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TREATMENT FOR
ACUTE KIDNEY FAILURE
A
key part of the immediate assessment and management of any
patient who is very ill, which will include many of those with
acute
kidney
failure, is to make a correct assessment of the intravascular
volume status and to resuscitate rapidly and effectively.
Fluid
Many patients with acute
kidney
failure are volume-depleted at the time of presentation. An
urgent priority is to correct such depletion rapidly. Once this
has been achieved—as judged by an improvement in peripheral
perfusion, a fall in pulse rate, loss of postural drop in blood
pressure, and a rise in jugular venous pressure—the perspective
changes.
In
the absence of normal
kidney
function the greatest care must be taken to regulate the intake
of fluids and electrolytes to match losses in the urine, from
the gastrointestinal tract, and from other 'insensible' sources.
As a working rule, fluid intake is limited to the volume of the
previous day's urine output and gastrointestinal losses, plus
500 ml, but this allocation may need to be substantially
increased in the presence of fever or in hot environments, when
insensible losses may be much increased.
However, as discussed above, fluid-balance charts are frequently
inaccurate and unthinking adherence to the 'output plus 500 ml'
rule can lead to grief. There is no substitute for careful,
twice-daily clinical examination for signs of intravascular
volume depletion or excess, supplemented by accurate daily
weighing to gauge the overall net fluid balance, and an
intelligent flexible response to the findings.
Sodium
In
the patient who is not being dialysed, the intake of sodium must
also be matched to output. Requirements are usually very small
in those who are oliguric, perhaps only 15 to 30 mmol/day, but
if the patient is polyuric the requirements can be considerable,
with a danger of volume depletion if these are not met. The
urine of a patient with polyuric
kidney
failure will usually contain sodium at a concentration of 50 to
70 mmol/l, hence if urine output is 3 litres/day then over 200
mmol of sodium may be required.
On
occasion, the urine output in polyuric acute
kidney
failure can be massive (even up to 1 litre/hour)—if the response
is to administer an even greater quantity of fluid (output plus
insensible losses), then it is possible to contrive a vicious
cycle whereby an ever-increasing urinary output is rewarded by
ever-increasing fluid infusion.
To
avoid this situation in the patient with polyuria it is best to
limit input to urinary output alone, thus allowing other fluid
losses to establish a mild overall negative balance, only
increasing fluid input if the patient develops significant
postural hypotension, which should be checked for twice daily.
For unknown reasons, an excess of sodium and water in patients
with tubular necrosis leads to peripheral or pulmonary oedema,
whereas in those with glomerulonephritis it tends to produce
hypertension.
Potassium
Because hyperkalaemia is one of the most important problems in
the management of acute
kidney
failure, it is essential to check plasma potassium levels at
least daily, and in those with hypercatabolism or
gastrointestinal bleeding, or who require surgery, more frequent
estimations are advisable. In oliguric cases, dietary
consumption should be limited to the minimum compatible with an
adequate intake of protein and amino acids (20–30 mmol/day).
Diuretics that work on the distal tubule (for example,
spironolactone, amiloride, and triamterene) promote potassium
retention: they should never be used in renal failure, and it is
important when reviewing the drug chart to remember that these
agents are frequent constituents of tablets containing a
combination of diuretic/antihypertensive compounds. Intravenous
preparations of antimicrobial agents that contain large amounts
of potassium should also be avoided whenever possible.
Excretion of potassium can sometimes be enhanced in those who
are oliguric by the use of high doses of furosemide (0.5–1 g
daily). Oral potassium-exchange resins (e.g. Calcium Resonium),
prescribed concurrently with a laxative, can be useful in
controlling serum potassium for a few days or weeks, but they
are not effective treatments for acute severe hyperkalaemia and
are usually found to be unpalatable for long-term use. By
contrast, in polyuric acute
kidney
failure substantial losses of potassium can occur and need to be
replaced. Measurement of the urinary potassium concentration can
be helpful in estimating how much potassium is required.
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