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.

Normothermic ex situ liver perfusion (NEsLP) offers the opportunity to assess biomarkers of graft function and injury. We investigated NEsLP parameters (biomarkers and markers) for the assessment of liver viability in a porcine transplantation model. Grafts from heart‐beating donors (HBD), and from donors with 30 minutes (donation after cardiac death [DCD]30′), 70 minutes (DCD70′), and 120 minutes (DCD120′) of warm ischemia were studied. The HBD, DCD30′, and DCD70′‐groups had 100% survival. In contrast, 70% developed primary nonfunction (PNF) and died in the DCD120′‐group. Hepatocellular function during NEsLP showed low lactate (≤1.1 mmol/L) in all the groups except the DCD120′‐group (>2 mmol/L) at 4 hours of perfusion (P = .04). The fold‐urea increase was significantly lower in the DCD120′‐group (≤0.4) compared to the other groups (≥0.65) (P = .01). As for cholangiocyte function, bile/perfusate glucose ratio was significantly lower (<0.6) in all the groups except the DCD120′‐group (≥0.9) after 3 hours of perfusion (<0.01). Bile/perfusate Na+ ratio was significantly higher (≥1.2) after 3 hours of perfusion in all the groups except for the DCD120′‐group (≤1) (P < .01). Three hours after transplantation, the DCD120′‐group had a significantly higher international normalized ratio (>5) compared to the rest of the groups (≤1.9) (P = .02). Rocuronium levels were higher at all the time‐points in the animals that developed PNF during NEsLP and after transplantation. This study demonstrates that biomarkers and markers of hepatocellular and cholangiocyte function during NEsLP correlate with the degree of ischemic injury and posttransplant function.

Our case series demonstrates a high incidence of complications in this subpopulation, mainly postoperative. Extreme postoperative vigilance is required and recovery in a high dependency unit is highly recommended.

Describe the physiology of iron and its importance for mammalian health and function. Discuss which groups of patients require further investigation for iron deficiency anaemia, including those with normal serum ferritin values in whom a response to iron therapy is seen. Explain the rationale and pitfalls of laboratory tests in assessing iron status. Optimise iron status, particularly in patients scheduled for surgery. Iron is an essential bioelement in human physiology. It has key roles in cellular respiration: facilitating the formation of Adenosine triphosphate (ATP), oxygen transport through iron-containing haem groups (haemoglobin [Hb] and myoglobin), and protection against infection via iron withholding in the immune system. Iron excess results in toxicity, most notably to the heart and liver. Iron deficiency (ID) affects more than 2 billion people worldwide and remains the leading cause of anaemia. This review gives an overview of the physiology of iron metabolism and its impact on key groups of patients presenting for surgery, and summarises how to investigate and treat ID. Iron homeostasis The human body contains approximately 3e4 g iron in males and 2.5 g in females; 2.5e3.5 g of this in males is contained as Hb, 0.3e0.4 g as myoglobin, 100 mg as haem/non-haem Stuart Cleland BSc FRCA is a consultant in anaesthesia with clinical interests in upper gastrointestinal, hepatobiliary, and obstetric anaesthesia, and the preoperative assessment and optimisation of high-risk patients. He chairs his hospital's transfusion committee, and is the departmental lead for the management of perioperative anaemia. Wayne Thomas BSc (Hons) MRCP FRCPath is a consultant haematologist with a subspecialty interest in haemostasis, thrombosis, and iron deficiency. He is the laboratory lead for general haematology for his Trust, and clinical lead for blood transfusion. He is exchairman of the British Society of Haematology general haematology guidelines committee, and chairman of the UKNEGAS steering committee for haematology.