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Calcified catheter "cast" found on radiologic studies after central venous catheter removal is a rare complication that has been reported twice. Both cases were associated with thrombus. In this case report, we present a 15-year-old boy with acute lymphoblastic leukemia who demonstrated on CT scan a radiopacity in his left brachiocephalic vein after removal of an implanted venous access device. This was initially thought to be a retained catheter fragment. Diagnostic studies, including venogram, excluded the presence of a retained catheter fragment. Additional procedures to retrieve a nonexistent catheter fragment were thus avoided. Therefore, a catheter "cast" should be considered as part of the differential diagnosis when calcification is found on an imaging study after removal of an implantable venous access device to prevent an unwarranted surgical exploration.

Children with acquired immunodeficiency syndrome (AIDS) are at an increased risk for lymphoproliferative and neoplastic disorders. Included among these are smooth muscle neoplasms such as leiomyomas and leiomyosarcomas. There have been at least 15 reported cases of smooth muscle tumors in the approximately 8,000 children with AIDS, however the incidence in immunocompetent children is only two per ten million. The lesions in children with human immunodeficiency virus infection are usually found in the lung, liver, and gastrointestinal tract. Here, we present an unusual case of a 12-year-old African American girl with vertically acquired AIDS who presented to the pediatric emergency department with severe diffuse abdominal pain. She was ultimately found to have an appendiceal leiomyoma on abdominal exploration, the first reported case. Our report suggests that smooth muscle tumors of the appendix be included in the differential diagnosis of abdominal masses in children with AIDS.

Persistent interstitial pulmonary emphysema (PIPE) is a syndrome characterized by air-leakage in the perivascular tissues of the lung, primarily affecting mechanically ventilated neonates. Reports in the literature of infants developing PIPE with no history of respiratory distress syndrome (RDS) or mechanical ventilation are scarce. Here, we present a case of a 3-month-old former full term male infant with no history of RDS or mechanical ventilation who presented with focal cystic lung disease associated with spontaneous tension pneumothorax. He was ultimately found to have PIPE based on pathologic evaluation of the resected cystic region. We believe that focal PIPE should be included in the differential diagnosis of cystic lung disease in a full term, unventilated infant, even when spontaneous pneumothorax is the presenting entity.

Bacterial translocation (BT) may be a normal physiologic process that is important for mucosal antigen sampling in the gut. However, physiologic insults such as endotoxemia, hemorrhagic shock, or necrotizing enterocolitis (NEC) may lead to pathologic BT and thus contribute to the pathogenesis of nosocomial infection. The mechanism may involve accelerated enterocyte apoptosis at the intestinal villus apex resulting, at least transiently, in a "bare area" at the villus tip where bacteria can attach and traverse the epithelium. Evidence suggests that sustained upregulation of the inducible isoform of nitric oxide synthase (NOS-2) co-localizes with enterocyte apoptosis and immunoreactivity to 3-nitrotyrosine, the footprint of peroxynitrite (ONOO-), a potent oxidant formed by the reaction of nitric oxide (NO) with superoxide. We propose that the bare area at the villus apex is caused by apoptosis of enterocytes that have migrated from the base of the crypts to the villus apex and are shed into the intestinal lumen. These bare areas, and thus the degree of BT, may be the result of an imbalance between enterocyte proliferation and apoptosis. We postulate that normal enterocyte apoptosis is mediated by the caspase cascade, whereas enterocyte proliferation and differentiation in the crypt may be regulated by tyrosine kinase-dependent signaling pathways. Both of these cellular pathways may be influenced by overproduction of NO and its metabolite ONOO-. Therefore, sustained NO production and ONOO- formation occurring in inflammatory states may differentially accelerate apoptosis in the villus apex and/or inhibit proliferation at the base of the crypts resulting in expanded extrusion zones at the villus tip and accelerated BT.

Nitric oxide (NO) appears to play a paradoxical role in intestinal physiology. Although NO has potent bactericidal effects, a growing body of evidence suggests that it mediates intestinal injury and breakdown of gut barrier function. Data from our lab and others show an increased incidence of bacterial translocation following endotoxin challenge, and upregulation of inducible NO synthase (iNOS) mRNA and protein in the intestine. These phenomena co-localize with enterocyte apoptosis at the tips of the intestinal villi and immunoreactivity to nitrotyrosine. Electron microscopy reveals swollen mitochondria, implicating these organelles as putative targets for NO or its reactive nitrogen intermediates. We review some of the literature and discuss our current work in trying to define this mechanism.