Neoplastic obstruction of the inferior vena cava (IVC) constitutes a rare but formidable challenge in both vascular and oncologic surgery. It may arise from primary tumors originating within the vessel wall, such as leiomyosarcomas, or more frequently as secondary invasion or tumor thrombus from adjacent malignancies, including renal cell carcinoma, hepatocellular carcinoma, or adrenal cortical carcinoma. The anatomic complexity of the IVC, its proximity to vital structures, and the hemodynamic consequences of obstruction demand a thorough understanding of tumor characteristics, precise preoperative imaging, and meticulous surgical planning. This chapter provides a comprehensive review of the classification, diagnostic workup, and detailed surgical techniques used to manage neoplastic IVC obstruction. We explore the roles of segmental resection, reconstruction techniques, and the use of advanced bypass methods, including cardiopulmonary bypass for intracardiac tumor extension. Outcomes, complications, and long-term prognosis are discussed, emphasizing the importance of an aggressive, multidisciplinary approach to optimize patient survival and quality of life.
Cancer can cause inferior vena cava (IVC) obstruction. Usually, an oncologic resection is not possible and palliative treatment is needed. An endovascular procedure can be performed in most cases under local anesthesia plus sedation through a percutaneous approach. Stenting is a safe and the most effective technique and provides excellent technical and clinical success rates with immediate improvement of symptoms. Despite the short life expectancy of these patients, the technique allows them a far better quality of life. On the other hand, treatment of venous sequalae of carcinological treatment can give good long-term results.
Popliteal entrapment (compression) syndrome is a rare disease affecting principally young people, without atherosclerotic involvement. It is due to extrinsic compression of the neurovascular bundle at the popliteal fossa. There is no consensus or guidelines for the diagnosis or management, especially for functional popliteal entrapment. Compression of the popliteal vein manifests itself symptomatically in dynamic situations, such as prolonged standing or physical exercises. These symptoms are not specific, and clinical examination does not identify specific signs either. The ultrasound (US), in supine position, is usually nondiagnostic. Actually, a normal US in patients who complain of symptoms, related to venous insufficiency, should evoke venous compression as a possible diagnostic. Dynamic imaging by US is the key to visualizing the conflict between veins and anatomical structures. If a surgical treatment is considered, magnetic resonance imaging and/or dynamic phlebography are necessary. Nonsurgical procedures for light or mild cases include stretching exercises and botulinic toxin, under US-assisted injection. In more symptomatic patients, and depending on the etiology of compression, several surgical options can be offered: direct decompression through popliteal fossa dissection, aponeurectomy, isolated or combined with lengthening of gastrocnemius and soleus muscles. An often-overlooked syndrome is the chronic venous insufficiency described by Dijkstra and colleagues in patients with morbid obesity: weight loss is able to stabilize or improve venous return without direct vascular interventions and even allows healing of chronic ulcers.
Venous thoracic outlet syndrome (VTOS) is a vascular disorder caused by extrinsic compression of the axillary-subclavian vein, leadingto impaired venous drainage of the upper extremity. Compression most commonly occurs at the costoclavicular junction (CCJ) and, less frequently, at the pectoralis minor space, either independently or as part of a combined "double crush" mechanism. This venous compression may be initially asymptomatic, discovered only incidentally in high-risk populations, but it can evolve into symptomatic disease-manifesting as intermittent swelling and venous congestion, or progressing to acute thrombosis with significant morbidity. VTOS is clinically categorized into 4 subtypes: asymptomatic compression, nonthrombotic VTOS (McCleery syndrome), thrombotic VTOS (Paget-Schroetter syndrome), and postthrombotic VTOS. The diagnostic process requires a high index of suspicion and dynamic imaging under provocative conditions. Advances in duplex ultrasound, magnetic resonance venography, and intravascular ultrasound (IVUS) have improved the detection and characterization of both positional and chronic venous obstruction. Contemporary management emphasizes early thrombus removal, timely surgical decompression, and venous reconstruction in selected cases. Prompt diagnosis and intervention are critical to prevent progression to postthrombotic syndrome and irreversible functional impairment. This review offers a comprehensive overview of VTOS, including its pathophysiology, classifications, diagnostic pathways, and management algorithms, supported by current literature.
May-Thurner syndrome (MTS), also known as iliac vein entrapment syndrome, is caused by extrinsic compression of the left common iliac vein-most often by the right common iliac artery-leading to venostasis and potential development of deep vein thrombosis (DVT). Though historically underdiagnosed, its recognition has increased with the routine use of cross-sectional imaging and intravascular ultrasound (IVUS), which now serves as the gold standard for diagnosis and procedural guidance. MTS primarily affects young women and often presents with unilateral leg swelling, recurrent DVT, or chronic pelvic symptoms. Diagnosis relies on duplex ultrasound, computed tomography or magnetic resonance venography, venography, and IVUS, which can detect subtle intraluminal abnormalities and guide precise stent placement. Endovascular treatment with dedicated venous stents has largely replaced open surgical options due to superior safety, efficacy, and durability. Proper stent selection and IVUS-guided sizing are essential to avoid complications such as restenosis or migration. Postprocedural management includes anticoagulation and patient-specific follow-up. Ongoing research focuses on novel stent technologies, AI-enhanced imaging, and longterm outcome data from registries like the European Venous Registry. Early identification and intervention improve long-term outcomes and quality of life, underscoring the importance of clinical awareness and multidisciplinary care.
Chronic venous disease is one of the most frequent consultations in our daily practice, so we must consider the management of complications and special cases that are more frequent than expected. If as physicians we seek to improve patients' quality of life, we need multidisciplinary management to achieve this goal.
Atrophie blanche (AB) is a distinctive dermatological finding characterized by stellate, porcelain-white, atrophic plaques, commonly located on the lower extremities. Although traditionally regarded as a permanent sequela of chronic venous insufficiency (CVI), AB may also arise from diverse etiologies including livedoid vasculopathy, vasculitis, and medication-induced vascular damage. This review aims to clarify the clinical significance of AB, emphasizing the importance of accurate diagnosis and etiology-based management. AB is not a diagnosis itself but a marker of underlying vascular pathology; thus, a thorough clinical assessment- including duplex ultrasound and, in some cases, histopathological and immunological studies-is essential. Management strategies differ depending on the cause: compression therapy and venous interventions for CVI; anticoagulation for livedoid vasculopathy; and drug cessation in cases of hydroxyurea-induced ulcers. Adjunctive treatments such as punch grafting and advanced wound care can enhance healing and reduce pain of ulcerated AB. Multidisciplinary care is critical for optimal outcomes. Although AB is often associated with difficult-to-heal ulcers, emerging evidence suggests that, with targeted treatment, reversal of lesions might be possible. Further research is needed to better understand the pathophysiology and to establish standardized therapeutic protocols.
Chronic venous disease changes the hemodynamics of venous return, causing intraluminal hydrostatic hypertension and congestion. All of this triggers inflammation, tissue damage, and possible nerve damage due to low oxygen levels. Prevalence of neuropathy was identified in patients with chronic venous insufficiency. In a transversal descriptive study, a nonprobability sample of 370 adult patients with chronic venous insufficiency classified as CEAP 3 to 6 (according to clinical, etiological, anatomical, pathophysiological classification) were evaluated in 4 clinics in Guatemala City where they were assessed for neuropathy via the DN4 scale (douleur neuropathique questionnaire). The prevalence of neuropathy in patients with chronic venous insufficiency (CEAP 3 to 6) was 44.6% [95% CI, 28.9-39.9]. No significant differences were observed in the prevalence of neuropathy by sex and age (P=0.655 and P=0.463, respectively); but according to CEAP classification (P<0.001), the higher the degree of CEAP, the higher the prevalence of neuropathy. It was concluded that more than two-fifths of patients with chronic venous insufficiency may develop neuropathy, with this prevalence being higher in patients with more advanced venous disease.
Lipedema is a very frequent chronic disease, frequently underdiagnosed and misdiagnosed and whose pathophysiology is still under research. Patients, most of them women, present with evident disproportion in the distribution of fat between the upper and lower part of the body, swelling, easy bruising, and pain in the lower limbs, and sometimes in the upper limbs. The major aims of its management are to reduce symptoms such as heaviness and pain, reshape the affected limbs, control weight, improve mobility, and improve the quality of life. Setting realistic expectations is important for both patient and medical care providers. Depending on the stage, treatment includes physical therapies, compression garments, exercise, diet, psychological support, and surgical treatment in selected cases. The approach must be integrative and multidisciplinary, looking for a change in patients' habits. Although there is no scientific evidence to support the additional value of using compression garments for managing lipedema, some reports do show benefits in reducing pain in lipedema patients. Clinical guidelines and consensus documents state that compression therapy should be part of the conservative treatment for lipedema, and that patients with lipedema should receive compression garments as part of theirtreatment. The lowest compression class that alleviates the patient's symptoms should be preferred. Further research is needed.
Chronic venous disease is a widespread condition, with telangiectasias and reticular veins (C1 disease according to the CEAP classification) among its most frequent and cosmetically concerning early manifestations. Whereas sclerotherapy remains the gold standard for their treatment, newer approaches have emerged aiming to optimize results and reduce complications. Among them, the combination of transdermal long-pulsed 1064-nm Nd:YAG laser with sclerotherapy has gained growing attention, particularly in the form of the cryo-laser cryo-sclerotherapy (CLaCS) technique, which merges laser-induced vessel damage with sclerotherapy, enhanced by cryo-cooling and augmented reality guidance. Additionally, the sequential use of transdermal laser following foam sclerotherapy has also shown clinical value in improving outcomes. Evidence from randomized trials and long-term follow-up cases points to higher clearance rates, better aesthetic outcomes, and fewer adverse effects when laser and sclerotherapy are used in tandem. The evolving literature, supported by international guideline mentions, reflects increasing clinical acceptance of these multimodal strategies. Drawing from both personal clinical experience and recent studies, this review takes a closer look at the growing evidence behind CLaCS and other laser-sclerotherapy combinations, exploringtheir mechanisms, clinical data, and practical advantages as a patient-centered evolution in phlebology, offering effective minimally invasive solutions that align with what today's patients are really looking for.
Chronic venous disease (CVD) signs and symptoms include heaviness, aching, swelling, throbbing, and itching (HASTI). Advanced stages of CVD include swelling, hyperpigmentation, and venous ulcer. Treatment improves most of the signs and symptoms including healing of venous ulcers. Resolution of swelling is often not achieved and can be due to a variety of reasons. After venous intervention, inconsistent rates of reduction in swelling can be due to misdiagnosis, persistent venous disease, and burnout of the lymphatic system. Patients require comprehensive evaluation to identify potential treatment options. Failure to identify other causes of swelling after venous intervention should prioritize lymphatic health using conservative therapies like compression, exercise, and, potentially, venoactive drugs. The addition of lymphedema management techniques such as manual lymphatic drainage and intermittent pneumatic compression are recommended. Further research is needed to clarify the factors influencing swelling resolution, optimize treatment strategies, and establish evidence-based guidelines for post-intervention care, ultimately improving patient outcomes and quality of life.
Deep venous thrombosis (DVT) is a source of morbidity by way of shortterm, disabling symptomatology and mid-long-term postthrombotic syndrome (PTS), particularly when involving the iliofemoral segment. Catheter-directed interventions for acute iliofemoral DVT have been increasingly used over the past decade to alleviate early symptoms and reduce the incidence and severity of PTS. To achieve these clinical benefits in a safe and durable way certain steps need to be applied involving patient selection, technique of thrombus removal, stenting (or not), and follow-up.
Residual edema is often found after venous interventions. Although several reports mention residual edema, it has not been studied thoroughly and is frequently underreported. There are many reasons for which residual edema occurs and why it is often not emphasized. Such edema is obvious after the intervention, and it can worsen with time. One important reason is the treatment itself that can be inadequate, incomplete, or even inappropriate. Continuity of care, addressing remaining disease, and using compression and medication to reduce inflammation and edema play an important role too. Venous disease may have been long-standing, leading to phlebolymphedema, which is not fully reversible as the lymphatic vessels are permanently damaged. Systemic conditions that are associated with edema are also responsible. Furthermore, patient factors such as lack of physical activity, obesity, and musculoskeletal issues limiting mobility and impairing the muscle pump function contribute as well. Use of different types of medications that are responsible for causing edema should also be considered. The coexistence of lymphedema and lipedema with venous disease can explain the limited response of venous interventions. In a good number of patients, there is idiopathic edema that can be unrelated to venous disease. A good evaluation should be performed, and the practitioners should set the right expectations for patients treated for chronic venous disease
Chronic venous obstruction (CVO) is a debilitating condition affecting millions of individuals, leading to significant morbidity and reduced quality of life. This review aims to explore innovative strategies and evidence- based approaches to enhance the management and long-term outcomes of patients with CVO. Accurate diagnosis and assessment of CVO severity is crucial for guiding appropriate treatment. Noninvasive techniques like duplex ultrasonography, computed tomography (CT) venography, and magnetic resonance (MR) venography can provide detailed information about the venous system. Invasive venography remains the gold standard for evaluating the extent and severity of venous obstruction. Conventional conservative treatments, such as compression therapy, play a crucial role in CVO management. Compression stockings can improve venous return, reduce edema, and alleviate symptoms. Compression therapy has also been shown to enhance the effectiveness of other interventions, such as endovascular procedures. Emerging treatment modalities, including endovascular venous reconstruction and adjunct surgical endophlebectomy, offer promising alternatives for patients with CVO. Endovascular techniques, such as stenting and angioplasty, can effectively restore venous patency and improve clinical outcomes. Surgical endophlebectomy may be considered in complex cases where endovascular options are limited. Multidisciplinary care, involving vascular specialists, wound care experts, and physical therapists, is essential for optimizing patient outcomes. Ongoing research and clinical trials are further exploring innovative strategies to improve the management and long-term prognosis of individuals with CVO.
Over the last few decades, knowledge of microcirculation has expanded in its pathophysiological and molecular bases and its correlations with clinical practice. By observing images of the cutaneous circulation, it is possible to identify the degree of microangiopathy and associate its findings with the evolution of chronic venous disease (CVD). With the progression of venous disease, the cutaneous capillaries lose their typical hairpin shape of healthy individuals and early stages of the disease, become progressively enlarged and tortuous, and form masses or tangles described as glomerulus-like capillaries. In more advanced stages of CVD, there is a reduction in functional capillary density. This reduction in the number of capillaries begins to be observed in C3 and is more important in classes C4, C5, and C6. The result is the replacement of healthy capillaries by large coiled vascular masses, reduced skin perfusion, and the replacement of healthy connective tissue by a chronic fibrosing inflammatory process characteristic of lipodermatosclerosis found in class C4, which eventually leads to skin ulceration. There is currently a consensus that these evolutionary changes in microcirculation are caused by the association of different hemodynamic forces and an intricate inflammatory cascade that results in a vicious cycle of proteolytic remodeling of the venous wall and further inflammation, as well as degradation of the protective endothelial glycocalyx, producing a broad spectrum of clinical symptoms ranging from varicose veins to venous ulcers.
The increased recognition of iliac vein stenosis in the causative effect of venous origin-chronic pelvic pain has led to an ongoing debate of the evaluation, diagnosis, and treatment of patients with pelvic venous disease (PeVD) who present with both iliac venous stenosis and ovarian vein reflux. While ovarian reflux has been thought to play a primary role in the pathophysiology of this disease process, increased evidence suggests that iliac vein stenosis can also lead to chronic pelvic pain and other associated conditions present in these patients, such as chronic venous disease and postural orthostatic tachycardia. Moreover, patient evaluation is confronted by associated nonspecific pelvic symptoms and various anatomical presentations, which are becoming more diagnosable. This is leading to an increase in incidence of patients presenting with combined patterns, which poses a challenge in choosing a treatment algorithm. This article will describe insights to accurately diagnose the disease with its different clinical and anatomical presentations, focusing on the management of combined iliac vein stenosis and ovarian vein reflux in patients with nonthrombotic disease.
The vein known as the "vein of Giacomini" or "Giacomini vein" is part of the venous network of the lower limb and is involved in the drainage of the posterior part of the thigh. This vein owes its name to the Italian professor of anatomy who was the first to describe it in 1873. Giacomini observed that this vein acts as a proximal extension of the small saphenous vein and may follow multiple anatomical courses. Moreover, its most intriguing feature is that it can have more than 1 hemodynamic pattern depending on its valve arrangement and, most interesting, it leads to 2 different types of reflux when this vein becomes incompetent. Minimally invasive surgical options for this vein insufficiency include thermal ablation or ultrasound-guided foam sclerotherapy. These options allow for focused treatment of the leak point for both types of reflux. This article reviews the anatomy of the Giacomini vein, its hemodynamics and reflux variations, and the current treatment modalities for Giacomini-vein-related venous insufficiency.
Obstruction of the inferior vena cava (IVC) is a significant contributor to chronic venous insufficiency (CVI). Patients may present with a wide range of symptoms, from being asymptomatic to suffering from severely debilitating conditions. The causes of IVC obstruction can be congenital, related to malignancies, or nonmalignant. Among these, nonmalignant causes are the most common. The protocol for selecting patients for cava recanalization and stenting must be strict. The clinical basis should guide the procedural approach for inferior cava obstruction. The endovascular technique for addressing proximal deep vein obstruction is now well standardized. Special care should be taken to reconstruct the confluence when applied in the IVC. Considering the low complication rates, satisfactory patency rates, and symptom improvement, the endovascular approach is worth considering to enhance the quality of life for these patients. Although additional high-quality evidence is needed, the benefits outweigh the drawbacks for cava recanalization in selected individuals.
After discontinuing anticoagulation, the risk of recurrent venous thromboembolism (VTE) in patients suffering an episode of unprovoked or weakly provoked VTE ranges between 30% and 50%, the rate being higher in patients with primary deep venous thrombosis (DVT). Baseline parameters that increase this risk are male sex, obesity, carriership of thrombophilia, proximal location of DVT, and renal failure. While the latest international guidelines suggest indefinite anticoagulation for most such patients, new scenarios are being offered through the availability of risk stratification models that have the potential to identify patients in whom anticoagulation can be safely discontinued because of a low risk of recurrence, and those in whom extending anticoagulation is undesirable because of a high risk of bleeding. Low-dose apixaban and rivaroxaban are the mainstay of extended treatment of VTE in all patients, except those who are carriers of the antiphospholipid syndrome. As an alternative, low-dose aspirin and sulodexide have been reported to decrease the risk of recurrent events by 30% to 50% without increasing the bleeding risk
On the basis that in the presence of isolated calf deep venous thrombosis (DVT) fatal pulmonary emboli (PE) did not occur while the patient was in hospital, there was one school of thought that routine anticoagulation was unnecessary and that ultrasound surveillance would suffice, reserving anticoagulation for those in whom the thrombus extends into the popliteal or more proximal veins. However, another school of thought, based on the realization that local damage to the venous valves with the development of reflux and skin changes, and symptoms of persistent pain and edema in 10% to 23% of patients leading to CEAP C4-C6 classes and a DVT recurrence rate of up to 14%, believed anticoagulation should be routine in such patients unless there were serious contraindications. Recent evidence from randomized controlled trials and meta-analyses indicates that isolated calf DVT should be treated. A key message from studies addressing the comparison between direct oral anticoagulants (DOACs) and conventional therapy for the initial and short-term therapy (3-6 months) is that treatment of acute isolated calf DVT with DOACs is as effective as standard therapy; also, it's associated with a statistically significant reduction in the risk of major bleeding complications, clinically relevant as intracranial and fatal bleeding are the most reduced types.
