Vaginal birth after cesarean delivery: results of a 5-year multicenter collaborative study.

Cesarean delivery has become the most frequently performed major operation in the United States. Widespread use of vaginal birth after previous cesarean delivery could potentially eliminate up to one-third of cesareans. However, many physicians have been reluctant to adopt this policy without large studies conclusively demonstrating its safety. This study evaluated the maternal and perinatal outcomes of over 5000 cases of labor after previous cesarean delivery. This multicenter study began in 1984 and initially included nine California hospitals. During the first 2 years, there were 1776 trials of labor resulting in 1314 vaginal births. In January 1986 two additional hospitals joined the collaborative project. Over the next 3 years, there were 3957 trials of labor resulting in 2977 vaginal births at the 11 participating hospitals. During the entire study period, 5733 patients opted for a trial of labor and 4291 (75%) delivered vaginally. There were no maternal deaths in the trial-of-labor group, and perinatal mortality was not significantly different from that of the general obstetric population. These results support the findings of numerous smaller studies that have concluded that the policy of routine repeat cesarean delivery should be abandoned.

Megacolon in myotonic dystrophy caused by a degenerative neuropathy of the myenteric plexus.

A 32-yr-old man with myotonic dystrophy had a left hemicolectomy performed because of a megacolon. The colonic mucosa, smooth muscle, and connective tissue appeared normal by hematoxylin and eosin and trichrome stains and transmission electron microscopy. In contrast, the myenteric plexus had markedly fewer neurons than normal on the hematoxylin and eosin stains. Silver staining of the plexus revealed degeneration and decreased numbers of argyrophilic neurons, which were smaller and had fewer processes and a more uneven staining quality than controls. Many axons were fragmented, and increased numbers of glial cell nuclei were present in the plexus. Degenerative changes in the neurons were present in a patchy distribution on transmission electron microscopy. Immunohistochemistry revealed a decrease of the substance P- and enkephalin-immunoreactive fibers in the muscularis externa. This suggests that colonic motor dysfunction associated with myotonic dystrophy may be caused by a visceral neuropathy that involves the substance P- and enkephalin-immunoreactive fibers of the smooth muscle.

There are no morphologic abnormalities of the gastric wall or abdominal vagus in patients with diabetic gastroparesis.

Because there is evidence for vagal autonomic neuropathy as the cause of diabetic gastroparesis, we hypothesized that this disorder should be associated with morphologic abnormalities of the abdominal vagus nerve or gastric myenteric plexus, or both. We studied the smooth muscle and myenteric plexus of the stomach in 18 nondiabetic controls and 16 patients with long-standing diabetes. Five of the diabetics had gastroparesis and 11 did not. We utilized conventional histology and Smith's silver technique for visualizing the myenteric plexus. Neurons within the myenteric plexus were quantified in sections stained with each technique. The abdominal vagus nerves from 5 diabetics (2 with gastroparesis) and 12 nondiabetic controls were stained with hematoxylin and eosin, Gomori trichrome, luxol-fast blue, and Holmes' silver stains. There were no abnormalities in the numbers or appearance of neurons or axons in the myenteric plexus of the stomach of diabetics, with or without gastroparesis. Also absent were abnormalities of the smooth muscle or vagus nerve. Thus, no morphologic abnormalities of the gastric wall or abdominal vagus were identified in diabetic gastroparesis.