519 HYPOTHESIS: CONGENITAL MAGNESIUM (Mg) DEFICIENCY IN THE PATHOGENESIS OF THE RESPIRATORY DISTRESS SYNDROME (RDS)

Abstract

A shock lung is the most visible pathology of severe Mg deficiency in the very young mammal; this hypothesis suggests that RDS is a human counterpart. The mean plasma Mg value of 165 premature infants with RDS was 1.51±0.02 mEq/L. with 76% of values betweeh 1.0 and 1.6 mEq/L (mean, 1.42), despite acidosis or hypoxemia, both of which increase plasma Mg. (The Hospital's normal range for Mg is 1.6-2.2 mEq/L). Low income adolescent multipara, who are at highest risk for RDS infants, are also at high risk for Mg deficiency because of Mg-poor diet and high metabolic demand for Mg during adolescent growth and successive pregnancies. RDS incidence is high in premature infants, with highest rates at the lowest birth weights; infants of mothers with diabetes mellitus (DM);and twins. These, are at risk for Mg deficiency: Prematurity contributes to Mg deficiency, since the Mg concentration of the 20-week fetus is 62% that of the term infant (Widdowson & Dickerson, 1964); DM is associated with urinary loss of Mg.; twins have fetal-fetal competition for Mg. Secondary metabolic effects of Mg deficiency such as hypocalcemia and increased intracellular water and sodium are problems in RDS. Partutition in Mg deficient animals is prolonged and stressed. Stress, plus deficiency in Mg in respect to calcium, favors the release of stored catecholamines and histamine (Douglas, 1968). An exaggerated release of epinephrine and/or histamine leads to acute pulmonary edema, often with hemorrhage. As in anaphylactic shock, the episode is self-limited with a potential for spontaneous resolution or death. Cortisone therapy prior to delivery may be protective.