Page 513 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Fluid Therapy in Endocrine and Metabolic Disorders 501

quantity of free fatty acids is oxidized to ketone bodies for 1 to 2 hours after fluid therapy is instituted, particu-
under the influence of glucagon, although cortisol, epi- larly when hyperglycemia is severe, hypotension is pres-
nephrine, and growth hormone also play a role in ent, or clinically relevant hypokalemia exists. Reduction
stimulating ketogenesis. Anorexia that is usually present of blood glucose concentration before replacement of
in patients with DKA contributes to the hormonal intravascular volume could result in loss of water from
changes mentioned above and lack of substrate for ana- the intravascular space along with glucose and worsening
bolic functions. Use of ketones is impaired in DKA as of hypotension. Severe hyperglycemia and hypotension
well, contributing to their increased concentration. are likely. A substantial reduction of blood glucose will
Low serum insulin and elevated serum glucagon occur despite a delay in insulin administration because
concentrations are correlated with increasing serum fluid therapy alone reduces insulin resistance, increases
ketone concentrations in dogs with diabetes mellitus. 23 insulin availability at peripheral tissues such as skeletal
muscle, dilutes the blood glucose, and enhances urinary
Fluid and Electrolyte Metabolism loss subsequent to an increase in glomerular filtration rate
Dehydration is a consistent finding in dogs and cats with (GFR). 76 After initial rehydration, consideration should
DKA. 15,17,20,53 It occurs because of osmotic diuresis sec- be given to the decrease in the plasma effective osmolality
ondary to glycosuria and ketonuria, and as a result of gas- and thus the plasma volume that occurs after reduction of
trointestinal losses associated with vomiting and diarrhea. the blood glucose concentration, necessitating adminis-
Electrolyte loss also occurs in these patients because of tration of fluids at a higher rate than would be needed
the diuresis and the cation excretion that accompanies in a euglycemic patient. After hydration status has been
ketoacid excretion. 43 Insulin deficiency also results in loss normalized and blood glucose concentration reduced,
of electrolytes because insulin is required for normal additional fluid administration should be based on the
sodium, chloride, potassium, and phosphorus reabsorp- calculation of maintenance needs plus ongoing losses
tion in tubular epithelial cells. Loss of sodium, potassium, from the gastrointestinal tract (e.g., vomiting, diarrhea)
chloride, magnesium, phosphorus, and calcium occur to and in urine (i.e., polyuria caused by continued glycos-
a substantial degree in DKA. However, the resulting elec- uria). Aggressive treatment is not necessary in dogs or cats
trolyte abnormalities are reflected variably in plasma with ketonuria if metabolic acidosis and signs of systemic
concentrations. 15,17,20,53 Hyponatremia is reported in illness are not present. The presence of a concurrent dis-
40% to 54% of dogs and 34% to 81% of cats with ease, present in most dogs and cats with DKA, may neces-
DKA, 15,20,37,45,69 but correction of the serum sodium sitate modification of the fluid therapy plan.
concentration for hyperglycemia reduces the prevalence
of this finding. 45 Because glucose has an osmotic effect Fluid Composition
in the plasma, hyperglycemia results in a shift of water Because of the marked deficits of water and sodium pres-
into the intravascular space, diluting the plasma sodium. ent in animals with DKA, 0.9% saline is the fluid of choice
This effect can be corrected by adding 1.6 mEq/L to the for initial management. Administration of an isotonic
measured sodium concentration for each 100 mg/dL solution allows for rapid expansion of intravascular vol-
that the plasma glucose exceeds 100 mg/dL. ume in patients with severe dehydration or hypovolemic
shock.
Acid-Base Changes Serum osmolality usually is high in animals with DKA,
Loss of ketoacids in urine results in buffering by plasma often moderately to markedly so. The median measured
bicarbonate. Urinary bicarbonate excretion contributes osmolality in 23 cats with DKA was 353 mOsm/kg (ref-
to the metabolic acidosis induced by accumulation of erence range, 280 to 300 mOsm/Kg), and the median
ketoacids. 43 Retention of these unmeasured anions results calculated osmolality in 19 other cats was 333 mOsm/
15
inanincreasedaniongap.TheprognosisofdogswithDKA kg. An increase in the calculated osmolality was con-
37 45
is negatively affected by a worsening base deficit. firmed in another recent study of 13 cats with DKA.
The hyperosmolality is attributable primarily to hypergly-
TREATMENT cemia, azotemia, and ketone bodies. Because treatment
Fluid Therapy rapidly resolves these abnormalities, the osmolality would
The goals of fluid therapy in DKA are to restore be expected to decrease predictably without the use of
circulating volume, replace water and sodium deficits, hypotonic solutions. Cerebral edema has been
correct electrolyte imbalances, improve tissue delivery documented in humans, particularly children during
of nutrients, and decrease the blood glucose concentra- treatment of DKA. Clinical signs of cerebral edema are
46
tion. Initial fluid therapy should improve intravascular rare despite its common occurrence. Rapid reduction
volume, reduce secretion of counter-regulatory in plasma osmolality is a major factor in development
hormones, and enhance tissue delivery of insulin. It is of cerebral edema. Cerebral edema is caused in part by
recommended that insulin administration be delayed the accumulation of idiogenic osmoles in the central