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Disorders of Potassium,
FOCAL POINT
Phosphorus, and
★Intensive management of
critically ill animals can lead to
Magnesium in
severe electrolyte and acid–base
abnormalities. Critical Illness
KEY FACTS
Auburn University
■ Hyperkalemia can cause life- Douglass K. Macintire, DVM, MS
threatening cardiac arrhythmia.
■ Imbalances of potassium,
phosphorus, and magnesium
must be corrected cautiously
to avoid severe side effects.
P otassium, phosphorus, and magnesium are primarily intracellular ions.
Their serum concentrations are maintained within a narrow range by
strict homeostatic mechanisms. When imbalances of these ions occur in
critical illness, the results can be life threatening.
safely be accomplished by the oral route if the patient is ATPase, and proton pumps. It is essential for many
not exhibiting severe clinical signs. The phosphorus con- metabolic functions, including ATP production and
tent of cow’s milk is 0.029 mmol/ml.20 Calcium phos- synthesis of nucleic acids and proteins. It helps regulate
phate tablets containing 580 mg of calcium, 450 mg of smooth muscle vascular tone and may influence lym-
phosphorus, and 400 IU of vitamin D3 are also available. phocyte activation and cytokine production.
Hyperphosphatemia Hypomagnesemia
Increases in serum phosphorus levels are most com- Magnesium deficiency may result from decreased in-
monly seen in veterinary patients with renal failure.18 take, increased losses, or alteration of distribution. Crit-
Decreased glomerular filtration rate results in phospho- ically ill animals may be predisposed to hypomagne-
rus retention. Other causes include massive cellular semia because of stress, catabolic illness, nasogastric
damage (tumor lysis syndrome, rhabdomyolysis, suctioning, peritoneal dialysis, total parenteral nutri-
snakebite, thromboembolism), hypoparathyroidism, tion, diuretics, massive blood transfusion, or aggressive
and poisoning from hypertonic sodium phosphate ene- intravenous fluid therapy with magnesium-deficient
mas26 or vitamin D toxicity. Iatrogenic causes include fluids.31 Because similar conditions cause hypokalemia
overzealous phosphorus replacement or overdose of and/or hypophosphatemia, magnesium deficiency may
phosphorus-containing urine acidifiers. Mild elevations be unrecognized and overlooked. In fact, concurrent
of phosphorus are considered normal in young, grow- hypokalemia may be refractory to aggressive potassium
ing dogs. replacement until the magnesium deficit is corrected.28
Clinical findings include diarrhea, hypocalcemia, Clinical signs of hypomagnesemia include cardiac ar-
tetany, hyperosmolality, hypernatremia, and an in- rhythmia, muscle weakness, tremors, seizures, altered
creased tendency toward metastatic calcification of soft mentation, esophageal motility disorders, and respirato-
tissues when the calcium–phosphorus product exceeds ry muscle paralysis.31 Normal serum magnesium con-
58.18 Hyperphosphatemia also contributes to the pro- centrations range from 1.89 to 2.51 mg/dl.29 If an ani-
gression of renal disease by stimulating renal secondary mal exhibits clinical signs (cardiac arrhythmia, muscle
hyperparathyroidism.19 Hyperphosphatemia is treated tremors, refractory hypokalemia) and serum magne-
with intravenous fluids to correct acidosis and promote sium levels are 1.2 mg/dl or lower, magnesium supple-
phosphorus excretion. Fluids containing dextrose pro- mentation can be considered.
mote translocation of phosphorus into cells. Animals Mild deficits can be corrected by intravenous fluids
with renal failure should receive a low-phosphorus diet, that contain magnesium. In cases of severe magnesium
and intestinal phosphate binders should be given with depletion, magnesium chloride or magnesium sulfate
food to decrease absorption. can be added to 5% dextrose in water at an initial dose
of 0.75 to 1.0 mEq/kg/day and continued at half of the
DISORDERS OF MAGNESIUM BALANCE initial dose for 3 to 5 days.31 For life-threatening ven-
Recent reports in human critical care medicine indi- tricular arrhythmia, digitalis-induced arrhythmia, or
cate a high incidence (>50%) of hypomagnesemia.27,28 cardiac arrest, a dose of 0.15 to 0.3 mEq/kg (50 to 100
Although serum magnesium in veterinary patients is mg/kg) can be diluted in 5% dextrose or 0.9% saline
seldom measured, certain critically ill animals are prob- and administered slowly intravenously over 5 to 15
ably also at risk for magnesium imbalance. A recent re- minutes to raise the ventricular fibrillation threshold.
port documented that magnesium imbalance was the Even when serum magnesium levels are normal,
most common electrolyte abnormality in 101 critically magnesium infusion should be considered for some an-
ill dogs admitted to the intensive care unit at Colorado imals with refractory tachyarrhythmia, especially when
State University: 30% had hypermagnesemia and 20% conventional therapy has failed.32 The lack of a reliable
had hypomagnesemia.29 measure of total body magnesium tends to make thera-
Magnesium is the second most abundant intracellu- py somewhat empirical.
lar cation. Most of the total body magnesium is present Potential side effects of intravenous magnesium
in bone and skeletal muscle. Only 1% is in the serum. therapy include hypocalcemia, hypotension, and car-
Unfortunately, because of the dynamic nature of mag- diac conduction abnormalities (atrioventricular and
nesium homeostasis, serum magnesium measurements bundle-branch blocks). Overdoses can be treated with
may not accurately reflect total body stores.30 In fact, calcium gluconate (10 to 50 mg/kg intravenously).31
serum levels can be normal despite magnesium deple- Fortunately, it is difficult to cause prolonged hyper-
tion or excess. magnesemia because the kidneys can eliminate most
Magnesium is a coenzyme for Na+,K+-ATPase, Ca++- of the excess magnesium.27
Magnesium (1 to 2 mEq/kg/day) can also be given tion of hydrogen ions with varying degrees of metabolic aci-
orally. It is available as oxide or hydroxide. dosis. J Clin Invest 36:373–382, 1957.
10. Macintire DK: Emergency therapy of diabetic crises: Insulin
overdose, diabetic ketoacidosis, and hyperosmolar coma. Vet
Hypermagnesemia Clin North Am Small Anim Pract 25:639–650, 1995.
At present, hypermagnesemia is not considered to be 11. Schunk KL: Feline polymyopathy. Proc ACVIM:197–200,
clinically significant in critically ill animals unless there 1984.
are associated signs of hypocalcemia. The most com- 12. Dow SW, Le Couteur RA, Fettman MJ, et al: Potassium
mon cause is renal failure combined with overuse of depletion in cats: Hypokalemic polymyopathy. JAVMA
191:1563–1568, 1987.
magnesium-containing antacids. 13. Dow SW, Le Couteur RA, Fettman MJ, et al: Hypokalemia in
cats: 186 cases (1984–1987). JAVMA 194:1604–1608, 1989.
CONCLUSION 14. Tannen RL: Relationship of renal ammonia production and
Intensive management of critically ill animals, in- potassium homeostasis. Kidney Int 11:453–465, 1977.
cluding such interventions as total parenteral nutrition, 15. Tolins JP, Hostetter MK, Hostetter TH: Hypokalemic
enteral nutrition, intravenous insulin, aggressive fluid nephropathy in the rat: Role of ammonia in chronic tubular
injury. J Clin Invest 79:1447–1458, 1987.
therapy, nasogastric suctioning, massive blood transfu- 16. Tilley LP: Essentials of Canine and Feline Electrocardiography,
sion, and peritoneal dialysis, can lead to severe elec- ed 2. Philadelphia, Lea & Febiger, 1985, pp 82, 86.
trolyte and acid–base abnormalities. Veterinarians must 17. Drobatz KJ: Serum electrolytes in cats with urethral obstruc-
closely monitor potassium, phosphorus, and magne- tion. Proc 5th Annu Int Vet Emerg Crit Care Symp:24–27,
sium levels to detect and correct any life-threatening 1996.
18. Chew DJ, Meuten DJ: Disorders of calcium and phosphorus
imbalances in these patients.
metabolism. Vet Clin North Am Small Anim Pract 12:
411–438, 1982.
About the Author 19. Berner VN, Shike M: Consequences of phosphate imbal-
Dr. Macintire is affiliated with the Department of Small ance. Annu Rev Nutr 8:121–148, 1988.
20. Solomon SM, Kirby DF: The refeeding syndrome: A review.
Animal Surgery and Medicine, College of Veterinary
J Parenter Enteral Nutr 14:90–97, 1990.
Medicine, Auburn University, Alabama, and is a Diplo- 21. Justin RB, Hohenhaus AE: Hypophosphatemia associated
mate of the American College of Veterinary Internal with enteral alimentation in cats. J Vet Intern Med 9:
Medicine and the American College of Veterinary Emer- 228–233, 1995.
gency and Critical Care. 22. Adams LG, Hardy RM, Weiss DJ, Bartges JW: Hypophos-
phatemia and hemolytic anemia associated with diabetes
mellitus and hepatic lipidosis in cats. J Vet Intern Med
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