Page 562 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

550 FLUID THERAPY

OUTPATIENT FLUID THERAPY ELECTROLYTE

Despite widespread use of subcutaneous fluid therapy, its ABNORMALITIES
role in managing kidney disease has never rigorously been
evaluated. Empirically, chronic dehydration or persistent SODIUM AND CHLORIDE
signs of uremia are rational indications for chronic subcu-
taneous fluid administration. Dose is empirical, based on The serum sodium concentration may be normal, ele-
subjective assessment of the patient’s well-being and on vated, or decreased with renal failure. Hypernatremia
hydration status. A typical starting dose for cats is 100 before fluid therapy indicates excessive free-water loss.
to 150 mL daily to every other day. Cats subjectively seem Administration of sodium bicarbonate or hypertonic
to respond more favorably to subcutaneous fluid therapy saline may cause hypernatremia. Hyponatremia may indi-
compared with dogs. Lactated Ringer’s solution or 0.9% cate excess sodium loss associated with vomiting or pan-
saline are appropriate fluids choices. Dextrose containing creatitis, or transient dilutional hyponatremia after
fluids increase the risk of abscess formation, and administration of mannitol, hypertonic dextrose, or col-
Plasmalyteisreportedtosting.Manyownerscanbetaught loid solutions. Hyponatremic solutions (5% dextrose,
to administer the fluid dose at home, using a new needle total parenteral nutrition, enteral formulations) may
for each administration. An administration tube can be cause hyponatremia. In many situations, initial dehydra-
implanted in the subcutaneous space for fluid administra- tion is caused by isonatremic fluid loss with a normal
10,13
tion without a needle, but this method increases the risk of sodium concentration.
infection at the site where the tube exits the skin, and sub- The initial fluid deficit should be replaced by an
cutaneous fibrosis with subsequent pain during adminis- isonatremic solution such as lactated Ringer’s solution,
tration and decreased capacity has been observed. 0.9% saline, or Plasmalyte 148. Continued administration
of these solutions over several days may lead to
NUTRITIONAL SUPPORT hypernatremia. A lower sodium fluid, such as one half
Renal failure is a highly catabolic disease. Although it is strength LRS or 0.45% saline, with 2.5% dextrose to
hard to clearly identify the contribution of nutritional maintain isotonicity, is a more appropriate fluid choice
managementtooutcome,poornutritionalstatusisamajor after the initial rehydration phase. The serum sodium
factor in increasing patients’ morbidity and mortality. 63 concentration should be monitored regularly and the
Early enteral feeding can help preserve gastrointestinal fluid choice adjusted as needed.
mucosal integrity. 32 Although renal diets, characterized Clinical signs of sodium disorders are unlikely unless
by restricted phosphorus and restricted quantities of high rapid changes occur in the sodium concentration, and
quality protein, are indicated for treating chronic kidney the signs are generally related to neurologic dysfunction.
disease, the ideal diet for acute renal failure has not been The rate of sodium change should not be more than
17
identified. 27,48 In the absence ofinformation, enteral diets 1 mEq/L/hr. Chloride changes tend to parallel
for critically ill animals or people have been used. 10 sodium changes.
Anorexia is a common problem in the hospitalized POTASSIUM
renal failure patient. If the appetite does not return within
a few days of therapy, feeding tube placement may allow Hypokalemia
administration of an appropriate quantity of the desired Hypokalemia is more likely to be present in chronic kid-
diet, easy administration of oral medications, and is ney disease compared to acute kidney injury, and is more
strongly recommended in animals not voluntarily con- likely in cats compared with dogs. In cats with CKD, 20%
suming adequate calories.. If vomiting cannot be con- to 30% of cats are hypokalemic. 16,19,31 Multiple
trolled, partial or total parenteral nutrition (PPN or mechanisms may contribute to the development of hypo-
TPN) may be necessary. kalemia, including excessive renal wasting associated with
Whether supplementation is enteral or parenteral, the polyuria. Alkalemia worsens hypokalemia as potassium
volume that can be administered may be limited in shifts intracellularly in response to translocation of hydro-
patients who are anuric or oliguric. Most liquid diets suit- gen ions out of the cells. Vomiting and loop diuretics
able for use in a nasoesophageal or nasogastric tube have a cause further potassium loss. Decreased oral intake alone
caloric density around 1 kcal/mL. 33 Provision of 100% of generally does not cause hypokalemia, but prolonged
the basal energy requirements generally will require a vol- anorexia exacerbates hypokalemia. Hypokalemia may be
ume of about twice the insensible fluid requirements. present at admission, particularly with polyuric CKD,
Common formulas for calculation of total parenteral or it may develop during hospitalization, particularly in
nutrition will also encompass almost twice the insensible the diuretic phase of recovery from acute kidney injury
9
fluid requirements. The need for nutritional support is or with effective diuretic therapy. Hypokalemia is both
an indication for fluid removal via dialysis in the oliguric a cause and effect of renal dysfunction; hypokalemia
patient. interferes with urinary concentrating ability, but the renal