Handbook of Venous Thromboembolism

Jecko Thachil, Catherine Bagot, Jecko Thachil, Catherine Bagot, Catherine Bagot

• Publisher: Wiley-Blackwell
• Year: 2017
• Print ISBN: 9781119095576
• eBook ISBN: 9781119095583
• Edition: 1
• Topic: Medicine
• Subtopic: Emergency Medicine & Critical Care

A clinically oriented handbook providing up-to-date recommendations for mastering the practical aspects of patient management for venous thromboembolism

Venous thromboembolism (VTE) is associated with high morbidity and mortality both in and out of the hospital setting, and is one of the commonest reasons for hospital attendances and admissions. Designed as a practical resource, the Handbook of Venous Thromboembolism covers the practical aspects of venous thromboembolism management in short and easily followed algorithms and tables. This important text helps physicians keep up-to-date with the latest recommendations for treating venous thromboembolism in clinic-oriented settings. Experts in fields such as the radiological diagnosis of pulmonary embolism and thrombophilia testing, give a succinct summary of the investigation, diagnosis and treatment of venous thromboembolism and include evidence-based guidelines.

With contributions from a team on internationally recognized experts, Handbook of Venous Thromboembolism is a source of information that specialists in the field can recommend to non-specialists and which the latter will be able to review to assist in their education and management of this wide-spread condition. This vital resource:

• Comprises of a clinically focused handbook, useful as a daily resource for the busy physician
• Offers a handbook written by an international team of specialists offering their experience on the practical aspects of venous thromboembolism management
• Addresses venous thrombosis prevention, a major focus for healthcare providers
• Includes coverage on controversies in the management of venous thromboembolism so clinicians can understand how experts are practicing in real scenarios

Written for hematology trainees, emergency and acute medicine physicians, junior doctors, and primary care physicians, Handbook of Venous Thromboembolism covers the basics for treating patients with venous thromboembolism and offers guidelines from noted experts in the field.

Section V
Unusual Site Thrombosis

21
Cerebral Venous Thrombosis

Christian Weimar

Department of Neurology and Stroke Center, University Duisburg‐Essen, Germany

Although a rare cause of stroke, cerebral venous thrombosis (CVT) is increasingly diagnosed because of greater clinical awareness, more sensitive neuroimaging techniques, and the survival of patients with previously lethal diseases that confer a predisposition to CVT. The incidence of CVT in adults was investigated in two Dutch provinces, serving 3.1 million people, and was found to be 1.32 per 100 000 person years (95% CI 1.06–1.61) with an incidence of 2.78 (95% CI 1.98–3.82) among women between the ages of 31 and 50 years (Coutinho et al., 2012). The most common condition associated with CVT in women is pregnancy/puerperium, with an incidence of around 10 in 100 000 deliveries in high‐income countries, accounting for 5–20% of all CVT (Bousser and Crassard, 2012). The incidence in Canadian children was estimated at 0.67 per 100 000 (95% CI 0.55–0.76), but is likely higher in developing countries due to infective diseases (deVeber et al., 2001).

Aetiology

There are multiple predisposing factors of CVT, which are very similar to those causing extracerebral venous thrombosis, except for a number of local causes. In about 15% of patients, no cause of CVT can be found, but follow‐up may detect an underlying disease up to several months later (Ferro et al., 2004). Oral hormonal contraception remains the sole predisposing factor in about 10%, but is also frequently found in combination with coagulation disorders. Coagulation disorders are common causes of CVT, in particular the Factor‐V‐Leiden mutation, with APC resistance accounting for 10–25% of cases (Dentali et al., 2006; Pai et al., 2012).

Other coagulopathies associated with CVT include: prothrombin mutation G 20210 A; antithrombin III deficiency; protein C and protein S deficiency; antiphospholipid antibody syndrome; plasminogen deficiency; hyperhomocysteinaemia; dysfibrinogenaemia; disseminated intravasal coagulation; heparin‐induced thrombocytopenia type 2 (Kenet et al., 2010; Saposnik et al., 2011). Additional causes include malignancies (meningeoma, carcinoma, lymphoma, carcinoid, leukaemia), haematological disorders (polycythaemia, sickle cell disease, paroxysmal nocturnal haemoglobinuria, immune‐mediated haemolytic diseases, thrombocytaemia), collagenosis (systemic lupus erythematodes, Sjögren’s syndrome) and vasculitis (Behcet’s disease, Wegener’s granulomatosis, sarcoidosis) (Saposnik et al., 2011).

Other rare causes of CVT include: intracranial hypotension; cerebral concussion; neurosurgical interventions; obstructive hydrocephalus; impaired venous drainage (central venous catheter, dural arteriovenous malformation, strangulation); medication poisoning (asparaginase, other chemotherapeutics, steroids, erythropoietin, drugs, vitamin A overdose); metabolic disorders (diabetes, thyrotoxicosis, uraemia, nephrotic syndrome); gastrointestinal disorders (liver cirrhosis, chronic inflammatory bowel disease); and heart disease (heart failure, cardiomyopathy). Septic CVT can be found in up to 18% of all cases in developing countries (Khealani et al., 2008), and is associated with localised infections such as mastoiditis, otitis media, sinusitis, tonsillitis, retropharyngeal abscess with thrombosis of adjacent jugular vein, oral or cerebral abscess, and meningitis. Potential generalised infectious causes include bacterial septicaemia, endocarditis, hepatitis, encephalitis, measles, tuberculosis, typhus, malaria, and aspergillosis.

Pathophysiology

Two separate pathophysiological mechanisms need to be distinguished: thrombosis of cortical veins and thrombosis of the major sinus. The latter are needed for the clearance of cerebrospinal fluid (CSF). This process is mediated by so‐called Pacchioni’s granulations, which constitute arachnoid protrusions into the cerebral sinus, and enable transport of CSF from the subarachnoid space into the blood. Thrombosis of the cerebral sinus thus results in intracranial hypertension (Brunori et al., 1993). Occlusion of a cerebral vein obstructs the drainage of blood from brain tissue, causing an increase in venous and capillary pressure and breakdown of the blood‐brain barrier, which results in parenchymal damage (Ungersbock et al., 1993).

Clinical Presentation

CVT may often remain asymptomatic, due to numerous ways of venous drainage and reversal of venous flow. Headache is the initial symptom in more than 70%, and remains the only symptom in about 16% (Gameiro et al., 2012). It can be associated with other common symptoms, such as nausea/vomiting, seizures, reduced consciousness or confusional state and focal neurological deficits (Ferro et al., 2004). Papilledema can be found in about 40%, mainly in patients with a chronic course or delayed diagnosis. Initial presentation with focal or generalised epileptic seizures occurs in 30–40% of cases. Other less frequent symptoms include thunderclap headache, subarachnoid haemorrhage, cranial nerve palsy, transient ischemic attacks, migraine with aura, psychiatric disturbances and tinnitus.

Neurological findings and type of focal seizures are determined by the localisation of CVT and the associated lesions. The common thrombosis of the superior sagittal sinus (60% of cases) causes headache, papilledema, seizures, motor deficits and impaired consciousness, whereas thrombosis of the cavernosus sinus is associated with ocular nerve palsies and ipsilateral ocular affection (chemosis, proptosis, papilledema). Patients with isolated thrombosis of the lateral sinus present mostly as isolated intracranial hypertension or aphasia, if the left transverse sinus is occluded. Occlusion of the deep cerebral venous system more likely causes coma, motor deficits or aphasia. Bilateral venous congestion of the thalamic region causes decreased consciousness as a major finding, and minor transient cognitive impairment, rather than...

Table of contents

• Cover
• Title Page
• Table of Contents
• List of Contributors
• Foreword
• Section I: Clinical Overview
• Section II: Diagnosis
• Section III: Treatment
• Section IV: Special Situations
• Section V: Unusual Site Thrombosis
• Section VI: Long‐term Sequelae of VTE
• Section VII: Controversies
• Section VIII: Prevention
• Index
• End User License Agreement