Myonecrosis in umbilical cord and chorionic plate blood vessels

Abstract

Objectives: The term myonecrosis is used to refer to necrotic/degenerative changes of the myocytes in the vessel walls of the umbilical cord and/ or in the chorionic plate. Myonecrosis is usually considered to be a consequence of meconium toxicity in cases of prolonged meconium exposure. However, degenerative changes of the myocytes may also occur in the absence of meconium due to autolysis of the umbilical cord and fetal surface vessels after intrauterine fetal death. We hypothesized that the patterns of myonecrosis in these two instances would differ with changes of meconium myonecrosis involving the portions of vessel walls adjacent to the amniotic cavity, the outer layers of the vessel walls more than the inner layers and the arteries (carrying less well oxygenated blood) more than the veins. This preferential patterning was not expected to be seen in autolysis. Methods:We examined the umbilical cord vessels of the placentas from 10 stillborn term fetuses with myonecrosis to determine its distribution. As a control group we used 4 term fetuses terminated by KCl injection because of severe brain anomalies. The location and extent of myonecrosis was assessed by dividing each umbilical cord vessel into 4 quadrants, two facing the amniotic cavity and two towards the centre, and then applying a semi-quantitative score to evaluate the extent. Results:Myonecrosis involved the arteries affecting first the portion of the vessel wall facing the amniotic cavity and extending from the outer to the inner layers. The vein wall showed the same pattern, but tended to be spared in the quadrants towards the centre of the cord. Meconium laden macrophages were only abundant in Wharton's jelly in two cases. In the other cases, myonecrosis presented with a variable degree of involvement of inner and outer vessel wall involving the whole vessel circumference. Myonecrosis in the chorionic plate was seen in 3/10 cases and was only seen in association with meconium. The history in some of the stillbirth cases without meconium pointed to hypoxic ischemic conditions in utero as causing or contributing to myonecrosis. In 2/4 KCl control cases the cord vessels showed degenerative changes involving the whole circumference, but in the other two, myonecrosis was present in the quadrants facing the amniotic cavity with a variable degree of extension through the wall. Conclusion: We conclude that myonecrosis may or may not be associated with meconium and, whether associated with meconium or autolysis alone, its location and extension also reflect oxygen levels in the fetal blood and in the amniotic fluid.