Page 212 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

202 ELECTROLYTE DISORDERS

TABLE 7-2 Preparations for Phosphate Supplementation (Preparations for
Parenteral Use)
Composition Osmolality Phosphate Sodium Potassium
Compound (per mL) pH (mOsm/kg) (mmol/mL) (mEq/mL) (mEq/mL)
Sodium phosphate 142 mg Na 2 HPO 4 , 5.70 5580 3.000 4.0 0
276 mg
NaH 2 PO 4 •H 2 O
Potassium phosphate 236 mg K 2 HPO 4 6.60 5840 3.003 0 4.36
224 mg
KH 2 PO 4

TABLE 7-3 Preparations for Phosphate Supplementation (Preparations for Oral Use)
Phosphorus Phosphate Potassium
Product Composition mg mEq mg mEq mg mEq Company Prep

K-Phos Dibasic sodium phosphate, 250 14.1 45 1.1 298 13 Beach Tablets
Neutral monobasic potassium phosphate,
monobasic sodium phosphate
Uro-KP Dibasic sodium phosphate, 250 14.1 49 1.3 250 11 Star Tablets
Neutral monobasic potassium phosphate,
monobasic sodium phosphate
Neutra-Phos Dibasic sodium phosphate, 250 14.1 278 7.1 164 7.1 Ortho- Powder
monobasic potassium phosphate, McNeill
monobasic sodium phosphate
Neutra- Dibasic potassium phosphate, 250 14.1 556 14.2 0 0 Ortho- Powder
Phos-K monobasic potassium phosphate McNeill
K-Phos Monobasic potassium phosphate 114 3.7 144 3.7 0 0 Beach Tablet
Original
K-Phos M.F. Monobasic potassium phosphate, 126 4.0 45 1.1 67 2.9 Beach Tablet
monobasic sodium phosphate
K-Phos No. 2 Monobasic potassium phosphate, 250 8.0 88 2.2 134 5.8 Beach Tablet
monobasic sodium phosphate

Amounts given per tablet or per 75 mL of reconstituted liquid.
Prep, preparation.

calcification of organs, including the heart and lungs 166 CAUSES OF HYPERPHOSPHATEMIA
may occur and can be fatal. Acute hyperphosphatemia
Hyperphosphatemia in dogs and cats is primarily caused
(such as can occur after ingesting oral sodium phosphate
by decreased renal excretion, but increased intake and
solutions in preparation for colonoscopy) has been 169
translocation also may be responsible (Box 7-2).
associated with acute renal failure in patients without Translocation occurring during treatment of
prior hypercalcemia, 118 and a direct toxic effect of phos-
hemolymphatic malignancies may cause tumor lysis syn-
phate on renal tubular cells has been hypothesized. In
drome (i.e., hyperphosphatemia, hypocalcemia,
human end-stage renal disease patients, hyperphos-
hyperkalemia, hyperuricemia, and oliguric acute renal
phatemia is associated with increased cardiovascular mor-
36 failure). Myeloblasts and lymphoblasts may contain up
tality. After phosphate administration, deposition of to four times as much phosphate as normal cells, and
calcium and phosphate in bone and soft tissue may con- destruction of these cells causes release of phosphate. This
tribute to hypocalcemia. The magnitude of hypocalcemia syndrome is uncommon in small animal practice. In one
is related to the rate at which serum phosphorus concen- study of dogs with multicentric lymphosarcoma, serum
tration increases, but the exact relationship is unpredict-
phosphorus concentrations were normal before therapy
able. The risk of soft tissue mineralization increases when 120
and did not change after treatment. Urinary phospho-
the [Ca] [Pi] solubility product exceeds 60 to 70.
rus excretion increased but probably because urine volume