Vol. 19, No.
1 January 1997 V HEINZ SYMPOSIUM 1996
Continuing Education Article
FOCAL POINT
★Intensive management of
critically ill animals can lead to
severe electrolyte and acid–base
abnormalities.
KEY FACTS
■ Hyperkalemia can cause life-
threatening cardiac arrhythmia.
■ Imbalances of potassium,
phosphorus, and magnesium
must be corrected cautiously
to avoid severe side effects.
■ Hypophosphatemia can cause
acute hemolysis in recovering
diabetics and malnourished
patients receiving nutritional
support.
■ Unexplained decreases in serum
phosphorus should prompt a
search for infection, p. 44.
■ Until the magnesium deficit
is corrected, concurrent
hypokalemia may be refractory
to aggressive potassium
replacement.
Disorders of Potassium,
Phosphorus, and
Magnesium in
Critical Illness
Auburn University
Douglass K. Macintire, DVM, MS
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.
DISORDERS OF POTASSIUM BALANCE
Potassium is the primary intracellular cation; 95% of total body potassium is
within cells.1 Potassium maintains intracellular volume and normal membrane
potential. If the ratio between intracellular and extracellular potassium is dis-
turbed, the membrane potential of excitatory tissue (heart, nerve, and muscle)
is affected; conduction disturbances result.2 In normal animals, daily potassium
intake equals daily losses.
Hypokalemia
Hypokalemia is probably the most common electrolyte abnormality recog-
nized in critically ill veterinary patients. Clinical signs include muscle weak-
ness, cramping, lethargy, myocardial depression, ileus, urine retention, inability
to concentrate urine, and mild hyperglycemia from decreased insulin se-
cretion.1,2 Severe potassium depletion can result in death from paralysis of res-
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
production (it is a cofactor
for glycolysis and is needed
to form ATP) and cell mem-
brane maintenance (it is a
component of phospholipid
membrane and is required
to form 2,3-diphosphoglyc-
erate). Serum phosphorus
concentration is regulated
by dietary intake, renal ex-
cretion, factors that pro-
mote ion translocation into
or out of cells (e.g., insulin,
glucose, blood pH), and in-
teractions of the regulatory
hormones vitamin D and Figure 3—An unexplained drop in hematocrit accompanied
parathyroid hormone. by hemolysis in recovering diabetics or malnourished ani-
mals receiving nutritional
Hypophosphatemia phatemia.
Until recently, clinically
significant decreases in
serum phosphorus levels were considered uncommon.
Now hypophosphatemia is increasingly being recog-
nized as a problem in critically ill humans and animals.
Clinical sequelae of hypophosphatemia include hemol-
ysis (Figure 3), skeletal muscle weakness, leukocyte dys-
function, and poor oxygenation of tissue as a result of
reduced 2,3-diphosphoglycerate levels.19
Nutritional recovery syndrome was first recognized in
prisoners of war after World War II.20 Aggressive feed-
ing after prolonged malnutrition resulted in a syn-
drome of lethargy, depression, diarrhea, and multiple
electrolyte abnormalities. It was later found that mal-
nourished patients are prone to hypophosphatemia
upon refeeding. Glucose and phosphorus are transport-
ed into cells as a result of insulin secretion. Phosphorus
is a cofactor for glycolysis and is rapidly consumed,
sometimes dropping to dangerously low levels.
The same syndrome can be seen in veterinary pa-
tients that receive enteral nutrition or intravenous
dextrose solutions after a period of malnutrition. 21
Hypophosphatemia can be prevented by gradually in-
creasing feeding to the full caloric requirements over
several days and avoiding overzealous feeding of high-
carbohydrate diets.
Another cause of clinically significant hypophos-
phatemia is insulin therapy in patients with diabetic ke-
toacidosis.22,23 The problem usually manifests as acute
hemolysis, lethargy, and weakness several days after in-
sulin and fluid therapy begin.
Hypophosphatemia may be caused or enhanced by
aluminum hydroxide products that bind phosphorus in
the gut, thereby decreasing its absorption.24 Sucralfate
NUTRITIONAL RECOVERY SYNDROME ■ SEPSIS ■ POTASSIUM PHOSPHATE
The Compendium January 1997
also binds to phosphorus.
These agents should be
discontinued if the patient
has hypophosphatemia and
should not be used in ani-
mals prone to hypophos-
phatemia. For example,
male cats with postobstruc-
tive diuresis may initially
exhibit hyperphosphatemia
and azotemia; however, hy-
pophosphatemia may devel-
op later as a result of exces-
sive renal losses. Therefore,
the use of phosphate binders
in these animals should be
avoided.
support suggests hypophos- Although the mechanism
is unclear, hypophosphate-
mia can be an early sign of
sepsis. Unexplained decreas-
es in serum phosphorus should therefore prompt a
search for infection.24 The decline in phosphorus may
be secondary to the hypermetabolic state or respiratory
alkalosis, both of which occur early in sepsis.
When hypophosphatemia is causing clinical signs or
when serum phosphorus levels drop below 1.0 mg/dl,
the hypophosphatemia should be treated with intra-
venous replacement. Complications of intravenous re-
placement can include hyperphosphatemia, hypocal-
cemia, tetanic seizures, soft tissue mineralization, and
hypotension secondary to rapid infusion.24
Phosphorus must be administered slowly and cau-
tiously, and serum levels should be monitored every 6
hours. Replacement can be discontinued when serum
levels reach 2.0 to 2.5 mg/dl.
Potassium phosphate is available in a solution con-
taining 3 mmol of phosphate (93 mg) and 4.3 mEq of
potassium per milliliter. Most veterinary references rec-
ommend a dosage of 0.01 to 0.03 mmol/kg/hr to be
given for 6 hours and continued for another 6 hours if
the phosphorus levels remain low.21–24 This dosage is safe
but may be inadequate for animals with severe deple-
tion. A recommended dose for humans is 7.7 mg/kg/hr
(0.025 mmol/kg/hr) administered over 4 hours.25
Potassium phosphate must be administered in calci-
um-free solutions, such as 0.9% saline instead of lactat-
ed Ringer’s solution. Although some texts recommend
giving half of the potassium requirement as potassium
phosphate, this protocol can result in phosphorus over-
dose because the potassium deficit greatly exceeds the
phosphorus deficit in most patients.22
Phosphorus replacement (0.5 to 2 mmol/kg/day) can
The Compendium January 1997
safely be accomplished by the oral route if the patient is
not exhibiting severe clinical signs. The phosphorus con-
tent of cow’s milk is 0.029 mmol/ml.20 Calcium phos-
phate tablets containing 580 mg of calcium, 450 mg of
phosphorus, and 400 IU of vitamin D3 are also available.
Hyperphosphatemia
Increases in serum phosphorus levels are most com-
monly seen in veterinary patients with renal failure.18
Decreased glomerular filtration rate results in phospho-
rus retention. Other causes include massive cellular
damage (tumor lysis syndrome, rhabdomyolysis,
snakebite, thromboembolism), hypoparathyroidism,
and poisoning from hypertonic sodium phosphate ene-
mas26 or vitamin D toxicity. Iatrogenic causes include
overzealous phosphorus replacement or overdose of
phosphorus-containing urine acidifiers. Mild elevations
of phosphorus are considered normal in young, grow-
ing dogs.
Clinical findings include diarrhea, hypocalcemia,
tetany, hyperosmolality, hypernatremia, and an in-
creased tendency toward metastatic calcification of soft
tissues when the calcium–phosphorus product exceeds
58.18 Hyperphosphatemia also contributes to the pro-
gression of renal disease by stimulating renal secondary
hyperparathyroidism.19 Hyperphosphatemia is treated
with intravenous fluids to correct acidosis and promote
phosphorus excretion. Fluids containing dextrose pro-
mote translocation of phosphorus into cells. Animals
with renal failure should receive a low-phosphorus diet,
and intestinal phosphate binders should be given with
food to decrease absorption.
DISORDERS OF MAGNESIUM BALANCE
Recent reports in human critical care medicine indi-
cate a high incidence (>50%) of hypomagnesemia.27,28
Although serum magnesium in veterinary patients is
seldom measured, certain critically ill animals are prob-
ably also at risk for magnesium imbalance. A recent re-
port documented that magnesium imbalance was the
most common electrolyte abnormality in 101 critically
ill dogs admitted to the intensive care unit at Colorado
State University: 30% had hypermagnesemia and 20%
had hypomagnesemia.29
Magnesium is the second most abundant intracellu-
lar cation. Most of the total body magnesium is present
in bone and skeletal muscle. Only 1% is in the serum.
Unfortunately, because of the dynamic nature of mag-
nesium homeostasis, serum magnesium measurements
may not accurately reflect total body stores.30 In fact,
serum levels can be normal despite magnesium deple-
tion or excess.
Magnesium is a coenzyme for Na+,K+-ATPase, Ca++-
GLOMERULAR FILTRATION RATE ■ ARRHYTHMIA ■ REFRACTORY TACHYARRHYTHMIA
Small Animal
ATPase, and proton pumps. It is essential for many
metabolic functions, including ATP production and
synthesis of nucleic acids and proteins. It helps regulate
smooth muscle vascular tone and may influence lym-
phocyte activation and cytokine production.
Hypomagnesemia
Magnesium deficiency may result from decreased in-
take, increased losses, or alteration of distribution. Crit-
ically ill animals may be predisposed to hypomagne-
semia because of stress, catabolic illness, nasogastric
suctioning, peritoneal dialysis, total parenteral nutri-
tion, diuretics, massive blood transfusion, or aggressive
intravenous fluid therapy with magnesium-deficient
fluids.31 Because similar conditions cause hypokalemia
and/or hypophosphatemia, magnesium deficiency may
be unrecognized and overlooked. In fact, concurrent
hypokalemia may be refractory to aggressive potassium
replacement until the magnesium deficit is corrected.28
Clinical signs of hypomagnesemia include cardiac ar-
rhythmia, muscle weakness, tremors, seizures, altered
mentation, esophageal motility disorders, and respirato-
ry muscle paralysis.31 Normal serum magnesium con-
centrations range from 1.89 to 2.51 mg/dl.29 If an ani-
mal exhibits clinical signs (cardiac arrhythmia, muscle
tremors, refractory hypokalemia) and serum magne-
sium levels are 1.2 mg/dl or lower, magnesium supple-
mentation can be considered.
Mild deficits can be corrected by intravenous fluids
that contain magnesium. In cases of severe magnesium
depletion, magnesium chloride or magnesium sulfate
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
initial dose for 3 to 5 days.31 For life-threatening ven-
tricular arrhythmia, digitalis-induced arrhythmia, or
cardiac arrest, a dose of 0.15 to 0.3 mEq/kg (50 to 100
mg/kg) can be diluted in 5% dextrose or 0.9% saline
and administered slowly intravenously over 5 to 15
minutes to raise the ventricular fibrillation threshold.
Even when serum magnesium levels are normal,
magnesium infusion should be considered for some an-
imals with refractory tachyarrhythmia, especially when
conventional therapy has failed.32 The lack of a reliable
measure of total body magnesium tends to make thera-
py somewhat empirical.
Potential side effects of intravenous magnesium
therapy include hypocalcemia, hypotension, and car-
diac conduction abnormalities (atrioventricular and
bundle-branch blocks). Overdoses can be treated with
calcium gluconate (10 to 50 mg/kg intravenously).31
Fortunately, it is difficult to cause prolonged hyper-
magnesemia because the kidneys can eliminate most
of the excess magnesium.27
Small Animal
Magnesium (1 to 2 mEq/kg/day) can also be given
orally. It is available as oxide or hydroxide.
Hypermagnesemia
At present, hypermagnesemia is not considered to be
clinically significant in critically ill animals unless there
are associated signs of hypocalcemia. The most com-
mon cause is renal failure combined with overuse of
magnesium-containing antacids.
CONCLUSION
Intensive management of critically ill animals, in-
cluding such interventions as total parenteral nutrition,
enteral nutrition, intravenous insulin, aggressive fluid
therapy, nasogastric suctioning, massive blood transfu-
sion, and peritoneal dialysis, can lead to severe elec-
trolyte and acid–base abnormalities. Veterinarians must
closely monitor potassium, phosphorus, and magne-
sium levels to detect and correct any life-threatening
imbalances in these patients.
About the Author
Dr. Macintire is affiliated with the Department of Small
Animal Surgery and Medicine, College of Veterinary
Medicine, Auburn University, Alabama, and is a Diplo-
mate of the American College of Veterinary Internal
Medicine and the American College of Veterinary Emer-
gency and Critical Care.
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