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Round ligament varices (RLV) are an important clinical entity as they may cause hernia-like symptoms in the absence of a true hernia. When this condition is diagnosed correctly, unnecessary intervention may be prevented. We aimed to determine the significance and anatomy of RLV in pregnancy and to review and describe their clinical and sonographic appearance. We followed prospectively five patients who presented during pregnancy with clinical symptoms suspicious of an inguinal hernia. All patients were diagnosed with RLV on ultrasound examination. All patients were managed conservatively and in all five cases, RLV resolved spontaneously postpartum. The diagnosis of RLV should be considered in pregnant women presenting with a groin mass. Sonography is diagnostic and can save unnecessary surgical exploration and associated morbidity.

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Percutaneous placement of large-diameter dialysis catheters via the Seldinger technique can be technically challenging in patients with coagulopathy, difficult anatomy, or several previous central line insertions. We describe a method for achieving safer access by combining an open approach to delineate the venous anatomy of the chest wall, with a micropuncture device and smaller diameter guidewire to gain intravascular access to the cephalic vein or its major tributaries. Serial dilation of otherwise unusable vessels can then permit successful and safer hemodialysis catheter insertion in these difficult cases.

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HYPOTHESIS: Cinematic technetium Tc 99m red blood cell ((99m)Tc-RBC) scans, in which real-time scanning is performed and analyzed, can accurately localize gastrointestinal bleeding and thus direct selective surgical intervention. DESIGN: Retrospective medical record review with historical controls. SETTING: Large, university-affiliated public hospital in urban setting. PATIENTS: Twenty-six patients presenting with upper and lower gastrointestinal hemorrhage who underwent cinematic (99m)Tc-RBC scan examinations between 1990 and 1997 and required surgical intervention to control the bleeding. INTERVENTIONS: All patients with gastrointestinal bleeding underwent open surgical procedures to provide cessation of bleeding and resection of appropriate abnormalities. MAIN OUTCOME MEASURES: Patient outcome was based on correlation between preoperative RBC scans and intraoperative findings, surgical pathology, and postoperative clinical course. RESULTS: Twenty-five (96%) of 26 scans were interpreted as positive for gastrointestinal bleeding. In 22 of these 25 scans, the site of bleeding was correctly identified for a sensitivity of 88%. One or more additional diagnostic tests were performed on 19 (73%) of 26 patients, and included angiography and flexible endoscopy. The most common operation performed to control bleeding was a hemicolectomy (14/26). Diverticulosis was the most prevalent diagnosis (46%). Two patients (8%) experienced rebleeding after operation. The overall mortality rate was 19% (5/26). CONCLUSIONS: Cinematic (99m)Tc-RBC scintigraphy is a sensitive, noninvasive alternative to mesenteric angiography for accurately localizing the site of gastrointestinal hemorrhages. As such, this technique can be reliably used to direct selective surgical intervention.

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BACKGROUND: Cirrhosis is characterized by the accumulation of collagen within the extracellular matrix (ECM) of the liver and progressive hepatocellular dysfunction. Since recent studies have shown that the ECM can modulate cellular function, we examined whether the ECM could contribute to hepatocellular dysfunction. To address this question we examined hepatocyte behavior in two different ECM environments. MATERIALS AND METHODS: Primary rat hepatocytes were cultured as a monolayer on collagen or as multicellular aggregates (spheroids) within a laminin-rich ECM. Hepatocytes were then compared for viability, response to proinflammatory cytokines, and their capacity to activate a heat shock response and adopt a thermotolerant phenotype. In addition, we compared the ability of prior heat shock exposure to protect hepatocytes from tumor necrosis factor (TNF) alpha/actinomycin-D-induced apoptosis in the two different ECM environments. RESULTS: Hepatocytes cultured as a monolayer on collagen exhibited decreased viability, underwent spontaneous apoptosis, and displayed an attenuated cytokine-stimulated nitric oxide production compared to hepatocytes cultured as spheroids. In response to heat, hepatocytes in both ECM environments expressed inducible heat shock protein 70 (hsp72). But, only the hepatocyte spheroids exhibited thermotolerance in response to a subsequent thermal challenge. In contrast to previous reports, induction of the heat shock response failed to protect hepatocytes against TNFalpha-induced apoptosis. CONCLUSIONS: These data demonstrate that the ECM can play an integral role in specific hepatocellular behaviors. Furthermore, the progressive deposition of collagen within the ECM, which is characteristic of fibrotic liver diseases, may directly contribute to the progressive hepatocellular dysfunction observed in cirrhosis. Hepatocellular viability, response to proinflammatory cytokines, heat shock response, and thermotolerance were all altered depending on the composition of the ECM. In contrast, TNFalpha-induced apoptosis was independent of the composition of the ECM.

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Bacterial endotoxin (LPS) elicits dramatic responses in the host including elevated plasma lipid levels due to the increased synthesis and secretion of triglyceride (TG)-rich lipoproteins by the liver, and the inhibition of lipoprotein lipase. This cytokine-induced hyperlipoproteinemia, clinically termed the "lipemia of sepsis", was customarily thought to represent the mobilization of lipid stores to fuel the host response to infection. However, since lipoproteins can also bind and neutralize LPS, we hypothesize that TG-rich lipoproteins (VLDL and chylomicrons) are also components of an innate, non-adaptive host immune response to infection. Herein we review data demonstrating the capacity of lipoproteins to bind LPS, protect against LPS-induced toxicity, and modulate the overall host response to this bacterial toxin. Lastly, we propose a pathway whereby lipoprotein-bound LPS may represent a novel, endogenous mechanism for regulating the hepatic acute phase response.

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