We report a case of fatal hypermagnesemia in a 53-year-old woman admitted for acute exacerbation of chronic obstructive pulmonary disease and with a history of chronic constipation treated regularly with magnesium-containing laxatives. On admission, her magnesium level was 2.0mg/dL, which rose to a peak of 10.8mg/dL despite hydration and diuresis in the presence of a normal kidney function. Continuous renal replacement therapy was promptly initiated, which reduced her serum magnesium levels, but her condition continued to deteriorate precipitously progressing to shock leading to oligoanuric renal failure, and she died 2 days later. A review of the literature shows that though rare and often unsuspected, severe hypermagnesemia frequently results in death even in individuals with normal renal function despite renal replacement therapy. In patients with constipation, retention of magnesium-based laxative in the gut apparently serves as a reservoir for continuous magnesium absorption and contributes to mortality.

Short bowel syndrome (SBS) is the predominant cause of intestinal failure and is thus associated with a high degree of morbidity and mortality. One of the reasons this occurs is the dramatic reduction in nutrient absorptive capacity. Of the many causes of SBS, the most common cause is extensive surgical resection. The impressive ability of the bowel to adapt functionally and morphologically is critical for decreasing morbidity and mortality in these patients. The degree of adaptation is vital in decreasing the dependence on parenteral nutrition (PN) and for improving patient quality of life and long-term outcome. Provision of appropriate and sufficient nutritional and fluid support is essential for the management of these patients. The primary goal is to prevent or eliminate the need for PN. Recent developments have promoted a greater understanding of the process of intestinal adaptation. Various intestinal trophic factors have been recognized. These efforts have led to the early development of hormonal therapy to stimulate intestinal adaptation and enhance intestinal absorption. Intestinal transplantation remains an option for those who have developed life-threatening complications from PN and cannot be managed using more conservative techniques.

Hypermagnesemia is a rare cause of coma in a patient with normal renal function. When present, it is often because of iatrogenic medication overdose. We report a fatal case of chronic Epsom salt gargles for halitosis that produced a serum magnesium of 23.6 mg/dL (9.8 mmol/L) and resulted in coma. We review the wide presentation of hypermagnesemia from subtle neurologic and cardiovascular signs to the major life-threatening clinical manifestations of shock, dysrhythmias, coma, and cardiopulmonary arrest despite emergency dialysis.

Magnesium is an essential cation, involved in many enzymatic reactions, as a cofactor to adenosine triphosphatases. It is critical in energy-requiring metabolic processes, as well as protein synthesis and anaerobic phosphorylation. Serum Mg concentration is maintained within a narrow range by the kidney and small intestine since under conditions of Mg deprivation both organs increase their fractional absorption of Mg. If Mg depletion continues, the bone store contributes by exchanging part of its content with extracellular fluid (ECF). The serum Mg can be normal in the presence of intracellular Mg depletion, and the occurrence of a low level usually indicates significant Mg deficiency. Hypomagnesemia is frequently encountered in hospitalized patients and is seen most often in patients admitted to intensive care units. The detection of Mg deficiency can be increased by measuring Mg concentration in the urine or using the parenteral Mg load test. Hypomagnesemia may arise from various disorders of the gastrointestinal tract, conditions affecting Mg renal handling, or cellular redistribution of Mg. The gastrointestinal causes include the following: protein-calorie malnutrition, the intravenous administration of Mg-free fluids and total parenteral nutrition, chronic watery diarrhea and steatorrhea, short bowel syndrome, bowel fistula, continuous nasogastric suctioning, and, rarely, primary familial Mg malabsorption. The renal causes include Bartter's and Gitelman's syndrome, post obstructive diuresis, post acute tubular necrosis, renal transplantation, and interstitial nephropathy. Many therapeutic agents cause renal Mg wasting and subsequent deficiency. These include loop and thiazide diuretics, aminoglycosides, cisplatin, pentamidine, and foscarnet. Magnesium deficiency is seen frequently in alcoholics and diabetic patients, in whom a combination of factors contributes to its pathogenesis. Hypomagnesemia is known to produce a wide variety of clinical presentations, including neuromuscular irritability, cardiac arrhythmias, and increased sensitivity to digoxin. Refractory hypokalemia and hypocalcemia can be caused by concomitant hypomagnesemia and can be corrected with Mg therapy. The dose and route of administration of Mg in the treatment of hypomagnesemia is dictated by the clinical presentation, the degree of Mg deficiency, and the renal function.

This is a case of magnesium intoxication in a neonate produced by an oral magnesium cathartic. A review of the literature revealed there are very few cases that have been reported of magnesium toxicity due to cathartics. There is no recommended dose for magnesium cathartics in neonates or data on their safety. A review of the management of magnesium intoxication is presented.

Concentration and voltage dependence of unidirectional Mg fluxes across the rat colon ascendens were measured in a modified Ussing chamber. Mucosa (M) to serosa (S) Mg flux exhibits a cellular component, whereas SM flux is totally diffusive. At all the concentrations between 0.125 and 8 mmol/liter MS Mg transport is higher than the flux in the opposite direction, resulting in Mg absorption. In contrast to Mg, in Ca transport a cellular component is involved in both directions across the tissue, 1 alpha, 25-Dihydroxyvitamin D3 has no influence on the Mg transport. Mg (5 mmol/liter) remarkably decreases MS Ca flux and reduces Ca absorption by 70%. The parallel decrease in MS Ca flux with that of the simultaneously measured paracellular marker mannitol and the voltage clamp experiments reveal that Mg has no influence on cellular Ca transport but only reduces diffusive MS Ca flux, possibly by decreasing transepithelial fluid absorption. The experiments demonstrate that the colon ascendens of the rat is capable of absorbing Mg at rates comparable to that found for Ca. There is evidence that Mg and Ca are transported by separate cellular mechanisms. Diffusive movement across the paracellular route plays an important role on net transport of both earth alkali ions.

Concentration and voltage dependence of unidirectional magnesium fluxes across the rat descending colon were measured in a modified Ussing-chamber. Mucosa to serosa (ms) magnesium flux exhibits a saturable component, whereas serosa to mucosa (sm) flux is linearly related to the magnesium concentration from 0.125 to 8 mmol/L. At all the concentrations used, ms magnesium transport is higher than the flux in the opposite direction, resulting in net magnesium absorption. Only ms magnesium transport has a voltage-independent, i.e., cellular-mediated component. Magnesium flux from serosa to mucosa, however, is totally voltage-dependent, i.e., purely diffusive and probably constrained to the paracellular pathway. The cellular-mediated fraction of ms magnesium transport is comparable to that found for calcium. Calcium (5 mmol/L) has no influence on ms flux or on the magnesium flux in the opposite direction. Magnesium (5 mmol/L) has no influence on the sm calcium flux but abolishes calcium absorption by decreasing ms calcium flux. The voltage clamp experiments reveal that magnesium has no influence on the cellular-mediated ms calcium transport but exclusively decreases diffusive calcium flux in this direction. Pretreatment with 1 alpha,25-dihydroxyvitamin D3 (250 ng/kg s.c. daily given for 4 days) has no effect on ms magnesium flux but it remarkably stimulates ms calcium transport. These findings suggest that both earth alkaline ions in the descending colon are transported by separate cellular-mediated mechanisms. On the other hand, the similarity of the kinetic parameters as well as the similarity of the voltage-independent ms fluxes would support the assumption that both ions are absorbed by the same mechanism. Hence, the question of whether both ions are absorbed by the same or by distinct transport processes cannot be answered by the present experiments. Diffusive movement across the paracellular route plays an important role in net transport of both ions. Diffusive magnesium flux is equal in both directions. In contrast, for calcium an asymmetry in the paracellular fluxes with a prevalence of the diffusive sm flux over the diffusive fraction of the flux from mucosa to serosa has been reported. The different behavior with respect to the paracellular movement can be explained by the radius of the hydrated magnesium ion, which is smaller than calcium with its hydration shells.

We describe a patient who survived a peak serum magnesium level of 9.5 mmol/L (23.0 mg/dL) after an oral cathartic overdose. The patient presented in coma but regained full consciousness over the next six hours with supportive therapy. His serum magnesium had returned to near-normal levels by the following morning at the time of his hospital discharge. This case represents an unprecedented extent of ingestion-related hypermagnesemia in a surviving patient, given that serum levels of more than 8 mmol/L are frequently associated with death from cardiac arrest.

A wide variety of pharmacologic agents have been implicated in a number of electrolyte disorders. The present review focuses on abnormalities of sodium, potassium, calcium, magnesium, and phosphate. Several mechanisms are involved in the pathogenesis of these disorders. These involve stimulation and modulation of other hormones (e.g., antidiuretic hormone, renin-angiotensin system, parathyroid hormone), damage to renal tubules, and, in some cases, a combination of factors. Recognition of these abnormalities is important because their presence may be life threatening or may aggravate the side effects of the drug itself.

Magnesium imbalance is clinically significant. It is common, treatable, and frequently overlooked. We review the literature describing magnesium deficit and excess syndromes and formulate specific treatment protocols.

The case history of a patient with severe muscular weakness resulting from magnesium intoxication following oral and rectal administration of magnesium citrate cathartics is reported. The findings of the electrophysiologic studies were characteristic of the neuromuscular blockade seen in this disorder, including marked reduction in evoked muscle action potential amplitude which progressively decline on nerve stimulation at low rates, and a striking degree of facilitation of evoked muscle action potential after exercise or on high-frequency stimulation. When the hypermagnesemia was corrected, strength returned to normal.