Whole-body lymphangioscintigraphy and SPECT/CT in children with lymphatic complications after surgery for complex congenital heart disease.

The number of patients surviving repair of complex congenital heart disease (CCHD) has increased due to improved surgical techniques, post operative management and outpatient care. Likewise, this growing patient population has demonstrated an increasing number and complexity of complications involving the lymphatic system. To evaluate the peripheral and central lymphatic system, whole-body lymphangioscintigraphy (LAS) is considered as the initial imaging evaluation of choice. To date, very few publications exist on the value of lymphatic imaging techniques in infants and small children with lymphatic complications following surgery for congenital heart disease. A retrospective review of medical records from 2008 to 2018 was performed for pediatric patients referred for lymphatic complications after CCHD surgery at an academic medical center. LAS and SPECT/CT was performed using intradermal bipedal injections of Tc 99m labeled filtered sulfur colloid, and in some patients also bilateral hand injections, followed by dynamic imaging and whole- body planar imaging typically up to 180 minutes post injection. Clinical decision making and outcomes were recorded. LAS and SPECT/CT were performed without complication in pediatric patients with prior surgery for CCHD. LAS successfully localized various lymphatic abnormalities such as lymphatic obstruction, reflux, and leaks, which were further delineated by SPECT/CT. LAS findings directed further evaluation with more definitive studies, management and prognosis. Five of the ten patients had follow up outcome data - 2 years and up to 10 years. LAS and SPECT/CT are safe and effective techniques for the initial evaluation of lymphatic abnormalities in pediatric patients with CCHD. LAS, particularly with further 3D localization by SPECT/CT, provides functional imaging of peripheral and central lymphatic flow and thus provides guidance for medical therapy, non operative interventional management, and surgical therapy for these diverse, debilitating, and often life threatening disorders.

Neonatal Lymphedema from Thoracic Duct Obstruction Complicating Percutaneous Intravenous Central Catheterization.

Percutaneous intravenous central catheter (PICC) complications are not common and generalized edema and anasarca in neonates as a complication of PICC malposition is even rarer. Documentation of the pathomechanisms of lymphedema in cases of severe anasarca in neonates is not often done. Here we document thoracic duct obstruction as the cause of lymphedema in a neonate with severe nonpitting generalized edema. Most PICC procedures should ideally be guided by point-of-care bedside ultrasound (US), and this precaution may prevent malposition of PICC lines although it will not detect subsequent migration or extravasation.

Frontal ventricular dimensions of the brain in infants and children.

Four hundred computerized tomographic scans of the brain in infants and children from birth to 15 years of age were reviewed. Of these, 142 were judged to exhibit normal ventricular dimensions as determined by the biventricular (V/H) index, the length of a line drawn between the heads of the caudate nuclei (V) relative to the width of the cerebral hemispheres (H) at the same level. When all scans were analyzed collectively, the V/H index followed a Gaussian distribution (mean, .11 +/- .03) [SD]; range, .00 to .20). The index did not increase with advancing age within the pediatric population (0 to 15 years), as it does in adults.

Perioperative neonatal methemoglobinemia and transcutaneous oxygen monitoring.

Two premature neonates who suffered severe perioperative methemoglobinemia are reported. Simultaneous transcutaneous oxygen monitoring revealed adequate blood oxygen tension. Continuous transcutaneous monitoring may give a false sense of security by reflecting normal blood oxygen tension in the absence of adequate oxygen unloading capacity.

Hepatic metabolism of orally administered prostaglandin F2 alpha in suckling and weanling rats.

Suckling (12- to 14-day-old) and weanling (30-day-old) rats were sacrificed 2 h after oral administration of 3H-labeled prostaglandin F2 alpha. Although radioactivity recovered from the stomach and small intestine (including contents) was slightly higher in sucklings (28.3 +/- 3.7%; n = 10) than in weanling rats (21.3 +/- 5.3%; n = 7), the liver of sucklings contained significantly higher amounts of counts (11.0 +/- 1.1 vs. 3.3 +/- 0.5%). Combined column and thin-layer chromatography of liver extracts showed more authentic prostaglandin F2 alpha in sucklings (11.0 +/- 0.5% of the liver counts) than in weanlings (7.0 +/- 1.1%). The liver of suckling rats contained a higher percentage of more polar metabolites (43.3 +/- 1.6 vs. 34.3 +/- 3.0%). These studies demonstrate differences in processing of oral prostaglandin F2 alpha in the early postnatal period.

Indomethacin fails to induce ulceration in the gastrointestinal tract of newborn and suckling rats.

Little is known about the role of oral prostaglandins and maintenance of intestinal epithelial cell membrane integrity in suckling animals. The presence of prostaglandins in milk suggests that they may have potential cytoprotective effects. Thus, experiments were performed to determine whether indomethacin causes inflammation in the gastrointestinal tract of suckling animals. Rats were treated with daily intraperitoneal injections of indomethacin (10 mg/kg) starting on the 1st day of life. Unlike adult animals which develop intestinal lesions within 72 h, these rats did not develop intestinal ulcerations until weaning started on days 15 to 16. Indomethacin-treated suckling animals prevented from weaning did not develop intestinal lesions until they had access to solid food on day 23. Indomethacin-treated rats had large reductions in jejunal prostaglandin E2 content. In addition, prostaglandin E2 was present in rat milk in relatively large concentration as determined by radioimmunoassay. These studies suggest that exogenous prostaglandins present in milk may protect the intestine of suckling rats from indomethacin-induced inflammation; however, once weaning commences, prostaglandin insufficiency may develop leading to intestinal lesions. We speculate that suckling rats treated with indomethacin did not develop ulcerative lesions, despite a marked reduction in intestinal prostaglandin content, possibly due to prostaglandins present in milk.

Gastrointestinal processing of gastrically administered prostaglandin F2 alpha in suckling and weanling rats.

In view of the presence of prostaglandins in milk, studies were performed to determine if maturational differences are present in the gastrointestinal processing of exogenous prostaglandin F2 alpha. Suckling (10- to 14-day-old) and weanling (30-day-old) rats were gastrically fed 3H-labeled prostaglandin F2 alpha and killed 2 h later. Characterization of radioactivity present in the stomach from animals of both age groups revealed low prostaglandin F2 alpha metabolism. Analyses of proximal, middle, and distal intestinal segments revealed age-related differences in prostaglandin metabolism. The amount of unmetabolized PGF2 alpha in intestinal segments of suckling rats ranged from 11.4 to 13.5%. In weanling rats, there was a tendency toward increased amounts of intact PGF2 alpha in proximal (16.3 +/- 1.6%) and middle (17.6 +/- 2.2%) regions; however, 25.9 +/- 1.9% of the tissue radioactivity present in the distal small intestine of weanling rats was authentic PGF2 alpha, significantly greater than that of the distal segment of suckling rats. The intestine of weanling rats contained greater amounts of less polar metabolites. These results indicate that orogastrically fed prostaglandin can pass through the gastrointestinal tract of developing rats and be delivered to the distal intestinal mucosa intact.

Epidermal growth factor potentiates cortisone-induced cleft palate in the mouse.

Epidermal growth factor (EGF) injected into pregnant mice increased the frequency of cleft palate (CP) in cortisone-treated mouse fetuses. EGF alone produced proliferation and thickening of the epithelium of the palatal processes, but CP was not significantly increased over saline injected controls. Cortisone alone produced thinning of the palatal epithelium and caused CP in 61 percent of formed fetuses. The combination of EGF and cortisone treatment induced CP in 100 percent of formed fetuses; epithelial thickening still occurred with the combination treatment. Thus, EGF may be teratogenic under special circumstances. These observations suggest that the relative thickness of the palatal shelf epithelium may not be a critical factor in the fusion of the palatal shelves.

In vitro intestinal processing of prostaglandin F2 alpha in rats: developmental aspects.

Cytoprotective prostaglandins (PGs) such as PGF2 alpha are present in milk and can be absorbed intact from the gastrointestinal tract. Developmental differences in gastrointestinal PG metabolism in vivo have been previously reported. To evaluate the role of small intestinal tissue, detailed analysis of PG processing in vitro of small intestinal segments of suckling and weanling rats using everted sacs was performed. Sacs were incubated in Krebs-Ringer bicarbonate buffer, pH 7.4, at 37 degrees C. Bathing mucosal fluid contained [3H]PGF2 alpha. Proximal and middle intestinal segment everted sacs of suckling rats exhibited greater transfer of radioactivity in comparison with those of weanling rats. Whereas in suckling rats transfer of radioactivity decreased from proximal to distal regions of the intestine, no segmental differences were seen in weanlings. Maturational differences were also present in the capacity for PG catabolism. Suckling rat everted sacs had a greater proportion of radioactivity present as intact, unmetabolized PGF2 alpha present in sac tissue and serosal fluid in all intestinal segments in comparison with those of weanling rats. Weanling everted sacs contained greater amounts of less polar metabolites. These results indicate that there are quantitative and qualitative age-related differences in transfer and processing of exogenous PGF2 alpha in small intestinal tissue of developing rats.

Intact biliary excretion of gastrically administered prostaglandin F2 alpha in rats: developmental differences.

Tritium-labeled prostaglandin F2 alpha was administered via orogastric tube to bile duct-cannulated suckling and weanling rats to determine if maturational differences were present in the biliary excretion of prostaglandin F2 alpha and metabolites. Animals were killed 2 h after radioactivity administration. Characterization of radioactivity present in bile revealed age-related differences in biliary prostaglandin F2 alpha excretion. Suckling rats had a greater proportion of radioactivity migrating in chromatographic regions of greater polarity than prostaglandin F2 alpha. Compared with the weanling, a significantly greater amount of radioactivity cochromatographed with intact, unmetabolized prostaglandin F2 alpha (33.08 +/- 1.99 vs. 21.38 +/- 1.46). These results indicate that orogastrically administered prostaglandin F2 alpha can be absorbed from the gastrointestinal tract, transported to the liver, and subsequently excreted into bile and detected in an unmetabolized form in suckling and weanling rats. The enterohepatic circulation of milk-derived prostaglandin present in bile may contribute to the overall content of intestinal prostaglandins.

Prostaglandin stability in human milk and infant gastric fluid.

Prostaglandins are present in breast milk and may protect and maintain intestinal epithelial cell integrity in developing mammals. In view of their very short half-life in other body tissues and fluids, studies were performed to determine prostaglandin stability in milk and gastric fluid. Tritiated prostaglandins E2 and F2 alpha were incubated for 30 min in whole milk, milk cells, and milk plasma obtained from mothers delivering at term and prematurely, and in preterm infant gastric fluid. Radioactivity chromatographic analysis revealed minimal degradation of PG in milk preparations and gastric fluid. Thus, milk may serve as an effective natural medium for PG delivery to the gastrointestinal tract. The cytoprotective effect of prostaglandins on the gastrointestinal tract may be related to their stability and lack of degradation in milk and gastric digestive juices.