Etiology

Tetany is a disease whose etiology is incompletely understood. It was originally associated with calcium deficiency and more recently with magnesium deficiency, although it can also be produced by alkalosis. The disease can follow the removal or incapacity of the parathyroid glands and can be a complication of alcoholism and a consequence of prolonged diarrhea and vomiting. Protein-energy malnutrition (PEM) may also precipitate the disease.

As a rule, neonatal tetany strikes during the first 14 days of life, and the spasms, twitches, rigid body, and turned-down corners of the mouth (carp mouth) that it produces are nearly identical to the symptoms of neonatal tetanus. Full-term newborn infants generally have significantly higher levels of serum calcium than do their mothers. However, these levels fall rapidly during the first 2 or 3 days of life, and perhaps the high phosphorus content of cow's milk places the bottle-fed baby at special risk from tetany because it impairs the alimentary absorption of calcium. Another contributing factor is, doubtless, parathyroid immaturity, whereas still another can be the poor nutritional status of the mother. Maternal tetany can develop in malnourished and muciparous mothers whose serum calcium falls with each succeeding pregnancy. Thus there is a positive correlation among frequent pregnancies, maternal dietary deficiency, and hypocalcemic (or hypomagne-semic) convulsions in infants.

At greatest risk are infants born prematurely, born with low birth weights, and born of muciparous or diabetic mothers as well as those who are products of a difficult labor. Males are much more susceptible than females, suggesting that an androgen may be involved. The peak incidence of neonatal tetany for full-term infants occurs about the sixth day of life, and the disease seldom appears before the third day. In those who are born prematurely or whose mothers suffered a difficult birth, the condition frequently develops within the first 24 hours.

Infantile tetany, the most common form of the disease, occurs chiefly between 6 months and 2 years of age and is the most prevalent between 4 and 8 months of age. As with neonatal tetany, males again predominate among the victims, and bottle-fed babies are at substantially greater risk than their breast-fed counterparts. In neonatal tetany, vitamin D has the para doxical effect of raising the incidence of hypocalcemia, perhaps because of its suppressive effect on the parathyroid glands. But a deficiency of vitamin D to promote the absorption of calcium is strongly implicated in the etiology of infantile tetany, and indeed, evidence of rickets is nearly always present. The disease is much more frequent during the winter months when sunlight and, thus, vitamin D are in shortest supply. Because of pigment, black children in temperate zones have in the past proved the most susceptible to rickets during these months. Doubtless they are also more susceptible to infantile tetany than are their white counterparts.

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