The Effect of Chronic Mechanical Obstruction on Ureteral Peristalsis

THE JOURNAL OF UROLOGY

Vol. 85, No. 4 April 1961 Copyright© 1961 by The Williams & Wilkins Co. Printed in U.S.A.

THE EFFECT OF CHRONIC MECHANICAL OBSTRUCTION ON URETERAL PERISTALSIS FRANK G. DELUCA, ORVAR SWENSON

AND

BRIAN SMYTH

From the Department of Surgery, Boston Floating Hospital, Boston, Mass.

One cause of megaloureter is diminished or absent peristalsis. In reviewing the literature there are suggestions that the etiology of the peristaltic defects may be due to congenital causes, infection, and mechanical obstruction.' No evidence has so far been published to define the exact role of mechanical obstruction as an etiologic factor .2 The object of this study was to determine, experimentally, the role of mechanical obstruction in producing ureteral dilatation and disturbances in ureteral peristalsis. METHOD

Sixteen adult female mongrel dogs were used in the experiments. Preliminary excretory urograms were made in 14 of 16 dogs prior to the obstruction of one ureter. In the remaining two, this examination was performed one to four days following the obstruction. "Gnder sterile conditions a suprapubic incision was made and the bladder and ureters were identified. The bladder was opened and the ureteral orifices were cannulatcd with polyethylene catheters. Manometric tracing of uretcral peristalsis was then made by attaching the polyethylene catheters to a low pressure transducer and graphic recordings were obtained on a Grass polygraph. The polyethylene catheters were removed after an aluminum band had been placed loosely around the lower encl of one ureter in order to produce a partial mechanical obstruction. In the last six experiments a cellophane band was used to partially obstruct the ureter. The bladder and abdominal wall were closed without drainage. Urinalysis and urine cultures were performed on all dogs at monthly intervals. Followup exAccepted for publication July 26, 1960. 1 Swenson, 0., Fisher, J. H. and Smyth, B.: Studies of normal and abnormal ureteral peristalsis. Med. J. Austral., 2: 805, 1959. 2 Bradford, R.: Observations made upon dogs to determine whether obstruction of the ureter would cause atrophy of kidney. Brit. Med. J., 2: 1720, 1897. 497

cretory urograms were performed 2 weeks following obstruction and at 6-month intervals for the remainder of the experiments. The animals were all explored on the average of three to five months following the initial obstructive operation. During the procedure the size of the kidney and the amount of dilatation and obstruction of the ureter were recorded. The bladder was opened and polyethylene catheters inserted into the ureteral orifices bilaterally. Ureteral peristalsis was recorded by the method described previously. The bladder and abdominal wall were closed around the ureteral catheter. Three to 5 cc, 30 per cent urokon was injected into the catheters and cinefluoroscopic studies were performed. After a period of 18 to 23 months, 9 clogs survived and were subjected to an intravenous urogram, exploration and ureteral peristaltic studies of the obstructed ureter. In order to evaluate ureteral patency, 7 clogs were studied by inserting a size 100 T-tube polyethylene catheter proximal to the obstruction. The free edges of the ureterostomy were approximated around the T-tube with interrupted 5-0 silk sutures according to the method described by Scott and DeLuca. 3 By recording from the T-tube, it was possible to detect changes in ureteral peristalsis related to increasing bladder pressure. Bladder pressures were recorded by attaching the Foley catheter to a transducer which was connected to a channel on the Grass polygraph. Prior to sacrificing the animals, tissue for histological sections was obtained from the bladder, both ureters and kidneys. RESULTS

Preliminary ureteral peristaltic studies and intra venous urograms were performed on all 16 dogs and interpreted as normal. Cinefluoroscopic studies were performed in several clogs prior to obstruction for comparison with the 3 Scott, J. and DeLuca, F.: Study of lower end of ureter and ureterovesical junction. Brit. J. Urol., in press.

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Fm. 1. Dog No. 159-57. Initial peristaltic study of left ureter, January 16, 1958

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Fm. 2. Dog No. 102-58. Obstruction of left ureter, March 11, 1958. Ureteral peristalsis 140 days after obstruction; note elevation of baseline pressure to 10 to 20 cm. of H 20. cine studies after the ureteral obstruction. Normal intraureteral resting pressures ranged from 2 to 5 cm. of H20 and ureteral contractions generated pressures ranging from 20 to 50 cm. of H,O. The average frequency was 6 to 8 waves per minute (:fig. 1). The subjects were followed for a minimum of 115 days and a maximum of 698 days. From a total of 16 dogs with unilateral obstructed ureters, ureteral dilatation developed in 15. Ten of the 15 dogs presented with gross, tortuous megaloureters. In this latter group, six were obstructed with a cellophane cuff. This technique produced a tortuous megaloureter more rapidly than the aluminum band, presumably due to a denser :fibrosis at the point of application. One animal 4 months after obstruction had a slight degree of hydronephrosis, dilatation and aperistalsis of the obstructed ureter. Urine

from this ureter contained over one million E. coli per ml. The aluminum band was removed at the time of infection. Four months later an intravenous urogram, cinefluoroscopic and manometric ureteral peristalsis studies demonstrated a return of peri~talsis, normal sized ureter and kidney still slightly hydronephrotic. Urine culture at this time revealed no growth of bacteria. In 13 of the 16 dogs postmortem examination revealed four atrophic kidneys and nine hydronephrotic kidneys. The four atrophic kidneys had ureters which were moderately dilated but not tortuous. In the group of nine hydronephrotic kidneys, eight presented with tortuous megaloureters. The remaining hydronephrotic kidney had megaloureter, aperistalsis and infection at one time. These changes returned to normal with removal of obstruction. Ureteral peristalsis was studied bilaterally in

EFFECT OF MECHANICAL OBSTRUCTION ON URETERAL PERISTALSIS

all 16 dogs by the direct manometric graphic technique and by cinefluoroscopy 4 to 5 months after obstruction. The intraureteral resting pressures were elevated and varied from 10 to 20 cm. H20. The amplitude of the peristaltic wave ranged from 15 to 50 cm. H20 and frequency rate was from 4 to 8 per minute (fig. 2). After 3 to 4 months of partial to complete obstruction, there was practically no change in the characteristics of the waves except for an elevated

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intraureteral resting pressure. Cinefluoroscopy in all cases confirmed the results of the manometric technique and also documented the apparent "to and fro" peristaltic wave of a completely obstructed ureter. Final peristaltic studies were performed in 7 dogs by placing a size 100 T-tube polyethylene catheter in the ureter approximately 2 cm. from the point of obstruction. A urethral catheter permitted filling of the bladder. The catheters 810

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FIG. 3. Dog No. 109-58. Obstruction of left ureter, March 13, 1958. Final peristaltic study, October 20, 1959. First graph represents bladder pressure and second, ureteral peristalsis. Third graph is a time signal, and fourth is bladder volume in cubic centimeters. Peristalsis present, with elevation of baseline pressure but no increase in amplitude or frequency with increasing bladder pressure. Megaloureter completely obstructed.

FIG. 4. Dog No. 159-57. Obstruction of left ureter, January 16, 1958. Final peristaltic study on October 19 1959, 698 days of partial obstruction. First graph for bladder pressure and second graph for ureteral pe~istalsis. Some increase in frequency and amplitude of ureteral peristalsis with increasing bladder pressure.

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were connected to two separate transducers and channels on the recorder. In six of the 7 dogs we were able to record ureteral peristalsis on the obstructed side with elevated baseline pressures varying from 20 to 30 cm. H20. The initial base-

Fm. 5. Dog No. 108-58. Hydronephrotic kidney and megaloureter with grossly infected foul smelling, thick urine. Peristalsis absent on final studies. Note pseudomembrane covering bladder mucosa.

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line pressure was first recorded by inserting a size 24 needle into the ureters. The amplitude of the peristaltic wave varied from 15 to 50 cm. of H20. No changes in frequency or amplitude of ureteral peristalsis were recorded in a completely obstructed ureter by filling the bladder with saline and increasing its pressure gradually or rapidly to 45 cm. of H20 (fig. 3). Changes in frequency and amplitude were demonstrated by rapid bladder filling in experiment 159-57 in which the dog, after approximately 698 days, demonstrated only partial obstruction and some renal function by intravenous urogram (fig. 4). In spite of huge megaloureter, initial and final peristaltic studies do not differ greatly. In one of the 7 dogs with a large hydronephrotic kidney and megaloureter, there was a lack of peristalsis. The urine was thick and foul smelling and a growth of over five million Staphylococcus albus per ml. was recorded. The urinary bladder, ureter, and large cystic kidney were lined with a thick pseudomembrane (fig. 5). This is the second case in this series of chronic, mechanically obstructed ureters presenting with hydronephrosis, megaloureter and infection which demonstrated a lack of normal peristalsis (fig. 6). Another interesting finding was the "to and fro" movement of an obstructed ureter. In one experiment the lower ureter was apparently completely obstructed by a large fibrous mass and while recording manometrically the uretera

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EFFECT OF MECHANICAL OBSTRUCTION ON URETERAL PERIS'rALSIS

peristalsis, one could actually see the upper and lower ureter alternately constrict and dilate. No urine was ejected into the bladder. It was decided to inject 3 cc air into the ureter and by doing this one could see the movement of the air bubble in the distended large ureter. The air bubble would appear at the obstructed point of the ureter and at times in the proximal ureter. The large, dilated ureter would contract but the air bubble would unpredictably appear in the proximal or distal portion of the ureter. A possible explanation of this is that the urine in front of the contraction wave fails, because of the obstruction, to enter the bladder. As the ureter relaxes the air bubble moves upward. It has been postulated that a reverse peristaltic wave is present, but such a contraction is not required to explain this retrograde movement of urine. This phenomenon warrants further investigation. DISCUSSION

As early as 1897, casual reference to a distended ureter was made by Professor Rose Bradford2 while performing experiments on whether an obstructed ureter would cause atrophy of the kidney. We noticed that gradual and progressive obstruction was of importance in producing huge and tortuous ureters. This was well brought out by comparing the sizes of the ureters obstructed with a cellophane cuff and those obstructed with an aluminum band. There is no doubt that the ureters obstructed with the aluminum band were distended to some extent; but the ureters obstructed with the cellophane cuff became huge and tortuous. The cellophane material produced a progressive and severe inflammatory reaction as noted at postmortem examination. This reaction produced a gradual partial obstruction and differs from the type of immediate partial obstruction produced by the aluminum band. Fourteen out of the 15 megaloureters were capable of demonstrating peristalsis even after a period of 365 days of obstruction. A completely obstructed ureter did not show an increase in amplitude and/or frequency of peristalsis when bladder pressure was increased as demonstrated by Scott and DeLuca. 3 We feel that this response of ureteral peristalsis was not produced because there was a complete obstruction of the lower ureter. Another factor, which undoubtedly influences ureteral peristalsis, was either partially or completely lacking in some experiments and that

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was the production of urine by the kidney. In several of our experiments, in which the intravenous pyelogram demonstrated minimal renal function after 2 hours, we were able to produce an increase in frequency and amplitude of ureteral peristalsis by slowly perfusing the renal pelvis with H20 or saline. Chronic complete or partial mechanical obstruction alone, therefore, did not cause an absence in ureteral peristalsis. One may compare the megaloureter secondary to mechanical obstruction to that of the megacolon. The dilatation in both cases is a normal response of the cellular elements to increasing capacity and work. In both cases there will be some return to normal size with the elimination of the obstruction. In two of the 16 experin1ents, mechanical obstruction was associated with severe infection. In both cases ureteral peristalsis was not demonstrated by the manometric catheterization technique and by cinefluoroscopy. In one of the 2 cases, 4 months after the mechanical obstruction was eliminated, there was a return of the ureter to normal size and a return of peristalsis confirmed both by the manometric catheterization technique and cinefluoroscopy. On intravenous urography there was still some persistent hydronephrosis. In the other case, because of persistent obstruction and infection, peristalsis was still lacking after 580 days. We realize that 2 cases are not sufficient evidence from which to conclude that infection alone or mechanical obstruction with infection is an important factor in causing an aperistaltic ureter. The constant elevation of pressure ranging from 10 to 30 cm. of water pressure within the obstructed ureter is important since normally this is below 5 cm. It is believed that pressure above 15 to 20 cm. of water pressure is sufficient to produce hydronephrosis. It would seem that the "high" resting pressure is the direct cause of the hydronephrosis. SUMMARY

Partial ureteral obstruction produces a megaloureter. No significant changes in the frequency or amplitude of ureteral contractions are produced by partial obstruction. The resting intraureteral pressure which is normally zero is increased to 10 to 30 cm. of water pressure. This apparently is the factor which produces hydronephrosis. Infection may play the more important role in destroying ureteral peristalsis,