Ahmed Shafik

Department of Surgery and Experimental Research, Faculty of Medicine, Cairo University, Cairo, Egypt

Received 3/20/98 Accepted 4/30/98

4- RESULTS AND DISCUSSION

The tests were completed and evaluated in all the volunteers with no adverse effects. The mean basal pressures are shown in table 1.

4.1 Effect of renal pelvic distension on the anal and rectal pressures

The effect of rapid renal pelvic distension in increments of 2 ml of saline on the pressures in the renal pelvis, rectum and anal canal is shown in figure 1. The renal pelvic pressure increased significantly (p < 0.05) on distension with 6 ml of saline. The more the renal pelvis was distended, the more the renal pelvic pressure increased whereas the rectum did not record significant pressure changes (p > 0.05). Meanwhile, the anal canal pressure increased significantly on renal pelvic distension with 10 and 12 ml of saline (p < 0.05; figure 1). We did not try distension of the renal pelvis with more than 12 ml of saline due to possibility of injury.

Figure 1: Effect of rapid renal pelvic distension in increments of 2 ml of saline on the pressure in the renal pelvis, rectum and anal canal.

The subjects felt renal and anal pain only on rapid renal pelvic distension with 10 and 12 ml of saline (table 2); no pain was felt with 2-8 ml distension. The renal pain occurred in the flank and was a dull ache while the anal pain was felt in the anus and lower pelvic area as a sharp stabbing ache. The severity of the flank and anal pain increased with more renal pelvic distension, was felt as long as the distension was maintained and disappeared upon release of the distension.

Table 2: Incidence of flank and anal pain on rapid renal pelvic distension

Slow renal pelvic distension led to rise in renal pelvic pressure with volumes greater than 6 ml (p < 0.05). However, the pressure rise was significantly lower than that produced by rapid distension (p < 0.05; figure 2). No significant rectal or anal pressure changes occurred (p > 0.05; figure 2). Flank pain was felt with 10 to 12 ml distension, but anal pain did not occur.

Figure 2: Effect of slow renal pelvic distension in increments of 2 ml of saline on the pressure in the renal pelvis, rectum and anal canal.

4.2 Effect of ureteric distension on the anal and rectal pressure

Rapid distension of the upper third of the ureter showed significant ureteric pressure rise with 0.5, 0.75 and 1 ml distension (p < 0.05; p < 0.05; p < 0.01, respectively; figure 3). The ureteric pressure continued to rise as the ureteric distension increased. While the rectum exhibited no significant pressure rise (p > 0.05) upon ureteric distension, a significant pressure increase was recorded in the anal canal with 0.75 and 1 ml distension (p < 0.05; p < 0.05, respectively; figure 3). Flank and anal pain were felt on ureteric distension with 0.75 and 1 ml of saline. The flank pain occurred as a dull ache while the anal pain was sharp and stabbing and was felt in the anus and lower pelvic area. The flank pain occurred with a distending ureteric volume less than that of the anal pain. Both the flank and anal pain disappeared with the release of the ureteric distension.

Figure 3: Effect of rapid ureteric distension in increments of 0.25 ml of saline on the pressure in the ureter, rectum and anal canal.

Slow ureteric distension caused ureteric pressure rise with 0.75 and 1 ml of saline and led to flank pain (figure 4). Meanwhile, no significant rectal or anal pressure changes (p > 0.05) occurred and no anal pain was felt. The ureteric pressure rise was significantly lower (p < 0.05) than that caused by rapid ureteric distension (figures. 3-4).

Figure 4: Effect of slow ureteric distension in increments of 0.25 ml of saline on the pressure in the ureter, rectum and anal canal.

Distension of the middle and lower third of the ureter produced results similar to those produced by the upper third distension with no significant difference (p > 0.05). We did not try ureteric distension with more than 1 ml in view of possibility of injury.

4.3 Effect of renal pelvic and ureteric distension on the external anal sphincter EMG

The basal activity of the external anal sphincter showed a mean amplitude of motor unit action potentials of 102.4 ± 26.2 µV (range 80-121). This basal EMG showed no significant change of activity on rapid renal pelvic distension up to 8 ml (figure 5). A significant increase of EMG activity occurred with 10 and 12 ml distension and the activity was more on distension with 12 ml than with 10 ml (figure 5). The motor unit action potentials recorded a mean of 586.3 ± 82.8 µV (range 418-750) at 10 ml renal pelvic distension and 674.6 ± 94.5 µV (range 533-890) at 12 ml. The EMG activity returned to the basal value on release of distension. The increased external anal sphincter activity was associated with anal and lower pelvic pain which disappeared upon release of renal pelvic distension.

Figure 5: The EMG activity of the external anal sphincter on rapid renal pelvic distension with a) 2, b) 4, c) 6, d) 8, e)10 and f)12 ml of saline.

The external anal sphincter exhibited increased EMG activity only with 0.75 and 1 ml rapid distension of the upper third of the ureter (figure 6). It recorded mean motor unit action potentials of 528.6 ± 78.2 µV (range 427-780) with 0.75 ml distension and 612.8 ± 88.5 µV (range 508-863 µV) with 1 ml distension. The increased external anal sphincter EMG activity was associated with anal and lower pelvic pain. No increased activity occurred on ureteric distension with volumes lower than 0.75 ml. The external anal sphincter EMG actvity returned to the basal level upon release of distension. These findings also occurred with no significant difference (p > 0.05) on distension of the middle and lower third of the ureter.

Figure 6: The EMG activity of the external anal sphincter on rapid ureteric distension with a) 0.25, b) 0.5, c) 0.75 and d) 1 ml of saline.

Slow renal pelvic or ureteric distension caused no significant change in the EMG activity of the external anal sphincter (p > 0.05); no anal pain was felt.

4.4 Effect of renal pelvic and ureteric distension on the anesthetised renal pelvis, ureter and external anal sphincter

Rapid and slow distension of the renal pelvis or ureter, 20 minutes after having been anesthetised did not cause significant pressure changes in the renal pelvis, ureter, rectum or anal canal (p > 0.05). No flank or anal pain was felt. Distension after two hours, when the anesthetic effect had worn out, produced pressure response as well as flank and anal pain similar to that observed before anesthetisation with no significant difference (p > 0.05). Distension of the renal pelvis or ureter after saline administration produced pressure responses in the renal pelvis, ureter, rectum and anal canal similar to those before saline administration (p > 0.05).

The external anal sphincter EMG activity, as well as rectal and anal canal pressures did not respond to rapid or slow renal pelvic or ureteric distension 20 minutes after external anal sphincter anesthetisation; the subjects did not feel anal pain. Two hours later, when the anesthetic effect had waned, the external anal sphincter showed increased activity; the anal canal pressure was elevated on rapid renal pelvic or ureteric distension as mentioned previously and flank and anal pain was felt.

In the current study, we performed rapid renal pelvic and ureteric distension in an attempt to simulate the distending effect of a calculus impacted in the ureteropelvic junction or ureter. The effect of slow renal pelvic or ureteric distension could be compared with that of partial obstruction of the renal pelvis or ureter.

Rapid renal pelvic or ureteric distension caused an increase of both the anal pressure and external anal sphincter EMG activity as well as flank and anal pain. The flank pain occurred with significant distension of the renal pelvis and appears to be due to the increase of the renal pelvic pressure. The anal pain is presumably caused by external anal sphincter contraction as evidenced by the increase of its EMG activity on renal pelvic or ureteric distension. Alternatively, it might be caused by the high anal pressure which occurs on renal pelvic or ureteric distension. The elevated anal pressure and the anal pain may be due to increased contractile activity of the internal anal sphincter. However, the fact that the anal canal pressure did not increase and the anal pain was not felt on renal pelvic or ureteric distension while the external anal sphincter was anesthetised, does not support such a conclusion and confirms that the external anal sphincter is the source of these findings. Furthermore, the increased EMG activity of the external anal sphincter on renal pelvic or ureteric distension is another evidence that this sphincter is the source of the elevated anal canal pressure.

The present findings demonstrate a previously unrecognized relationship between renal pelvic or ureteric distension and the external anal sphincter . The external anal sphincter response to renal pelvic or ureteric distension affirms the hypothesis of the possible involvement of a reflex which we term "reno-anal reflex". This reflex relationship is evidenced by reproducibility and its absence on anesthetizing either of the renal pelvis and ureter or the external anal sphincter , both presumably representing the 2 arms of the reflex arc.

We do not know yet the role of the reno-anal reflex which might be evoked by rapid renal pelvic or ureteric distension as for example by means of a calculus impacted in the ureteropelvic junction or in the ureter. The external anal sphincter contraction might confine the bowels and thus could explain the abdominal distension which occurs in subjects who are passing a stone down the ureter or have an impacted calculus in the ureteropelvic junction. Although in such cases, the urinary symptoms commonly overshadow the anal pain and abdominal distension, the latter symptoms could be misleading when outstandingly present.

Slow distension of the renal pelvis or ureter did not cause anal pressure elevation or pain, nor an increase of the external anal sphincter EMG activity.