Hypomagnesemia in relation to digoxin intoxication in children

Singh, Ram B.; Dubé, Karine; Srivastav, Priyanka

doi:10.1016/s0002-8703(76)80248-7

Cited by 29 publications

(15 citation statements)

References 18 publications

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“…Hypokalaemia has been a relatively common finding, but recent studies suggest that a high level of awareness of this has led to widespread treatment of patients receiving digoxin with potassium supplements or potassium sparing drugs. Hypomagnesaemia may now be more common than hypokalaemia in adults (Whang et al, 1985), children (Singh et al, 1975) and the elderly (Martin et al, 1988) who are being treated with digoxin.…”

Section: Discussionmentioning

confidence: 99%

Magnesium status and digoxin toxicity.

Young,

Goh,

McKillop

et al. 1991

Brit J Clinical Pharma

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1. Eighty‐one hospital patients receiving digoxin were separated into groups with and without digoxin toxicity using clinical criteria. Serum digoxin, sodium, potassium, calcium, creatinine, magnesium and monocyte magnesium concentrations were compared. 2. Subjects with digoxin toxicity had impaired colour vision (P less than 0.0001, Farnsworth‐ Munsell 100 hue test) and increased digoxin levels (1.89 (1.56‐2.21) vs 1.34 (1.20‐1.47) nmol l‐1, P less than 0.01) (mean (95% confidence limits], though there was considerable overlap between two groups. 3. Subjects with digoxin toxicity had lower levels of serum magnesium (0.80 (0.76‐0.84) vs 0.88 (0.85‐0.91) mmol l‐1, P less than 0.01) and monocyte magnesium (6.40 (5.65‐7.16) vs 8.76 (7.81‐9.71) mg g‐1 DNA, P less than 0.01), but there were no significant differences in other biochemical parameters. A greater proportion of toxic subjects were receiving concomitant diuretic therapy (20/21 vs 37/60, P less than 0.05). 4. Magnesium deficiency was the most frequently identified significant electrolyte disturbance in relation to digoxin toxicity. In the presence of magnesium deficiency digoxin toxicity developed at relatively low serum digoxin concentrations.

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Section: Discussionmentioning

confidence: 99%

Magnesium status and digoxin toxicity.

Young,

Goh,

McKillop

et al. 1991

Brit J Clinical Pharma

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“…The arrhythmogenic dose of acetylstrophanthidin was significantly lower in hypomagnesemia, but normal sinus rhythms were reestablished when magnesium sulfate was administered. Singh et al [4] ob served a 55% incidence ofdigoxin toxicity in hypomagnesemic children who had received furosemide and potassium supplements. Ad ditionally, Singh et al [3] induced hypomag nesemia in dogs via furosemide administra tion and reported a 36% reduction in the ar rhythmogenic dose of ouabain.…”

Section: Discussionmentioning

confidence: 99%

“…However, in addi tion to sodium and water loss, other electro lyte imbalances may develop with this regi men [1], Hypomagnesemia has been demon strated with diuretic therapy, and this condi tion has been associated with altered toxicity of digitalis [2][3][4][5].…”

Section: Introductionmentioning

confidence: 99%

Enhanced Sympathetic Activity as a Mechanism for Cardiac Glycoside Toxicity in Hypomagnesemia

Tackett¹

1986

Pharmacology

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Hypomagnesemia was induced in dogs by administration of furosemide (20 mg/ kg/day) for 7 days. Following replacement of a concomitant loss of potassium, ouabain was infused at 1 μg/kg/min until death. The inotropic response, sustained ventricular arrhythmias, and death all occurred at significantly lower ouabain doses in hypomagnesemic animals than in normomagnesemic dogs. Additionally, hypomagnesemic dogs exhibited an abrupt sympathetic discharge which could be interrupted by bilateral ablation of the stellate ganglia. These results suggest that the neuroexcitatory effects of cardiac glycosides are enhanced during hypomagnesemia.

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“…verapamil or diltiazem). If the patient has a digoxin level above the therapeutic range (0.8-2.0 ng/ml; toxicity >2.4 ng/ml), then temporizing measures depending on the arrhythmia (magnesium, phenytoin, lidocaine) [40] should be used until definitive treatment with digoxin Fab is initiated. Management of calcium channel blocker toxicity may require infusions of calcium gluconate, glucagon, insulin and dextrose.…”

Section: Treating Reversible Causesmentioning

confidence: 99%