Page 563 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Managing Fluid and Electrolyte Disorders in Renal Failure 551

dysfunction is generally reversible with normalization of To calculate the amount to administer, subtract the
the potassium concentration. 43 patient [K] from the desired [K] of 3 mEq/L. Calculate
Signs of hypokalemia include muscle weakness (stiff the blood volume (8% of body weight in kilograms in
stilted gait in hind legs, cervical ventroflexion, respiratory dogs, 6% in cats), and multiply the blood volume by
muscle paralysis). Cardiac changes occur inconsistently 60% to estimate the plasma volume. Multiply the plasma
but may include ventricular and supraventricular volume by the difference between the measured and
arrhythmias. Rarely are U waves noted on the electrocar- desired potassium concentration to determine the num-
diogram. Other signs include fatigue, vomiting, anorexia, ber of milliequivalents of KCl to administer as an IV bolus
and gastrointestinal ileus. 13,49 Clinical signs of hypokale- over 1 to 5 minutes through a central vein. Check the
mia are likely when the concentration is less than serum potassium 5 minutes later. A second bolus, calcu-
2.5 mEq/L; a concentration of less than 2.0 may be life lated from the new [K], can be administered, but use cau-
threatening. 10,13 tion and administer more slowly as the serum [K]
Hypokalemia is diagnosed by a low serum potassium approaches 3 mEq/L. 49
concentration. Evaluation of the fractional excretion of Once oral intake is possible, potassium gluconate can
potassium may help distinguish renal potassium loss (frac- be administered. A dose of 5 to 10 mEq per day divided
tional excretion >4%) from nonrenal loss (fractional into 2 to 3 doses is used to replenish potassium, followed
excretion <4%). 15,18 by 2 to 4 mEq/day for maintenance. 18 Potassium citrate
Because excretion of potassium may be impaired with (40 to 60 mg/kg/day divided into 2 to 3 doses) is an
renal failure, treatment in this setting requires judicious alternative to potassium gluconate that also helps to cor-
supplementation with careful monitoring. However, as rect acidosis. Potassium chloride can be added to subcu-
normalization of hypokalemia can improve renal function taneous fluids up to a concentration of 35 mEq/L.
and decrease clinical signs, treatment of hypokalemia For patients on intravenous potassium supplementa-
should not be overlooked. 43 In the hospitalized patient tion, frequent monitoring (once to multiple times daily)
unable to tolerate oral medications, potassium chloride is recommended. During potassium repletion on an out-
may be added to the intravenous fluids. The rate of sup- patient basis, monitoring every 7 to 14 days until a stable
plementation is based on the patient serum potassium maintenance dose is reached is recommended. 43 If hypo-
concentration, based on an empirically derived scale kalemia remains refractory to standard supplementation,
(Table 22-1). The rate of potassium supplementation hypomagnesemia may be present, and magnesium sup-
should not exceed 0.5 mEq/kg/hr. The serum potas- plementation may be necessary.
sium concentration might decrease during initial fluid
therapy despite supplementation because of extracellular Hyperkalemia
fluid volume expansion, increased distal tubular flow, and Renal excretion is the major mechanism for removing
cellular uptake, especially if administered with dextrose. potassium from the body, and chronic hyperkalemia is
In situations with an immediately life-threatening unlikely to occur with normal renal function.
hypokalemic emergency (i.e., respiratory muscle weak- Hyperkalemia is more likely to develop in oliguric or
ness with hypoventilation, hypokalemic cardiac anuric acute renal failure, and usually does not occur in
arrhythmias), some recommend administering an intra- chronic kidney disease unless oliguria or severe metabolic
venous bolus of KCl. This should only be undertaken acidosis are present. 10 Metabolic acidosis from mineral
with constant EKG monitoring because a rapid potassium acids (e.g., NH 4 Cl, HCl) but not organic acids (e.g., lac-
bolus could potentially cause a fatal arrhythmia. tic acid, ketoacids) causes translocation of potassium out
of cells as hydrogen ions enter the cells. CKD patients
may have a reduced ability to tolerate an acute potassium
load and may take 1 to 3 days to reestablish external
TABLE 22-1 Sliding Scale of potassium balance after a potassium load. 15 Mild
Potassium hyperkalemia seems relatively common in stable patients
Supplementation on angiotensin converting enzyme inhibitor therapy; my
experience is that most do not exceed 6.5 mEq/L, but
Serum Potassium Potassium clinical significance of this is uncertain. Hyperkalemia
Concentration Concentration in and azotemia are common with hypoadrenocorticism
(mEq/L) Fluids (mEq/L) and acute tumor lysis syndrome. 18
Hyperkalemia can be an immediately life-threatening
3.5-4.5 20 electrolyte disorder. The increase in extracellular potas-
3-3.5 30
2.5-3 40 sium changes the electrical potential of excitable cells.
2-2.5 60 The myocardium is relatively resistant compared to the
<2 80 conduction cells. Typical EKG changes include bradycar-
dia; tall, spiked T waves; shortened QT interval; wide