 51.2 per cent or 72 operative cases in their se~ies of 123 with a mortality of 3.2 per cent. Sixty-four one hundredths
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A. RAVICH
per cent mortality in 640 cases were reported from the Mayo Clinic by Bumpus and Scholl, 2 per cent by Rafin (18), 4 per cent by Israel, 9 per cent by Rovsing and 1 death reported by Joly in the 32 cases operated on at the St. Peter's Hospital for stone in London from 1915-1924. There had been no mortality in the author's 68 operative cases. SUMMARY AND CONCLUSION
Of all the etiological theories that had been advanced, urinary stasis seems to be the only constant factor necessary for a stone to form in the urinary passages. The chemical character of the stone seems to depend upon the pH of the urine which may change from time to time and accounts for the different laminae so often demonstrated in stones. Calculi seem to form when as a result of urinary stagnation some change occurs in the secretory function of the tubular epithelium causing coalescence or diminution of the protective colloids and consequent precipitation of the unattached crystalloids. Trauma, faulty diet, infection and foreign bodies are often contributory causative factors in the presence of stasis. The 2: 1 ratio of ureteral calculi in males and the 80 per cent incidence in adults of twenty-one to fifty years of age corresponds with the greatest incidence of inflammatory conditions of the adnexa in males and females. This is borne out by the fact that of the 393 prostatic examinations recorded, only 82 or 21 per cent had what appeared to be normal prostates and seminal vesicles, the remainder showing some degree of recognizable pathology. The passage of ureteral stones is hindered by physiological narrowings, kinks, strictures, fixation of the ureter and atony of the ureteral musculature. Of the 758 cases of ureteral calculi privately treated during the past ten years, about 69.8 per cent were in males and 30.2 per cent in females. X-ray was positive in approximately 90 per cent and most of the remainder were diagnosed by wax tip catheter which is considered a very important diagnostic measure. Approximately 83.6 per cent required cystoscopic manipulation, 6.3 per cent passed their calculi spontaneously, and 11.2 per cent
CRITICAL STUDY OF URETERAL CALCULI
185
were operated without a single mortality. Three and four tenths per cent recurrence was noted, chiefly in those ·who refused follow up treatment by ureteral dilatation. In presenting this report the author wishes to express his appreciation for the laborious statistical work so ably performed by his assistant, Dr. M. Goldberg.
101 Lafayette Avenue, Brooklyn, N. Y. REFERENCES (1) JoLY: Stone and Calculus Disease of the Urinary Organs. C. V. :.VIosby Company, 1929. (2) VAN LEERSUM: Jour. Biol. Chem., 1928, lxxvi, 137. (3) RosT: Arch. f. Klin. Chir., 1930, clxii, 701. (4) RANGANATHAN: Indian Jour. Med. Res., 1930, xviii, 599. (5) NEWCOMB: Indian Jour. Med, Res., 1930, xviii, 275. (6) KEYSER: Arch. Surg., 1923, vi, 529. (7) MEYER, J.: Zeitsch. f. Klin . .:V[ed., 1929, iii, 613. (8) YAGISHITA: Jap. Jour. Derm. and Urol., 1931, xxxi, 5. (9) SQUIER: Lewis' Practice of Surgery. W. F. Prior Company, Vol. VIII, Chapter X. (10) JEANBRAU: Encyclop. franc. d'Urol., 1914, iii, 815. (11) GROSSMAN, W.: Zeit. f. Urol. Chir., 1930, xxix, 187. (12) BUMPUS AND SCHOLL: Surg. Clin. North America, 1925, v, no. 3,813. (13) BUMPUS AND THOMPSON: Surg., Gynecol. and Obstet., 1930, 1, 106. (14) TANDLER AND ZucKERKANDL: Stud. z. Anat. und Klinik d. Prostatahypertrophie, Julius Springer, Berlin, 1922. (15) SQUIRES, C. B.: Jour. Urol., 1930, xxiv, 461. (16) DouRMASHKIN: Jour. Amer. :\1ed. Assoc., 1932, xcviii, 276. (17) BARNEY AND CHUTE, R.: Jour. Urol., 1931, xxv, 173. (18) RAFIN: Jour. d'Urol., 1921, ix, 428.
A stone of the urinary bladder having been discovered by Prof. Elliot Smith in the grave of a prehistoric Egyptian boy of about sixteen, computed to have lived about 7000 years ago makes calculous disease of the urinary tract one of the oldest ailments known to man (1). Stone specialists flourished long before the time of Hippocrates, yet in spite of such a hoary existence the etiology of urinary calculus is still controversial. Until the advent of the cystoscope some forty-five years ago, its prevention and cure had not been materially improved upon. With the combined use of the cystoscope and x-ray however, some of the predisposing causes have been ascertained and their correction facilitated. ETIOLOGY
The brilliant advances of physiological chemistry during the past two decades have added considerably to our knowledge of calculus deposition. It remains for the modern urologist however, to evaluate and correlate the physio-chemical factors with the clinical data to arrive at some definite conclusions about the etiology of calculous disease. Various theories have been advanced from time to time only to succumb under the onslaught of more advanced scientific researches. Thus, a theory which appears perfectly logical today may be disproved entirely tomorrow. Accordingly race, climate, geography, food, water, vitamines, etc., which at one time or another held sway as the most important causative factors in kidney stone formation have been dropped one by one into their proper places in the light of recent experimentation. 1 Read at the Twenty-ninth Annual l\Ieeting of the American Urological Association, Toronto, Canada, l\Iay 31, 1932.
171
172
A. RAVICH
Many of the previously recognized etiological factors referred to bladder stones, to which rats, the most commonly used experimental animal, are particularly susceptible during captivity. It had been shown that vitamin deficient diets have a deleterious effect on the organism by making the individual less resistant to infection and more prone to stasis. Van Leersum (2) believes there is a connection between vitamin A deficiency and the formation of phosphatic calculi by keraOn the other hand, Rost tinization of the tubular epithelium. (3) substantiates the contention of Perlman and Weber that the formation of phosphatic stones should not be considered merely an avitaminosis but agrees with McCollum and Simmonds that they are due to some deficiency in diet. Ranganathan (4) thinks there is a close relationship between diet and the chemical composition of stones. Newcomb (5) seems to feel that the degree of acidity or alkalinity of the urine exerts some influence on the precipitation of stone-forming salts. Normal urine is a strongly supersaturated solution but in certain pathological conditions the concentration and saturation may be greatly increased. Urinary salts do not obey the ordinary laws of chemical solutions. If the total amount of salts found in normal urine were mixed with water, only a small percentage would be found in solution, the remainder being precipitated. Uric acid, for instance is ten to twenty times more soluble in urine than in pure water. The abnormal solubility of stoneforming salts seems to depend upon the protective action of certain colloids which in normal urine prevents their precipitation into calculi. In stagnant concentrated urine, there seems to be a disproportionate increase in the number of crystals with a relative diminution in the number of colloids necessary to keep all the salts in solution. The solubility of the stone-forming salts depends on the state of subdivision of the urinary colloids. During the process of "aging" the colloids coalesce and become larger and larger, thereby rapidly reducing their total surface area and with it diminishing their surface energy. The sparingly soluble salts not being retained in a state of adsorption in relation to the
CRITICAL STUDY OF URETERAL CALCULI
173
"aging" colloids, the watery parts of the urine become supersaturated and a crystalline precipitate forms. This seems to be the phenomenon that occurs when strongly uratic urine is permitted to stand in a test tube. After a time the macroscopic uric acid gravel which Beer calls uric acid showers adheres to the side walls or falls to the bottom. Lichtwitz claims that urinary stagnation may cause inflammatory changes which precipitate the colloids in the tubules in the form of a "gel" that acts as a nucleus for a stone. Crystalloid precipitation then occurs with incrustations around these precipitated colloids. This contention is borne out by the modern concept of the physiology of the kidney which recognizes that the filtrate found in Bowman's capsule by osmosis contains no colloids. During the passage of this fluid through the tubules however, colloids are added. Since urinary colloids are entirely different from those found in blood serum, it is reasonable to suppose that the former must be secreted by the secretory epithelial cells that line the tubules. The amount of colloid in the urine seems to depend upon the diet and is increased when this is rich in protein. With a deficient diet, the protective action of the colloids is diminished and the excess of free salts is precipitated with a resulting formation of urinary calculi. On the other hand, calculi have been produced in animals by greatly increasing the crystalline content of the urine thereby disturbing the quantitative crystalloid-colloid relationship (6). J. Meyer (7) considers urine as a simple aqueous supersaturated solution of various salts which follows the ordinary laws of ionization and concentration. The concentration of the salts in solutions varies with their hydrogen ion concentration (pH). As this swings from the alkaline to the acid side, the concentration of the phosphates, oxalates, urates and uric acid increases in the order named. As the concentration of the various salts in urine increases in the presence of stasis the tendency to precipitation around some nucleus is increased regardless of the chemical composition of the urine. Yagishita (8) in a recent article on his experimental investiga-
174
A. RAVICH
tions of the ongm of kidney stones based on a series of 564 rabbits concludes that by far the most important element in their causation is a gradually increasing moderate urinary blockage without which stones practically never form. In the presence of blockage, however, the formation of calculi is assisted materially by other factors, the most important of which, he believes is the increased excretion of stone-forming salts in the urine. Squier (9) states that faulty drainage causes retention of crystals, a colloid crystalloid imbalance and precipitation and coalescence of the crystals. When Keyser and Braasch produced oxamide calculi in rabbits they were usually found in the tiny pocket behind the cusp of the free margin of the calices, where it is probable that the urinary stream exerts less force in washing the crystalline material forward. They also point out that the smaller concrements found in the human kidney generally lie in the minor calices. Mechanical interference with urinary drainage may be responsible for lowering the local resistance of the kidney to infection and may produce conditions favorable to the retention of crystals precipitated from the urinary solution. Infection, congenital malformations and anatomical abnormalities, trauma and prolonged confinement to bed following fractures are some of the contributing factors. The great majority of urinary calculi seem to arise in a clinically uninfected urine. In a fairly large clinical experience in his office and in hospitals the author can truthfully state that he has never seen a primary calculus in the kidney, ureter or bladder without more or less concomitant urinary stasis in these organs. The great majority of renal calculi are apparently passed out into the ureter before they attain a size sufficiently large to be retained within the kidney. Although the reproductive organs of males and females are entirely different, their relationship to the lower ends of the ureter is quite analogous. In both sexes the kidneys are alike, which seems to account for the fact that in my private series of 350 cases of renal calculus during the past ten years, 176 were in females and 174 in males. This corresponds more or less to the statistics presented by other writers. The increased tendency to
CRITICAL STUDY OF URETERAL CALCULI
175
nephroptosis and pyelitis in females may account for the relative increase in the number of renal calculi in this sex as compared with the preponderance of ureteral calculi in males. Thus, whereas there were only 55 infected urinef; in 174 renal calculi in males, there were 96 infected urines in the 176 females. Although the bladders of both sexes are intrinsically alike, physiologically, the influence exerted extrinsically by the collarlike prostate around the vesical neck with the tendency to incomplete emptying of the bladder, as contrasted with the relative freedom from obstruction in the female urethra, apparently accounts for the wide difference in the number of vesical calculi in males and females. The presence of stagnant urine in the bladder so common among male adults seems to produce an increasing concentration of the urine in which the urinary salts increase more rapidly than the colloids and are precipitated and welded into a stone. It seems that the lower calyx of the kidney does not drain off as readily as the middle or upper calyces unless these are obstructed by congenital or acquired infundibular constriction. Joly claims that the lower calyx is the most frequent site of stone formation in the kidney. Ureteral calculi usually originating in the lower calyx are either washed down or forcibly ejected from this pool by some sudden jolt or peristaltic contraction into the ureter. If the calculus is small enough and the ureteral lumen is sufficiently patent, the stone easily finds its way into the bladder and out through the urethra. All too often however the calculus becomes impacted and must be removed either by cystoscopic manipulation or operation. Since most ureteral obstructions occur in the pelvic portion of the ureter, calculi are most frequently impacted in this location as shown by the following table from the author's series of 758 cases of ureteral calculi treated during the past ten years. Location of calculus at first examination Kidney·......................................................... 19 Lumbar ureter down to synchondrosis. . . . . . . . . . . . . . . . . . . . . 148 Upper half of pelvic ureter. . . . . . . . . . . . ................ 130 Lower half of pelvic ureter....... . . . . . . . .................. 287
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A. RAVICH
At ureteric orifice . . . . ... In bladder . . . . . . . . . . . .. Position not stated .... Passed before examination. In urethra .............. .
. ................ .................
24 20
.... .....
81 44 5
In most of the statistical studies on this subject males are more frequently afflicted with ureteral calculi than females. In the above series, 529 or 69.8 per cent ·were in males and 229 or 30.2
FIG.
1.
ROENTGEN OGRAM SHOWING BILATERAL HYDROURETER CAUSED BY UTERINE FIBROID
per cent in females. Of 220 cases reported by Jeanbrau (10), 61 per cent were males and 39 per cent females. W. Grossman (11) in a study of 380 cases of ureteral calculi reported 242 or 63.7 per cent in males and 138 or 36.3 per cent in females. Bumpus and Scholl (12) reported 880 cases at the Mayo Clinic from 1901-1924 in which 68 per cent were males and 32 per cent females. Israel and others report about the same proportion.
y_
P. p, L
FIG.
2.
RELATION OF THE HYPERTROPHIED PROSTATE TO THE CAPSULE, POSTERIOR URETHRA, URETERS, SEMINAL VESICLES AND VAS DEFERENS
(From Tandler and Zuckerkandl)
Fm.
3.
PosTERIOR Vrnw OF BLADDER SHOWING LATERAL DISPLACEMENT OF VAs DEFERENS AND SEMINAL VESICLES WITH EFFECT ON URETERS CAUSED BY PROSTATIC HYPERTROPHY
(From Tandler and Zuckerkandl)
177
~~--··--·--~
178
---------
A. RAVICH
Bumpus and Thompson (13) reporting on 1001 cases of ureteral ,calculi at the Mayo Clinic in the ten years from 1919 to 1928 base their principal argument against ureteral obstruction as an
FIG. 4.
POSTERIOR Vrnw SHOWING TREMENDOUS HYPERTROPHY OF PROSTATE WITH !TS EFFECT ON VAS DEFERENS AND URETERS
(From Tandler and Zuckerkandl)
etiological factor in stone formation upon the fact that since pelvic inflammation in females is admittedly an important cause for ureteral obstruction which they claim is not present in males, they conclude that ureteral obstruction therefore cannot play much of a role in the causation of ureteral stone (fig. 1). The
179
CRITICAL STUDY OF URETERAL CALCULI
author however begs to take exception to this conclusion. Anatomically there is a very close relationship between the prostate and seminal vesicles and the lower end of the ureter (14) (figs. 2, 3, 4, and 5), and any pathology present in these organs will exert either a mechanical or inflammatory effect on the ureter .
.[
FIG. 5.
DILATATION OF THE URETERS DUE TO CHRONIC VESICAL NECK OBSTRUCTION
(From Tandler and Zuckerkandl)
The great bulk of ureteral calculi occur in adults between twentyone and fifty years of age, as shown by the following table: Age incidence 11-20 years....................................................... 16 21-30 years . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 190 31-40 years. . . . . ........... . . . . . . . . . . . . . . . . . . . . . . . . . . . . 260 41-50 years . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 177 51-60 years.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83 61-70 years................. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19 Over 70 years . . . . ............... ............................ 4 Not stated . . . . . . . ......... 9 Youngest 11 years; oldest 74 years.
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A. RAVICH
It is well known that the sexual life of the males in the above mentioned age group leads to engorgement and inflammation of the prostate and seminal vesicles. In this series the condition of the prostate and seminal vesicles was noted in 393 of the 529 male cases shown in the following table: Condition of prostate and seminal vesicles
N"ormal..... . . . . ................................... 82 Slightly enlarged. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 173 11oderately enlarged... . ................. 112 Very large..................... . . . . . . . . . . . . . . . . . 14 Median prostatic bars. . . .............................. 12
Whereas ureteral calculi when first seen are preponderately associated with clear uninfected urine and may accordingly be classed as primary calculi, renal and vesical calculi however being more frequently associated with pyuria and infection may be considered as secondary calculi. This secondary nature of stone formation being more frequent in the kidney than in the ureter may account for the fact that whereas of the 758 ureteral calculi in this series there were 685 single and 73 multiple stones, of the 350 renal calculi cited above 235 were single against 115 multiple. The causative agency was apparently equal on both sides as shown by the following: 342 ureteral calculi on right side 404 ureteral calculi on left side 12 ureteral calculi were bilateral SYMPTOMS
The following table is interesting: History of colic
78 gave no history of colic 157 came in for first attack 141 had two attacks 382 had multiple attacks
::\Iany of these patients complain of typical colic starting in the kidney and radiating downwards along the ureter and terminating in the iliac region, groin, scrotum, penis or vulva and occasionally along the inner side of the thigh and leg. At times when the
CRITICAL STUDY OF URETERAL CALCULI
181
pain radiates anteriorly and not downwards and is more or less continuous, one often finds the calculus impacted at the ureteropelvic junction. The colic seems to be initiated by the sudden over-distension of the renal pelvis with urine stretching the capsule and the nerves supplying it. Calculi impacted at the lower end of the ureter may simulate prostatitis. At times patients are erroneously treated for lumbago, sacro-iliac disease and subluxation. Some of these are actually put in plaster casts and sciatic nerves stretched and injected only to be relieved by the discovery and elimination of a ureteral calculus. Pain on the right side fairly typical of appendicitis is quite frequent as shown by appendectomies in 226 of the 1001 cases reported by Bumpus and Thompson and 30 reported by Cabot in his series of 143 ureteral calculi. W. Grossman reports 15 of his 380 cases treated for appendicitis of which 8 had appendectomies. In the author's series 36 had been treated for appendicitis of which 28 had appendectomies. This would seem to indicate that the careful surgeon of today requests a urological survey before operation in all doubtful cases of right-sided pain. Owing to the marked abdominal distension occasionally present with stones of the upper ureter, a number of patients were treated for acute intestinal obstruction, pancreatitis, gastric ulcer, gall bladder disease, etc. One hundred and thirty-five patients presented marked gastric distress over varying periods. One hundred and eighty-five had gross hematuria. DIAGNOSIS
Ureteral calculus although relatively simple to diagnose with the aid of the x-ray may at times necessitate a very extensive examination. In this series 684 cases gave positive evidence of stone on the x-ray film, whereas 74 were negative. Of those that were negative, 54 showed a scratch on the wax tip catheter. Of the remaining 20, 8 were found projecting from the ureter opening, 2 were diagnosed from the appearance of the orifice, 1 presented a filling defect in the urogram and 9 were free in the bladder. AL times the grating noted on withdrawal of the catheter assisted in making the diagnosis. In the author's
------- -
----~----------------
182
---
A. RAVICH
practice the wax-tipped catheter was as important a diagnostic measure as x-ray and in uric acid stones was often the only means whereby a diagnosis could be made. RECURRENCE
The number of recurrences in this series amounted to 20 on the same side. 12 developed stones on the opposite side, and 6 on both sides. Most of these were in cases that failed to follow
FIG.
6.
AUTHOR'S
IRRIGATING URETERAL BOUGIES
up correction of the existing ureteral obstruction. Bumpus and Thompson report 3.2 per cent recurrence in their cases, whereas Bumpus and Scholl reported 10 per cent recurrences in their series. TREATMENT
Manipulative cystoscopic measures were necessary in most of the cases in this series. Included in these procedures were (a) simple passage of a ureteral catheter to dislodge the stone, (b)
CRITICAL STUDY OF URETERAL CALCULI
183
dilatation of the ureter by indwelling single or multiple catheters or by the author's irrigating ureteral bougies (fig. 6), (c) extraction of stones impacted within the ureteric orifice or intramural portion of the ureter by the Howard Spiral stone dislodger, (d) enlargement of the ureteric orifice by either an electric cutting current or scissors, and (e) lithotripsy of a growing bladder stone by the author's lithotriptoscope. In the remaining cases the stones were either passed spontaneously or required open operation. The accompanying table presents the end results of the cases studied: Results of treatment 48 456 37 20 9 8 3 3 38 40 3 17 68 5 3
passed calculus spontaneously. passed calculus after simpler cystoscopic manipulations. extracted from ureteric orifice. found in bladder and extracted. required cutting of orifice with cystoscopic scissors. required fulguration of orifice. brought out imbedded in wax bulb. required lithotripsy for stones passed and remaining in bladder. not heard from. still under treatment or observation. had multiple calculi in whom the smaller were removed cystoscopically followed by operative removal of the larger stones. were advised operation and wandered off. were operated by author. extracted from posterior urethra. died of other causes.
Combining the 17 who were advised operation with the 68 operated cases yields an operative incidence of 11.2 per cent as against 9.5 per cent reported by Claude B. Squires (15) of 606 cases reported from the Crowell Clinic from 1915-1930. Bumpus and Thompson report that 480 of their 1001 cases or 48 per cent were subjected to operation with a mortality of 0.2 per cent. Dourmashkin (16) reports 79 operative cases or 13.4 per cent in his series of 589. W. Grossman operated on 126 of his 380 cases with a mortality of 3 per cent. Jeanbrau had a mortality of 1.4 per cent in his operative cases and Barney and Richard Chute (17) reported 51.2 per cent or 72 operative cases in their se~ies of 123 with a mortality of 3.2 per cent. Sixty-four one hundredths
184
A. RAVICH
per cent mortality in 640 cases were reported from the Mayo Clinic by Bumpus and Scholl, 2 per cent by Rafin (18), 4 per cent by Israel, 9 per cent by Rovsing and 1 death reported by Joly in the 32 cases operated on at the St. Peter's Hospital for stone in London from 1915-1924. There had been no mortality in the author's 68 operative cases. SUMMARY AND CONCLUSION
Of all the etiological theories that had been advanced, urinary stasis seems to be the only constant factor necessary for a stone to form in the urinary passages. The chemical character of the stone seems to depend upon the pH of the urine which may change from time to time and accounts for the different laminae so often demonstrated in stones. Calculi seem to form when as a result of urinary stagnation some change occurs in the secretory function of the tubular epithelium causing coalescence or diminution of the protective colloids and consequent precipitation of the unattached crystalloids. Trauma, faulty diet, infection and foreign bodies are often contributory causative factors in the presence of stasis. The 2: 1 ratio of ureteral calculi in males and the 80 per cent incidence in adults of twenty-one to fifty years of age corresponds with the greatest incidence of inflammatory conditions of the adnexa in males and females. This is borne out by the fact that of the 393 prostatic examinations recorded, only 82 or 21 per cent had what appeared to be normal prostates and seminal vesicles, the remainder showing some degree of recognizable pathology. The passage of ureteral stones is hindered by physiological narrowings, kinks, strictures, fixation of the ureter and atony of the ureteral musculature. Of the 758 cases of ureteral calculi privately treated during the past ten years, about 69.8 per cent were in males and 30.2 per cent in females. X-ray was positive in approximately 90 per cent and most of the remainder were diagnosed by wax tip catheter which is considered a very important diagnostic measure. Approximately 83.6 per cent required cystoscopic manipulation, 6.3 per cent passed their calculi spontaneously, and 11.2 per cent
CRITICAL STUDY OF URETERAL CALCULI
185
were operated without a single mortality. Three and four tenths per cent recurrence was noted, chiefly in those ·who refused follow up treatment by ureteral dilatation. In presenting this report the author wishes to express his appreciation for the laborious statistical work so ably performed by his assistant, Dr. M. Goldberg.
101 Lafayette Avenue, Brooklyn, N. Y. REFERENCES (1) JoLY: Stone and Calculus Disease of the Urinary Organs. C. V. :.VIosby Company, 1929. (2) VAN LEERSUM: Jour. Biol. Chem., 1928, lxxvi, 137. (3) RosT: Arch. f. Klin. Chir., 1930, clxii, 701. (4) RANGANATHAN: Indian Jour. Med. Res., 1930, xviii, 599. (5) NEWCOMB: Indian Jour. Med, Res., 1930, xviii, 275. (6) KEYSER: Arch. Surg., 1923, vi, 529. (7) MEYER, J.: Zeitsch. f. Klin . .:V[ed., 1929, iii, 613. (8) YAGISHITA: Jap. Jour. Derm. and Urol., 1931, xxxi, 5. (9) SQUIER: Lewis' Practice of Surgery. W. F. Prior Company, Vol. VIII, Chapter X. (10) JEANBRAU: Encyclop. franc. d'Urol., 1914, iii, 815. (11) GROSSMAN, W.: Zeit. f. Urol. Chir., 1930, xxix, 187. (12) BUMPUS AND SCHOLL: Surg. Clin. North America, 1925, v, no. 3,813. (13) BUMPUS AND THOMPSON: Surg., Gynecol. and Obstet., 1930, 1, 106. (14) TANDLER AND ZucKERKANDL: Stud. z. Anat. und Klinik d. Prostatahypertrophie, Julius Springer, Berlin, 1922. (15) SQUIRES, C. B.: Jour. Urol., 1930, xxiv, 461. (16) DouRMASHKIN: Jour. Amer. :\1ed. Assoc., 1932, xcviii, 276. (17) BARNEY AND CHUTE, R.: Jour. Urol., 1931, xxv, 173. (18) RAFIN: Jour. d'Urol., 1921, ix, 428.