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Metabolic Disorders
Disorders of Magnesium Metabolism
Subclinical Hypomagnesemia in Critically Ill Animals
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Sections in Veterinary Professionals
  • Behavior
  • Circulatory System
  • Clinical Pathology and Procedures
  • Digestive System
  • Emergency Medicine and Critical Care
  • Endocrine System
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Chapters in Metabolic Disorders
  • Metabolic Disorders Introduction
  • Congenital Erythropoietic Porphyria
  • Disorders of Calcium Metabolism
  • Disorders of Magnesium Metabolism
  • Disorders of Phosphorus Metabolism
  • Disorders of Potassium Metabolism
  • Equine Metabolic Syndrome
  • Fatigue and Exercise
  • Fever of Unknown Origin
  • Hepatic Lipidosis
  • Ketosis in Cattle
  • Malignant Hyperthermia
  • Transport Tetany in Ruminants
Topics in Disorders of Magnesium Metabolism
  • Overview of Disorders of Magnesium Metabolism
  • Hypermagnesemia
  • Hypomagnesemic Tetany in Cattle and Sheep
  • Subclinical Hypomagnesemia in Critically Ill Animals
 
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Subclinical Hypomagnesemia in Critically Ill Animals

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

Low serum Mg concentrations have been reported to occur in 65% of critically ill people, 39–46% of dogs and cats in the intensive care unit (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 the equine and small animal diet is 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 therapy with IV fluids unsupplemented with Mg.

Hypocalcemia is also frequently observed 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 therapy unless the low serum Mg levels are identified and corrected. Despite the precise regulation of serum Mg concentration by the kidney, 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, glucagons, and calcium concentrations do influence Mg absorption and excretion to some degree.

Mild hypocalcemia and hypomagnesemia stimulate PTH release, but 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 therapy is required to support an inappetent animal in the ICU, Mg should be supplemented. A constant rate infusion of 50–150 mg/kg/day, IV, of Mg sulfate (0.1–0.3 mL/kg/day of the 50% solution) provides daily requirements.

Last full review/revision July 2011 by Allison J. Stewart, BVSC (Hons), MS, DACVIM-LA, DACVECC

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