Evaluation of pectus bar position and osseous bone formation.

PURPOSE: Minimally invasive repair has become a popular approach for pectus excavatum (PE). The bar is secured to the thoracic wall and left for approximately 2 years. The authors have noticed an intense bone formation (BF) around some of these bars at removal. A review of children undergoing bar removal was performed to better understand this BF in relation to bar placement. METHODS: A retrospective review of children undergoing bar removal after PE repair since January 1998 was performed. Chart review included age at bar insertion and removal, bar insertion position (subcutaneous [SC] v submuscular [SM]), BF on Chest x-ray and at bar removal, operating time, and estimated blood loss (EBL). RESULTS: Thirty-six patients underwent bar removal during the study period (16 SC and 20 SM). Chest x-ray evaluation was possible in 27 patients (16 SM, 11 SC). No difference existed for length of time the bar was in place or age at insertion/removal between groups. EBL was higher in the SM (18.3 v 8.8 mL, not significant). BF was seen radiographically in 15 SM and 3 SC patients (P <.001). BF was encountered at removal in 19 SM patients and a single SC patient (P <.001). Operating time was statistically longer (P <.01) for the SM group (30.2 v 15.6 min). CONCLUSIONS: Bar position during repair of PE is important. SM positioning virtually always results in BF with increased EBL and statistically longer operating time at removal. Careful placement of the bar in the SC position without violating the fascia should be used to avoid these undesirable effects.

Fibroblast growth factor signaling in the developing tracheoesophageal fistula.

BACKGROUND/PURPOSE: The Adriamycin-induced rat model of esophageal atresia and tracheoesophageal fistula (EA/TEF) provides a reliable system for the study of EA/TEF pathogenesis. The authors previously hypothesized that faulty branching lung morphogenesis pathways were a critical component of its pathogenesis. The authors have found evidence for faulty fibroblast growth factor (FGF) signaling related to epithelial-mesenchymal interactions in the fistula tract. To better define FGF signaling, the differential expression of FGF ligands and their receptors between lung, fistula tract, and esophagus are described. METHODS: Time-dated pregnant, Sprague-Dawley rats were injected with Adriamycin (2 mg/kg intraperitoneally) on days 6 through 9 of gestation. Tissues were processed for histology and reverse transcriptase polymerase chain reaction. FGF-1, -7 and -10 were measured from whole lung, fistula tract, and esophagus of TEF or normal embryos. Expression of FGF2RIIIb and FGF2RIIIc receptors was measured in isolated epithelium and mesenchyme of lung and fistula tract of TEF embryos as well as lung and esophagus from normal controls. RESULTS: FGF-1 mRNA was present in the fistula tract and normal and Adriamycin-exposed lung but absent from whole esophagus. Interestingly, FGF-7 mRNA was present only in normal lung. FGF-10 was present in all tissues examined. FGF2RIIIb mRNA was absent in fistula mesenchyme but present in all other tissues examined. However, the splice variant FGF2RIIIc mRNA was present in all tissues examined. CONCLUSIONS: These findings support defective FGF signaling in the rat model of EA/TEF. Absence of FGF-7 mRNA in Adriamycin-exposed tissues suggests the primary effect of Adriamycin may be to inhibit FGF-7 expression. Moreover, absence of FGF2RIIIb in fistula mesenchyme may be caused by loss of positive feedback from FGF-7, its normal obligate ligand. Understanding these specific defects in FGF signaling may provide insight into faulty mechanisms of EA/TEF.

Organogenesis particularly relevant to fetal surgery.

In utero surgical intervention is an exciting frontier in medicine. Fetal surgeons strive to treat congenital anomalies definitively while organogenesis is still occurring. Many of these anomalies pose such a threat to the viability of the affected fetus that waiting until after the child is born to treat them is frequently not satisfying and too often unsuccessful. We review the embryology of selected systems that have associated aberrancies of development for which fetal surgery is particularly applicable. The surgeon can more effectively launch an assault against congenital anomalies when armed with a solid appreciation of normal development. Recognizing the critical period for the development of a system allows him or her to formulate the optimal time and mode of intervention.

Complete discontinuity of the distal fistula tract from the developing gut: direct histologic evidence for the mechanism of tracheoesophageal fistula formation.

The embryogenesis of tracheoesophageal anomalies remains controversial. The purpose of this study was to better define the embryogenesis of developing esophageal atresia with tracheoesophageal fistula (EA/TEF), with specific attention to the controversial issue of whether a discontinuity exists in the foregut during its development of EA/TEF. Pregnant outbred rats were injected with adriamycin (2 mg/kg i.p.) on days 6-9 of gestation (E6-E9). At E12.5 and 13.5, microdissection of the entire foregut was performed. Foreguts were examined by phase microscopy, and serial, precisely transverse sections were created for hematoxylin and eosin (H&E) staining. Gross microdissection of the developing foregut at E12.5 (n = 9) revealed a blind-ending, bulbous fistula tract arising from the middle branch of the tracheal trifurcation (as seen by direct and phase microscopy). No connection with the gut could be appreciated at E12.5, but by E13.5 (n = 10) there was an obvious connection between the fistula and the stomach. Serial H&E transverse sections also demonstrated a blind-ending fistula tract arising from the trachea at E12.5. This fistula tract was clearly discontinuous from the developing stomach, which appeared much further caudal to the end of the fistula tract. These results strongly support a model of experimental TEF wherein the fistula tract arises from a trifurcation of the trachea, and (only during a specific gestational window between days 12.5 and 13.5) there is discontinuity between the fistula tract and the stomach. By day 13.5, the fistula joins with the stomach anlage. These observations in the developing EA/TEF should help to resolve the controversy about the mechanism of EA/TEF formation.

Lectin as a marker for staining and purification of embryonic pancreatic epithelium.

The embryonic pancreatic epithelium, and later the ductal epithelium, is known to give rise to the endocrine and exocrine cells of the developing pancreas, but no specific surface marker for these cells has been identified. Here, we utilized Dolichos Biflorus Agglutinin (DBA) as a specific marker of these epithelial cells in developing mouse pancreas. From the results of an immunofluorescence study using fluorescein-DBA and pancreatic specific cell markers, we found that DBA detects specifically epithelial, but neither differentiating endocrine cells nor acinar cells. We further applied this marker in an immunomagnetic separation system (Dynabead system) to purify these putative multi-potential cells from a mixed developing pancreatic cell population. This procedure could be applied to study differentiation and cell lineage selections in the developing pancreas, and also may be applicable to selecting pancreatic precursor cells for potential cellular engineering.