By Christopher M. Loftus
This publication is an updated reference on all facets of anticoagulation and hemostasis in neurosurgery. After a gap part on simple ideas and drug periods in present use, exact attention is given to coagulation concerns appropriate to all sufferers, not only neurosurgical ones. The insurance contains, for instance, deep vein thrombosis, pulmonary embolism, and disseminated intravascular coagulation. quite a few vital concerns particular to neurosurgical perform are then addressed, and a precis of present instructions and most sensible practices is supplied. via bringing jointly the most recent wisdom from around the self-discipline, this booklet will function a valid foundation for knowledgeable choice making in surgical perform. will probably be of day-by-day worth for neurosurgeons and trainees around the globe and also will be of curiosity to emergency room physicians, surgeons ordinarily, severe care physicians, neurologists, and sanatorium medication specialists.
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Extra resources for Anticoagulation and Hemostasis in Neurosurgery
LMWH is derived from UFH to produce molecules that are one-third the molecular weight of UFH . LMWHs and their smaller chains do not bind other plasma proteins as signiﬁcantly as UFH thus making their pharmacokinetics much more predictable and thereby eliminating the need for routine monitoring in most situations . The decreased binding of non-AT molecules also confers less risk of heparin-induced thrombocytopenia (HIT) and less bone loss. 1) that confers upon LMWH the ability to inhibit thrombosis without producing signiﬁcant anticoagulant activity [27– 29].
Using a blood pressure cuff inﬂated to 40 mmHg, a controlled puncture wound is made with a calibrated spring-loaded lancet triggered on the volar surface of the forearm, and the resulting wound is blotted every 30 s until bleeding stops. A prolonged bleeding time signals a functional platelet disorder such as von Willebrand disease (VWD), a vascular disorder such as vasculitis, or therapy with aspirin and other nonsteroidal anti-inﬂammatory drugs (NSAIDs). Because the bleeding time test is affected by non-platelet variables (intra-capillary pressure, skin thickness, size and depth of the wound), and it has inadequate predictive value, it has been largely discontinued.
A mutation in the factor V gene substitutes glutamine for arginine at position 506 of the factor V molecule (FV R506Q; FV Leiden). The arginine molecule is a normal cleavage site for APC; the substitution slows or resists APC hydrolysis. The resistant factor Va remains active and raises the production of thrombin, leading to thrombosis. The APC resistance clot-based assay is used to screen for FV Leiden. This is a PTT-based assay that incorporates factor V-depleted plasma and APC. A ratio of PTT results between an aliquot with or without APC determines if there is abnormal factor V activity (APC resistance).