Page 517 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Fluid Therapy in Endocrine and Metabolic Disorders 505

cause hypocalcemia, hyperphosphatemia, tetany, soft tis- convert to bicarbonate. Therefore patients that have
sue mineralization, and renal failure. 29,33 Because phos- hyperchloremic metabolic acidosis may be more likely
4
phate deficits vary widely and are not necessarily to benefit from bicarbonate administration. Potential
reflected by serum phosphorus concentrations, phos- complications of bicarbonate administration in animals
phate administration should be guided by repeated serum with ketoacidosis include impaired ketone use, paradoxi-
phosphorus measurements during treatment. Potassium cal intracellular or CNS acidosis, and contribution to
phosphate should be administered by constant-rate infu- cerebral edema. The most common detrimental effect
sion at an initial dosage of 0.01 to 0.06 mmol/kg/hr. of bicarbonate is likely to be worsening of hypokalemia
Higher infusion rates can be administered as necessary. because concurrent intravenous fluid therapy and insulin
Monitoring should consist of measurement of serum administration cause a decrease in serum potassium
potassium, phosphorus, and calcium concentrations concentration.
every 8 to 12 hours during phosphate administration. Recommendations for bicarbonate therapy are to
Hyperphosphatemia, clinically relevant hypocalcemia, administer a conservative dose when acidosis is severe.
and hyperkalemia are indications to discontinue phos- If the blood pH is less than 7.0 or the plasma bicarbonate
phate administration. Treatment also should be concentration is less than 8 mEq/L, bicarbonate treat-
discontinued when the serum phosphorus concentration ment should be instituted. The bicarbonate deficit in
is normal and the animal is eating. Some have suggested milliequivalents can be estimated by the following for-
that potassium phosphate be routinely administered to mula: 0.3 body weight (kg) (24 patient bicarbon-
animals with DKA regardless of the initial serum phos- ate). One fourth to one half of this dose is administered
phorus concentration, but there is no evidence in veteri- over 2 to 4 hours. Blood gases should be measured after
nary or human medicine that such treatment is completion of bicarbonate administration with additional
beneficial. 29 bicarbonate administered if the blood pH remains less
than 7.2 or the plasma bicarbonate concentration is less
Magnesium Supplementation than 12 mEq/L. If blood gases are not available, bicar-
Magnesium deficiency is present in some cats with DKA bonate should not be administered.
as reflected by measurement of ionized magnesium
concentrations. 60 However, total magnesium HYPERGLYCEMIC
concentrations were high in many of the same cats, and HYPEROSMOLAR STATE
the widely available total magnesium concentration is
unlikely to reflect active plasma magnesium status. 60 Formerly named hyperglycemic hyperosmolar
Because clinical signs such as arrhythmia, weakness, nonketotic coma, hyperglycemic hyperosmolar state
seizures, and refractory hypocalcemia and hypokalemia (HHS) is defined as diabetes mellitus with a blood glu-
have not been documented to result from hypomagnese- cose concentration greater than 600 mg/dL and serum
mia in dogs or cats with DKA, magnesium supplementa- osmolality more than 350 mOsm/kg in the absence of
tion is not recommended. ketonuria. 26,44 In humans, acidosis is mild if present,
but acidosis may be more common in dogs and cats with
Bicarbonate Administration HHS. 43,44 The pathogenesis of this syndrome is similar
The acidosis of DKA typically is a high anion gap acidosis, to that of ketoacidosis, but it is thought that plasma insu-
although hyperchloremic acidosis also can be present at lin concentrations are higher in HHS than in DKA. 43
presentation. The unmeasured anions are ketoacids that This difference results in insulin activity sufficient to pre-
act as precursors of bicarbonate during treatment with vent ketosis but inadequate to prevent hyperglycemia.
insulin because insulin enhances use of ketones and Reductions in secretion or activity of growth hormone,
inhibits further production of ketoacids by decreasing glucagon, or both also may play a role in development
18,43
lipolysis. Because of this, the acidosis associated with of HHS. Loss of water in urine and decreased water intake
DKA does not usually need to be treated with bicarbon- cause dehydration with subsequent decreased renal per-
ate, although animals with severe acidosis may benefit fusion and resultant retention of glucose. The stress of
from treatment. Studies in humans have not shown a ben- concurrent illness that usually is present results in
eficial effect of bicarbonate administration in DKA. 35,57 increased counter-regulatory hormones, which contrib-
However, few patients with severe acidosis have been ute to further increases in blood glucose concentration.
studied, and it is currently recommended to administer Clinical signs are related to diabetes mellitus, concur-
bicarbonate to individuals with a blood pH less than rent disease, and hyperosmolality. Dehydration, hypo-
7.0, particularly if the pH does not improve after the first thermia, and abnormalities of mentation ranging from
hour of intravenous fluid administration. 43 Humans with depression to stupor or coma are common. 44 Other neu-
hyperchloremic metabolic acidosis have a slower recovery rologic signs include weakness, abnormal pupillary light
from acidosis compared with those with a high anion gap, reflexes, cranial nerve deficits, and seizures. Neurologic
probably because they have relatively less ketoacid to signs likely result from intracellular dehydration of the