·

 

Readers who wish more detailed information are referred to Clinics of North America, May, 1998, pp598; Proceedings of AAHA, 1997, pp 187; Proceedings of the 6th International Symposium of Veterinary Critical Care Symposium, 1998,pp338, pp754. The following "discussion" will, where possible, be honed to essentials...

 

 

 

The basics of magnesium homeostasis are:

Redistribution:

insulin therapy
catecholamines
pancreatitis (e.g. deposition of Mg ⁺² complexes in fat)

 

 

Homeostasis...................Causes...............Consequences............Diagnosis..............Treatment

 

 

 

Magnesium is a key component of, literally, hundreds perhaps thousands of enzyme and transport systems and hormonal activities..involving virtually every major body system..Therefore, the clinical manifestations of hypomagnesemia can be single or multi-systemic and in many instances, the details of these are incompletely understood. A summary outline follows. Where an explanation or hypotheses to explain the observed phenomenon is reasonable, one will be offered.

Cardiovascular

Increased Suseptibility to Digoxin-related arrythmias

Increased incidence of atrial .....fibrillation
Arrythmias resulting from secondary .....hypokalemia, hypocalcemia that are refractory to antiarrythmic medication
Hypertension

Metabolic

Refractory hypokalemia...responsive ONLY to Mg⁺²
supplementation, e.g. diabetic ketoacidosis, ..................(More thoughts on these soon)

Refractory hypocalcemia responsive ONLY to Mg⁺²
supplementation

Neuromuscular

Seizure/Coma
Tetany
General weakness
Ataxia...........................................................................(More thoughts on these too...soon)
Dyspnea .......(weakness affects respiratory muscles)
Dysphagia
Depression
Hyperreflexia ...(secondary to hypocalcemia?)

 

Metabolic

Refractory hypokalemia...

...responsive only to Mg ⁺² supplementation, e.g in diabetic ketoacidosis;
...possibly due to decreased functionality of Mg-dependent Na/K-ATPase .......and/or impairment of renal potassium resorption

Refractory hypocalcemia...

...responsive only to Mg ⁺² supplementation (or only transiently responsive ........to calcium infusion;
...Hypomagnesemia--> impaired release of PTH
...Hypomagnesemia--> impaired action of PTH at level of bone

Hypophosphatemia..

...possibly secondary to impaired renal tubular resorption/retension

 

Gastrointestinal

Adynamic ileus (-->Nausea/anorexia/emesis)

 

Hematological

Hemolysis, anemia

Platelet aggregation

 

 

 

 

 

 

1.Measure serum Magnesium: Suffice it to say that total body magnesium is very difficult to assess from serum [Mg ⁺² ] determinations. Remember, only 0.3% is in the serum!

Published [Mg ⁺² ] are (normal ranges) for serum

Dog: 1.7-2.4 mg/dl (0.697-1.0 mmol/L) *

Cat: 1.0-2.5 mg/dl (0.41-1.02mmol/L) *

*..note that mmol/L x 2.44 = ~ mg/dl

To correct for the bound magnesium fraction:

Corrected [Mg ⁺² ]= Total [Mg ⁺² ] + 0.005( 40-{Albumin})
....where [Mg ⁺²] is in mmol/L
....and where {Albumin}= serum albumin in g/L

 

2.Assess Total Body Magnesium Measurement:....a cumbersome procedure is described (Cl of NA article) involving determination of percent retension (from % urine excretion measurement) of administered magnesium over a 24 hour period. Readers who are interested in the specifics of the procedure are referred to that article.

 

3."Guestimate" Technique:

Any of the following crisis situation should be considered presumptive evidence of hypomagnesemia, possibly warranting treatment, accordingly.

 

Homeostasis...................Causes...............Consequences............Diagnosis..............Treatment

 

 

 

For Ventricular Arrythmias

 

For other Crises:

*(MgSO₄ comes as 50% (500mg/ml; 4.06meq/ml) solution)

 

 

MONITORING TREATMENT OF HYPOMAGNESEMIA:

 

 

 

Homeostasis...................Causes...............Consequences............Diagnosis..............Treatment

 

 

Chronic hypomagnesemia can result for the reasons described earlier...renal tubular diseases, diuretic and other drug therapies (e.g digoxin), in particular. In these cases, it may be prudent to supplement the treatment with oral magnesium . Empirically, a dose of 1-2 meq/kg per day is recommended. Keeping in mind the possibility of adverse effects (unlikely but possible with oral supplementation), rechecking the patient within a week or two after commencement of treatment is also wise.

Note also that many oral preparations of magnesium are cathartic, and can cause diarrhea in some patients. The gluconate salt or amino acid-chelated elemental magnesium forms are usually better tolerated and are, therefore, recommended.

 

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