The earliest clinical indication of hypermagnesemia is loss of deep tendon reflexes. States of magnesium excess are characterized by generalized neuromuscular depression. Clinically, severe hypermagnesemia is rarely seen except in those patients with advanced renal failure treated with magnesium-containing antacids. However, hypermagnesemia is produced intentionally by obstetricians who use parenteral magnesium sulfate (MgSO4 ) to treat preeclampsia. MgSO4 is administered until depression of the deep tendon reflexes is observed, a deficit that occurs with modest hypermagnesemia (over 4 mEq/L). Greater elevations of magnesium produce progressive weakness, which culminates in flaccid quadriplegia and in some cases respiratory arrest due to paralysis of the chest bellows mechanism. Hypotension may occur because of the direct aeriolar relaxing effect of magnesium. Changes in mental status occur in the late stages of the syndrome and are characterized by somnolence that progresses to coma.