Venous hypertension, caused by venous reflux, often leads to heaviness, swelling, and pain in the legs. However, the hemodynamics of venous flow are complex and incomprehensible, with a frequently unclear correlation between reflux and symptoms. Regarding treatment options, removal of saphenous veins (SVs) based on a few seconds of reflux can adversely affect patients. Further, indiscriminate removal of SVs in aging populations may complicate future treatment of arterial diseases. Patients should be treated selectively based on ultrasound examinations and hemodynamic principles. The CHIVA strategy, which involves treating patients without removing SVs, is a potential treatment option for patients with mild chronic venous insufficiency. In this context, we introduce the Teupitz shunt classification, which forms the basis for hemodynamic correction.

Although varicose veins are known to have a very high prevalence, there are many different treatment methods available. The optimal extent of treatment for the incompetent great saphenous vein has not yet been clearly established. Recent guidelines recommend the proper extent and method of treatment based on expert opinion. Considering complications and subjective data, such as symptoms and quality of life, above-the-knee treatment could be suggested. However, in terms of recurrence and objective data, below-the-knee treatment might be preferred. It would be better to approach treatment on a customized basis for each patient by carefully analyzing the results based on both subjective and objective data.

Varicose veins are consistent with physically dilated superficial veins ≥3 mm. Physiologically, chronic venous insufficiency is an advanced chronic venous disease with functional abnormalities. Essentially, the shape of the vein is directly influenced by hydrostatic pressure. Ambulatory venous pressure is increased as shunt formation and vein will be dilated by the connection with deep venous refluxes. Hydrostatic parodox in varicose veins is that the ambulatory venous pressure is not directly related with vein diameter but with shunt formation with valve insufficiency. Mean ambulatory venous pressure of 10–30 mmHg is considered as normal, 31–45 mmHg as intermediate and >45 mmHg as severe venous hypertension. Diameter measurement is used in the diagnosis of varicose veins, but treatment need to be more focused to remove hydrostatic pressure rather than diameter of vein in respect to improve symptoms related with varicose veins. Nevertheless, there are some concerns for the treatment of large veins. From the guidelines endothermal ablation is recommended than non-thermal ablation for >10 mm large varicose vein. Large veins might increase the incidence of endothermal heat induced thrombosis. Caprini score more than 7 will be benefited from chemoprophylaxis for large vein. For the compression therapy, inelastic compression is recommended than elastic compression to improve the function of calf muscle pump.

Venous thromboembolism (VTE), a severe condition comprising deep vein thrombosis and pulmonary embolism, requires prompt treatment. Traditional therapies include heparin, low-molecular-weight heparin, and warfarin. Direct oral anticoagulants (DOACs) such as dabigatran, rivaroxaban, apixaban, and edoxaban has revolutionized VTE management. Clinical trials show that DOACs are as effective as traditional anticoagulants in preventing recurrent VTE, with similar or lower rates of major bleeding. However, DOAC use is complex in vulnerable populations—those with comorbidities, chronic kidney disease, cancer, and advanced age—due to higher VTE and bleeding risks from polypharmacy and altered pharmacokinetics. Trials have shown promising results for DOACs, but these studies often include few patients from these high-risk groups. Moreover, while DOACs are validated for atrial fibrillation, these findings may not apply directly to patients with VTE due to different dosing. In this study, we aimed to address this gap by reviewing the literature on the efficacy and safety of DOACs in these vulnerable populations.

Venous flow normally circulates from the skin to superficial veins, which drain into the deep veins and the heart. Venous reflux refers to blood flow that flows in the opposite direction. Venous reflux is caused by gravity and valvular insufficiency. Diagnosing venous reflux is important to determine treatment for lower extremity venous disease. Unlike arteries, venous reflux is greatly affected by the relative position of the probe and the vessel. Standardized ultrasound images are required to verify venous reflux using ultrasound. It is important to perform the reflux provocation test using the standardized posture and method.

The calf muscle pump is the motive force enhancing venous blood return from the lower extremity to the heart. It causes displacement of venous blood in both vertical and horizontal directions, generates ambulatory pressure gradient between the thigh and lower leg veins, and bidirectional streaming within calf perforators. Ambulatory pressure gradient triggers venous reflux in incompetent veins, inducing ambulatory venous hypertension in the lower leg and foot. Bidirectional flow in calf perforators enables quick pressure equalization between deep and superficial veins of the lower leg; the outward (into the superficial veins) oriented component of the bidirectional flow taking place during calf muscle contraction is not a pathological reflux but a physiological centripetal flow streaming via the great saphenous vein into the femoral vein. Calf perforators are communicating channels between both systems, making them conjoined vessels; they are not involved in generating pathological hemodynamic situations and do not cause ambulatory venous hypertension. Pressure gradient arising during calf pump activity between the femoral vein and the saphenous remnant after abolishing saphenous reflux triggers biophysical and biochemical events, which might induce recurrence. Thus, abolishing saphenous reflux removes the hemodynamic disturbance but simultaneously generates a precondition for reflux recurrence and the return of the previous pathological situation; this chain of events has been termed the hemodynamic paradox. But this review showed that varicose veins could be improved quickly through lower leg muscles (especially calf muscle) regeneration by increasing mitochondrial cellular energy (adenosine triphosphate) of leg muscles without removing varicose veins.

In the patient with chronic venous disease, venous hypertension occur which result in inability of calf pumps and conduits in the venous system to maintain a normal pressure and normal flow towards the heart. Venous hypertension is caused by venous reflux, obstruction, a combination of reflux and obstruction or arterio-venous fistula. Compensation for obstruction are the development of collateral vein circulation and lymphatic drainage. The clinical symptoms and signs are a result of the venous hypertension and the lack of compensation. Inability to quantitate these factors in individual patients contributes to an incomplete understanding of the pathophysiology, leading to controversies and significant challenges in managing chronic venous disease.

The clinical importance and optimal management of chronic Gastrocnemius vein (GCV) incompetence have rarely been discussed. In case of an incompetent GCV with varicose degeneration, surgical management of intramuscular varicose vein may be challenging. Combined treatment using endovenous laser ablation and ultrasound-guided foam sclerotherapy for tortuous and dilated left lateral gastrocnemius vein incorporating distal muscular trunk as well as proximal main trunk, showed acceptable early outcome. Longer-term follow-up is warranted to verify the benefits from this novel non-surgical approach for deep-seated vein abnormalities.

Iliofemoral venous outflow obstruction, arising from nonthrombotic iliac vein lesions (NIVLs) or post-thrombotic disease (PTs), is a frequent culprit behind chronic venous signs and symptoms. In response, the adoption of deep venous stenting has gained traction, demonstrating commendable technical success and acceptable complication rates in the management of both acute and chronic venous obstruction. However, the focus on venous stent failure has intensified due to concerns related to in-stent restenosis or thrombosis. Such complications elevate the risks of symptom recurrence and thrombosis relapse, necessitating a judicious approach. The identified contributors to venous stent failure encompass multifaceted factors, including insufficient coverage of the affected area, inadequate vein inflow, inappropriate stent sizing, suboptimal drug therapy, patient non-compliance, stent migration, or fracture. This paper provides a comprehensive exploration of these factors associated with venous stent failure, shedding light on the complexities surrounding the efficacy and longevity of deep venous stenting in the context of iliofemoral venous outflow obstruction.