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CHAPTER 26
sphincter. Moreover, the scars as a result of the operation in the ischial area may facilitate
the development of pressure sores.
(6) Hydronephrosis—pyonephrosis
Non-obstructive hydronephrosis following spinal cord injuries above the thoraco-
lumbar junction may be caused by neurogenic spasms of muscle fibres of the pelvi-
ureteric junction or calyces. Just as early infection of the bladder may elicit detrusor
spasms once the heightened reflex-activity of the isolated cord has developed, so may
spasms of the pelvi-ureteric junction and/or calyces be caused by early ascending infec
tion, resulting in alteration of the normal rhythm of relaxation and contraction between
the calyces system and pelvi-ureteric junction. Under normal circumstances, the calyces
eject their contents into the renal pelvis which in turn empties itself into the ureter.
Disturbances of the emptying mechanism at the pelvi-ureteric junction, due to obstruc
tion, will result in stagnation of urine in the pelvis resulting in, what is called, pelviectasis
or pelvic type of hydronephrosis. In these cases, the I.V.P. will show dilatation of the
renal pelvis, while the calyces may be of normal shape and size.
However, if the pelvis is intrarenal, its capacity for enlargement is limited and a
calyceal type of hydronephrosis will predominate. In the majority of our cases, the
hydronephrosis commenced in the calyces system, as revealed by dilatation of individual
or all calyces varying in size from clubbing to *cannon-balP deformity. In the great
majority, hydronephrosis following spinal cord lesions, except where caused by congenital
defects and abnormalities, is the result of obstruction which may occur within any section
of the urinary tract. Hydrodynamic dysfunction resulting from structural alteration in
urethra, bladder or ureter, may develop without infection of the urinary tract. However,
the main cause of hydronephrosis is ascending infection from the bladder which could
be prevented by proper management from the start as reported earlier.
Attention has been drawn in my monograph of 1953 to the development of hydro
nephrosis caused by periureteritis and panureteritis setting up inflammatory adhesions
between the various segments of the ureter—mainly the lower and upper ones—and the
surrounding tissues, resulting in ureter-kinking in coronal and sagittal directions and in
certain cases producing strictures of the ureter. Patients, admitted with long-standing
infection, have shown grotesque forms of hydroureter and hydronephrosis, and one
wondered, sometimes, how it was possible not only to survive but even lead an active
and useful life with such renal pathology for so many years. In this connection, the
following case is indeed an instructive example:
On 25 August 1953 a man, aged 38 years, was admitted, who on 27 October 1943 nac^
sustained a fracture-dislocation of Ti2/Li, resulting in an incomplete transverse spinal
cord syndrome below Tn with only partial motor paralysis of the distal muscles of the
left foot and analgesia from Tn-L3 on the left and 84/5 on the right, dribbling inconti
nence and a residual urine of 8 oz but being able to pass 20 oz of urine by expression. The
urine was infected with
B. proteus,
and an I.V.P. revealed a bilateral hydronephrosis with
a very large dilatation of the right pelvis and a kink of the right ureter at the uretero-
pelvic junction (Fig. 176). Unfortunately, there was no record of any I.V.P. done else-
