Tissue PO2 and reperfusion injury in the transplanted liver after application of aprotinin.
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Biomedical subjects
Publications and source records attributed to R Pichlmayr.
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The incidence of arterioportal fistulas (APFs) following percutaneous transhepatic procedures is quoted to be between 5 and 20%; the majority of them remain clinically asymptomatic and do not require any treatment. However, an APF large enough to cause a reversal of blood flow in the portal vein is rather uncommon especially in a transplanted liver where it may have potentially hazardous consequences. We report on a 21-year-old female patient who received a liver transplantation on account of a Budd-Chiari syndrome. Following a liver biopsy, a large APF developed in the right lobe of the graft. Despite the known risks associated with catheterization of graft vessels, a successful coil occlusion of the fistula could be carried out thus rendering surgery unnecessary.
The therapy of severe hepatic trauma requires complex surgical procedures. Our current surgical management of these injuries is described, including liver transplantation for the treatment of potentially lethal hepatic trauma.
In order to investigate the diagnostic value in differential diagnosis of primary liver tumors, color Doppler sonography was used preoperatively in 30 patients. Without difference, tumor hypervascularization was found in patients with hepatocellular carcinoma (2 of 4), cholangiocellular carcinoma (4 of 4), hemangioma (3 of 8), focal nodular hyperplasia (8 of 8), adenoma (3 of 4), and neuroendocrine tumor (n = 1). No vascular signal could be detected in 1 case of adenomatous hyperplasia and 2 cases of hepatocellular carcinoma, one after previous chemoembolization. Hemangioma appeared hypo- or even avascular in 5 of 8 patients. Therefore, according to our experience, the yield of color Doppler sonography is rather low for differential diagnosis and prediction of the tumor dignity. With regard to the surgical procedure, valuable information about tumor extension can be obtained particularly in central lesions close to hilar structures or liver vein confluence. Further indications result from follow-up of tumor vascularization after chemoembolization and chemotherapy.
Experimental investigations have shown alterations of the ileal mucosal surface after specific fat diets resembling early changes in Crohn's disease. An animal experiment in pigs has been conducted. After creation of an anisoperistaltic segment these were fed either a specific fat diet containing chemically processed, partially hydrogenated fats or a low fat control diet over a period of 3 months. Defined areas of the ileal lamina propria were examined by transmission electron microscopy with the underlying question to what extent ultrastructural alterations could be compared to Crohn's disease. In comparison to the control group these areas were characterized by a dense infiltration of "inflammatory" cells like lymphocytes, histiocytes, macrophages and plasma cells indicating a hyperplasia and activation of lympho-plasmocytotic cells. Additionally, a focal prominent infiltration of mast cells with degranulation was observed as well as a dilatation of axons with depletion of axonal organelles in half of the animals after fat-feeding. Compared to patients with Crohn's disease the results show obvious similarities. It is concluded, that chemically processed fats could cause direct stimulation of immunologically-specific and non-specific cells in the lamina propria mucosae or directly injure the intestinal mucosa with secondary infiltration of inflammatory cells into the lamina propria.
Recently it has become clear that the inflammatory response of immune cells to target cells and extracellular matrix is regulated by several receptor-ligand molecules. Three main classes of molecules mediating intercellular adhesion and activation processes have been identified: the integrin, immunoglobulin and selectin families. This study surveys the expression of adhesion molecules on resident and infiltrating cells in human liver grafts. The patterns of cellular expression and inducibility in different pathological conditions of the graft are described. Our results show organ-specific regulation of the different adhesion molecules during alloreactive reactions and other types of inflammatory reactions. No rejection-specific patterns were detected on comparison with reperfusion damage or infectious transplant inflammation. Major differences were noted in the composition of the portal tract and sinusoid with regard to endothelial and parenchymal cell expression of cell-cell and cell-matrix adhesion molecules. Intravascular and interstitial differences in the expression patterns of leukocyte adhesion receptors support a concept of stepwise expression. The implications for the appearance of inflammatory reactions in human liver in immunosuppressive and therapeutic interventions are discussed.
BACKGROUND: Cystic enlargement of the extrahepatic bile duct system is a rare abnormal finding. A congenital origin is usually supposed; however, the pathogenesis is unknown. We report on our experience with extrahepatic bile duct cysts with special regard to cause, treatment, and recurrent disease. METHODS: From 1976 to 1991, 13 patients, 35 to 74 years of age, were treated for extrahepatic bile duct cysts. Seven patients had previously undergone cholecystectomy. Two patients were admitted because of recurrent disease; neither had undergone curative resection. RESULTS: In 11 patients a biliojejunal anastomosis with a Roux-en-Y was created after cyst resection; one patient underwent a diverticular stalk resection with end-to-end anastomosis of the choledochal duct. After a mean follow-up of 68 months eight of 10 patients were alive, two of whom complained about cholangitis. Recurrent diffuse dilatation of the remaining choledochus developed in one patient; one other patient died of cholangiocellular carcinoma 2 years after operation. CONCLUSIONS: In patients who had undergone previous cholecystectomy or with recurrent disease an acquired malformation cannot be excluded. Surgical treatment is always indicated because of imminent complications and should aim at complete resection of cystic tissue. Periodic postoperative evaluation is necessary to detect recurrent disease and malignant transformation.
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BACKGROUND: Changes in energy substrate metabolism, as well as those in arterial ketone body ratio (KBR; acetoacetate/3-hydroxybutyrate), were investigated to follow energy status of hepatic allograft. METHODS: Plasma concentrations of energy substrates were measured immediately after 35 orthotopic liver transplantations in 32 adult patients. RESULTS: Twenty-three patients left the intensive care unit within 1 month (group A), six patients were forced to stay in the intensive care unit longer than 1 month (group B), and the other six grafts failed within 1 month (group C). In group B the KBR was significantly lower than in group A 6 hours after reperfusion of the grafts (0.70 +/- 0.09 vs 1.21 +/- 0.10, mean +/- SEM; p < 0.05). In group C the KBR remained significantly lower than in group A at 6 hours (0.65 +/- 0.04 vs 1.21 +/- 0.10; p < 0.01), on the first postoperative day (0.64 +/- 0.03 vs 1.36 +/- 0.10; p < 0.001), and on the second postoperative day (0.65 +/- 0.02 vs 1.58 +/- 0.11; p < 0.01). Total ketone body concentration (TKB) was significantly higher in group B than in group A at 4 hours (462.9 +/- 105.0 mumol/L vs 201.6 +/- 32.6 mumol/L; p < 0.01), 6 hours (483.4 +/- 102.1 mumol/L vs 125.5 +/- 25.9 mumol/L; p < 0.001), and the first postoperative day (481.1 +/- 196.6 mumol/L vs 123.9 +/- 24.1 mumol/L; p < 0.001). No increase in TKB was observed in group C. CONCLUSIONS: It is suggested that low values in KBR accompanied with low levels of TKB should be regarded as a strong indicator of graft failure and fatty acid oxidation and ketogenic pathways are accelerated to compensate for energy deficits in patients with low values in KBR and high levels of TKB until KBR recovers immediately after orthotopic liver transplantation.
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