There are two main causes of perioperative bleeding. The first, surgical bleeding is due to a failure to surgically control bleeding vessels at the operative site and has been discussed earlier in this chapter. This bleeding usually occurs at a single site and is confined to the operative field. Physical measures, such as, pressure, liga clips, tamponade, or diathermy are required to control blood loss. Non-surgical or haemostatic bleeding, on the other hand, results from a failure of haemostasis. This might be due to pre-existing undetected bleeding disorder or massive blood transfusion. Additionally it may be caused by haemostatic abnormalities secondary to the surgery. Often, it results from a combination of pathologies. There may be associated hypothermia, acidosis and hypovolaemia. There may be evidence of generalised bleeding and oozing and manifestations of disordered haemostasis including petechiae, purpura, and oozing from venepuncture sites, central venous catheter sites, urinary catheters, and nasogastric tubes.
In this setting, there are several components to the management of bleeding. It is essential to identify high-risk patients preoperatively. In many of these instances measures such as discontinuation of relevant medication or appropriate blood product cover preoperatively, will substantially diminish operative bleeding risk. An understanding of perioperative haemostatic changes is also essential. This may be related to the underlying pathology as well as the consumption of coagulation factors, platelets, and natural anticoagulants that follow significant blood loss. Massive blood transfusion constitutes blood loss that requires the replacement of the complete blood volume in less than 24 hours. In such a situation it is vital to monitor the full blood count and coagulation tests regularly and transfuse the appropriate blood products. It is usually necessary to transfuse appropriate doses of packed red cells, FFP (15 ml/kg), and platelets to ensure haemostasis. Platelet counts should be kept above 100 x 109 in the neurosurgical setting. If fibrinogen levels are low (less than 1.0 g/dl) transfusion of cryoprecipitate should also be considered. Hypothermia must be avoided as a fall of body core temperature may result in deranged coagulation.
Pharmacological interventions may also be used for prevention and treatment of perioperative bleeding.4,17 These agents may improve primary haemostasis, stimulate fibrin formation, or inhibit fibrinolysis. Anti-fibrinolytic drugs include aprotinin and lysine analogues such as tranexamic acid. The haemostatic effects of these agents depend upon inhibition of fibrinolysis as well as, in the case of aprotinin, a protective effect on platelets. Aprotinin is a 58 amino acid polypeptide of bovine origin, which directly inhibits various serine proteases, including plasmin. Adverse effects are rare but hypersensitivity reactions have been reported including anaphylaxis. The use of aprotinin is contraindicated in disseminated intravascular coagulation and in patients with renal failure. Aprotinin's usefulness has been demonstrated in various surgical settings, particularly cardiac surgery and liver transplantation where prospective studies show significant decrease in bleeding and transfusion requirements. The efficacy and safety of the aprotinin has also been established in patients having intracranial surgery. In a study of 100 patients requiring surgery for an intracranial meningioma or a vestibular schwannoma, intra-operative blood loss was halved by the use of prophylactic high dose intravenous aprotinin. Although there is a theoretical risk ofincreased thrombosis with the use of prohaemostatic agents, in clinical practice thrombotic complications are rare. Local haemostasis may also be improved by the use of fibrin sealants, which usually consist of a thrombin source added to fibrinogen concentrates in the presence of calcium. This mimics the final steps of the physiological clotting cascade to form a fibrin clot. The use of these topical agents is now well described in neurosurgery. They reduce local blood loss and incidence of CSF leaks. In patients with severe bleeding unresponsive to conventional measures, recombinant factor VIIa may help achieve haemostasis.9 This haemostatic agent was developed from our understanding of the key role of tissue factor/factor VII in activating the coagulation pathway in vivo. Recombinant factor VIIa acts primarily via a tissue factor-dependent mechanism that limits its action to the site ofbleeding, although some tissue factor-independent effects may also be involved, particularly on the platelet surface. There are anecdotal reports of successful use in neurosurgical and trauma patients, but the role of this costly therapy remains to be defined.
The use of near patient testing enables a convenient and dynamic global assessment of haemostasis in surgical patients.4 One of the main methodologies is thromboelastography (TEG), which is a dynamic viskokinetic monitoring device that analyses whole blood coagulation and fibrinolysis parameters. It provides sequential information about initial clot time, clot strength, and the degree of fibri-nolysis. A study of TEG in neurosurgery patients has demonstrated progressive hypercoagulability over the course of surgery. This begins with induction of anaesthesia and increases over the course of surgery with the most dramatic increases during the early stages and, then, after tumour removal or aneurysm clipping. In this small study, young females who underwent craniotomy were the most hypercoagulable. In addition to defining global haemostasis, TEG may be used to optimise blood product support in bleeding patients, perioperatively. Another near patient device finding increasing utility in evaluating haemostasis in the surgical setting is the platelet function analyser (PFA-100™).
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