Page 958 - Small Animal Internal Medicine, 6th Edition

930 PART VII Metabolic and Electrolyte Disorders

Clinical Features
Hyperphosphatemia is a marker of underlying disease. By BOX 53.9
VetBooks.ir itself, hyperphosphatemia usually does not cause clinical Causes of Hypophosphatemia in Dogs and Cats
signs. An acute increase in serum phosphorus may cause
hypocalcemia and its associated neuromuscular signs. Sus-
tained hyperphosphatemia can cause secondary hyperpara- Decreased Intestinal Absorption
Phosphate binders*
thyroidism, fibrous osteodystrophy, and mineralization of Vitamin D deficiency
soft tissues. Fortunately, most causes of hyperphosphatemia Decreased dietary intake
cause a decrease in serum calcium concentration so that the Malabsorption, steatorrhea
calcium-phosphorus solubility product ([Ca] × [Pi]) remains
less than 60. The risk of soft tissue mineralization increases Increased Urinary Excretion
when the [Ca] × [Pi] solubility product exceeds 60. Chronic Primary hyperparathyroidism*
kidney disease is the most common cause of sustained Humoral hypercalcemia of malignancy*
hyperphosphatemia and an increase in the solubility product DKA*
Renal tubular disorders (Fanconi syndrome)
above 60. History, physical examination, and results of CBC, Diuretics
serum biochemistry panel, urinalysis, and serum T 4 concen- Eclampsia
tration (cats) will usually reveal the cause.
Transcellular Shifts
Treatment Insulin administration, especially for DKA*
Hyperphosphatemia usually resolves with correction of the Respiratory and metabolic alkalosis
underlying disease. In dogs and cats with kidney disease, Sodium bicarbonate administration*
hyperphosphatemia can initially be lowered with aggressive Parenteral glucose administration*
fluid therapy. Low-phosphorus diet with orally administered Parenteral nutritional solutions
phosphate binders is the most effective way to treat sus- Hypothermia
tained hyperphosphatemia caused by kidney disease (see Laboratory Error
Chapter 41).
DKA, Diabetic ketoacidosis.
*Common causes.
HYPOPHOSPHATEMIA Modified from DiBartola SD, Willard MD: Disorders of phosphorus:
hypophosphatemia and hyperphosphatemia. In DiBartola SP,
editor: Fluid, electrolyte, and acid-base disorders in small animal
Etiology practice, ed 4, St Louis, 2012, Saunders Elsevier.
Hypophosphatemia is present when the serum phosphorus
concentration is less than 3 mg/dL in the dog and cat,
although reference ranges may vary between laboratories. or only mildly decreased because metabolic acidosis of DKA
Hypophosphatemia usually is not clinically worrisome until results in a shift of phosphorus from the intracellular to the
the serum phosphorus concentration is less than 1.5 mg/dL. extracellular compartment.
Hypophosphatemia results from decreased phosphorus
absorption in the intestinal tract, increased urinary phos- Clinical Features
phorus excretion, or translocation from the extracellular to Clinical signs may develop when the serum phosphorus
the intracellular compartment. Hypophosphatemia is com- concentration is less than 1.5 mg/dL, although signs are
monly associated with humoral HHM (i.e., lymphoma), variable and severe hypophosphatemia is clinically silent
primary hyperparathyroidism, and aggressive therapy for in many animals. Hypophosphatemia primarily affects the
DKA (Box 53.9). Clinically significant hypophosphatemia is hematologic and neuromuscular systems in the dog and cat.
most likely to occur within the first 24 hours of therapy for Hemolytic anemia is the most common sequela to hypo-
diabetic ketoacidosis, when a shift of potassium and phos- phosphatemia. Hypophosphatemia decreases the eryth-
phorus from the extracellular to the intracellular compart- rocyte concentration of adenosine triphosphate (ATP),
ment occurs. The nature of the translocation of phosphorus which increases erythrocyte fragility, leading to hemo-
between intracellular and extracellular compartments is lysis. Hemolysis usually is not identified until the serum
similar to that seen with potassium. Factors that promote a phosphorus concentration is 1 mg/dL or less. Hemo-
shift of potassium into the intracellular compartment (e.g., lytic anemia can be life-threatening if not recognized and
alkalosis, insulin, glucose infusion) promote a similar shift treated. Neuromuscular signs include weakness, ataxia, and
in phosphorus. During therapy for DKA, the serum phos- seizures, as well as anorexia and vomiting secondary to
phorus concentration can decline to severe levels (i.e., intestinal ileus.
<1 mg/dL) as a result of the dilutional effects of fluid therapy
and the intracellular shift of phosphorus after initiation of Treatment
insulin and bicarbonate therapy. It is interesting to note that For most dogs and cats, hypophosphatemia resolves after
the initial serum phosphorus concentration usually is normal correction of the underlying cause. Phosphate therapy