F- CLINICAL ASPECTS OF SPINAL CORD INJURIES
419
complaining of backache, and eventually it was found that he had developed abscesses
involving his spine and caused by aspergillosis. It was this disease with its complications
which eventually led to his death on n June 1972. The day before he died the blood urea
level was 52 mg per cent and the plasma creatinine 2-1 mg per cent and the kidney
transplant was functioning well right up to the time of death. It is really a tragedy having
regard to the good function of the transplanted kidney that he had to die from asper
gillosis. It is hoped that in future paraplegics who need kidney transplantation for renal
deficiency as a result of pyelonephritis will not be excluded from this new treatment.
Urine analysis and urine culture as well as detailed blood analysis and diastolic blood
pressure are the key to the diagnosis of early and progressive renal deficiency. Moreover,
positive results of rectal biopsies will ascertain whether chronic renal deficiency is
associated with amyloidosis, although negative rectal biopsies do not exclude renal
amyloidosis, as shown by the histological findings in this case following nephrectomy of the
right kidney.
Multiple factors are often operative in causing deterioration of renal function, and
amongst them occult sepsis from chronic tonsillitis and tooth decay or osteomyelitis
resulting from pressure sores may be mentioned. The importance of proper dental
hygiene and care cannot be overstressed, and patients with early renal deficiency should
have regular dental check-ups and septic teeth should be removed immediately. Toxic
agents are also instrumental in causing acceleration of renal deficiency and indeed acute
renal failure. The case of chronic renal deficiency, who developed acute renal failure,
following Renacidin treatment, mentioned earlier (page 397) is a striking example in this
respect, and the constant use of pain-killing drugs, especially those containing Phenacetin
should also be mentioned in this connection. Products of protein catabolism also have
toxic effects and, therefore, protein intake should be reduced in acute exacerbation of
chronic renal failure, associated with oliguria or anuria, and replaced by carbohydrate
diet. The special protein and mineral free diet consisting of glucose, peanut or olive oil
and vitamins, introduced by Bull
et al.
(1949,1953)? which we used to prescribe for these
patients in previous years, has been abandoned because it was too nauseating even when
given by stomach tube.
Mineral metabolism.
Particular attention has been paid in recent years to potassium
hemostasis and its disturbances in chronic renal failure, whereby protein catabolism and
metabolic acidosis play an essential part. Paeslack (1965) found hyperkalaemia in 5 cases
and hypokalaemia in 2 cases with progressed renal deficiency amongst 36 paraplegics, in
whom detailed investigations of the mineral metabolism had been carried out. Hypo
kalaemia may result from increased loss of potassium due to diarrhoea, vomiting, anorexia
and diuretics, and this may cause adverse cardiac effects (Tucker
et
a/., 1963). In some
cases, especially where renal failure is due to chronic pyelonephritis, hypokalaemia may
result from failure of renal conservation of potassium and the excretion of large amounts
of this ion in the urine. On the other hand, metabolic acidosis may cause hyperkalaemia
in oliguric patients with acute renal failure (see page 414).
Treatment consists of control of acidosis by sodium bicarbonate and adequate
glucose intake, and in cases of persistent vomiting and diarrhoea, a slow intravenous
