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Veterinary Clinics: Magnesium: A Quick Reference

This document summarizes key information about magnesium, including: - Magnesium is primarily stored in bones and muscles, with 1% in extracellular fluid. The kidneys control magnesium balance through reabsorption in different parts of the nephron. - Magnesium deficit can result from gastrointestinal issues, renal diseases, certain drugs, and more. Deficiency manifests in cardiovascular, neuromuscular, and electrolyte disturbances. - While the best diagnostic assay is unclear, low serum magnesium levels consistent with clinical signs suggest deficit. Treatment involves oral or parenteral magnesium supplementation depending on the severity and situation.

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0% found this document useful (0 votes)
37 views4 pages

Veterinary Clinics: Magnesium: A Quick Reference

This document summarizes key information about magnesium, including: - Magnesium is primarily stored in bones and muscles, with 1% in extracellular fluid. The kidneys control magnesium balance through reabsorption in different parts of the nephron. - Magnesium deficit can result from gastrointestinal issues, renal diseases, certain drugs, and more. Deficiency manifests in cardiovascular, neuromuscular, and electrolyte disturbances. - While the best diagnostic assay is unclear, low serum magnesium levels consistent with clinical signs suggest deficit. Treatment involves oral or parenteral magnesium supplementation depending on the severity and situation.

Uploaded by

Danilo Jimenez
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd
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Vet Clin Small Anim 38 (2008) 467–470

VETERINARY CLINICS
SMALL ANIMAL PRACTICE
Magnesium: A Quick Reference
Shane W. Bateman, DVM, DVSc
Department of Veterinary Clinical Sciences, The Ohio State University,
601 Vernon L. Tharp Street, Columbus, OH 43210–1089, USA

DISTRIBUTION OF MAGNESIUM
 In human beings, 1% of the total body magnesium is in the extracellular fluid
(ECF), whereas the remaining 99% is intracellular.
 Approximately two thirds of body magnesium is stored with calcium and phos-
phorus in bones, 20% in muscles, and 11% in soft tissues other than muscles.
 Like calcium, extracellular magnesium is present in three forms:
 Ionized or free form (55%) thought to constitute the biologically active fraction
 Protein-bound form (20%–30%)
 Complexed form (15%–25%)
 Magnesium is only 20% to 30% bound to protein, being less affected by
changes in albumin concentration than calcium.

MAGNESIUM HANDLING
 The primary site of magnesium absorption seems to be the ileum, but the jeju-
num and colon also contribute substantially to net absorption.
 The kidneys control and regulate magnesium balance.
 Various segments of the nephron play an important role in magnesium homeo-
stasis. Of the filtered magnesium:
 10% to 15% of magnesium is reabsorbed within the proximal tubule.
 60% to 70% is reabsorbed in the cortical thick ascending limb of the loop
of Henle.
 10% to 15% is reabsorbed in the distal convoluted tubule.
 The final concentration of magnesium in the urine is determined at the
distal convoluted tubule under hormonal and nonhormonal control.

MANIFESTATIONS AND CAUSES OF MAGNESIUM DEFICIT


 Refer to Box 1.
 Cardiovascular
 Intracellular and extracellular magnesium concentrations play an impor-
tant role in cardiac excitability, contraction, and conduction through reg-
ulatory effects on calcium movement.

E-mail address: [email protected]

0195-5616/08/$ – see front matter ª 2008 Elsevier Inc. All rights reserved.
doi:10.1016/j.cvsm.2008.01.014 vetsmall.theclinics.com
468 BATEMAN

Box 1: Causes of magnesium deficit


Gastrointestinal
Reduced intake, starvation, or malnutrition
Chronic diarrhea
Gastric suction
Malabsorption syndromes
Short bowel syndrome
Gastric bypass surgery
Colonic neoplasia
Familial or inherited
Renal
Diabetes mellitus or diabetic ketoacidosis
Diuretics (except potassium-sparing agents)
Osmotic agents (including hyperglycemia)
Intrinsic renal causes of diuresis
Postobstructive
Polyuric acute failure
Hyperaldosteronism
Hyperthyroidism
Renal tubular acidosis
Concurrent electrolyte disorders
Hypokalemia
Hypercalcemia or hyperparathyroidism
Hypophosphatemia
Drugs
Gentamicin
Carbenicillin
Ticarcillin
Cyclosporin
Cisplatin
Postrenal transplantation
Familial or inherited
Miscellaneous
Excessive loss from lactation
Redistribution
Acute myocardial infarction
Acute pancreatitis
Insulin
Catecholamine excess
Idiopathic

Data from Bateman SW. Disorders of magnesium: magnesium deficit and excess. In: Dibartola
SP, editor. Fluid, electrolyte and acid-base disorders in small animal practice. 3rd edition.
Philadelphia: Elsevier; 2006. p. 218.
MAGNESIUM: A QUICK REFERENCE 469

Table 1
Dose ranges for magnesium salts
Rapid mEq of Mg/g mEq/kg/d mEq/kg/h mg/kg/h
replacement of salt
MgSO4 8.12 0.75–1 0.03–0.04 3.7–4.9
MgCl2 9.25 0.75–1 0.03–0.04 3.2–4.3
Slow mEq of Mg/g mEq/kg/d mEq/kg/h mg/kg/h
replacement of salt
MgSO4 8.12 0.3–0.5 0.013–0.02 1.6–2.5
MgCl2 9.25 0.3–0.5 0.013–0.02 1.4–2.2
Emergency/ mEq/kg mg/kg Duration
loading MgSO4 0.15–0.3 19–37 5 min–1 h
(emergency)
24 h (loading)
MgCl2 0.15–0.3 16–32 5 min–1 h
(emergency)
24 h (loading)
Oral mEq/kg/d
Several 1–2
Abbreviations: h, hour; Mg, magnesium; min, minutes.
Data from Bateman SW. Disorders of magnesium: magnesium deficit and excess. In: Dibartola SP, editor.
Fluid, electrolyte and acid-base disorders in small animal practice. 3rd edition. Philadelphia: Elsevier;
2006. p. 222.

 Magnesium may act as an antiarrhythmic agent by limiting intracellular


calcium overload.
 Neuromuscular
 Magnesium depletion enhances neuronal excitability and neuromuscular
transmission.
 Magnesium acts as an analgesic by blocking N-methyl-D-aspartate
(NMDA) receptors within the central nervous system.
 Electrolyte disturbances
 Depletion of magnesium has a permissive effect on potassium exit from
the cells leading to extracellular accumulation of potassium, which is sub-
sequently lost from the body.
 Frequently, this potassium deficiency is refractory to supplementation until
the magnesium deficit also has been corrected.
 Hypocalcemia also occurs in human beings as a concurrent electrolyte
abnormality when a magnesium deficit is present.

DIAGNOSIS OF A MAGNESIUM DEFICIT


 Currently, there is no consensus regarding the best assay for diagnosis.
 Serum magnesium does not correlate well with magnesium deficit based
on clinical signs or with serum ionized magnesium.
 Ionized serum magnesium and total serum magnesium may be useful
when results are low and are consistent with clinical suspicion of a mag-
nesium deficit.
 The magnesium retention test may be helpful in the future.
470 BATEMAN

MAGNESIUM SUPPLEMENTATION
 Clinical situations in which magnesium supplementation may be considered
 Cardiac arrhythmias
 Torsade de pointes, digitalis toxicity, ventricular ectopy
 Metabolic
 Diabetic ketoacidosis, hypokalemia refractory to supplementation,
hypocalcemia refractory to supplementation
 Use with caution if renal insufficiency is present.
 Refer to Table 1.

Further Readings
Bateman SW. Disorders of magnesium: magnesium deficit and excess. In: Dibartola SP, editor.
Fluid, electrolyte and acid-base disorders in small animal practice. 3rd edition. Philadelphia:
Elsevier; 2006. p. 210–26.
Cortes YE, Moses L. Magnesium disturbances in critically ill patients. Compend Contin Educ Pract
Vet 2007;29(7):420–7.

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