Venous Insufficiency


Article Author:
Shivik Patel


Article Editor:
Scott Surowiec


Editors In Chief:
Paul DiCesare


Managing Editors:
Frank Smeeks
Scott Dulebohn
Erin Hughes
Pritesh Sheth
Mark Pellegrini
James Hughes
Richard Ciresi
Phillip Hynes


Updated:
11/18/2018 8:58:00 PM

Introduction

Chronic venous insufficiency (CVI) typically refers to lower extremity edema, skin trophic changes, and discomfort secondary to venous hypertension. Chronic venous insufficiency is a prevalent disease process. Disability-related to chronic venous insufficiency attributes to diminished quality of life and loss of work productivity. In most cases, the cause is incompetent valves. Each year approximately 150,000 new patients are diagnosed with chronic venous insufficiency, and nearly $500 million is used in the care of these patients. The CEAP classification (clinical, etiology, anatomy, and pathophysiology) has been developed to guide decision-making in chronic venous insufficiency evaluation and treatment. The system has shown to predict the patient quality of life and severity of their symptoms.[1][2][3]

Etiology

The etiology of chronic venous insufficiency can also be classified as either primary or secondary to deep venous thrombosis (DVT). Primary chronic venous insufficiency refers to the symptomatic presentation without a precipitating event and is due to congenital defects or changes in venous wall biochemistry. Recent studies suggest that approximately 70% of patients have primary chronic venous insufficiency and 30% have the secondary disease. Studies into primary chronic venous insufficiency have identified reduced elastin content, increased extra-cellular matrix remodeling and inflammatory infiltrate. The culmination of which alters the integrity of the vein promoting dilation and valvular incompetence. Secondary chronic venous insufficiency occurs in response to a DVT which triggers an inflammatory response subsequently injuring the vein wall. Irrespective of the specific etiology, chronic venous insufficiency promotes venous hypertension. The most common non-modifiable risk factors are female gender and non-thrombotic iliac vein obstruction (May-Thurner syndrome). Several studies have also suggested a genetic component contributing to vein wall laxity. Modifiable risk factors include smoking, obesity, pregnancy, prolonged standing, DVT, and venous injury.[4][5]

Epidemiology

An estimated six to seven million people within the United States have an existing diagnosis of advanced venous disease and meet diagnostic criteria for chronic venous insufficiency. Results across studies suggest that in the general population between 1% to 17% of men and 1% to 40% of women may experience chronic venous insufficiency. Despite this wide range, non-western countries appear to have a lower overall prevalence. Among all chronic venous insufficiency patients, approximately 1% to 2.7% will develop a venous stasis ulcer. Formation of an ulcer carries a poor prognosis, with 40% of patients developing recurrence despite standard treatment. Management of chronic venous insufficiency accounts for approximately 2% of the United States total healthcare.[6][7]

Pathophysiology

Chronic venous insufficiency pathophysiology is either due to reflux (backward flow) or obstruction of venous blood flow. Chronic venous insufficiency can develop from the protracted valvular incompetence of superficial veins, deep veins or perforating veins which connect them. In all cases, the result is venous hypertension of the lower extremities. Superficial incompetence is usually due to weakened or abnormally shaped valves or widened venous diameter which prevents normal valve congruence. Deep vein dysfunction is usually owing to the previous DVT which results in inflammation, valve scarring and adhesion, and luminal narrowing. Perforating vein valvular failure allows a higher pressure to enter the superficial venous system. The subsequent dilation prevents the proper closure of the valve cusps in the superficial veins. Most patients will also have the disease in the superficial veins. The resting venous pressure is a summation of the outflow obstruction, capillary inflow, valve function, and muscle pump function. Regardless of the cause, the persistently elevated venous hydrostatic pressure may result in lower extremity pain, edema, and venous microangiopathy. Some patients develop permanent skin hyperpigmentation from hemosiderin deposition as red blood cells extravasate into the surrounding tissue. Many of these patients will also have lipodermatosclerosis, which is skin thickening from fibrosis of subcutaneous fat. As the disease progresses, the perturbed microcirculation and dermal weakening can result in ulcer formation.[8]

History and Physical

Patients with chronic venous insufficiency commonly present initially with a combination of dependent pitting edema, leg discomfort, and fatigue, and itching. Although there can be variation in presentation among patients, certain features are more prevalent: pain, cramping, itching, prickling, and throbbing sensation. Patients may describe symptoms that improve with rest and leg elevation, and with no association for exercise. This latter feature can be used to distinguish venous from arterial claudication. As their disease progresses, the presence of varicose veins and tenderness can be noted along with refractory edema and skin changes. Patients with advanced disease will present with a severe blanched skin lesion, dermal atrophy, hyperpigmentation, dilated venous capillaries, and ulcer formation most commonly overlying the medial malleolus. The physical exam must involve a detailed assessment of any ulcers, distal pulses, and neuropathy. A thorough history should note any hypercoagulable condition, oral contraceptive use, previous DVT or intervention, the level of physical activity, and occupation. The patient’s presentation should carefully be distinguished from other pathologies with similar symptoms: diabetic ulcers, ischemic ulcers, and dermatologic conditions including cancer.

Evaluation

In addition to a full history and physical exam, initial evaluation should include objective stratification. Venous reflux testing can identify regions affected and give some indication of the etiology and pathophysiology. Duplex ultrasonography, particularly B-mode imaging, can be helpful for identifying the regions of the affected anatomy. Insufficiency within a venous segment is defined as reflux of more than 0.5 seconds with distal compression. Invasive venography can be used in patients who may require surgery or have suspicion for venous stenosis. Other modalities which may be employed are: ankle-brachial index to exclude arterial pathology, air or photoplethysmography, intravascular ultrasound, and ambulatory venous pressures, which provides a global assessment of venous competence.[9][10]

Treatment / Management

Patients with chronic venous insufficiency should be treated based on their severity and nature of the disease. The treatment goals include reducing discomfort and edema, stabilizing skin appearance, removing painful varicose veins and healing ulcers. Most patients should initially be treated conservatively with leg elevation, exercise (which improves calf muscle pump), weight management, and compression therapy. Ulcers are treated best with compression bandaging systems. Chronic venous ulcerations entail a risk of infection and cancerous transformation (Marjolin ulcer). Compression therapy should be used with caution in patients with the coexisting peripheral arterial disease. Significant arterial insufficiency should be treated before instituting a compression regimen. Patients whose ulcers fail to respond to compression may ultimately need surgical intervention. Superficial vein reflux can be managed with foam sclerotherapy, endovenous thermal ablation, or stripping. Deep vein reflux may be treated with valve reconstruction or valve transplant. Perforator reflux can either be managed with sclerotherapy, endovenous thermal ablation, or with subfascial endoscopic perforator surgery (SEPS). It should be noted, however, that compression therapy regimens that are adhered to are highly effective in treating all forms of venous pathophysiology.[3][11][12]

Differential Diagnosis

  • Lymphedema
  • Cellulitis
  • Stasis dermatitis
  • Varicose veins

Complications

  • Venous ulcer
  • Leg discoloration
  • Thrombophlebitis
  • DVT
  • Pulmonary embolism
  • Bleeding

Enhancing Healthcare Team Outcomes

CVI is best managed by a team of healthcare professionals that include a wound care nurse, vascular surgeon, general surgeon, bariatric nurse, and physical therapist. Most cases of CVI can be treated, but the key is compliance. Patients should be encouraged to wear compression stockings, unless there is a contraindication. Just the use of stockings alone can markedly improve the symptoms and appearance. In addition, the patient should be encouraged to lose weight and avoid standing in one position for prolonged times. [13][14](Level V)

Outcomes

CVI if left untreated leads to very high morbidity and disability. Without treatment, the condition is progressive, ultimately leading to skin breakdown and ulcer formation. And these ulcers are difficult to heal leading to significant pain and increased costs of healthcare. Many patients end up in wound clinics where they are treated for months and years, without any significant benefit. These patients are also at an increased risk for deep vein thrombus and pulmonary embolism. In addition, any minor trauma is associated with torrential bleeding that can sometimes be fatal. [15][16](Level V)


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Venous Insufficiency - Questions

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Which of the following is the best treatment for patients with chronic venous insufficiency?



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In adults, what is the most common cause of chronic, unilateral lower extremity edema?



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Which of the following is NOT a treatment of chronic venous insufficiency?



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62-year-old multiparous female with a history of smoking presents with an ulcer on her left lower extremity. On physical exam, she also has significant edema, dark-brown skin discoloration, and palpable dorsalis pedis and posterior tibial pulses. What is the mechanism of her disease?



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A 55-year-old male, with a long-standing history of chronic venous insufficiency treated with compression stockings, leg elevation, and exercise, presents with a recent 1.5 cm x 1 cm ulcer proximal to his right medial malleolus. He denies any trauma to the area. On physical exam, he also has patchy white angulated scarring surrounding the ulcer. What is the most appropriate next step in managing this patient?



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A 59-year-old female presents for evaluation of her chronic lower extremity discomfort and swelling. Her past medical history is significant for smoking, oral contraceptive use, and obesity. She has a remote history of deep venous thrombosis that was treated medically. On physical exam, she has bilateral swelling and multiple tender varicose veins. Prior to developing a treatment plan, what should be done?



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Venous Insufficiency - References

References

Chamanga ET, Understanding venous leg ulcers. British journal of community nursing. 2018 Sep 1     [PubMed]
Garcia R,Labropoulos N,Gasparis AP,Elias S, Present and future options for treatment of infrainguinal deep vein disease. Journal of vascular surgery. Venous and lymphatic disorders. 2018 Sep     [PubMed]
Schwahn-Schreiber C,Breu FX,Rabe E,Buschmann I,Döller W,Lulay GR,Miller A,Valesky E,Reich-Schupke S, [S1 guideline on intermittent pneumatic compression (IPC)]. Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete. 2018 Aug     [PubMed]
Sutzko DC,Obi AT,Kimball AS,Smith ME,Wakefield TW,Osborne NH, Clinical outcomes after varicose vein procedures in octogenarians within the Vascular Quality Initiative Varicose Vein Registry. Journal of vascular surgery. Venous and lymphatic disorders. 2018 Jul     [PubMed]
Kavousi Y,Al Adas Z,Karamanos E,Kennedy N,Kabbani LS,Lin JC, Men present with higher clinical class of chronic venous disease before endovenous catheter ablation. Journal of vascular surgery. Venous and lymphatic disorders. 2018 Jul 28     [PubMed]
DePopas E,Brown M, Varicose Veins and Lower Extremity Venous Insufficiency. Seminars in interventional radiology. 2018 Mar     [PubMed]
Taylor J,Hicks CW,Heller JA, The hemodynamic effects of pregnancy on the lower extremity venous system. Journal of vascular surgery. Venous and lymphatic disorders. 2018 Mar     [PubMed]
Mutlak O,Aslam M,Standfield NJ, Chronic venous insufficiency: a new concept to understand pathophysiology at the microvascular level - a pilot study. Perfusion. 2018 Aug 1     [PubMed]
Knupfer J,Reich-Schupke S,Stücker M, [Conservative management of varicosis and postthrombotic syndrome]. Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete. 2018 May     [PubMed]
Butaney M,Thirumavalavan N,Hockenberry MS,Kirby EW,Pastuszak AW,Lipshultz LI, Variability in penile duplex ultrasound international practice patterns, technique, and interpretation: an anonymous survey of ISSM members. International journal of impotence research. 2018 Oct     [PubMed]
null Update on Current Care Guideline: Venous insufficiency of the lower limb. Duodecim; laaketieteellinen aikakauskirja. 2017     [PubMed]
Appelen D,van Loo E,Prins MH,Neumann MH,Kolbach DN, Compression therapy for prevention of post-thrombotic syndrome. The Cochrane database of systematic reviews. 2017 Sep 26     [PubMed]
Bozkurt AK,Balkanay OO, [Approach to venous diseases in the elderly]. Turk Kardiyoloji Dernegi arsivi : Turk Kardiyoloji Derneginin yayin organidir. 2017 Sep     [PubMed]
Freisinger E, Compression therapy for deep vein thrombosis - why, yes! VASA. Zeitschrift fur Gefasskrankheiten. 2017 Aug     [PubMed]
Tessari M,Tisato V,Rimondi E,Zamboni P,Malagoni AM, Effects of intermittent pneumatic compression treatment on clinical outcomes and biochemical markers in patients at low mobility with lower limb edema. Journal of vascular surgery. Venous and lymphatic disorders. 2018 Jul     [PubMed]
Xu Z,Hsia HC, The Impact of Microbial Communities on Wound Healing: A Review. Annals of plastic surgery. 2018 Jul     [PubMed]

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