Best practice & research. Clinical anaesthesiology
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One of the greatest disappointments associated with a successful surgical procedure is a thrombotic or thrombo-embolic complication in the postoperative period. Morbidity and mortality of the perioperative period are related, to a relevant degree, to perioperative thrombo-embolic events. Ranging from simple deep venous thrombosis to pulmonary embolism or arterial thrombosis, this class of complication invariably increases length of hospital stay or may result in mortality. The purpose of this review is to identify the procedures and patient populations noted to have thrombophilia in the postoperative period, link the changes in circulating and in situ haematological/biochemical substrates most likely responsible for morbidity, identify the clinical diagnostic modalities that detect recent/impending thrombosis and, lastly, consider the rational therapeutic approaches recommended for minimising postoperative thrombotic complications.
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Best Pract Res Clin Anaesthesiol · Mar 2010
ReviewPerioperative coagulation management--fresh frozen plasma.
Clinical studies support the use of perioperative fresh frozen plasma (FFP) in patients who are actively bleeding with multiple coagulation factor deficiencies and for the prevention of dilutional coagulopathy in patients with major trauma and/or massive haemorrhage. In these settings, current FFP dosing recommendations may be inadequate. However, a substantial proportion of FFP is transfused in non-bleeding patients with mild elevations in coagulation screening tests. ⋯ FP24 and thawed plasma are alternatives to FFP with similar indications for administration. Both provide an opportunity for increasing the safe plasma donor pool. Although prothrombin complex concentrates and factor VIIa may be used as alternatives to FFP in a variety of specific clinical contexts, additional study is needed.
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Best Pract Res Clin Anaesthesiol · Mar 2010
ReviewNew insights into acute coagulopathy in trauma patients.
Abnormal coagulation parameters can be found in 25% of trauma patients with major injuries. Furthermore, trauma patients presenting with coagulopathy on admission have worse clinical outcome. Tissue trauma and systemic hypoperfusion appear to be the primary factors responsible for the development of acute traumatic coagulopathy immediately after injury. ⋯ This coagulopathy can then be exacerbated by subsequent physiologic and physical derangements such as consumption of coagulation factors, haemodilution, hypothermia, acidemia and inflammation, all factors being associated with ongoing haemorrhage and inadequate resuscitation or transfusion therapies. Knowledge of the different mechanisms involved in the pathogenesis of acute traumatic coagulopathy is essential for successful management of bleeding trauma patients. Therefore, early evidence suggests that treatment directed at aggressive and targeted haemostatic resuscitation can lead to reductions in mortality of severely injured patients.
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Best Pract Res Clin Anaesthesiol · Dec 2009
ReviewHyperglycaemia as part of the stress response: the underlying mechanisms.
Stress hyperglycaemia is a distinctive clinical feature of critical illness. Stress mediators, namely stress hormones, cytokines and the central nervous system, interfere with normal carbohydrate metabolism, especially in the liver and skeletal muscle. Central insulin resistance, defined as increased hepatic gluconeogenesis and glucose output despite abundant endogenous insulin levels, appears pivotal to the occurrence of stress hyperglycaemia. ⋯ Still, exogenous insulin administration normalises blood glucose levels in this setting. Insulin treatment may counteract hepatic insulin resistance during acute critical illness. During prolonged critical illness, therapeutic insulin effects seem mediated by increased skeletal muscle glucose uptake and use.