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Vol. 19, No.

1 January 1997 V HEINZ SYMPOSIUM 1996

Continuing Education Article

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.

■ Hypophosphatemia can cause DISORDERS OF POTASSIUM BALANCE


acute hemolysis in recovering Potassium is the primary intracellular cation; 95% of total body potassium is
diabetics and malnourished within cells.1 Potassium maintains intracellular volume and normal membrane
patients receiving nutritional potential. If the ratio between intracellular and extracellular potassium is dis-
support. turbed, the membrane potential of excitatory tissue (heart, nerve, and muscle)
is affected; conduction disturbances result.2 In normal animals, daily potassium
■ Unexplained decreases in serum intake equals daily losses.
phosphorus should prompt a
search for infection, p. 44. Hypokalemia
Hypokalemia is probably the most common electrolyte abnormality recog-
■ Until the magnesium deficit nized in critically ill veterinary patients. Clinical signs include muscle weak-
is corrected, concurrent ness, cramping, lethargy, myocardial depression, ileus, urine retention, inability
hypokalemia may be refractory to concentrate urine, and mild hyperglycemia from decreased insulin se-
to aggressive potassium cretion.1,2 Severe potassium depletion can result in death from paralysis of res-
replacement. piratory muscles.
Hypokalemia can result from decreased intake, excessive losses, or transloca-
tion of potassium to the intracellular space. Animals with anorexia, vomiting,
and diarrhea are prone to hypokalemia, especially if they are given intravenous
fluids deficient in potassium. Animals with pancreatitis, peritonitis, parvoviral
enteritis, and other causes of vomiting generally require potassium supplemen-
tation to maintain normal serum levels.2
Fluids containing 14 to 20 mEq/L usually maintain serum potassium levels
and prevent them from dropping precipitously in conditions in which
Small Animal The Compendium January 1997

decreased intake or ex- TABLE I Potassium depletion


cessive losses are expect- Potassium Replacement can worsen progressive
ed. Excessive renal losses renal damage through
can be seen in patients Serum Potassium Chloride decreased ability to au-
with chronic renal fail- Potassium Added to Fluid Maximum Infusion Rate a toregulate glomerular
ure,3–5 during the recov- (mEq/L) (mEq/L) ml/lb/hr ml/kg/hr filtration rate and in-
ery or diuretic phase of creased ammoniagene-
acute renal failure, and 3.6–5.0 20 11 25 sis, which can be toxic
during the diuresis that 3.1–3.5 30 8 17 to tubule and interstitial
often follows relief of uri- 2.6–3.0 40 5.5 12 cells.14,15 Therefore, cats
nary obstruction in male 2.1–2.5 60 4 8 with chronic renal fail-
cats.2 Serum potassium <2.0 80 3 6 ure and other condi-
levels in these patients tions associated with in-
should be checked fre- aSo as not to exceed 0.5 mEq/kg/hr. creased potassium losses
quently. If hypokalemia should receive oral po-
occurs, potassium sup- tassium gluconate (2 to
plementation can be administered according to the slid- 4 mEq/day).
ing scale6 in Table I. Cats accept potassium gluconate fairly readily, but
Intravenous potassium supplementation must not ex- oral potassium chloride liquid is generally unpalatable
ceed 0.5 mEq/kg/hr (Table I); otherwise, serious ar- to cats and may cause vomiting. Enteric-coated tablets
rhythmia or asystole may occur. If the animal is eating, are poorly absorbed and may cause gastrointestinal irri-
oral potassium supplementation is safe and effective. tation. If the cat is eating, potassium gluconate powder
Diabetic animals, particularly those with ketoacido- can be mixed in the food. Supplemental potassium can
sis, are also prone to hypokalemia.7,8 The body stores of also be safely given in subcutaneous fluids at concentra-
potassium in sick diabetic animals are often depleted tions of up to 30 mEq/L. Higher concentrations may
through increased urinary and gastrointestinal losses cause skin sloughs.
and decreased intake. Serum potassium levels appear Inappropriate loss of potassium via urine can be doc-
falsely elevated in animals with acidosis because potassi- umented by measuring fractional excretion (FEK ) from
um has moved out of cells. For each 0.1 change in a single urine sample and concurrent serum sample ac-
blood pH, an inverse change in serum potassium of ap- cording to the following formula:
proximately 0.6 mEq/L can be expected because of
translocation.9
U /S
Serum potassium levels can drop precipitously after FEK = K K × 100
UCR /SCR
insulin treatment and correction of acidosis. Potassium
levels in sick diabetic patients must therefore be closely
monitored. If hypokalemia is present, potassium sup- where U K = urine potassium (mEq/L), S K = serum
plementation should be instituted before aggressive in- potassium (mEq/L), UCR = urine creatinine (mg/dl),
sulin treatment is begun.10 and SCR = serum creatinine (mg/dl). Values over 4% to
Feline hypokalemic polymopathy syndrome was first 6% are consistent with inappropriate loss of potassium.
reported in 1984.11 Clinical signs include generalized Animals with increased losses, especially geriatric cats,
muscle weakness, cervical ventroflexion (Figure 1), ele- should receive oral potassium supplementation daily.
vated creatine kinase levels, and severe hypokalemia.
These signs remit after potassium supplementation.12,13 Hyperkalemia
Most affected cats were geriatric and had evidence of Elevated serum potassium levels can be a life-threat-
chronic renal disease. Many commercial feline diets ening emergency because of the effect on the myocardi-
were found to provide inadequate potassium for cats um (Figure 2). Progressive abnormalities appear on the
with increased losses resulting from chronic renal dis- electrocardiogram.16 Mild hyperkalemia is associated
ease. with peaked T waves, decreased amplitude of the R
Most diets today contain adequate amounts of potas- wave, and prolongation of the P–R interval. As serum
sium (0.6% to 0.7% of dry weight), and the syndrome potassium levels increase, flattening of the P wave,
has become infrequent. Nevertheless, cats with chronic bradycardia, prolongation of the Q–T interval, and
renal disease and other causes of increased losses or de- widening of the QRS complex can occur. Severe life-
creased intake are at risk of hypokalemia.13 threatening hyperkalemia can cause a sinoventricular

FELINE HYPOKALEMIC POLYMYOPATHY ■ FRACTIONAL EXCRETION ■ ELECTROCARDIOGRAM


The Compendium January 1997 Small Animal

rhythm, ventricular fibrilla- to 0.5 U/kg) combined with


tion, asystole, and cardiac glucose (2 g/U) diluted to a
arrest. 10% solution. Dextrose
Causes of hyperkalemia in (2.5% to 5%) should be
veterinary patients include added to subsequent fluids
hypoadrenocorticism (Addi- to prevent hypoglycemia.
son’s disease), acute oliguric The third option for treat-
renal failure, ruptured blad- ing animals with life-threat-
der or urethral tear, urethral ening hyperkalemia is 10%
obstruction, severe crushing calcium gluconate (50 to
injuries, heatstroke, massive 100 mg/kg; 0.5 to 1.5 ml/kg)
cellular destruction (snake- given by slow intravenous
bite, tumor lysis syndrome, bolus while monitoring
overwhelming infection, heart rate and the electro-
thromboembolism), Tri- Figure 1—This cat has cervical ventroflexion secondary to cardiogram. Calcium pro-
churis vulpis infection, and hypokalemia (serum potassium 2.0 mEq/L), which result- tects the myocardium from
body cavity effusion. Hyper- ed from extreme polyuria after exposure to a toxin. Clini- the arrhythmogenic effects
kalemia can also be iatro- cal signs resolved after potassium supplementation. of hyperkalemia.
genic (overdose of potassi- After the underlying cause
um-sparing diuretics or of hyperkalemia is removed,
overzealous potassium sup- continued diuresis is gener-
plementation). ally required to enhance re-
When the hyperkalemia is nal potassium excretion.
not life-threatening, the ani- Animals with acute oliguric
mal generally requires no renal failure may require
specific therapy for reducing peritoneal dialysis or hemo-
hyperkalemia, other than re- dialysis if urine flow cannot
moval of the underlying be initiated by pharmaco-
cause and dilutional fluid logic means.
therapy. Life-threatening The choice of fluid for
hyperkalemia is treated by hyperkalemic animals is
removing the underlying somewhat controversial.
cause and taking immediate Potassium-free fluids are of-
steps to stabilize cell mem- ten recommended (5% dex-
branes and promote intra- Figure 2—Electrocardiographic tracings from a male cat trose in water, 0.9% sodium
cellular translocation of with urethral obstruction (lead 2, 50 mm/sec). Ventricular chloride), but these fluids
potassium. This can be ac- tachycardia (top) was associated with a serum potassium may worsen sodium imbal-
level of 9.2 mEq/L. Normal sinus rhythm (bottom) was re-
complished through three ance. Also, because they are
2 stored by a slow intravenous bolus of sodium bicarbonate
different mechanisms. Some (2.2 mEq/kg). not buffered, they do not
animals require all three help correct acidosis.
treatments to stabilize the If the hyperkalemia is se-
myocardium. vere (>10 mEq/L), a potassium-free fluid should be
First, a slow intravenous bolus of sodium bicarbonate chosen for initial fluid therapy. Otherwise, lactated
(1 to 2 mEq/kg) can be administered. This is the treat- Ringer’s solution (which has a potassium content of 4
ment of choice for animals with Addison’s disease. It is mEq/L) appears to be the most physiologic choice for
also effective in most feline cases of urinary obstruc- animals with normal renal function once the underly-
tion, but it may promote hypocalcemia in some cases. ing cause of hyperkalemia is removed. The hyper-
Cats with urinary obstruction often have low serum kalemia usually resolves with dilution, restoration of
calcium levels secondary to high phosphorus levels.17 In- perfusion, and enhanced renal excretion.
travenous sodium bicarbonate lowers ionized calcium
levels and may cause tetany or muscle tremors. The pre- DISORDERS OF PHOSPHORUS BALANCE
ferred method for lowering serum potassium in these Like magnesium and potassium, phosphorus is pri-
patients is an intravenous bolus of regular insulin (0.25 marily an intracellular ion.18 It is important for energy

BICARBONATE ■ INSULIN AND GLUCOSE ■ CALCIUM GLUCONATE


Small Animal The Compendium January 1997

production (it is a cofactor also binds to phosphorus.


for glycolysis and is needed These agents should be
to form ATP) and cell mem- discontinued if the patient
brane maintenance (it is a has hypophosphatemia and
component of phospholipid should not be used in ani-
membrane and is required mals prone to hypophos-
to form 2,3-diphosphoglyc- phatemia. For example,
erate). Serum phosphorus male cats with postobstruc-
concentration is regulated tive diuresis may initially
by dietary intake, renal ex- exhibit hyperphosphatemia
cretion, factors that pro- and azotemia; however, hy-
mote ion translocation into pophosphatemia may devel-
or out of cells (e.g., insulin, op later as a result of exces-
glucose, blood pH), and in- sive renal losses. Therefore,
teractions of the regulatory the use of phosphate binders
hormones vitamin D and Figure 3—An unexplained drop in hematocrit accompanied in these animals should be
parathyroid hormone. by hemolysis in recovering diabetics or malnourished ani- avoided.
mals receiving nutritional support suggests hypophos- Although the mechanism
Hypophosphatemia phatemia. is unclear, hypophosphate-
Until recently, clinically mia can be an early sign of
significant decreases in sepsis. Unexplained decreas-
serum phosphorus levels were considered uncommon. es in serum phosphorus should therefore prompt a
Now hypophosphatemia is increasingly being recog- search for infection.24 The decline in phosphorus may
nized as a problem in critically ill humans and animals. be secondary to the hypermetabolic state or respiratory
Clinical sequelae of hypophosphatemia include hemol- alkalosis, both of which occur early in sepsis.
ysis (Figure 3), skeletal muscle weakness, leukocyte dys- When hypophosphatemia is causing clinical signs or
function, and poor oxygenation of tissue as a result of when serum phosphorus levels drop below 1.0 mg/dl,
reduced 2,3-diphosphoglycerate levels.19 the hypophosphatemia should be treated with intra-
Nutritional recovery syndrome was first recognized in venous replacement. Complications of intravenous re-
prisoners of war after World War II.20 Aggressive feed- placement can include hyperphosphatemia, hypocal-
ing after prolonged malnutrition resulted in a syn- cemia, tetanic seizures, soft tissue mineralization, and
drome of lethargy, depression, diarrhea, and multiple hypotension secondary to rapid infusion.24
electrolyte abnormalities. It was later found that mal- Phosphorus must be administered slowly and cau-
nourished patients are prone to hypophosphatemia tiously, and serum levels should be monitored every 6
upon refeeding. Glucose and phosphorus are transport- hours. Replacement can be discontinued when serum
ed into cells as a result of insulin secretion. Phosphorus levels reach 2.0 to 2.5 mg/dl.
is a cofactor for glycolysis and is rapidly consumed, Potassium phosphate is available in a solution con-
sometimes dropping to dangerously low levels. taining 3 mmol of phosphate (93 mg) and 4.3 mEq of
The same syndrome can be seen in veterinary pa- potassium per milliliter. Most veterinary references rec-
tients that receive enteral nutrition or intravenous ommend a dosage of 0.01 to 0.03 mmol/kg/hr to be
dextrose solutions after a period of malnutrition. 21 given for 6 hours and continued for another 6 hours if
Hypophosphatemia can be prevented by gradually in- the phosphorus levels remain low.21–24 This dosage is safe
creasing feeding to the full caloric requirements over but may be inadequate for animals with severe deple-
several days and avoiding overzealous feeding of high- tion. A recommended dose for humans is 7.7 mg/kg/hr
carbohydrate diets. (0.025 mmol/kg/hr) administered over 4 hours.25
Another cause of clinically significant hypophos- Potassium phosphate must be administered in calci-
phatemia is insulin therapy in patients with diabetic ke- um-free solutions, such as 0.9% saline instead of lactat-
toacidosis.22,23 The problem usually manifests as acute ed Ringer’s solution. Although some texts recommend
hemolysis, lethargy, and weakness several days after in- giving half of the potassium requirement as potassium
sulin and fluid therapy begin. phosphate, this protocol can result in phosphorus over-
Hypophosphatemia may be caused or enhanced by dose because the potassium deficit greatly exceeds the
aluminum hydroxide products that bind phosphorus in phosphorus deficit in most patients.22
the gut, thereby decreasing its absorption.24 Sucralfate Phosphorus replacement (0.5 to 2 mmol/kg/day) can

NUTRITIONAL RECOVERY SYNDROME ■ SEPSIS ■ POTASSIUM PHOSPHATE


The Compendium January 1997 Small Animal

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

GLOMERULAR FILTRATION RATE ■ ARRHYTHMIA ■ REFRACTORY TACHYARRHYTHMIA


Small Animal The Compendium January 1997

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,
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18. Chew DJ, Meuten DJ: Disorders of calcium and phosphorus
imbalances in these patients.
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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-
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HYPERMAGNESEMIA ■ HYPOCALCEMIA ■ MONITORING