Deep Vein Thrombosis and Pulmonary Embolism: A guide for practitioners 2/ed
By Andrew Blann
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About this ebook
The new edition has details of the theory and practice of traditional drugs and the use of non-Vitamin K antagonist oral anticoagulants (NOACs) and overall the book will enable the practitioner to manage their patients with confidence
Contents include:
Introduction
What is deep vein thrombosis and pulmonary embolism and why are they important?
Who is at risk of these conditions and why?
Recognising and confirming DVT and PE
What have we got to treat these conditions?
Clinical practice of anticoagulation
Heparin and LMWH
Warfarin
Non-vitamin K antagonist anticoagulants (NOACs)
What happens if something goes wrong? – Haemorrhage
References
Answers to Consolidation notes and Case Studies
Dr Andrew Blann, Senior Lecturer and Consultant Clinical Scientist, Birmingham, UK
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Deep Vein Thrombosis and Pulmonary Embolism - Andrew Blann
Deep vein thrombosis and pulmonary embolism
A guide for practitioners
Dr Andrew Blann
Deep vein thrombosis and pulmonary embolism: a guide for practitioners 2nd edition
Andrew Blann
ISBN: 9781907830-33-4
First published 2009; this revised edition published 2015
All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without either the prior permission of the publishers or a licence permitting restricted copying in the United Kingdom issued by the Copyright Licensing Agency, 90 Tottenham Court Road, London, W1T 4LP. Permissions may be sought directly from M&K Publishing, phone: 01768 773030, fax: 01768 781099 or email: publishing@mkupdate.co.uk
Any person who does any unauthorised act in relation to this publication may be liable to criminal prosecution and civil claims for damages.
British Library Cataloguing in Publication Data
A catalogue record for this book is available from the British Library
Notice
Clinical practice and medical knowledge constantly evolve. Standard safety precautions must be followed, but, as knowledge is broadened by research, changes in practice, treatment and drug therapy may become necessary or appropriate. Readers must check the most current product information provided by the manufacturer of each drug to be administered and verify the dosages and correct administration, as well as contraindications. It is the responsibility of the practitioner, utilising the experience and knowledge of the patient, to determine dosages and the best treatment for each individual patient. Any brands mentioned in this book are as examples only and are not endorsed by the publisher. Neither the publisher nor the authors assume any liability for any injury and/or damage to persons or property arising from this publication.
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Contents
List of figures
List of tables
About the author
Introduction
Chapter 1: What are deep vein thrombosis and pulmonary embolism and why are they important?
Chapter 2: Who is at risk of these conditions and why?
Chapter 3: Recognising and confirming VTE
Chapter 4: What have we got to treat these conditions?
Chapter 5: Clinical practice of anticoagulation
Chapter 6: Use of LMWH
Chapter 7: Use of warfarin
Chapter 8: Use of NOACs
Chapter 9: What happens if something goes wrong? – Haemorrhage
Selected references
Answers to consolidation notes and case studies
Glossary
Index
Figures
1.1The coagulation system simplified
3.1A clinical approach to the diagnosis of possible DVT
3.2A clinical approach to the diagnosis of possible PE
5.1Anticoagulation management simplified
6.1Algorithm for general medicine
6.2General algorithm for the use of LMWH in non-orthopaedic surgical patients admitted the day before their operation
6.3Guidelines for Caesarean section
8.1Key aspects of the coagulation pathway showing the action of NOACs
8.2Management of the risk of VTE in AF
Tables
2.1Risk factors in 1231 patients with VTE
2.2Prevalence of inherited risk factors for VTE in Caucasians
2.3Risk factor stratification
4.1Comparison of LMWH and unfractionated heparin
5.1Risk factors for VTE
5.2Additional risk factors for surgical in-patients
5.3Contra-indications and cautions to heparin prophylaxis
5.4Contra-indications and cautions to OAC prophylaxis
5.5Contra-indications and cautions for the use of GECS
5.6Application of risk assessment tables for the use of LMWH/NOAC
7.1Target INRs and recommended duration of anticoagulation
7.2Daily dose of warfarin to achieve rapid induction of INR 2–3
7.3Daily dose of warfarin to achieve slow induction of INR 2–3, e.g. as out-patients
7.4Patient factors that influence the efficacy of warfarin
8.1Disadvantages of traditional anticoagulants
8.2NICE documents and the NOACs
8.3Renal function and the NOACs
8.4Selected drug interactions with NOACs
8.5Last intake of drug before elective surgical intervention
8.6Scoring systems for VTE management in AF
8.7Doses of NOACs for defined indications
9.1Degrees of haemorrhage
9.2Action in response to a high INR in an out-patient
9.3Action in response to a high INR in an in-patient
9.4Some drug interactions with warfarin
About the author
Dr Andrew Blann PhD FRCPath FCRP (Ed)
is Consultant Clinical Scientist and Honorary Senior Lecturer in Medicine
at University Department of Medicine, City Hospital, Birmingham, UK
Introduction
Venous thromboembolism
Many common problems in clinical medicine and general practice relate to arterial and venous thrombosis. Thrombosis in veins (i.e. venous thromboembolism: VTE*) is a permanent problem in various cancers and following surgery, especially orthopaedic. Other risk factors include diabetes, smoking and obesity. It has been estimated that deaths due to VTE in the European Community exceed those due to AIDS, breast cancer, prostate cancer and road traffic accidents combined.
Pathology
A clot (thrombus) may consist simply of blood platelets stuck together with the glue-like fibrin, although red blood cells and white blood cells may also get caught up in the clot. A thrombus may form in the blood, or may develop from, and stick to, the inside of the blood vessel, from which anchored point it may grow. However, fragments (emboli) of this anchored clot may break off and fly away into the blood to cause problems elsewhere.
Recognition
The problem areas are clots in veins of the leg (deep vein thrombosis: DVT) and clots in the lungs (pulmonary embolus: PE) – clearly, each have their own different sets of signs and symptoms. These conditions are very well recognised and there are several aids to diagnosis, such as probability scores and laboratory tests. Together, DVTs and PEs comprise 95% of all VTEs; the remaining clots are most commonly found in the veins of the arms and shoulders.
Prevention and treatment
Ideally, prevention of VTE is by the avoidance (or minimisation) of risk factors such as poor diet and lack of exercise, but if this is impossible (e.g. surgery, cancer), there are drug and non-drug treatments which are also used once a clot is present.
Anti-thrombotic agents have been developed and the many classes of agents that are available are an attempt to find solutions to the wide range of thrombus-related disorders needing treatment. Until recently, the agents most commonly used in prophylaxis and treatment of VTE are heparin, low molecular weight heparin (LMWH) and a vitamin K antagonist (almost always warfarin). However, a new class of drugs, the non-vitamin K antagonist oral anticoagulants (NOACs), also known as direct-acting oral coagulants (DOACs), are set to take over from these traditional drugs in several conditions. Another group of drugs, such as streptokinase, may be used in an attempt to destroy or lyse the clot once it has been formed (i.e. thrombolysis). In the UK, the National Institute for Health and Care Excellence (NICE) is the dominant regulatory body, issuing advice, appraisals and guidance on the diagnosis and management of VTE.
*Key words, when first mentioned, are formatted in bold and are explained in the Glossary (page 88).
Chapter 1
What are deep vein thrombosis and pulmonary embolism and why are they important?
Clots often get a bad press, but their place in physiology is essential in minimising blood loss (haemorrhage). The process of healthy clot formation, coagulation, is generally very tightly regulated, but when this control goes wrong it can lead to build-up of clot that can then lead to clinically important thrombosis, which may even be fatal, especially if in the lung.
How coagulation works
A clot (thrombus) is formed from the platelet and fibrin. Platelets are tiny bodies produced (like red and white blood cells) in the bone marrow. The glue-like fibrin is formed from fibrinogen, produced by the liver. Fibrinogen is converted into fibrin by the crucial clotting enzyme thrombin, a molecule so active that it cannot exist by itself in the plasma, but circulates in blood in an inactive form as prothrombin, which is also produced by the liver. Prothrombin is converted to thrombin by a collection of other coagulation factors (Factor VII, Factor X, calcium) and molecules that together are known as the prothrombinase complex.
Many of us will be aware of the most well-known bleeding disease, haemophilia. This is caused by the lack