Fluid treatment for renal failure (Proceedings) - Veterinary Healthcare


Fluid treatment for renal failure (Proceedings)


Kidney disease is classically compartmentalized into acute and chronic disease, which is a convenient way to view what are very frequently markedly different manifestations of kidney disease. There is some overlap, however, in that a decompensated patient with chronic kidney disease (CKD) has a superimposed acute kidney injury (AKI) that may require hospitalization for fluid therapy. Although significant renal disease can be present without azotemia, fluid therapy is generally not necessary in those situations. In fact, fluid therapy may not be necessary in compensated chronic renal failure with mild to moderate azotemia.

Normal fluid losses consist of insensible and sensible losses. Insensible losses are those that are not consciously perceived, such as water lost via respiration, normal stool or sweating. Sweating is a negligible volume in dogs and cats. There is variation in respiratory losses in dogs, which may lose considerable amounts of fluid by excessive panting, but 22 ml/kg/day is the average. The main sensible fluid loss in the normal patient is urine output. Additional sensible losses include the volume lost from vomiting, diarrhea, body cavity drainage, burns, etc. In healthy animals, these losses are replaced by drinking and the fluid contained in food. In sick animals, who may not be voluntarily consuming food or water, or who may be restricted from consumption due to vomiting, fluid therapy is necessary to replace these losses. With renal disease, urine volume is frequently abnormally high or low, or inappropriate for the situation, and fluid therapy is tailored for the individual patient to maintain fluid balance.

Fluid therapy for hospitalized patients

Many drugs have been evaluated for their benefit in treating AKI, and some are helpful in certain settings. However the most effective therapy of AKI is careful management of fluid balance, which involves thoughtful assessment of hydration, a fluid treatment plan personalized for the specific patient, repeated and frequent reassessment of fluid and electrolyte balance, with appropriate changes in the treatment plan in response to the rapidly changing clinical situation of the renal failure patient.

Assessing hydration

The key feature to an appropriate fluid plan is accurate determination of hydration status. A deficit of the extravascular fluid compartment (interstitial and intracellular) causes dehydration. A severe deficit may decrease the intravascular compartment, leading to poor perfusion. Dehydration of less than approximately 5% is difficult to detect clinically. A 5 to 6% deficit leads to sticky mucous membranes. Six to eight percent dehydration causes dry mucous membranes and decreased skin elasticity. By 8-10% dehydration, the eyes may be sunken, and over 12% dehydration, corneas are dry, mentation is dull, and perfusion is impaired. Overhydration may manifest as wet mucous membranes, increased skin elasticity (heavy or gelatinous), shivering, nausea, vomiting, restlessness, serous nasal discharge, chemosis, tachypnea, cough, dyspnea, pulmonary crackles and edema, pleural effusion, ascites, diarrhea, or subcutaneous edema (especially hock joints and intermandibular space). Uremic patients frequently have xerostomia, causing dry mucous membranes independent of hydration status. Hypoalbuminemia or vasculitis may cause interstitial fluid accumulation despite an intravascular volume deficit. Emaciation or advanced age decrease elasticity of the skin.

An accurate body weight recorded prior to illness is an invaluable aid to assessing hydration. Body weight should be measured several times a day on the same scale. A sick animal may lose up to 0.5-1% body weight per day due to anorexia; changes in excess of this amount are due to changes in fluid status. An increase in blood pressure may indicate a gain of fluid; conversely, a decrease in blood pressure may indicate a net loss of fluid. Because of the high percentage of patients with hypertension (80% of dogs with severe acute uremia and 20-30% of dogs and cats with CKD), the trend rather than the absolute value is of more utility in assessing changes in hydration status. Similarly, changes in trends for PCV and total solids may reflect changes in volume, in the absence of bleeding or blood transfusion. Central venous pressure (CVP) measurement through a centrally placed intravenous catheter may provide information about intravascular filling. A volume depleted animal will have a CVP less than 0 cm H20. A CVP over 10 cm H20 is consistent with volume overload or right sided congestive heart failure. However, pleural effusion falsely elevates the CVP. Because each parameter is impacted by aspects beyond hydration status, these factors must be viewed in aggregate.


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