Basic Concepts of Fluid and Electrolyte Therapy

Oliguria secondary to AKI
Although it is important not to give excess fluid, failure to recognize
and treat hypovolaemia (and pre-renal AKI) adequately may compromise
organ perfusion and result in intrinsic AKI. There is evidence that
patients with oliguric AKI have more severe tubular damage and a
worse outcome.
Once a diagnosis of AKI has been made the underlying cause must be
established (Chapter 9). The most common causes are hypovolaemia
and/or sepsis leading to hypoperfusion of the kidneys. Clinical examination
must be performed to establish the patient's volume status and
the source of sepsis must be identified and treated promptly. If the
patient is hypovolaemic then appropriate fluid therapy must be given
according to a documented management plan, which requires regular
review and defined endpoints (Fig. 9).
In a patient with hypovolaemia and oliguric AKI
consider insertion of a central venous pressure (CVP) line and urinary
catheter (not mandatory and could introduce infection) to aid
with the assessment of volume status
resuscitate with IV fluids (fluid challenge)
stat fluid bolus of 500 ml (250 ml if cardiac failure) of a balanced
crystalloid (e.g. Hartmann’s solution or Ringer’s lactate)
rapidly. If hyperkalaemia is present (K + >5.5 mmol/l) or suspected
oliguric AKI or rhabdomyolysis 0.9% saline is preferred initially
(no potassium in crystalloid). However, there is no evidence
that administration of crystalloids containing 3-5 mmol/l
of K + worsen the hyperkalaemia.
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