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Urinary tract calculi and ileal conduit diversion
Urinary Tract Calculi and Heal Conduit Diversion Stephen P. Dretler, MD, Boston, Massachusetts
During the late 1940’s and early 1950’s Bricker [I] popularized the ileal conduit as a means of permanent urinary diversion for patients undergoing pelvic exenteration. Since many of these patients had lifeshortening diseases, it was not readily evident that although the ileal conduit provided solutions for some problems, it created others not easily soluble. By 1960, after widespread experience with ileal diversion, it became apparent that formation of urinary tract calculi was one of the most common longterm consequences of ileal conduit diversion, occurring in 4.7 to 10 per cent of patients [2-J]. Recently, calculi have been reported to occur in as many as 30 per cent of patients undergoing ileal conduit diversion [6]. Despite the frequency of this complication and the publications citing calculus formation as a hazard of diversion, it is curious that only one study has appeared which attempts to define possible calculogenic factors. Parsons and Cordonnier [7] compared the mineralizing effect of urine from patients who underwent diversion with and without calculi on rachetic rat cartilage and found both to have mineralizing properties. Although urine from patients with diversion and calculi cannot be distinguished by its effect on rachetic rat cartilage, it is likely that some basic etiologic factor or factors underlie calculogenesis. The purpose of this study is to determine the clinical characteristics of patients with diversion in whom urinary tract calculi develop and how they differ from the patients with diversion in whom calculi do not form. Recognition of these differences will suggest the possible mechanism of calculus formation and provide a basis for further investigation and prevention. From the Department of Urology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114. Reprint requests should be addressed to Dr Dretler, Department of Urology, Massachusetts General Hospital, Fruit Street, Boston, Massachusetts 02114. Presented at the Fifty-Second Annual Meeting of the New England Surgical Society at Portsmouth, New Hampshire, September 30, October 1 and 2. 1971.
480
Material and Methods To determine the clinical circumstances in which calculus formation occurs, the records of 740 patients tiho underwent ileal conduit diversion at the Massachusetts General Hospital from 1953 to 1969 were reviewed. Selected from this group were all patients, without preoperative evidence of urinary calculi, in whom urinary tract calculi formed subsequent to diversion. The clinical characteristics of patients in whom calculi formed were compared with those of the remainder of the population in whom diversion had been performed. The following factors were considered: age and sex; disease process necessitating diversion; the presence of preoperative ureteral dilatation and clinically or roentgenographically evident pyelonephritis; the interval between conduit construction and recognized calculus fprmation; conduit residuum; chemical composition of the calculus as determined by pulverization and wet-ash analysis; predominant bacterial organism in the urine identified by plating on McConkey’s and 5 per cent horse blood agar; the presence of ureteroileal obstruction as documented by retrograde dye studies; the presence of hyperchloremia (serum chloride greater than 106 mEq/L) or systemic acidosis (serum COz less than 25 mEq/L) as determined on the autoanalyzer. Results Thirty-five adults and one child, without prior evidence of calculus disease, were recognized to have formed urinary tract calculi from three months to fifteen years after ileal conduit diversion. (Figure 1.) Twenty patients were female and sixteen were male. Two additional patients had formation of calculi on foreign bodies in the conduit, one on a piece of silk and the other on a small piece of wood. Because of the obvious etiology of these calculi, these two additional patients have been excluded from the study. Seventeen of the thirty-six patients (47 per cent) had diversion during therapy for neoplastic disease: bladder, eight patients; cervix, seven; prostate, one; and rectum, one. Nineteen patients (53 per cent) underwent diversion for non-neoplastic disorders of the
The American
Journal of Surgery
Calculi Formation after lleal Conduit Diversion
lower urinary tract. Of the 740 patients undergoing ileal conduit diversion, 35 per cent underwent diversion for non-neoplastic disease and 65 per cent during therapy for cancer. Although only 46 per cent of all patients undergoing diversion had ureteral dilatation or pyelonephritis prior to diversion, thirty of thirty-six patients (84 per cent) in whom calculi formed had preoperative ureteral dilatation and/or evidence of pyelonephritis. Urine cultures were available for thirty-four of the thirty-six patients in whom calculi formed. Although more than one organism was often present, Proteus was the predominant organism in the urine of thirtyone of thirty-four patients (91 per cent). Review of the urine cultures reported in the remainder of the patients undergoing diversion revealed Proteus to be present in 40 per cent. The volume of residual urine in the ileal conduit was documented in twenty-two patients having diversion in whom calculi formed. (Figure 2.) Nineteen of the twenty-two patients had residual urine of greater than 10 ml. The average amount of recorded conduit residual in all other patients undergoing diversion was 8 ml. Serum electrolyte determinations were available for thirty-one of the thirty-six patients in whom calculi formed. Unequivocal hyperchloremic acidoses was present in twenty-one patients (70 per cent) and another three patients (10 per cent) had borderline systemic acidosis. Eight of the twenty-one acidotic patients had normal renal function as determined by creatinine or blood urea nitrogen levels. Less than 10 per cent of all other patients with diversion were noted to have any degree of hyperchloremic acidosis. Renal function, determined by creatinine and blood urea nitrogen levels, was recorded in twentyseven patients in whom calculi formed. Thirteen patients had normal renal function and in fourteen patients elevation of blood urea nitrogen and/or creatinine suggested impairment. Ureteral obstruction, occurring as a result of extrinsic compression, strictures, or tumor, was documented to have occurred in forty-six of 740 patients who underwent diversion. In eight of these patients urinary tract calculi formed. In six patients calculi formed ipsilateral to the site of ureteral obstruction; a seventh patient had bilateral calculi and unilateral obstruction, and in another patient a calculus formed contralateral to the site of obstruction. Fifteen calculi were removed and analyzed. Fourteen were composed of struvite (calcium, magnesium ammonium phosphate) and one was pure calcium oxalate. The patient in whom the pure calcium oxalate calculus formed had none of the clinical characteristics found in the remainder of the patients
Volume
123,
April 1972
YEARS
AFTER
DIVERS/ON
Figure 1. Interval from ileal diversion to calculus recognition in thirty-six patients.
undergoing diversion and in whom calculi formed. His urine was uninfected, and he had normal serum electrolyte levels. He had no evidence of pyelonephritis or preoperative ureteral dilatation. He was found to have widespread bony metastases and hypercalciuria. Calculi were bilateral in thirteen patients. Two patients were noted to have calculi within the conduit (excluding those found on foreign bodies). The lower pole calyx was the most common site of calculus formation. Six patients had branched calculi. Three patients who underwent pyelolithotomy had the presence of parenchymal calcifications confirmed by microscopic examination of renal biopsy specimens. Comments Thirty-six patients in whom urinary tract calculi formed in a series of 740 ileal conduit diversions would indicate a crude incidence of only 4.8 per cent. However, if only adults in whom diversion was per-
CONDUIT
RESIDUAL
VOLUME
fmll
Figure 2. Volumes of conduit residual in twenty-two patients in whom urinary tract calculi formed.
481
Dretler
formed for non-neoplastic disease and who were followed for at least one year are considered, the occurrence of urinary tract calculi approaches 13 per cent. If all 740 of these patients with diversion had survived and were followed for fifteen years (longest interval between diversion and calculus recognition), the incidence of urinary tract calculi would probably be considerably higher. Analysis of these clinical data revealed that patients undergoing diversion in whom urinary tract calculi formed could be distinguished from the remainder of the population at risk by the frequent occurrence of the following: ureteral dilatation, and/or pyelonephritis (84 per cent) and impaired renal function; urea-splitting urinary tract organisms (91 per cent); large volumes of conduit residual (average 29 ml); and overt or borderline hyperchloremic acidosis (80 per cent). (Table I.) Some may propose that pyelonephritis and the presence of urea-splitting organisms provide sufficient cause for the precipitation of urinary tract calculi. In the patients with ureteral obstruction, ureasplitting infection, and ipsilateral calculus formation, this may be the case. Certainly, the fact that fourteen of fifteen calculi were composed of struvite suggests that infection does play a role in stone formation. However, proponents of this theory of calculogenesis would find it difficult to explain why calculi failed to form in other patients with diversion who had urea-splitting infection (40 per cent) and pyelonephritis (46 per cent) or why the twenty-eight patients who had both pyelonephritis and urea-splitting infection prior to diversion did not have formation of calculi until after the conduit was constructed. It seems more reasonable to contend that although pyelonephritis and urea-splitting organisms may play a role in calculus formation, another variable is present which is responsible for altering the physiologic environment and thus increasing vulnerability to calculus formation. That common variable is indiyidual ileal conduit function. It is knoti that calculus formation occurs as a complication of ureterosigmoidostomy [8], as well as ileal conduit diversion. It is also known that the ileum shares some of the physiologic properties of colon; specifically, the ability to exchange bicarbonate for chloride [9]. Based on this knowledge and the clinical characteristics shown to occur in patients undergoing diversion in whom calctili form, a reasonable hypothesis regarding calculi formation in patients with diversion may be formulated. The amount of exchange of chloride and bicarbonate in the ileum is determined by the length of contact of urine and intestinal mucosa. Patients with conduits with poor peristalsis, long conduits, or large
482
volumes of conduit residual are thus subject to an accelerated rate of chloride-bicarbonate exchange and the occurrence of systemic acidosis (bicarbonate deficit). Patients in whom calculi form were found to have large amounts of conduit residual (average 29 ml) and a high incidence of hyperchloremia and/or systemic acidosis (80 per cent). Patients who have severe or prolonged systemic acidosis utilize extracellular buffering mechanisms to maintain a normal blood pH. When both intracellular and extracellular buffers are depleted, bone-buffering mechanisms are necessary. This results in the release of calcium and subsequent hypercalciuria [l&12]. Patients with diversion who, because of large volume of conduit residual, develop systemic acidosis and depletion of plasma and intracellular buffers, maintain homeostasis by the release of both alkali and calcium from bone. Excess calcium is excreted in the urine. Hypercalciuria is the obvious result. Hypercalciuria in the presence of an alkaline urine (91 per cent Proteus infection) allows a situation to occur which is favorable to the precipitation of urinary tract calculi. (Figure 3.) The prevention of calculus formation in patients with diversion is accomplished by meticulous conduit construction and maintenance of proper conduit function. Conduits should be made as short as possible and have a straight, wide passage through the abdominal wall to prevent the accumulation of residual urine. However, experience has shown that a well constructed and well functioning conduit may not always remain so. Stoma1 obstruction, conduit lengthening or dilatation and areas of conduit fibrosis may all occur, impeding the flow of urine and facilitating chloride-bicarbonate exchange. Therefore, patients with ileal conduits require frequent evaluation with
TABLE I
Clinical Characteristics in Patients with Diversion in Whom Calculi Formed Compared with Those of the Remainder of the Population with Diversion
Clinical Characteristics Age and sex Cause for diversion Neoplasia Benign neoplasia Preoperative ureteral dilatation and pyelonephritis Proteus infection Average conduit residual Systemic acidosis
Patients in Whom Stones Formed No significant
Others difference
47% 53%
65% 35%
64% 91% 29 ml 80%
46% 40% 8ml 10%
The American Journal of Surgery
Cal&Ii Formation
undoit
Iarqe
residuun
Ialu~t paarly
peri!3talsincI
1-
I-cl-m
!3?esnic
Bale
conduit
lZX&mge 3
I
k xlosis
1
bufferinq
1
calciun wlea.=le
1
mrcalciuria
aU%l.ine urine
after Heal Conduit
Diversion
4. Creevy CD: Renal complications after ileac diversion of urine in non-neoplastic disorders. J Ural 83: 394, 1960. 5. Ellis LR. Udall DA, Hodges CV: Further clinical experience with intestinal segments for urinary diversion. J Ural 105: 354,197l. 6. Malek RS, Burke EC, DeWeerd JH: lleal conduit diversion in children. J Ural 105: 892, 1971. JJ: Calcification of cartilage by 7. Parsons RP, Cordonnier urine from patients with ileal conduit urinary diversion. J Ural 96: 892, 1966. 8. Williams DF, Burkholder GV, Goodwin WE: Ureterosigmoidostomy: a 15 year experience. J Ural 101: 168, 1969. acidosis fol9. Madsen PO: The etiology of hyperchloremic lowing urointestinal anastomosis: an experimental study. J Ural 92: 448, 1964. 10. Lemmon J, Litzow JR, Lennon EJ: Effects of chronic acid loads in normal man. Further evidence for the participation of bone mineral in the defense against chronic metabolic acidosis. J C/in /west 45: 1608, 1966. 11. Lemmon J; Litzow JR, Lennon EJ: Studies on the mechanism by which chronic metabolic acidosis augments ur/nary calcium in man. J C/in Invest46: 1318, 1967. 12. Irving L, Chute AL: The participation of the carbonates of bone in the neutralization of ingested acid. J Cell Comp Physiol2: 1932, 1957.
i, Discussion Figure 3. Proposed pathogenesis of calculi formation in patients wtto have undergone iteal conduit diversion.
determination of serum electrolytes, measurement of conduit residuum, and urine cultures. The findings of large amounts of conduit residual, systemic acidosis, and/or urea-splitting urinary tract infection dictate the need for aggressive therapy to prevent the progression of events that may lead to calculus formation.
Summary Patients in whom urinary calcui form after ileal conduit diversion were found to have preoperative pyelonephritis and ureteral dilatation (84 per cent), large volumes of conduit residual (average of 29 ml), urease-producing urinary tract organisms (91 per cent), and hyperchloremic acidosis (80 per cent). On the basis of these findings a theory of the pathogenesis of calculi formation is formulated and methods of calculi prevention proposed. References 1. Bricker EM: Bladder substitution after pelvic evisceration. Surg C/in N Amer 30: 1511, 1950. 2. Cordonnier JJ, Nickolai CH: An evaluation of the use of an isolated segment of ileum as a means of urinary diversion. J Ural 83: 834, 1960. 3. Jaffe EM. Bricker EM, Butcher HR: Surgical complications of ileal segment urinary diversion. Ann Surg 167: 367. 1968.
Volume 123, April 1972
Henry T. Randall (Providence, RI): Some years ago, at the Memorial Hospital in New York, Dr Alexander Brunschwig claimed that it was only necessary to place the ureters in the colon. Renal failure and acidosis developed in some patients. A fellow in urology, Dr Willy Mathiesen, found that filtration rates were uniformly low in the patients in whom hyperchloremic acidosis developed. Doctor Dretler, did you study filtration rates in patients with calculi as compared with your controls? Finally, your studies re-emphasize the importance of a short conduit, which is the sine qua non of an effective substitute for the bladder. Stephen Dretler (closing): Poor renal function is not a prerequisite to the development of systemic acidosis and calculus formation. Almost one half of the stone-forming patients had normal renal function. The acidosis resulted from prolonged contact of urine and intestinal mucosa. Certainly, those patients with poor renal function and less buffer reserve will be more susceptible to systemic acidosis and subsequent calculus formation. The situation is no different than that which occurred in patients who had ureterosigmoidostomies. Contrary to popular belief, hypokalemia and hyperchloremic and systemic acidosis may be a consequence of ileal conduit diversion. Attempts to administer oral agents to acidify the urine will be futile and will lead to more severe systemic acidosis. Until the conduit is shortened or urease-producing bacteria are eliminated, the urine will remain alkaline. Stoma1 stenosis may be the cause of conduit lengthening and dilatation in some instances, but as Minton, Kiser, and Ketchum pointed out, the stoma need not be very large to achieve conduit emptying. It is probable that a lack of ileal peristalsis is more at fault than stoma1 problems. This seems to be especially true in paraplegics.
483
During the late 1940’s and early 1950’s Bricker [I] popularized the ileal conduit as a means of permanent urinary diversion for patients undergoing pelvic exenteration. Since many of these patients had lifeshortening diseases, it was not readily evident that although the ileal conduit provided solutions for some problems, it created others not easily soluble. By 1960, after widespread experience with ileal diversion, it became apparent that formation of urinary tract calculi was one of the most common longterm consequences of ileal conduit diversion, occurring in 4.7 to 10 per cent of patients [2-J]. Recently, calculi have been reported to occur in as many as 30 per cent of patients undergoing ileal conduit diversion [6]. Despite the frequency of this complication and the publications citing calculus formation as a hazard of diversion, it is curious that only one study has appeared which attempts to define possible calculogenic factors. Parsons and Cordonnier [7] compared the mineralizing effect of urine from patients who underwent diversion with and without calculi on rachetic rat cartilage and found both to have mineralizing properties. Although urine from patients with diversion and calculi cannot be distinguished by its effect on rachetic rat cartilage, it is likely that some basic etiologic factor or factors underlie calculogenesis. The purpose of this study is to determine the clinical characteristics of patients with diversion in whom urinary tract calculi develop and how they differ from the patients with diversion in whom calculi do not form. Recognition of these differences will suggest the possible mechanism of calculus formation and provide a basis for further investigation and prevention. From the Department of Urology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114. Reprint requests should be addressed to Dr Dretler, Department of Urology, Massachusetts General Hospital, Fruit Street, Boston, Massachusetts 02114. Presented at the Fifty-Second Annual Meeting of the New England Surgical Society at Portsmouth, New Hampshire, September 30, October 1 and 2. 1971.
480
Material and Methods To determine the clinical circumstances in which calculus formation occurs, the records of 740 patients tiho underwent ileal conduit diversion at the Massachusetts General Hospital from 1953 to 1969 were reviewed. Selected from this group were all patients, without preoperative evidence of urinary calculi, in whom urinary tract calculi formed subsequent to diversion. The clinical characteristics of patients in whom calculi formed were compared with those of the remainder of the population in whom diversion had been performed. The following factors were considered: age and sex; disease process necessitating diversion; the presence of preoperative ureteral dilatation and clinically or roentgenographically evident pyelonephritis; the interval between conduit construction and recognized calculus fprmation; conduit residuum; chemical composition of the calculus as determined by pulverization and wet-ash analysis; predominant bacterial organism in the urine identified by plating on McConkey’s and 5 per cent horse blood agar; the presence of ureteroileal obstruction as documented by retrograde dye studies; the presence of hyperchloremia (serum chloride greater than 106 mEq/L) or systemic acidosis (serum COz less than 25 mEq/L) as determined on the autoanalyzer. Results Thirty-five adults and one child, without prior evidence of calculus disease, were recognized to have formed urinary tract calculi from three months to fifteen years after ileal conduit diversion. (Figure 1.) Twenty patients were female and sixteen were male. Two additional patients had formation of calculi on foreign bodies in the conduit, one on a piece of silk and the other on a small piece of wood. Because of the obvious etiology of these calculi, these two additional patients have been excluded from the study. Seventeen of the thirty-six patients (47 per cent) had diversion during therapy for neoplastic disease: bladder, eight patients; cervix, seven; prostate, one; and rectum, one. Nineteen patients (53 per cent) underwent diversion for non-neoplastic disorders of the
The American
Journal of Surgery
Calculi Formation after lleal Conduit Diversion
lower urinary tract. Of the 740 patients undergoing ileal conduit diversion, 35 per cent underwent diversion for non-neoplastic disease and 65 per cent during therapy for cancer. Although only 46 per cent of all patients undergoing diversion had ureteral dilatation or pyelonephritis prior to diversion, thirty of thirty-six patients (84 per cent) in whom calculi formed had preoperative ureteral dilatation and/or evidence of pyelonephritis. Urine cultures were available for thirty-four of the thirty-six patients in whom calculi formed. Although more than one organism was often present, Proteus was the predominant organism in the urine of thirtyone of thirty-four patients (91 per cent). Review of the urine cultures reported in the remainder of the patients undergoing diversion revealed Proteus to be present in 40 per cent. The volume of residual urine in the ileal conduit was documented in twenty-two patients having diversion in whom calculi formed. (Figure 2.) Nineteen of the twenty-two patients had residual urine of greater than 10 ml. The average amount of recorded conduit residual in all other patients undergoing diversion was 8 ml. Serum electrolyte determinations were available for thirty-one of the thirty-six patients in whom calculi formed. Unequivocal hyperchloremic acidoses was present in twenty-one patients (70 per cent) and another three patients (10 per cent) had borderline systemic acidosis. Eight of the twenty-one acidotic patients had normal renal function as determined by creatinine or blood urea nitrogen levels. Less than 10 per cent of all other patients with diversion were noted to have any degree of hyperchloremic acidosis. Renal function, determined by creatinine and blood urea nitrogen levels, was recorded in twentyseven patients in whom calculi formed. Thirteen patients had normal renal function and in fourteen patients elevation of blood urea nitrogen and/or creatinine suggested impairment. Ureteral obstruction, occurring as a result of extrinsic compression, strictures, or tumor, was documented to have occurred in forty-six of 740 patients who underwent diversion. In eight of these patients urinary tract calculi formed. In six patients calculi formed ipsilateral to the site of ureteral obstruction; a seventh patient had bilateral calculi and unilateral obstruction, and in another patient a calculus formed contralateral to the site of obstruction. Fifteen calculi were removed and analyzed. Fourteen were composed of struvite (calcium, magnesium ammonium phosphate) and one was pure calcium oxalate. The patient in whom the pure calcium oxalate calculus formed had none of the clinical characteristics found in the remainder of the patients
Volume
123,
April 1972
YEARS
AFTER
DIVERS/ON
Figure 1. Interval from ileal diversion to calculus recognition in thirty-six patients.
undergoing diversion and in whom calculi formed. His urine was uninfected, and he had normal serum electrolyte levels. He had no evidence of pyelonephritis or preoperative ureteral dilatation. He was found to have widespread bony metastases and hypercalciuria. Calculi were bilateral in thirteen patients. Two patients were noted to have calculi within the conduit (excluding those found on foreign bodies). The lower pole calyx was the most common site of calculus formation. Six patients had branched calculi. Three patients who underwent pyelolithotomy had the presence of parenchymal calcifications confirmed by microscopic examination of renal biopsy specimens. Comments Thirty-six patients in whom urinary tract calculi formed in a series of 740 ileal conduit diversions would indicate a crude incidence of only 4.8 per cent. However, if only adults in whom diversion was per-
CONDUIT
RESIDUAL
VOLUME
fmll
Figure 2. Volumes of conduit residual in twenty-two patients in whom urinary tract calculi formed.
481
Dretler
formed for non-neoplastic disease and who were followed for at least one year are considered, the occurrence of urinary tract calculi approaches 13 per cent. If all 740 of these patients with diversion had survived and were followed for fifteen years (longest interval between diversion and calculus recognition), the incidence of urinary tract calculi would probably be considerably higher. Analysis of these clinical data revealed that patients undergoing diversion in whom urinary tract calculi formed could be distinguished from the remainder of the population at risk by the frequent occurrence of the following: ureteral dilatation, and/or pyelonephritis (84 per cent) and impaired renal function; urea-splitting urinary tract organisms (91 per cent); large volumes of conduit residual (average 29 ml); and overt or borderline hyperchloremic acidosis (80 per cent). (Table I.) Some may propose that pyelonephritis and the presence of urea-splitting organisms provide sufficient cause for the precipitation of urinary tract calculi. In the patients with ureteral obstruction, ureasplitting infection, and ipsilateral calculus formation, this may be the case. Certainly, the fact that fourteen of fifteen calculi were composed of struvite suggests that infection does play a role in stone formation. However, proponents of this theory of calculogenesis would find it difficult to explain why calculi failed to form in other patients with diversion who had urea-splitting infection (40 per cent) and pyelonephritis (46 per cent) or why the twenty-eight patients who had both pyelonephritis and urea-splitting infection prior to diversion did not have formation of calculi until after the conduit was constructed. It seems more reasonable to contend that although pyelonephritis and urea-splitting organisms may play a role in calculus formation, another variable is present which is responsible for altering the physiologic environment and thus increasing vulnerability to calculus formation. That common variable is indiyidual ileal conduit function. It is knoti that calculus formation occurs as a complication of ureterosigmoidostomy [8], as well as ileal conduit diversion. It is also known that the ileum shares some of the physiologic properties of colon; specifically, the ability to exchange bicarbonate for chloride [9]. Based on this knowledge and the clinical characteristics shown to occur in patients undergoing diversion in whom calctili form, a reasonable hypothesis regarding calculi formation in patients with diversion may be formulated. The amount of exchange of chloride and bicarbonate in the ileum is determined by the length of contact of urine and intestinal mucosa. Patients with conduits with poor peristalsis, long conduits, or large
482
volumes of conduit residual are thus subject to an accelerated rate of chloride-bicarbonate exchange and the occurrence of systemic acidosis (bicarbonate deficit). Patients in whom calculi form were found to have large amounts of conduit residual (average 29 ml) and a high incidence of hyperchloremia and/or systemic acidosis (80 per cent). Patients who have severe or prolonged systemic acidosis utilize extracellular buffering mechanisms to maintain a normal blood pH. When both intracellular and extracellular buffers are depleted, bone-buffering mechanisms are necessary. This results in the release of calcium and subsequent hypercalciuria [l&12]. Patients with diversion who, because of large volume of conduit residual, develop systemic acidosis and depletion of plasma and intracellular buffers, maintain homeostasis by the release of both alkali and calcium from bone. Excess calcium is excreted in the urine. Hypercalciuria is the obvious result. Hypercalciuria in the presence of an alkaline urine (91 per cent Proteus infection) allows a situation to occur which is favorable to the precipitation of urinary tract calculi. (Figure 3.) The prevention of calculus formation in patients with diversion is accomplished by meticulous conduit construction and maintenance of proper conduit function. Conduits should be made as short as possible and have a straight, wide passage through the abdominal wall to prevent the accumulation of residual urine. However, experience has shown that a well constructed and well functioning conduit may not always remain so. Stoma1 obstruction, conduit lengthening or dilatation and areas of conduit fibrosis may all occur, impeding the flow of urine and facilitating chloride-bicarbonate exchange. Therefore, patients with ileal conduits require frequent evaluation with
TABLE I
Clinical Characteristics in Patients with Diversion in Whom Calculi Formed Compared with Those of the Remainder of the Population with Diversion
Clinical Characteristics Age and sex Cause for diversion Neoplasia Benign neoplasia Preoperative ureteral dilatation and pyelonephritis Proteus infection Average conduit residual Systemic acidosis
Patients in Whom Stones Formed No significant
Others difference
47% 53%
65% 35%
64% 91% 29 ml 80%
46% 40% 8ml 10%
The American Journal of Surgery
Cal&Ii Formation
undoit
Iarqe
residuun
Ialu~t paarly
peri!3talsincI
1-
I-cl-m
!3?esnic
Bale
conduit
lZX&mge 3
I
k xlosis
1
bufferinq
1
calciun wlea.=le
1
mrcalciuria
aU%l.ine urine
after Heal Conduit
Diversion
4. Creevy CD: Renal complications after ileac diversion of urine in non-neoplastic disorders. J Ural 83: 394, 1960. 5. Ellis LR. Udall DA, Hodges CV: Further clinical experience with intestinal segments for urinary diversion. J Ural 105: 354,197l. 6. Malek RS, Burke EC, DeWeerd JH: lleal conduit diversion in children. J Ural 105: 892, 1971. JJ: Calcification of cartilage by 7. Parsons RP, Cordonnier urine from patients with ileal conduit urinary diversion. J Ural 96: 892, 1966. 8. Williams DF, Burkholder GV, Goodwin WE: Ureterosigmoidostomy: a 15 year experience. J Ural 101: 168, 1969. acidosis fol9. Madsen PO: The etiology of hyperchloremic lowing urointestinal anastomosis: an experimental study. J Ural 92: 448, 1964. 10. Lemmon J, Litzow JR, Lennon EJ: Effects of chronic acid loads in normal man. Further evidence for the participation of bone mineral in the defense against chronic metabolic acidosis. J C/in /west 45: 1608, 1966. 11. Lemmon J; Litzow JR, Lennon EJ: Studies on the mechanism by which chronic metabolic acidosis augments ur/nary calcium in man. J C/in Invest46: 1318, 1967. 12. Irving L, Chute AL: The participation of the carbonates of bone in the neutralization of ingested acid. J Cell Comp Physiol2: 1932, 1957.
i, Discussion Figure 3. Proposed pathogenesis of calculi formation in patients wtto have undergone iteal conduit diversion.
determination of serum electrolytes, measurement of conduit residuum, and urine cultures. The findings of large amounts of conduit residual, systemic acidosis, and/or urea-splitting urinary tract infection dictate the need for aggressive therapy to prevent the progression of events that may lead to calculus formation.
Summary Patients in whom urinary calcui form after ileal conduit diversion were found to have preoperative pyelonephritis and ureteral dilatation (84 per cent), large volumes of conduit residual (average of 29 ml), urease-producing urinary tract organisms (91 per cent), and hyperchloremic acidosis (80 per cent). On the basis of these findings a theory of the pathogenesis of calculi formation is formulated and methods of calculi prevention proposed. References 1. Bricker EM: Bladder substitution after pelvic evisceration. Surg C/in N Amer 30: 1511, 1950. 2. Cordonnier JJ, Nickolai CH: An evaluation of the use of an isolated segment of ileum as a means of urinary diversion. J Ural 83: 834, 1960. 3. Jaffe EM. Bricker EM, Butcher HR: Surgical complications of ileal segment urinary diversion. Ann Surg 167: 367. 1968.
Volume 123, April 1972
Henry T. Randall (Providence, RI): Some years ago, at the Memorial Hospital in New York, Dr Alexander Brunschwig claimed that it was only necessary to place the ureters in the colon. Renal failure and acidosis developed in some patients. A fellow in urology, Dr Willy Mathiesen, found that filtration rates were uniformly low in the patients in whom hyperchloremic acidosis developed. Doctor Dretler, did you study filtration rates in patients with calculi as compared with your controls? Finally, your studies re-emphasize the importance of a short conduit, which is the sine qua non of an effective substitute for the bladder. Stephen Dretler (closing): Poor renal function is not a prerequisite to the development of systemic acidosis and calculus formation. Almost one half of the stone-forming patients had normal renal function. The acidosis resulted from prolonged contact of urine and intestinal mucosa. Certainly, those patients with poor renal function and less buffer reserve will be more susceptible to systemic acidosis and subsequent calculus formation. The situation is no different than that which occurred in patients who had ureterosigmoidostomies. Contrary to popular belief, hypokalemia and hyperchloremic and systemic acidosis may be a consequence of ileal conduit diversion. Attempts to administer oral agents to acidify the urine will be futile and will lead to more severe systemic acidosis. Until the conduit is shortened or urease-producing bacteria are eliminated, the urine will remain alkaline. Stoma1 stenosis may be the cause of conduit lengthening and dilatation in some instances, but as Minton, Kiser, and Ketchum pointed out, the stoma need not be very large to achieve conduit emptying. It is probable that a lack of ileal peristalsis is more at fault than stoma1 problems. This seems to be especially true in paraplegics.
483