The poor clinical conditions associated with end-stage cirrhosis, pre-existing pulmonary abnormalities, and high comorbidity rates in patients with high Model for End-Stage Liver Disease scores are all well-recognized factors that increase the risk of pulmonary complications after orthotopic liver transplantation (OLT) surgery. Many intraoperative and postoperative events, such as fluid overload, massive transfusion of blood products, hemodynamic instability, unexpected coagulation abnormalities, renal dysfunction, and serious adverse effects of reperfusion syndrome, are other factors that predispose an individual to postoperative respiratory disorders. Despite advances in surgical techniques and anesthesiological management, the lung may still suffer throughout the perioperative period from various types of injury and ventilatory impairment, with different clinical outcomes. Pulmonary complications after OLT can be classified as infectious or non-infectious. Pleural effusion, atelectasis, pulmonary edema, respiratory distress syndrome, and pneumonia may contribute considerably to early morbidity and mortality in liver transplant patients. It is of paramount importance to accurately identify lung disorders because infectious pulmonary complications warrant speedy and aggressive treatment to prevent diffuse lung injury and the risk of evolution into multisystem organ failure. This review discusses the most common perioperative factors that predispose an individual to postoperative pulmonary complications and these complications' early clinical manifestations after OLT and influence on patient outcome.

Dyskerin is a nucleolar protein, altered in dyskeratosis congenita, which carries out two separate functions, both fundamental for proliferating cells. One function is the pseudo-uridylation of ribosomal RNA (rRNA) molecules, necessary for their processing, and the other is the stabilization of the telomerase RNA component, necessary for telomerase activity. A significant feature of dyskeratosis congenita is an increased susceptibility to cancer; so far, however, no data have been reported on dyskerin changes in human tumours. Therefore, in this study, the distribution of dyskerin in a large series of human tumours from the lung, breast, and colon, as well as from B-cell lymphomas, was analysed by immunohistochemistry. Dyskerin proved never to be lost or delocalized outside the nucleolus. A quantitative analysis of dyskerin mRNA expression was then performed in 70 breast carcinomas together with the evaluation of telomerase RNA component levels and rRNA pseudo-uridylation. Dyskerin mRNA levels were highly variable and directly associated with both telomerase RNA component levels and rRNA pseudo-uridylation. Dyskerin gene silencing in the MCF-7 human breast carcinoma cell line reduced telomerase activity and rRNA pseudo-uridylation. Significantly, patients with low dyskerin expression were characterized by a better clinical outcome than those with a high dyskerin level. These data indicate that dyskerin is not lost in human cancers and that the levels of its expression and function are associated with tumour progression.

Advances in pre-transplant treatment of cirrhosis-related organ dysfunction, intraoperative patient management, and improvements in the treatment of rejection and infections have made human liver transplantation an effective and valuable option for patients with end stage liver disease. However, many important factors, related both to an increasing "marginality" of the implanted graft and unexpected perioperative complications still make immediate post-operative care challenging and the early outcome unpredictable. In recent years sicker patients with multiple comorbidities and organ dysfunction have been undergoing Liver transplantation; appropriate critical care management is required to support prompt graft recovery and prevent systemic complications. Early post-operative management is highly demanding as significant changes may occur in both the allograft and the "distant" organs. A functioning transplanted liver is almost always associated with organ system recovery, resulting in a new life for the patient. However, in the unfortunate event of graft dysfunction, the unavoidable development of multi-organ failure will require an enhanced level of critical care support and a prolonged ICU stay. Strict monitoring and sustainment of cardiorespiratory function, frequent assessment of graft performance, timely recognition of unexpected complications and the institution of prophylactic measures to prevent extrahepatic organ system dysfunction are mandatory in the immediate post-operative period. A reduced rate of complications and satisfactory outcomes have been obtained from multidisciplinary, collaborative efforts, skillful vigilance, and a thorough knowledge of pathophysiologic characteristics of the transplanted liver.

The analysis of litigation records and 'incident reports' has suggested that the choice of accurate proceeding and the use of protection aids could reduce the number of claims, insurance premiums and the costs of litigation process, thus improving physician-patient relationship.

Although the perioperative bleeding complications and the major side effects of blood transfusion have always been the primary concern in liver transplantation (OLT), the possible cohesion of an underestimated intrinsic hypercoagulative state during and after the transplant procedure may pose a major threat to both patient and graft survival. Thromboembolism during OLT is characterized not only by a complex aetiology, but also by unpredictable onset and evolution of the disease. The initiation of a procoagulant process may be triggered by various factors, such as inflammation, venous stasis, ischemia-reperfusion injury, vascular clamping, anatomical and technical abnormalities, genetic factors, deficiency of profibrinolytic activity, and platelet activation. The involvement of the arterial system, intracardiac thrombosis, pulmonary emboli, portal vein thrombosis, and deep vein thrombosis, are among the most serious thrombotic events in the perioperative period. The rapid detection of occlusive vascular events is of paramount importance as it heavily influences the prognosis, particularly when these events occur intraoperatively or early after OLT. Regardless of the lack of studies and guidelines on anticoagulant prophylaxis in this setting, many institutions recommend such an approach especially in the subset of patients at high risk. However, the decision of when, how and in what doses to use the various chemical anticoagulants is still a difficult task, since there is no common consensus, even for high-risk cases. The risk of postoperative thromboembolism causing severe hemodynamic events, or even loss of graft function, must be weighed and compared with the risk of an important bleeding. In this article we briefly review the risk factors and the possible predictors of major thrombotic complications occurring in the perioperative period, as well as their incidence and clinical features. Moreover, the indications to pharmacological prophylaxis and the current treatment strategies are also summarized.

Human intestinal infections by Shiga toxin (Stx)-producing Escherichia coli cause hemorrhagic colitis and hemolytic uremic syndrome (HUS), which represents the main cause of acute renal failure in early childhood. In HUS, Stx released in the gut enter the bloodstream and are targeted to renal endothelium. The mechanism of toxin delivery is still a matter of debate, although the role of polymorphonuclear leukocytes (PMN) as a Stx carrier has been indicated. The aim of this paper was to better define the interactions between Stx and human PMN. Direct and indirect flow cytometric analysis and binding experiments with radiolabeled toxins demonstrated that Stx bind to the surface of human mature PMN but not to immature PMN from G-CSF-treated donors. The use of the human myeloid leukemia cell (HL-60) model for inducible cell differentiation confirmed that the toxin binding occurs only after granulocytic differentiation. Stx binding caused a delay of the spontaneous apoptosis of PMN, as shown by the delayed appearance of apoptotic nuclei and activation of caspase 3 and by the higher number of cells negative to the annexin V-binding assay after 48 h. Moreover, flow cytometric analysis of mixed Stx-positive and Stx-negative PMN populations showed that the toxins were transferred from positive to negative PMN. The delayed, spontaneous apoptosis and the passage of the toxic ligand from older PMN to new, mature cells entering the circulation from the bone marrow may explain the previously reported persistence of Stx in the blood of children with HUS.

Extrapontine myelinolysis can be found isolated or associated with CPM in up to two of three liver transplanted patients with myelinolysis. A marked variation of perioperative serum Na remains the main risk factor even in patients without preexisting hyponatremia; however, isolated hypernatremia may be solely responsible in some cases.

These results demonstrate that inhibition of ribosome biogenesis does not hinder cell cycle progression in RB- and p53-deficient cells. A daily-repeated transitory inhibition of ribosome biogenesis leads to a progressive reduction of ribosome content with the consequent extinction of cancer cell population lacking RB and p53.