Umbilical hernia repair in children: is pressure dressing necessary.

The use of pressure dressing to cover the sutured surgical wound is usually considered a routine conclusion to the repair of umbilical hernias in children. The wound is usually left dressed for a minimum of 5-7 days. The main purpose of pressure dressing is prevention of a hematoma formation. The aim of this study was to compare the surgical outcome after umbilical hernia repair in children when the wounds were covered using pressure dressing or left exposed without dressing after the completion of wound closure. Ninety-six patients with umbilical hernia repair were prospectively randomized to receive pressure dressing (n=52) or have their wounds left exposed without any dressing (n=44) after the completion of wound closure. None of the hernias were huge umbilical hernia and none required an umbilicoplasty. In the group who received pressure dressing, one patient developed wound infection 1.9% while no patients developed wound infection in the group who had their wounds exposed without any dressing. In children, there was no significant difference in terms of wound infection, hematoma or seroma formation and recurrence rate after applying pressure dressing or leaving the surgical wounds exposed without any dressing after completion of wound closure. Pressure dressing after umbilical hernia repair may be unnecessary.

Pediatric clean surgical wounds: is dressing necessary?

BACKGROUND/PURPOSE: The covering of the sutured surgical wound with a sterile dressing is usually considered a routine conclusion to an aseptic operation. The wound is usually left dressed for a minimum of 3 to 5 days. The main purpose of dressing is protection of the wound against bacterial contamination that remains a significant source of postoperative morbidity. The aim of this study was to compare the infectious local risk when the clean pediatric surgical wounds were dressed or left exposed without dressing after the completion of wound closure. METHODS: Four hundred fifty-one patients with clean surgical wounds were randomized prospectively to receive dressing (n = 216) or have their wounds left exposed without any dressing (n = 235) after the completion of wound closure. RESULTS: In the group that received wound dressing, wound infection developed in 3 patients (1.4%), whereas in the group that had wounds exposed without any dressing, 4 patients (1.7%) developed wound infection. CONCLUSIONS: In children, there was no significant difference in terms of wound infection after applying dressing or leaving the clean surgical wounds exposed without any dressing after completion of wound closure. Dressing clean surgical wounds may be unnecessary.

Notochord-gut failure of detachment and intestinal atresia.

A spectrum of congenital anomalies have been described in an adriamycin-treated model with common features to the human pattern. Multiple intestinal atresias was part of this spectrum occurring in 25% of full-term experimental rat fetuses. The aim of this study was to examine the underlying developmental mechanism that results in intestinal atresia. Virgin timed-pregnant Sprague-Dawley rats were injected with Adriamycin i.p. at a dose of 2 mg/kg on days 6-9 of gestation. Embryos were removed on different gestational days during organogenesis and serial transverse histologic sections were examined and compared with control specimens. In experimental embryos, hindgut atresia was seen in day 12 embryos. Attachment of the intestine with the notochord was obvious observation resulting in abnormal position of the intestine. In some specimens the atretic intestine was splitting the dorsal aorta or even located behind the dorsal aorta. It is concluded that in the adriamycin-animal model, notochord-intestinal failure of detachment resulted in intestinal atresia during the beginning of organogenesis period. The possible underlying mechanisms are pinching of some endodermal cells as well as interference with normal intestinal circulation resulting in ischemic necrosis.

Single umbilical artery and the VATER-animal model.

BACKGROUND/PURPOSE: Vascular disruption is recognized as a cause of congenital malformations. The authors analyzed the significance of single umbilical artery (SUA) in the Adriamycin-animal model to find out if it was associated with organ malformations. METHODS: Pregnant SD rats were injected with Adriamycin intraperitoneally at a dose of 2 mg/kg on days 6 through 9 of gestation. Serial transverse sections of full-term fetuses were analyzed by light microscopy. Embryos also were removed on different gestational days during organogenesis, and serial transverse histologic sections were examined and compared with suitable controls. RESULTS: In experimental embryos (n = 47), presence of a SUA resulted from either persistence of the primitive umbilical arteries that joined each other ventral to the hind gut to give rise to one umbilical artery or from secondary atrophy of one of the definitive umbilical arteries. Malformations such as intestinal atresia were associated with anomalous fusion between the dorsal aorta and the persistent primitive umbilical arteries. CONCLUSIONS: SUA is a prominent feature of the Adriamycin-animal model. No obvious association was found between malformations and SUA that resulted from atrophy of one of the definitive umbilical arteries; however, it was associated with anomalies such as intestinal atresia when it resulted from persistence of the primitive umbilical arteries.

Embryogenesis of tracheo esophageal anomalies: a review.

The embryology of the normal esophagus and trachea is controversial. There are two main opinions regarding the role played by the tracheoesophageal (TE) septum. Similar controversy exists in explaining the embryology of anomalous TE development, mainly due to a lack of embryos demonstrating these anomalies at critical stages during development. Proposed theories can be divided into four main groups: intraembryonic pressure; epithelial occlusion; differential growth; and vascular occlusion. More recently, a new theory has been described based on analysis of anomalous TE development in adriamycin (doxorubicin)-exposed rat embryos. Impaired tracheal development, with the foregut developing into the trachea rather than the esophagus and associated with development of a dorsal pouch from the upper part of the foregut, gave rise to esophageal atresia with distal TE fistula. On the other hand, development of a ventral upper foregut pouch led to tracheal atresia. A laryngotracheo-esophageal cleft may result if no upper foregut pouches develop, with differentiation of the ventral half of the foregut into trachea and the dorsal half into esophagus. This review describes the basic theories of normal and abnormal TE development in mammalian embryos and presents new data related to this abnormality.

Embryogenesis of adriamycin-induced hindgut atresia in rats.

It was proposed that the pathogenesis of multiple intestinal atresias (MIA) in human fetuses is a consequence of malformative processes of the gastrointestinal tract rather than an ischemic process. Recently, MIA has been described in adriamycin-exposed rat fetuses. The aim of this study was to describe the embryogenesis of hindgut atresia (HA) in the adriamycin animal model. Timed-pregnant Sprague-Dawley rats were injected with adriamycin on days 6-9 of gestation. Embryos were removed on different gestational days during organogenesis and histologic sections were examined and compared with control specimens. In experimental embryos, HA was seen on day 13; however, the lumen was patent on day 12. HA was associated with abnormal vascular anatomy that was obvious on days 12 and 13. It is concluded that HA in adriamycin-exposed embryos occurs at the beginning of organogenesis. Although it was associated with an obvious vascular anomaly, further studies are required to find out whether it is ischemic in origin.