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Subclinical Hypomagnesemia in Critically Ill Animals

ByAllison J. Stewart, BVSc (Hons), PhD, DACVIM-LAIM, DACVECC
Reviewed/Revised Aug 2022

    Subclinical hypomagnesemia is common in critically ill horses and small animals and can increase the severity of systemic inflammatory response syndrome, worsen the systemic response to endotoxin, and lead to ileus, cardiac arrhythmias, refractory hypokalemia, and hypocalcemia.

    Low serum magnesium (Mg) concentrations have been reported to occur in 65% of critically ill humans, 39%–46% of dogs and cats in the ICU, 49% of hospitalized horses, 54% of equine surgical colic patients, and 78% of horses with enterocolitis. In human and canine ICU populations, hypomagnesemic patients had higher rates of concurrent hypokalemia and hyponatremia and a longer length of hospitalization. In another study, 54% of equine surgical colic patients had low iMg levels, and these horses had a significantly greater prevalence of postoperative ileus.

    Although diets for horses and small animals are rarely deficient in Mg, subclinical acute hypomagnesemia is very common in critically ill animals. Serum Mg concentration may be low as a result of altered Mg homeostasis, cellular or third-space redistribution, GI loss of Mg, or diuresis secondary to aggressive fluid treatment with IV fluids unsupplemented with Mg.

    Hypocalcemia is also frequently present in the equine ICU. Although the mechanism of action is unknown, serum Mg may influence serum calcium concentrations; human hypocalcemic patients with concurrent hypomagnesemia are often refractory to calcium treatment unless the low serum Mg levels are identified and corrected. Despite the precise regulation of serum Mg concentration by the kidneys, Mg does not have a complex homeostatic endocrine regulating mechanism. This is in contrast to calcium, which is tightly regulated by parathyroid hormone (PTH), calcitonin, and calcitriol. However, PTH, vitamin D, calcitonin, arginine vasopressin, glucagon, and calcium concentrations do influence Mg absorption and excretion to some degree.

    Mild hypocalcemia and hypomagnesemia stimulate PTH release; however, severe Mg depletion and acute hypermagnesemia decrease PTH release. Consequently, parallel determination of calcium and PTH concentrations is important in the investigation of Mg homeostasis.

    If longterm fluid treatment is required to support an inappetent animal in the ICU, Mg should be supplemented. A constant rate infusion of Mg sulfate at 50–150 mg/kg/day, IV (0.1–0.3 mL/kg/day of the 50% solution), provides daily requirements.

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