Page 516 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

504 FLUID THERAPY

Regardless of the initial insulin administration proto- TABLE 20-2 Potassium
col used, intermediate or long-acting insulin treatment Supplementation in
can be instituted when the animal is eating normally.
Intravenous Fluids
Potassium Supplementation
Serum Potassium Potassium
Regardless of the serum potassium concentration, almost Concentration Supplement (mEq) in 1 L
all patients with DKA have a deficit of total body potas- (mEq/L) Intravenous Fluid
sium. 18,43 Before treatment, hypokalemia is found in
approximately 30% to 45% of dogs and 55% to 67% of >3.5 20
cats, whereas hyperkalemia is found in less than 10% of 3.0-3.5 30
cases.* Hypokalemia occurs because of urinary potassium 2.5-3.0 40
losses caused by osmotic diuresis, deficient renal tubular 2.0-2.5 60
potassium absorption caused by insulin deficiency, and <2.0 80
excretion with ketoacids, as well as through gastrointesti-
nal losses from vomiting and diarrhea. Treatment of DKA
rapidly lowers plasma potassium concentration because
correction of acidosis causes a transcellular shift of potas- Phosphorus is lost in patients with DKA because of a shift
sium into cells, insulin enhances transport of potassium from the intracellular to the extracellular compartment
into cells, and intravenous fluid administration causes secondary to hyperosmolality that is followed by urinary
diuresis and dilution of plasma potassium. Hypokalemia loss, decreased cellular uptake causedby insulin deficiency,
is present at sometime during hospitalization in over inhibitionofrenaltubularphosphateabsorptioncausedby
90% of cases. 15,37 Hypokalemia can cause muscle weak- acidosis, and osmotic diuresis. 33,43 During treatment of
ness, arrhythmias, and impaired renal function. DKA, the reduction in osmolality and insulin administra-
Potassium should be supplemented in virtually all tion result in translocation of phosphate into the cell from
animals with DKA, but the initial dose rate is dependent the extracellular compartment. This translocation fre-
on the pretreatment serum potassium concentration. If quently causes a marked decrease in the plasma phospho-
the serum potassium concentration is above the reference rus concentration. However, clinically important
range, intravenous fluids should be administered without consequences of hypophosphatemia are noted only when
the addition of potassium for 2 hours, at which time the the serum phosphorus concentration is less than 1.0 to
serum potassium concentration should be rechecked if 1.5 mg/dL, and these signs are observed inconsistently.
possible. If the serum potassium concentration has Hemolysis, muscle weakness, seizures, depression, and
decreased into the normal range, supplementation is decreased leukocyte and platelet function leading to infec-
given according to Table 20-2. The dose rate of KCl tion and bleeding can result from hypophosphatemia. The
should not exceed 0.5 mEq/kg/hr because of the risk only abnormalities documented as caused by
of cardiac arrhythmia. If a serum potassium measurement hypophosphatemia in veterinary DKA patients are hemo-
is not available after initial treatment and urine output lytic anemia in cats and possibly stupor and seizures in a
appears adequate, 30 to 40 mEq KCl should be added dog. 1,15,77 Hemolysiscanoccurdespitephosphatesupple-
to each liter of fluids. Urine production should be moni- mentation and may have causes other than
tored closely to ensure that oliguric renal failure is not hypophosphatemia including oxidative injury. 15,19
present. In humans with hypokalemia before treatment, Hypophosphatemia is present at initial evaluation in 13%
it is recommended that insulin administration be delayed to48%ofcatsandin29%ofdogswithDKA. 15,20,37 Careful
until the serum potassium concentration can be increased monitoring of serum phosphorus concentration during
into the normal range because the potassium concentra- the initial 24 to 48 hours of management is important to
43
tion will decrease during insulin administration. A sim- identify severe hypophosphatemia necessitating phospho-
ilar recommendation is made for veterinary patients with rus supplementation.
substantial hypokalemia (<3.5 mEq/L). Serum potas- Treatment of hypophosphatemia is indicated when the
sium concentration should be monitored 4 hours after serum phosphorus concentration before treatment is less
initiating potassium supplementation and at least every than 1.5 mg/dL or if the serum phosphorus concentra-
8 to 12 hours thereafter, with dosage adjustments to tion is less than 1.0 mg/dL in the dog and less than
maintain normokalemia (see Table 20-2). 1.5 mg/dL in the cat at any time. Potassium phosphate
typically is the treatment of choice because potassium
Phosphorus Supplementation supplementation is also necessary in most cases, but
Similar topotassium,phosphateisdeficientinanimalswith sodium phosphate is also available for use. Potassium
DKA regardless of the serum phosphorus concentration. phosphate is available as a solution containing 3 mmol/
mL of phosphorus (99 mg/dL) and 4.36 mEq/mL of
*References 15, 17, 20, 26, 37, 45, 53. potassium. Excessive phosphate supplementation can