From its inception the success of liver transplantation has been associated with massive blood loss. Massive transfusion is classically defined as > 10 units of red blood cells within 24 h, but describing transfusion rates over a shorter period of time may reduce the potential for survival bias. Both massive haemorrhage and transfusion are associated with increased risk of mortality and morbidity (need for dialysis/surgical site infection) following liver transplantation although causality is difficult to prove due to the observational design of most trials. The blood loss associated with liver transplantation is multifactorial. Portal hypertension secondary to cirrhosis results in extensive collateral circulation, which can bleed during hepatectomy particular if portal pressures are increased. Avoiding volume loading and maintenance of a low central venous pressure together with the use of vasopressors have been shown to reduce blood loss and transfusion during liver transplantation, but may increase the risk of renal impairment post-operatively. Coagulation defects may be present pre-transplant, but haemostasis is often re-balanced due to a deficit in both pro- and anti-coagulation factors. Further derangement of haemostasis may develop in the anhepatic and neohepatic phases due to absent hepatic metabolic function, hyperfibrinolysis and platelet sequestration in the donor liver. Point-of-care tests of coagulation such as the viscoelastic tests rotation thromboelastometry/thromboelastometry allow and more accurate and rapid assessment of these derangements in coagulation and guide the use of factor replacement and antifibrinolytics. Transfusion protocols guided by these tests have been shown to reduce transfusion rates compared with conventional coagulation tests, but have not shown improvements in mortality or morbidity. Pre-operative factors associated with massive transfusion include previous surgery, re-do transplantation, the aetiology and severity of liver disease. Intra-operatively the use of piggy-back technique and avoiding veno-veno bypass has been shown to reduced blood loss.

SummaryCardiac complications are common after non-cardiac surgery. Peri-operative myocardial infarction occurs in 3% of patients undergoing major surgery. Recently, however, our understanding of the epidemiology of these cardiac events has broadened to include myocardial injury after non-cardiac surgery, diagnosed by an asymptomatic troponin rise, which also carries a poor prognosis. We review the causation of myocardial injury after non-cardiac surgery, with potential for prevention and treatment, based on currently available international guidelines and landmark studies. Postoperative arrhythmias are also a frequent cause of morbidity, with atrial fibrillation and QT-prolongation having specific relevance to the peri-operative period. Postoperative systolic heart failure is rare outside of myocardial infarction or cardiac surgery, but the impact of pre-operative diastolic dysfunction and its ability to cause postoperative heart failure is increasingly recognised. The latest evidence regarding diastolic dysfunction and the impact on non-cardiac surgery are examined to help guide fluid management for the noncardiac anaesthetist.

Our exploratory study suggests that the use of PCCs as part of a multifaceted coagulation management strategy may have blood-sparing effects. Their incorporation into clinical practice, however, must await determination of their risk-benefit profile via multicentre randomised trials.

Therapeutic, II.

No abstract

Purpose: Thromboelastography (TEG) evaluates the viscoelastic properties of whole blood to assess clot formation and hemostasis. When blood cannot be analyzed immediately, it is stored in citrated tubes to be analyzed after recalcification. In this study, we evaluated the results of TEG analysis performed on citrated blood and compared these results to values obtained from activated (kaolin and tissue factor) and non activated, fresh blood samples, obtained at various time intervals (one, two, and three hours). Methods: Four blood samples were collected from each of ten healthy volunteers. The following TEG analyses were performed on each sample: reaction time (r), k time (k), alpha angle (α), and maximum amplitude (MA). Studies were done using fresh, non citrated blood, obtained within five minutes of collection, and using citrated blood, one, two, and three hours after collection. Samples were analyzed, with and without activation, using kaolin and tissue factor. Results:Tissue factor activated and non activated, citrated samples had shorter r and k times (P = 0.03, P = 0.008, P < 0.0001, and P < 0.0001, respectively) and higher alpha angle and MA values (P < 0.0001, P < 0.0001, P = 0.79, and P = 0.03, respectively) compared to fresh, non citrated samples. These findings were consistent with a hypercoagulable state. Conversely, citrated samples, activated with kaolin, yielded results similar to those obtained from fresh, non citrated samples. The TEG measurements were similar among citrated samples stored from one to three hours. Conclusions:Our results demonstrate that TEG measures, performed on citrated blood samples, yield results that are consistent with a hyperocoagulable state. Using kaolin to activate citrated samples, on the other hand, yields results similar to those obtained from non citrated, fresh blood samples.

No abstract

TXA appears effective in reducing red blood cell transfusion requirements without increasing the risk of thromboembolic events across a wide variety of liver transplant recipients, including those at low risk of bleeding or high risk of thromboembolic complications. We did not detect evidence of an increased risk of thrombotic complications with TXA exposure.