Page 959 - Small Animal Internal Medicine, 6th Edition
P. 959

CHAPTER 53   Electrolyte Imbalances   931


            probably is not indicated for asymptomatic animals in which   causes of clinically significant hypomagnesemia in dogs and
            the serum phosphorus concentration is greater than 1.5 mg/  cats include disorders leading to small intestinal malassimi-
  VetBooks.ir  dL and is unlikely to decrease further. Phosphate therapy is   lation; renal disorders associated with high urine output; the
                                                                 osmotic diuresis of diabetic ketoacidosis; and the shift of
            indicated if clinical signs or hemolysis is identified, or if the
            serum  phosphorus  concentration  is  less  than  1.5 mg/dL,
                                                                 lular to the intracellular compartment that occurs within the
            especially if a further decrease is possible. Phosphate supple-  potassium, phosphorus, and magnesium from the extracel-
            mentation is not indicated in dogs and cats with hypercalce-  first 24 hours of therapy for DKA (Box 53.10). Magnesium
            mia, oliguria, or suspected tissue necrosis. If renal function   is predominantly an intracellular cation. The nature of the
            is in question, phosphorus supplementation should not be   translocation of magnesium between intracellular and extra-
            provided until the status of renal function and the serum   cellular compartments is similar to that of potassium in that
            phosphorus concentration are known.                  factors that promote a shift of potassium into the intracel-
              The goal of therapy is to maintain the serum phosphorus   lular compartment (e.g., alkalosis, insulin, glucose infusion)
            concentration greater than 2 mg/dL without causing hyper-  promote a similar shift of magnesium.
            phosphatemia. Injectable potassium phosphate solution is
            available; however, unless urgent due to severity, oral phos-  Clinical Features
            phate supplementation is preferred (e.g., K-Phos Neutral or   Hypomagnesemia is reported to be the most common elec-
            Phospha 250 Neutral); bovine milk contains 0.032 mmol/  trolyte disorder in critically ill dogs and cats, and magnesium
            mL of elemental phosphorous and can be used for oral   deficiency may predispose animals to a variety of cardiovas-
            phosphate supplementation, balanced commercial diets,   cular, neuromuscular, and metabolic complications. Clinical
            or  a  combination  of  these.  IV  phosphate  supplementation   signs of hypomagnesemia do not usually occur until serum
            is usually required to correct severe hypophosphatemia,   total and ionized magnesium concentrations are less than
            especially in animals with diabetic ketoacidosis. Potassium   1.0 mg/dL and 0.4 mmol/L, respectively, and even at these
            phosphate solutions are typically used. If potassium supple-  low levels many animals remain grossly asymptomatic.
            mentation is contraindicated, sodium phosphate solutions   However, magnesium deficiency can result in several non-
            can be substituted. Potassium and sodium phosphate solu-  specific clinical signs, including lethargy, anorexia, muscle
            tions contain 3 mmol of phosphate per milliliter and either   weakness (including dysphagia and dyspnea), muscle fas-
            4.4 mEq of potassium or 4 mEq of sodium per milliliter. The   ciculations, seizures, ataxia, and coma. Concurrent hypoka-
            initial dosage of phosphate is 0.01 to 0.03 mmol/kg/h, prefer-  lemia, hyponatremia, and hypocalcemia occur in animals
            ably administered by constant-rate infusion in calcium-free   with hypomagnesemia, although the prevalence of these
            IV fluids (i.e., 0.9% sodium chloride). In dogs and cats with   electrolyte abnormalities may differ between species. These
            severe hypophosphatemia, it may be necessary to increase   electrolyte abnormalities may also contribute to the develop-
            the dosage to 0.03 to 0.12 mmol/kg/h. Because the dose of   ment of clinical signs. Magnesium is a co-factor for all
            phosphate necessary to replete an animal and the animal’s   enzyme reactions that involve ATP, most notably the sodium-
            response to therapy cannot be predicted, it is important to   potassium ATPase pump. Deficiencies in magnesium may
            initially monitor the serum phosphorus concentration every   cause potassium-losing nephropathy and increased urinary
            4 to 8 hours and adjust the phosphate infusion accordingly.   potassium losses, and the resultant hypokalemia may be
            Adverse effects from overzealous phosphate administration   refractory to appropriate potassium replacement therapy
            include iatrogenic hypocalcemia and its associated neuro-  unless hypomagnesemia is corrected. Magnesium deficiency
            muscular signs, hypernatremia, hypotension, mineralization   may inhibit PTH secretion from the parathyroid gland and
            of soft tissues, and renal failure. Serum total or preferably   may promote calcium uptake into bone, resulting in hypo-
            ionized calcium concentration should be measured at the   calcemia. Magnesium deficiency also causes the resting
            same time as serum phosphorus concentration and the rate   membrane potential of myocardial cells to be decreased and
            of phosphate infusion decreased if hypocalcemia is identified.  leads to increased Purkinje fiber excitability, with conse-
                                                                 quent generation of arrhythmias. Electrocardiographic
                                                                 changes include a prolonged PR interval, a widened QRS
            HYPOMAGNESEMIA                                       complex, a depressed ST segment, and peaked T waves.
                                                                 Cardiac arrhythmias associated with magnesium deficiency
            Etiology                                             include atrial fibrillation, supraventricular tachycardia, ven-
            Hypomagnesemia is present if serum total and ionized     tricular tachycardia, and ventricular fibrillation. In addition,
            magnesium concentrations are less than 1.5 mg/dL and   hypomagnesemia predisposes animals to digitalis-induced
            0.4 mmol/L, respectively, although reference ranges may   arrhythmias.
            vary between laboratories. Hypomagnesemia results from
            decreased oral intake, increased loss from the gastrointestinal   Diagnosis
            tract (e.g., malabsorption syndromes), increased renal loss   Many disorders and predisposing factors in dogs and cats are
            (e.g., postobstructive diuresis), endocrine causes (e.g., diabe-  associated with hypomagnesemia (see Box 53.10). However,
            tes mellitus), or translocation of the cation from the extracel-  measurement of serum total vs. ionized magnesium is some-
            lular to the intracellular compartment. The most common   what controversial. Serum total magnesium represents 1% of
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