Page 520 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

508 FLUID THERAPY

Rate and Volume of Fluid Administration sodium succinate or phosphate (cortisol) probably is
Administration of a bolus of NaCl will not only be effec- the best initial glucocorticoid treatment, primarily
tive for treatment of hypovolemia but also will reduce because it has mineralocorticoid activity as well. Hydro-
cortisone should be administered as a constant-rate infu-
hyperkalemia and metabolic acidosis and subsequently
sion of 0.3 mg/kg/hr or as an initial intravenous bolus
increase heart rate, cardiac output, and blood pressure.
(given over 5 minutes) of 5 mg/kg followed by 1 mg/
Initially, fluids should be given at a rate of 40 to 27,47
kg every 6 hours. Alternatively, dexamethasone
80 mL/kg/hr for the first 1 to 2 hours depending on
the severity of hypotension and hyperkalemia. 27 Once sodium phosphate (0.1 to 0.2 mg/kg intravenously) or
prednisolone sodium succinate (1 to 2 mg/kg intrave-
an adequate response to the initial fluid therapy is
nously) can be administered if hydrocortisone is not avail-
observed, the fluid rate can be decreased to two to three 65,70
able. There is no evidence that the higher doses of
times maintenance, based on the estimated fluid deficit
dexamethasone commonly recommended are beneficial
and ongoing losses. It is crucial to note urine output to
and could contribute to gastrointestinal bleeding and
ensure that oliguric renal failure is not present as a
other deleterious effects. Subsequent treatment should
primary condition (rather than hypoadrenocorticism)
consist of subcutaneous administration of dexametha-
or has occurred because of inadequate renal perfusion
sone every 12 hours or prednisolone every 6 hours until
secondary to hypoadrenocorticism. Inadequate urine
output may be the result of continued volume depletion oral treatment with prednisone (0.4 to 0.6 mg/kg daily)
caused by inadequate fluid therapy or ongoing losses, or can be tolerated. The oral prednisone dosage should be
as the result of oliguric renal failure. If urine output reduced over 7 to 10 days to a maintenance dose of
appears inadequate, placement of a urinary catheter is approximately 0.2 mg/kg daily and then adjusted as nec-
indicated to document oliguria and institute treatment essary to control clinical signs. The glucocorticoid dosage
for acute renal failure if present. Rapid improvement is should be increased if stress or illness occurs in a dog with
generally seen in dogs treated appropriately, but the clini- hypoadrenocorticism.
cal response in cats occurs more slowly and may require Mineralocorticoid Replacement
several days before substantial improvement occurs.
Because electrolyte abnormalities are rapidly corrected
A rapid increase in serum sodium concentration and
with intravenous administration of normal saline, and a
osmolality in the patient with hyponatremia and
short-acting injectable mineralocorticoid preparation is
hypoosmolality may be associated with dehydration of
not available, specific mineralocorticoid treatment gener-
the brain and neurologic signs caused by myelinolysis.
ally is delayed until oral fludrocortisone (0.01 mg/kg
This complication is more likely to occur with chronic 27,41,70
twice daily) can be administered. Hydrocortisone
hyponatremia than with that of 24 hours’ duration or less.
has some mineralocorticoid activity and for this reason is
Myelinolysis appears to be rare during treatment of dogs
with hypoadrenocorticism. 10,54 However, in animals the preferred glucocorticoid replacement. Administra-
tion of the long-acting injectable mineralocorticoid
with severe hyponatremia, this potential complication
desoxycorticosterone pivalate (DOCP) should be
should be considered and treatment adjusted so that
reserved for use once a definitive diagnosis has been
the serum sodium concentration increases by not more
made, although it reportedly can be safely administered
than 0.5 to 0.75 mEq/L/hr. 27
to dogs with normal adrenocortical function. Serum
Hypoglycemia should be treated with an initial bolus
electrolyte concentrations should be monitored and
of 0.5 to 1 mL/kg 50% dextrose if clinical signs are pres-
ent. If signs are not present and hypoglycemia is mild to dosage adjustments of mineralocorticoids made as
41,51
moderate, sufficient 50% dextrose to make a 5% solution appropriate.
should be added to the normal saline.
Management of Hyperkalemia
Rarely is specific treatment of hyperkalemia indicated
Glucocorticoid Replacement because appropriate fluid therapy rapidly corrects this
Glucocorticoids should be administered after fluid ther- electrolyte abnormality by dilution of plasma, increasing
apy has corrected the severe hypovolemia. Because appro- urine output, and shift of potassium into cells during cor-
priate intravenous fluid administration alone is very rection of acidosis. Indications for more aggressive treat-
effective in resolving the most serious manifestations of ment of hyperkalemia are severe bradyarrhythmia or
the hypoadrenocortical crisis, glucocorticoid treatment failure to respond to initial appropriate fluid therapy.
can be delayed for several hours if necessary. Unless dexa- Sodium bicarbonate administration will correct acidosis
methasone is administered, glucocorticoid treatment and decrease serum potassium concentration. The bicar-
should be delayed until the ACTH response test is bonate deficit can be calculated as described in the section
completed because other glucocorticoids will interfere on DKA, and 25% of the deficit should be administered.
with the cortisol assay. A rapid-acting glucocorticoid Alternatively, 1 to 2 mEq/kg of sodium bicarbonate can
should be administered intravenously. Hydrocortisone be administered slowly intravenously. Another effective