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than the drug itself, are still in favour of this therapy for dissolving renal stones and during
1965 and 1967 succeeded in achieving complete dissolution in 30 out of 47 patients; in
11 patients the size of the stone was either reduced or further growth arrested, 3 patients
did not tolerate the treatment and 3 patients had stag-horn stones too old and too large
for Renacidin therapy. These authors have taken special precautions, such as restricted
flow rate, never exceeding 20 drops per minute, restricted flow duration of Renacidin of
i hr alternating with saline 3, 2 or i hr respectively depending on the patient's tolerance,
furthermore by using a Fr.N 4 or 5 urethral catheter as inflow channel and as outflow
channel a plastic catheter of minimum Fr.N 6. Moreover, if the patient shows malaise,
nausea or bloodstained fluid with either Renacidin or saline instillation, this is at once
stopped but is resumed after at least 24 hr of freedom from symptoms. In spite of these
precautions, I feel one should be very circumspect in the use of Renacidin in patients
with raised blood urea and other signs of renal deficiency combined with calculosis.
(5) Vesico-ureteric reflux
Changes of the hydrodynamics in bladder and ureter leading to vesico-ureteric reflux
have been of increasing interest during the last 15 years to nephrologists, spinal specialists
and urologists alike. Kjellberg
et al.
(1957) reported 37 per cent of reflux in a large series
of non-paraplegic children with urinary tract infection without demonstrable obstructive
lesion. Rosenheim (1963) and his team of co-workers found reflux in 76 per cent out of 55
non-paraplegic patients with radiological evidence of chronic pyelonephritis, and over a
period of 4 years 23 (64 per cent) out of 36 of his patients with apparent primary chronic
pyelonephritis had vesico-ureteric reflux.
The main cause of reflux in spinal cord lesions is the disorganization of the reciprocal
vesico-ureteric function as a result of ascending infection. It is generally agreed that the
lower portion of the ureter is particularly vulnerable to ascending infection from the
bladder and also to increased vesical pressure. As the intravesical section of the ureter
with its longitudinal muscle fibres plays an essential part in the prevention of back flow
of urine from the bladder, bacterial invasion of this region may easily lead to impairment
of the elasticity of the valve-like action of the ureteric orifice and disrupt the reciprocal
vesico-ureteric function and its hydrodynamics. Alterations in the juxta-ureteric bladder
wall was previously considered by Hutch (1958) as the cause of the development of reflux
whether congenital or acquired. Dilatation of the lower segment of the ureter has been
described by Talbot & Bunts (1949) as the first sign of a vesico-ureteric reflux, which we
confirmed in our own paraplegic patients.
Vesico-ureteric reflux may be transient or permanent. It occurs unilaterally and
bilaterally although more often unilaterally, and it may change from one side to another
in the course of alterations of the vesical dysfunction (Fig. 174).
The standard method of demonstrating reflux has been cystography which in recent
years has been supplemented or replaced by cinefluoroscopic or radioisotopic techniques
(Bitker & Pagnot, 1964). However, from all our experience, cystography still represents
an efficient standard method. Smith (1966) compared both methods in 145 children
and came to the conclusion that the cine method yielded only slightly better results than
