Page 211 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Disorders of Phosphorus: Hypophosphatemia and Hyperphosphatemia 201

parenteral) can cause morbidity (e.g., hypocalcemia, soft Theoretically, adding phosphorus to fluids containing
tissue calcification, renal failure). Interestingly, treatment calcium may cause precipitation of calcium phosphate,
of asymptomatic hypophosphatemia in diabetic people but this appears to depend on relative concentrations of
is controversial and recommended only when hypophos- calcium and phosphorus. Phosphorus usually is
phatemia is severe (<2.0 mg/dL). 85 However, clinical administered after diluting it in physiologic saline solu-
experienceinveterinary medicinesuggeststhatanticipatory tion. The volume of distribution for administered phos-
phosphorus supplementation is reasonable in some phate varies tremendously among hypophosphatemic
ketoacidotic cats. people, and redistribution of phosphate can occur rapidly.
If oral supplementation is suitable (which is uncom- Therefore, the dose necessary for repletion and the
mon in patients with severe hypophosphatemia), it may patient’s response to therapy cannot be predicted. In
be safer and therefore preferable to parenteral supplemen- two studies of hypophosphatemic cats, total amounts of
tation. 5,112 Oral phosphate administration is unaccept- phosphorus infused intravenously ranged from 0.138
able in vomiting patients and perhaps in patients with to 1.26 mmol/kg, indicating a wide range of total body
diarrhea. If the enteral route is chosen, feeding skim or phosphate deficits. 2,80
low-fat milk or a buffered laxative usually is effective. A conservative approach is to assume that intrave-
Patients symptomatic because of hypophosphatemia gen- nously administered phosphate remains in the ECF com-
erally need parenteral replacement therapy. Administering partment (actually much of it enters the intracellular
phosphate intravenously is potentially dangerous because fluid). Development of hyperphosphatemia is unlikely
it may cause hypocalcemia, tetany, soft tissue mineraliza- with this approach. Prophylactic parenteral phosphate
tion, renal failure, or hyperphosphatemia. 88 Therefore, therapy (such as may be used for patients with diabetic
phosphorus administration typically has consisted of ketoacidosis) may be reasonably estimated by giving
injecting small amounts slowly over hours to days and one fourth to one half of the supplemented potassium
monitoring the patient repeatedly (e.g., 0.01 to 0.06 as potassium phosphate and the rest as potassium chlo-
mmol/kg/hr in dogs and cats with measurement ride. However, decreased urinary phosphate excretion
of serum phosphorus concentration every 6 to that develops during hypophosphatemia may persist dur-
8 hours). 80,173 Although such caution is wise, it is note- ing treatment and predispose to hyperphosphatemia. The
worthy that more aggressive phosphorus administration products available for oral and parenteral use are
has been used in people (i.e., 0.16 to 0.64 mmol/kg over summarized in Tables 7-1 through 7-3.
4 to 12 hours in patients receiving total parenteral nutri-
tion). 32 Other groups have used similarly large doses over
even shorter times (e.g., 0.4 to 0.8 mmol/kg depending HYPERPHOSPHATEMIA
on the degree of hypophosphatemia over 30 minutes in
patients with cardiac disease), also without problems. 180
Sodium phosphate and potassium phosphate are com- CLINICAL EFFECTS OF
monly used, but administration of glucose phosphate also HYPERPHOSPHATEMIA
has been reported. 180 Selection of the particular form of Increased serum phosphorus concentration decreases
phosphorus to administer is based on the patient’s serum serum calcium concentration so that the calcium phos-
electrolyte concentrations. phate solubility product ([Ca] [Pi]) remains constant.
Currently, it seems safest to administer phosphate by Hypocalcemia (which may cause tetany) and soft tissue
constant-rate infusion at rates that have been used mineralization are the major clinical consequences of
successfully in dogs and cats and to monitor the serum hyperphosphatemia. 169 If hyperphosphatemia occurs in
phosphorus concentration every 6 to 8 hours. a hypercalcemic patient, systemic calciphylaxis (i.e., acute

TABLE 7-1 Oral Preparations of Compounds Used as Phosphate Binders

Name of Product Chemical Name Company Preparations

Basaljel Aluminum carbonate gel Wyeth-Ayerst Capsules, suspension, tablets
Aluminum hydroxide Aluminum hydroxide gel Various manufacturers Tablets, capsules, suspension
Calcium carbonate Calcium carbonate Various manufacturers Tablets, suspension
PhosLo Calcium acetate Braintree Tablets, capsules
Calcium citrate Calcium citrate Various manufacturers Tablets
Renepho Calcium acetate/magnesium carbonate Fresenius Medical Care
Renagel Sevelamer HCl Genzyme Tablets, capsules
Renalzin Lanthanum carbonate Bayer Suspension