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May 1944


Author Affiliations

From Sarah Morris Hospital for Children and the Department of Metabolism and Endocrinology of Michael Reese Hospital.

Am J Dis Child. 1944;67(5):360-364. doi:10.1001/archpedi.1944.02020050022004

Of the convulsive disorders none is more severe than tetanus. Its victim is conscious (except in the terminal stages) and suffers excruciating pain from generalized spasms so violent as frequently to cause compression fractures of the vertebrae. When these convulsions involve the respiratory muscles, as they commonly do, sudden death from acute asphyxia may ensue. Although the ultimate cause of death in tetanus may be organic changes in the brain1 or inhibition of some vital enzymatic action,2 the immediate cause appears clinically to be either respiratory spasms or a terminal aspiration bronchopneumonia.

The active treatment of tetanus is twofold and consists specifically in the injection of tetanus antitoxin to neutralize the unbound circulating toxin and symptomatically in the administration of sedatives (such as solution of tribromoethanol or one of the barbiturates) or anticonvulsants (magnesium sulfate, for example) to control the spasms. Unfortunately the administration of tetanus antitoxin does

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