Venous Interventional Radiology (eBook)

Laura K. Findeiss (Autor)

eBook Download: EPUB

2020 | 1. Auflage
172 Seiten
Georg Thieme Verlag KG
9781638531685 (ISBN)

Infos

<p><strong><em>A state-of-the-art guide on the interventional management of venous disease from renowned experts!</em></strong></p><p>The diagnosis and management of venous disorders is a core competency of interventional radiology, comprising up to 75% of an interventional radiologist's caseload in some institutions. <cite>Venous Interventional Radiology</cite> by prominent interventional radiologist Laura Findeiss and an impressive group of contributors is a highly practical vascular interventional radiology reference that covers a full spectrum of venous disease. The richly illustrated book starts with an opening chapter on venous anatomy, physiology, and epidemiology.</p><p>Disease-specific chapters cover common to complex disorders, from varicose veins and venous ulceration, to thromboembolic disease and pulmonary embolism. Each chapter presents the latest minimally invasive image-guided interventions for the diagnosis and management of a specific disease. Clinical cases provide discussion of patient presentation/symptoms, clinical evaluation, procedural and non-invasive management strategies, and follow-up, all of which are key to delivering comprehensive patient care.</p><p><strong>Key Highlights</strong><ul><li>Angiographic and cross-sectional imaging findings enhance knowledge of disease processes</li><li>A chapter dedicated to vascular/venous access provides guidance on this basic yet critical component of patient care</li><li>The classification, evaluation, and treatment of venous anomalies and syndromes</li><li>The authors discuss pitfalls and complications, including their own pearls of wisdom and unanswered questions</li></ul></p><p>This highly practical guide is a must-have resource for trainee and veteran interventional radiologists and vascular surgeons.</p><p>This book includes complimentary access to a digital copy on <a href='https://medone.thieme.com'>https://medone.thieme.com.</a></p>

Textauszug

2 Venous Thromboembolism

Matthew T. Rondina and Hanadi Farrukh

Summary

Venous thromboembolism has been increasingly recognized as a significant contributor to patient morbidity and mortality, and there has been rapid growth in the application of interventional techniques to the management of venous thrombotic disorders. For the physician managing a patient with a venous thrombosis, an excellent understanding of the mechanisms of disease, thrombosis physiology, pathophysiology of clotting disorders, data to support the application of different pharmacologic interventions, and risks and benefits of different therapies is critical to success. This chapter provides a thorough overview of the science and pharmacologic management of thrombosis, as well as details of patient evaluation, epidemiology, and expected outcomes of intervention.

Keywords: venous thromboembolism, pulmonary embolism, deep vein thrombosis, diagnosis, anticoagulation, DOAC, Treatment, Warfarin, D-dimer, ultrasound

2.1 Introduction

Venous thromboembolism (VTE) is a major public health burden globally and, after myocardial infarction and stroke, the third most common cardiovascular disease. The causes of VTE are complex and multifactorial and include both inherited and acquired factors. As our population ages and develops VTE risk factors, the incidence and prevalence of VTE will continue to increase—as likely will its attendant complications, including postthrombotic syndrome (PTS) and pulmonary hypertension. Thus, for providers in all settings, an understanding of VTE is warranted.

Starting with a clinical vignette, this chapter will review the pathophysiology and epidemiology of VTE, including common provoking risk factors and inherited thrombophilias. The appropriate use of algorithms to diagnosis deep vein thrombosis (DVT) and pulmonary embolism (PE) will be reviewed, including a discussion on potentially more complex and challenging diagnostic issues—such as recurrent ipsilateral DVT and when computed tomography pulmonary angiography (CTPA) is contraindicated in patients suspected of having acute PE. With the advent of the direct oral anticoagulants (DOACs), therapeutic options for the treatment of VTE have broadened. Accordingly, we will discuss central issues in the management of VTE, including acute antithrombotic therapy, thrombolytics for massive PE, and the duration of anticoagulation for provoked and unprovoked events.

2.2 Clinical Vignette

2.2.1 Patient Presentation

A 46-year-old white female presented to clinic with a 2-week history of progressive exertional dyspnea that had worsened over the past 2 days. She also had the onset of right pleuritic chest pain 1 day earlier and two episodes of presyncope with palpitations and chills. She denied fevers, cough, or wheezing. She had tried an albuterol inhaler prescribed by a friend without benefit. She was a lifetime nonsmoker. Her past medical history was notable for gastroesophageal reflux disease, irritable bowel syndrome, and menorrhagia. Her past surgical history included a remote left oophorectomy for an ovarian cyst. Her current medications included lansoprazole, oral contraceptive pills (taken for the past 2 years), and dicyclomine.

2.2.2 Physical Exam

She was a pleasant obese white female in no acute respiratory distress, although she appeared mildly anxious. Her body mass index was 42 kg/m2, blood pressure was 116/76 mm Hg, pulse was 91 beats per minute, respiratory rate was 16 breaths per minute, the temperature was 98.6°F, and her room air oxygen saturation was 96%. Her cardiovascular exam noted a jugular venous pulsation of 5 cm H2O, and there was a regular heart rate and rhythm without murmurs or gallops. Her lungs were clear to auscultation and her abdomen was soft, nontender, with normal bowel sounds and no masses or organomegaly. Her extremities were without edema, there was no calf tenderness to palpation, and distal pulses were intact.

2.2.3 Lab Evaluation

Complete blood count, prothrombin time and international normalized ratio (INR), partial thromboplastin time, and comprehensive metabolic panel were within normal range. The troponin-I was 0.03 ng/mL (normal: 0.0–0.03 ng/mL) and the D-dimer was elevated at 2.5 μg/mL (normal 0.0–0.04 μg/mL).

2.2.4 Noninvasive Testing

An electrocardiogram demonstrated normal sinus rhythm with a rate of 90 beats per minute and diffusely inverted T waves across precordial leads.

2.2.5 Imaging

A posteroanterior and lateral chest X-ray was normal. CTPA demonstrated bilateral filling defects involving both the right and left main pulmonary arteries and extending into the segmental and subsegmental arteries, with distention of the right ventricle suggestive of right heart strain. A transthoracic echocardiogram demonstrated normal left ventricular systolic function with an ejection fraction of 68%, normal right ventricular systolic function, and mildly elevated pulmonary artery systolic pressure.

2.2.6 Plan of Care

She was admitted to the hospital with a diagnosis of acute, submassive PE and was treated with antithrombotic therapy.

2.3 Pathophysiology and Epidemiology of Venous Thromboembolism

Venous thrombi are classically comprised largely of red blood cells, with some leukocytes and platelets, interwoven in a fibrin lattice (►Fig. 2.1a). The formation of venous thrombosis occurs commonly in settings where there is vessel wall injury or stasis (e.g., surgery, trauma, malignancy), systemic inflammation (e.g., lupus, sepsis), and/or a procoagulant state (e.g., inherited thrombophilia, antiphospholipid antibodies). Vessel wall injury exposes tissue factor and collagen, leading to activation of the coagulation cascade. Historically, the coagulation cascade has been divided into the intrinsic and extrinsic pathways (►Fig. 2.1b). More recently, a cell-based model of coagulation has been put forth, whereby activation of the coagulation cascade occurs on the cell surface in four overlapping steps: (1) initiation, (2) amplification, (3) propagation, and (4) termination. The primary event for initiation of this cascade is the interaction of activated factor VII (FVIIa) with exposed tissue factor, converting factor II (FII, also known as prothrombin) to thrombin (FIIa) and fibrinogen to fibrin.

The epidemiology of VTE—including PE and DVT of the leg, pelvis, and arm—has recently been reviewed.1,2 VTE carries a major global disease burden with respect to incidence, morbidity, mortality, and cost.3,4 After myocardial infarction and stroke, VTE is the third most common cardiovascular disease, with a lifetime risk after age 45 years of 8.1%.5 The age-adjusted annual incidence of VTE has increased by 80% from 1985 to 2009 to 1.7/1,000/year. While DVT incidence has remained stable, PE incidence has progressively increased, possibly due to a combination of an aging population, improved diagnostic techniques, and/or poorly defined increases in VTE risk factors.6

VTE results in some 550,000 hospitalizations per year in the United States—350,000 for DVT and 200,000 for PE7—with at least 44,000 deaths per year. Moreover, this mortality rate is likely an underestimate as 10 to 25% of PE patients in the community may present with sudden death prior to diagnosis.8 Other consequences of VTE include a VTE recurrence rate of 15% over 3 years and 30% over 5 to 10 years in the absence of anticoagulation2,9 and a 6% rate of major bleeding over 3 years.10 In addition, PTS (►Fig. 2.2) occurs in 20 to 50% of patients within 2 years of a first episode of proximal DVT.11 Severe PTS symptoms and/or venous ulceration develop in 5 to 10% of patients.12 There is also a 2.8% incidence of chronic thromboembolic pulmonary hypertension within 1.5 years of an episode of PE.13 The result is an estimated annual cost of VTE in the United States of $7 to 10 billion per year.3

Fig. 2.1 (a) Venous thrombi are classically comprised largely of red blood cells, with some monocytes, neutrophils, and platelets, interwoven in a fibrin lattice. (b) The coagulation comprises the intrinsic and extrinsic pathways, whereas the cell-based model of coagulation occurs on the cell surface in four sequential phases: (1) initiation, (2) amplification, (3) propagation, and (4) termination. The intrinsic pathway begins with activation of factor XII, driving subsequent activation of factors XI, IX, and X. The primary event for initiation of the extrinsic pathway is the interaction between FVIIa and tissue factor (TF). Both the intrinsic and extrinsic pathways result in the conversion of prothrombin (FII) to thrombin (FIIa), in the common pathway. Thrombin then converts fibrinogen to fibrin and fibrin strands are cross-linked and stabilized by activated factor XIII (FXIIIa), leading to venous thrombus formation.

Fig. 2.2 Postthrombotic syndrome (PTS) is a complication of acute deep vein thrombosis. While still incompletely understood, the pathophysiology is thought to involve damage to the valves in the deep venous system with resulting venous insufficiency and inflammation. Patients with PTS have typical, often intermittent symptoms of leg erythema, cramping, heaviness, aching, and, in severe cases, ulceration.

2.3.1 Risk Factors for Venous Thromboembolism

VTE results from the complex, multiplicative interaction of inherited and/or acquired predisposing risk factors, often superimposed by the appearance of temporary clinical risk factors (►Table 2.1).2,14,15...

Produkt-Details

• Erscheint lt. Verlag: 7.10.2020
• Verlagsort: Stuttgart
• Sprache: englisch
• Themenwelt: Medizin / Pharmazie ► Gesundheitsfachberufe
• Themenwelt: Medizinische Fachgebiete ► Radiologie / Bildgebende Verfahren ► Nuklearmedizin
• Themenwelt: Medizinische Fachgebiete ► Radiologie / Bildgebende Verfahren ► Radiologie
• Schlagworte: image-guided interventions • Interventional Radiology • thromboembolism • Vascular Radiology • venous access • Venous disease
• ISBN-13: 9781638531685 / 9781638531685