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Hypermagnesemia-induced multiorgan failure

2000; Elsevier BV; Volume: 108; Issue: 8 Linguagem: Inglês

10.1016/s0002-9343(00)00403-4

1555-7162

Behzad Razavi, Douglas Somers,

Pharmacological Effects and Toxicity Studies

A 71-year-old man was hospitalized for lethargy, vomiting, and a 3-day history of decreased colostomy output. Four years earlier he had been diagnosed with rectal adenocarcinoma and was treated with surgery, chemotherapy, and radiation therapy. He had a history of hypertension, for which he was treated with hydrochlorothiazide (12.5 mg daily); he was not taking any other medications. On admission, he was afebrile, his blood pressure was 180/66 mm Hg, his pulse was 95 beats per minute, and his respiratory rate was 20 breaths per minute. Examination of the skin, head, heart, and lungs was normal. The abdomen was distended and nontender; bowel sounds were absent. Neurologic examination showed generalized weakness and diminished deep tendon reflexes. Laboratory studies revealed a hematocrit of 42% and white blood cell count of 20.0 × 109/L with a left shift. Serum levels were calcium 8.1 mg/dL, sodium 128 mEq/L, potassium 2.3 mEq/L, chloride 65 mEq/L, bicarbonate 54 mEq/L, blood urea nitrogen 28 mg/dL, and creatinine 2.8 mg/dL. Four days before admission, his blood urea nitrogen level was 20 mg/dL and his serum creatinine level was 0.7 mg/dL. Thyroid function tests, serum aminotransferase levels, a urine toxicology screen, and a urinalysis were normal. An abdominal radiograph showed an ileus pattern. An electrocardiogram was unremarkable. Room-air arterial blood gas studies revealed a pH of 7.62, a pCO2 of 43 mm Hg, a pO2 of 50 mm Hg, and a bicarbonate of 50 mEq/L. A chest radiograph showed left lower lobe pneumonia. The patient was given saline, potassium chloride, and ceftriaxone. Ten hours after admission, he was hypotensive, stuporous, hypoventilating, and areflexic. Repeat arterial blood gas studies showed a pH of 7.54, a pCO2 of 71 mm Hg, a pO2 of 69 mm Hg, and a bicarbonate of 59 mEq/L on 2 L/min of oxygen. The serum magnesium level was 9.0 mEq/L. His hypermagnesemia was treated with hemodialysis, as he was also severely hypokalemic. After a 4-hour dialysis, the patient was awake with normal tendon reflexes, and his serum magnesium level was 4.2 mEq/L. He then revealed that he had been taking milk of magnesia for 2 weeks. His ileus resolved, and he was discharged 5 days later with a serum creatinine level of 0.7 mg/dL and a serum magnesium level of 1.3 mEq/L. Magnesium acts as a calcium channel blocker, causing cardiac conduction delay and hypotension (1Golzarian J. Scott H.W. Richards W.O. Hypermagnesemia-induced paralytic ileus.Dig Dis Sci. 1994; 39: 1138-1141Crossref PubMed Scopus (54) Google Scholar). Hypermagnesemia causes neuromuscular blockade by inhibiting the release of presynaptic acetylcholine, which results in flaccid paralysis and respiratory depression (1Golzarian J. Scott H.W. Richards W.O. Hypermagnesemia-induced paralytic ileus.Dig Dis Sci. 1994; 39: 1138-1141Crossref PubMed Scopus (54) Google Scholar). Although hypermagnesemia can cause decreased peristalsis (2Hill W.C. Gill P.J. Katz M. Maternal paralytic ileus as a complication of magnesium sulfate tocolysis.Am J Perinatol. 1985; 2: 47-48Crossref PubMed Scopus (17) Google Scholar), paralytic ileus has been rarely reported (1Golzarian J. Scott H.W. Richards W.O. Hypermagnesemia-induced paralytic ileus.Dig Dis Sci. 1994; 39: 1138-1141Crossref PubMed Scopus (54) Google Scholar). Hypermagnesemia is most common in patients with renal insufficiency who take magnesium-containing antacids and laxatives. Increasing blood levels of magnesium correlate with specific clinical signs. Drowsiness and hyporeflexia occur at a serum magnesium level >4.0 mEq/L; PR, QRS, and QT interval prolongation may occur with concentrations as low as 5.0 mEq/L; somnolence and hypotension occur at 6.0 to 7.0 mEq/L; and paralysis of voluntary muscles and areflexia occur at 10 mEq/L. Hyporeflexia indicates the severity of hypermagnesemia and predicts cardiac and respiratory toxicity. Severe cases of hypermagnesemia should be treated with parenteral calcium to reverse cardiovascular and respiratory toxicity (3Van Hook J.W. Hypermagnesemia.Crit Care Clin. 1991; 7: 215-223PubMed Google Scholar). Dialysis may be life-saving in patients with renal failure or massive overdose (3Van Hook J.W. Hypermagnesemia.Crit Care Clin. 1991; 7: 215-223PubMed Google Scholar, 4Oren S. Rapoport J. Zlotnik M. et al.Extreme hypermagnesemia due to ingestion of Dead Sea water.Nephron. 1987; 47: 199-201Crossref PubMed Scopus (19) Google Scholar). Our patient had no history of chronic renal insufficiency. Hyponatremia and metabolic alkalosis may have contributed to his ileus, but the laboratory and clinical course suggests that hypermagnesemia caused neurologic, respiratory, renal, and gastrointestinal toxicity, all of which were successfully treated with hemodialysis.