There is increasing adjunctive use of AE in patients managed both operatively and nonoperatively. Intra-abdominal complications are common in these salvaged patients with severe liver injuries. Those patients that underwent early-AE received significantly fewer blood transfusions and more commonly had sterile hepatic collections. Only 26% of patients required liver-related surgery after AE. Therefore, the integration of AE as an adjunctive modality for patients with high-grade liver injuries is a safe and effective therapeutic option.

Hepatofugal flow (ie, flow directed away from the liver) is abnormal in any segment of the portal venous system and is more common than previously believed. Hepatofugal flow can be demonstrated at angiography, Doppler ultrasonography (US), magnetic resonance imaging, and computed tomography (CT). The current understanding of hepatofugal flow recognizes the role of the hepatic artery and the complementary phenomena of arterioportal and portosystemic venovenous shunting. Detection of hepatofugal flow is clinically important for diagnosis of portal hypertension, for determination of portosystemic shunt patency and overall prognosis in patients with cirrhosis, as a potential pitfall at invasive arteriography performed to evaluate the patency of the portal vein, and as a contraindication to specialized imaging procedures (ie, transarterial hepatic chemoembolization and CT during arterial portography). Hepatofugal flow is generally diagnosed at Doppler US without much difficulty, but radiologists should beware of pitfalls that can impede correct determination of flow direction in the portal venous system.

SummaryWe have addressed the restriction elements involved in the interaction of lamina propria lymphocytes (LPL) and intestinal epithelial cells using the model of primary mixed cell culture reaction. Whereas peripheral blood T cells proliferate in response to both allogeneic non T cells and class II antigen-bearing intestinal epithelial cells (non T cells >> epithelial cells), LP T cells appear to proliferate preferentially in response to intestinal epithelial cells. The interaction between these cells does not appear to be restricted by conventional products of the major histocompatibility complex as neither monoclonal antibodies to class I nor to class II antigens inhibit the mixed cell cultures, whereas they are inhibitory in conventional mixed lymphocyte reactions. Furthermore, treatment of epithelial cells with interferon 3/fails to augment the cells' ability to induce proliferation of LPL while successfully enhancing proliferation of peripheral blood T cells in parallel cultures. Taken together, these data suggest that alternate restriction elements or mucosa-specific accessory molecules may exist on intestinal epithelial cells that are preferentially recognized by LPLs. Such a distinct regulatory network may be critical to the maintenance of immunologic homeostasis in the gut.