Search

Long-term extrahepatic cholestasis in the rat induces ductular proliferation and fibrosis in the liver, portal hypertension, splenomegaly, portosystemic collateral circulation, and ascites. These splanchnic alterations could have an inflammatory pathophysiology.We measured serum levels of hepatobiliary injury markers and the acute phase proteins, alpha-1-major acid protein (alpha(1)-MAP) and alpha-1-acid glycoprotein (alpha(1)-GPA) in rats 6 wk after microsurgical extrahepatic cholestasis. We also assayed Th(1) (TNF-alpha and IL-1beta) and Th(2) (IL-4 and IL-10) cytokine levels in the liver, ileum, spleen, and mesenteric lymph complex by enzyme-linked immunosorbent assay (ELISA) techniques. Liver fibrosis was measured by Sirius red stain and by using an image system computer-assisted method and mast cell liver infiltration by Giemsa stain.The cholestatic rats showed an increase (P0.001) in serum levels of bile acids, total and direct bilirubin, AST, ALT, AST/ALT index, gamma-GT, alkaline phosphatase, alpha(1)- MAP, alpha(1)-GPA, and LDH (P0.05) in relation to sham-operated rats. TNF-alpha, IL-1beta, IL-4, and IL-10 increased in the ileum (P0.01) and mesenteric lymph complex (P0.001), and decreased in the liver (P0.001). A marked bile proliferation associated with fibrosis (P0.001) and mast cell infiltration was also shown in the liver of cholestatic rats.The splanchnic redistribution of cytokines, with an increase of Th(1) and Th(2) production in the small bowel and in the mesenteric lymph complex, supports the key role of inflammatory mechanisms in rats with secondary biliary fibrosis.

Intracompartmental sepsis (IS) is a rare complication in burn patients. IS presents in patients with inadequate perfusion of intracompartmental tissues with subsequent ischaemic necrosis and infection. Contributing factors include high-volume resuscitation, delayed escharotomies and previous bacteraemias. We describe the profile of a series of patients who developed IS in our Intensive Care Burn Unit (ICBU). We carried out a retrospective chart review of patients admitted to an ICBU over a 5-year period. Seven patients of 659 admissions (1.0%) developed IS involving the extremities. Diagnosis was based on the identification of purulent drainage and local swelling associated with signs of sepsis of unknown origin. Total body surface area (TBSA) burned averaged 67.4% and full-thickness body surface area (FTBSA) burned averaged 48.4%. All patients were sedated and mechanically ventilated. The first 24-h fluid requirements averaged 6.0 ml kg–1 per %TBSA burn (range 3.5–7.0 ml kg–1 per %TBSA). Escharotomies were performed in five patients within the first 24 h of admission. Median time of diagnosis of IS was 23 days from admission (range 11–45 days). Four patients developed bacteraemia caused by the same microorganism infecting the soft tissue. In five cases, the infecting microorganism had previously colonised the overlying burned skin. Three patients required amputation of the affected limb. In coclusion, IS is a devastating infectious complication which appears late after large burns. Predisposing factors include high-volume resuscitation, delayed escharotomies, colonisation of the overlying skin and previous bacteraemias. Earlier diagnosis and management are needed to attain a better outcome. Sin financiación 1.718 JCR (2010) Q2, 27/55 Dermatalogy, 65/188 Surgery; Q3, 16/23 Critical care medicine UEM

We report the case of a 48-year-old male with an exposition of a femorofemoral crossover bypass in the inguinal region and superficial femoral occlusion. This was successfully treated using an anteromedial thigh (AMT) pedicled flap based on the perforator vessel of the descending branch of the lateral circumflex femoral artery. Our report focuses on: i) considering the AMT flap as a safe and easy option to cover the inguinal region in cases of bypass exposure; ii) describing the attachment of this flap to the deep femoral artery in a patient with superficial femoral occlusion, in spite of some literature controversy.

Obstructive cholestasis causes hepatic cirrhosis and portal hypertension. The pathophysiological mechanisms involved in the development of liver disease are multiple and linked. We propose grouping these mechanisms according to the three phenotypes mainly expressed in the interstitial space in order to integrate them. Experimental extrahepatic cholestasis is the model most frequently used to study obstructive cholestasis. The early liver interstitial alterations described in these experimental models would produce an ischemia/reperfusion phenotype with oxidative and nitrosative stress. Then, the hyperexpression of a leukocytic phenotype, in which Kupffer cells and neutrophils participate, would induce enzymatic stress. And finally, an angiogenic phenotype, responsible for peribiliary plexus development with sinusoidal arterialization, occurs. In addition, an intense cholangiocyte proliferation, which acquires neuroendocrine abilities, stands out. This histopathological finding is also associated with fibrosis. It is proposed that the sequence of these inflammatory phenotypes, perhaps with a trophic meaning, ultimately produces a benign tumoral biliary process – although it poses severe hepatocytic insufficiency. Moreover, the persistence of this benign tumor disease would induce a higher degree of dedifferentiation and autonomy and, therefore, its malign degeneration.