Page 614 - WSAVA2018
P. 614

 25-28 September, 2018 | Singapore
to maintain homeostasis and control clinical signs until the kidney recovers.
Hydration status
Animals with AKI are often dehydrated at presentation but may also be overhydrated, mostly due to previous medical treatment that included excessive fluid administration. Although changes in hydration and volemia often parallel, there are some exceptions. An overhydrated patient may be hypovolemic and vice versa. Assessment of hydration status is based mostly on the patient’s skin turgor and the mucous membranes, however in patients with uremia this assessment is
often challenging. Uremia can lead to decreased saliva production and dry mouth (xerostomia) or alternatively
to nausea and salivation. There are only few objective measures that can be used to assess the hydration status. The most readily available tool to assess changes in hydration status is serial measurements of body weight.
The initial treatment should focus in correcting
the patient hydration status. Unless there is a contraindication for rapid fluid administration (e.g., heart disease), dehydration should be corrected over 4-6 hours, using the following formula:
When calculating the amount of fluids to be administered thereafter, one has also to consider urine production, ongoing losses, and insensible losses. The maintenance requirements of patients with AKI cannot be extrapolated from the required maintenance fluids of normal patients, as some of the AKI patients are an/oliguric while others are polyuric. Therefore, fluids rate should be adjusted individually for each patient.
Patients with AKI should be weighed at presentation and routinely during the treatment period. Once a patient has reached its goal weight, it should be maintained
on this weight throughout the hospitalization time.
Fluid rate is determined by the rate of fluid loss (urine production, insensible losses and ongoing losses). Fluid administration without close monitoring may result in life threatening overhydration, especially in those patients with low urine production that cannot excrete the fluids administered. Clinical signs of overhydration include serous secretions from the nose, peripheral edema, lung edema, chemosis, pleural effusion and ascites. Overhydration is a common cause for morbidity and mortality in patients with AKI.
Recovery from AKI is often associated with the transition from anuria/oliguria to polyuria. This is a critical point, in which the risk for dehydration is high, and consequently further damage to the kidneys may occur. Polyuric patients may lose a substantial amount of fluids and typically do not drink enough to compensate for the fluid
loss, thus fluids have to be administered as needed to maintain normal hydration status.
Once the animal has reached normal hydration status and urine production is still low, the use of diuretics should be considered. Under no circumstances, diuretics should be used to promote urine production
in a dehydrated patient. The most commonly used diuretics are mannitol, furosemide and dopamine. Despite their wide use, there is no solid scientific evidence to advocate their use. In addition, like any other drug, diuretics may be associated with side effects, therefore their use should be considered for each case individually.
Mannitol is an osmotic diuretic; therefore, it is active along the entire nephron. Mannitol increases urine production, blood flow to the kidney, and promotes urea excretion. Mannitol is also a free radical scavenger. It is administered initially as a bolus (0.5-1.0 gr/kg over 20 minutes) which is followed by a constant rate infusion
at 1 mg/kg/min. Prior to Mannitol administration blood pressure should be controlled, as mannitol may increase the intravascular volume and worsen hypertension.
Furosemide is a potent loop diuretic, which acts on the thick ascending loop of Henle. Furosemide increases the blood flow to the kidney and promotes urea excretion, but it does not have any effect on the glomerular filtration rate. Furosemide is administered as an initial bolus or as a constant rate infusion. In addition to its diuretic effect, furosemide promotes potassium excretion.
The use of dopamine is highly controversial, both in human and veterinary medicine. The recommended dose for AKI is a low (0.5-3.0 μg/kg/min), which,
at least in theory, activates only the dopaminergic receptors without activation of α and β adrenergic receptors. Recent studies performed in human medicine demonstrated that although dopamine can increase urine production in some patients with AKI, its use
did not change the outcome of these patients (death
or the need for dialysis). Fenoldopam is a selective dopaminergic agonist which has been shown to promote urine production and solute excretion in normal animals but in a recent study did not change the outcome or kidney dysfunction in animals with heatstroke related AKI (1).
Controlling clinical and clinicopathologic signs associated with uremia
Gastrointestinal signs result from a direct effect of the uremic toxins on the chemoreceptor trigger zone and from gastrointestinal damage caused by these toxins (e.g., ulcers). The control of gastrointestinal signs is achieved by the use of gastrointestinal protectants (H2 blockers, proton pump inhibitors) and antiemetic

   612   613   614   615   616