Patency of the ductus arteriosus after birth: a new theory.

The cause of patent ductus arteriosus has not yet been established. Spitzer1 in his ontogenetic and phylogenetic explanation considers patent ductus arteriosus as a simple malformation due to an arrest of development. He was not aware that patency of the ductus can be accompanied by severe pulmonary hypertension (so-called reversed ductus) ‘ 5 7 even though in most cases the pressures of the lesser circulation are normal or slightly elevated.8’ #{176} 10 While his interpretation could be applied to the presence of isolated, uncomplicated ductus, there is no stage of normal development which corresponds to the conditions found in ductus with pulmonary hypertension. Kennedy ’ in 1942 stated that “uncomplicated persistent patency of the ductus should not be regarded as malformation, but should be attributed to defective oxygenation of the blood during birth or shortly after.” Several subsequent publications’2’ 13. 14, 1 demonstrated fetal distress at birth and shortly after birth in a great number of the cases of patent ductus which were investigated. In statistical studies performed by Alzamora and co-workers,’5 the occurrence of patent ductus in children born above 9,000 feet is strikingly high. Experimental studies also give’ ’ 12 good evidence that asphyxia at birth may delay the closure of the ductus. Undoubtedly, as Record and McKeown’2 state: “these observations . . . do not dispose of the objection that closure might be expected to follow relief of embarrassment unless the possibility of closure is limited to a short period after birth.” It has been shown that the ductus may be obliterated many months after birth, even in the presence of anoxia, like in cases of tetralogy of Fallot,17 but this observation may not have direct bearing on the normal mechanism of closure. Spontaneous closure of the ductus has been described by several observers many months, and even years, after birth.’8’ 20