"My Whole Body is Cramping, I ?m Weak and I Cannot Eat"

Estak Choudhury, MD and Thomica James, MD

July 01, 2003

EKG Interpretation
The EKG shows a sinus tachycardia with a rate of 114 beats per minute. The corrected QT interval is prolonged with a length of 0.522 seconds. Given the patient?s presentation and physical exam results, hypomagnesemia and hypocalcemia were suspected as the primary cause of her condition as described above.

The neurological exam was repeated and revealed a positive Chvostek sign that caused trismus, and Tousseau sign that caused carpopedal spasm. The patient received MgSO2, two grams I.V. over 15 minutes.

Laboratory Results

Magnesium	0.5mEq/L
Phosphate	4.8mg/dl
Calcium	5.5mg/dl
Corrected Calcium	7.0mg/dl
Albumin	5.5 g/dl
Sodium	133mmol/L
Potassium	3.9mmol/L
Chloride	92mmol/L
Bicarbonate	22mmol/L
BUN	10mg/dl
Creatinine	1.2mg/dl
Parathyroid hormone	104pg/ml (reference 12-72pg/ml)

Summary
Noteworthy points of this case include symptoms of low serum magnesium manifested by muscle tremors and fasciculations, tetany, seizures and dysphagia that prevented the patient from eating. All these signs and symptoms are manifestations of hypocalcemia and hypomagnesemia.

Hypomagnesemia is common in alcoholic patients admitted to the hospital. One study demonstrated a prevalence of 30%. Almost half of these patients had excessive renal excretion of magnesium most likely due to alcohol-induced tubular dysfunction. Magnesium and calcium homeostasis are closely interdependent. Unlike calcium, there is no known hormonal regulation system for magnesium. Common causes of magnesium deficiencies include malnutrition, GI losses, and renal losses. In this case, both calcium and magnesium levels were low, with an elevated PTH level. Hypocalcemia is a classic sign of hypomagnesemia. There is some evidence that hypomagnesemia decreases PTH secretion, which exacerbates hypocalcemia. Also, several findings demonstrate that low magnesium levels creates PTH resistance. PTH induced release of calcium is impaired with magnesium less than 0.8mEq/L, therefore increasing the level of PTH. Decreased PTH may occur later in the illness.

The prolongation of QTc interval is a feature shared by both hypocalcemia and hypomagnesemia. Other EKG changes that can occur with hypomagnesemia include prolongation of PR interval, ST segment depression, T-wave inversion, flattening or inversion of precordial P waves, widening of QRS, torsades de pointes, refractory atrial fibrillation (and other arrhythmias), and worsening of digitalis toxicity. EKG changes with hypocalcemia may include terminal T-wave inversion, heart blocks and ventricular fibrillation.

Treatment of symptomatic hypomagnesemia is MgSO4, one to two grams I.V. over 15 minutes. If torsades de pointes is present, administer MgSO4, two grams I.V. over one to two minutes. If seizures are present, administer MgSO4, two grams, I.V. over 10 minutes. Calcium gluconate administration (one gram) is usually appropriate because most patients with hypomagnesaemia are also hypocalcemic.

Pearls

• Hypomagnesemia is common in alcoholic patient because of associate malnutrition and renal losses.
• EKG can assist in suggesting a diagnosis of hypomagnesemia and hpocalcemia in a seizing alcoholic or malnourished patient.
• Intravenous MgSO4 should be administered to the hypomagnesemia symptomatic patient if no contraindication exists.

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