Introduction

In surgery there is a fine balance between bleeding and thrombosis. Although the haemostatic process helps to halt excessive blood loss it might, in a prothrombotic milieu, become pathological and lead to thrombosis. In the management of surgical patients, it is essential to minimise the risk of complications from bleeding. Perioperative bleeding in the neurosurgical setting may have devastating consequences and lead to blindness or paralysis. Hence the importance of meticulous haemostasis in all cranial and spinal operations. In addition, neurosurgical patients are at a risk of thromboembolism.1-3 Symptomatic deep vein thrombosis (DVT) is recorded in 20% of patients in the absence of any thromboprophylaxis. Fatal pulmonary embolism (PE) is reported in 1.5% to 5% of neurosurgical patients. A risk assessment of bleeding versus thrombosis must be performed preoperatively in every neurosurgical patient to ensure an optimum outcome. This permits the early use of prophylactic measures thus reducing the risk of thrombosis and bleeding.

Neurosurgery is unique in that postoperative bleeding can be devastating and result in death or disability. As a consequence absolute haemostasis is essential. Technical advances such as the operating microscope and bipolar coagulation allow the accurate control of bleeding from fine cortical vessels. Chemical haemostasis also plays a part in the control of bleeding from capillaries and veins. However unlike his colleagues in other specialties the neurosurgeon can rarely rely on drains to an operative site or use monopolar coagulation.

It is important to recognize that the brain also contains a higher concentration of thromboplastin than any other human tissue. The liberation of thromboplastin into the circulation institutes the extrinsic clotting cascade. Sufficient thromboplastin activation can be a factor in patients developing disseminated intravascular coagulation after a severe head injury. The triggering of the extrinsic cascade is also likely to be a factor in the development of vasospasm seen in patients after subarachnoid haemorrhage.

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