You are in: eMedicine Specialties > Vascular Surgery > MEDICAL TOPICS Chronic Venous InsufficiencyArticle Last Updated: Oct 5, 2006AUTHOR AND EDITOR INFORMATIONSection 1 of 12
  Author: Deron J Tessier, MD, Staff Surgeon, Kaiser Permanente Medical Center, Fontana, CA Deron J Tessier is a member of the following medical societies: American College of Surgeons and American Medical Association Coauthor(s): Russell A Williams, MBBS, Program Director, Professor, Department of Surgery, University of California Medical Center at Irvine Editors: William H Pearce, MD, Chief, Division of Vascular Surgery, Violet and Charles Baldwin Professor of Vascular Surgery, Department of Surgery, Northwestern University School of Medicine; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Vincent Lopez Rowe, MD, Assistant Professor of Surgery, Department of Surgery, Division of Vascular Surgery, University of Southern California Medical Center; Paolo Zamboni, MD, Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy; William H Pearce, MD, Chief, Division of Vascular Surgery, Violet and Charles Baldwin Professor of Vascular Surgery, Department of Surgery, Northwestern University School of Medicine Author and Editor Disclosure Synonyms and related keywords: CVI, superficial venous insufficiency, venous insufficiency, postphlebitic syndrome, postthrombotic syndrome lipodermatosclerosis, superficial venous incompetence, venous incompetence, valvular incompetence, hypercoagulability, Virchow triad, venous stasis, venous stasis ulcers, venous reflux, stasis dermatitis, stasis ulcer, venous ulcer, DVT, deep vein thrombosis, varicose veins, junctional high-pressure disease, perforator high-pressure disease, venous hypertension, varicosities, varicosity, telangiectasia, venectasia, spider vein, vein disease, venous disease, swollen veins, telangiectatic veins INTRODUCTIONSection 2 of 12
  Chronic venous insufficiency (CVI) is a common condition affecting 2-5% of Americans. Historically, CVI was known as postphlebitic syndrome and postthrombotic syndrome, both of which refer to the etiology of most cases. However, these names have been abandoned because they fail to recognize another common cause of the disease, the congenital absence of venous valves. History of the ProcedureIn 1914, Homans postulated that the relative hypoxia of static venous blood decreases the amount of oxygen reaching the skin, causing skin changes and ulcers characteristic of CVI. In 1930, Landis et al demonstrated the direct relationship between venous hypertension in the legs and increased capillary intraluminal pressures. In 1953, Piulacks et al theorized that arteriovenous fistulas in the skin of the lower extremities cause hypoxia, resulting in changes to the skin and tissues. In 1982, Burnand et al presented the fibrin cuff hypothesis, which describes the primary problem as venous hypertension in the lower extremities causing leakage of plasma proteins, particularly fibrinogen. A fibrin cuff encircles affected capillaries, decreasing oxygen diffusion to surrounding tissues. In 1988, Coleridge-Smith et al described the white-cell trapping theory, which hypothesizes that venous hypertension and resultant increased capillary pressures trap white blood cells in the capillaries, where they become activated and damage capillary beds. Increased capillary permeability allows seepage of plasma proteins and fibrinogen into the interstitium, where a fibrin cuff forms, thus decreasing oxygen diffusion to surrounding tissues. ProblemIn addition to poor cosmesis, CVI can lead to chronic life-threatening infections of the lower extremities. Pain, especially after ambulating, is a hallmark of the disease. CVI causes characteristic changes, called lipodermatosclerosis, to the skin of the lower extremities, which lead to eventual skin ulceration. FrequencyCVI is a significant public health problem in the United States. Of all Americans, estimates indicate that 2-5% have some changes associated with CVI. Approximately 24 million Americans have varicose veins. Approximately 6 million Americans have skin changes associated with CVI. Venous stasis ulcers affect approximately 500,000 people. The mean incidence for hospital admission for CVI is 92 per 100,000 admissions. Epidemiology: Peak incidence occurs in women aged 40-49 years and in men aged 70-79 years. EtiologyCongenital absence of or damage to venous valves in the superficial and communicating systems can cause CVI. Venous incompetence due to thrombi and formation of thrombi favored by the Virchow triad (venous stasis, hypercoagulability, endothelial trauma) also can cause CVI (see Image 1). Varicose veins rarely are associated with the development of CVI. Risk factors associated with chronic venous insufficiency
PathophysiologyTwo major mechanisms in the body prevent venous hypertension. First, bicuspid valves in the veins prevent backflow and venous pooling. DVTs commonly occur at these valves, causing irreversible damage to the valve. Second, during normal ambulation, calf muscles decrease venous pressures by approximately 70% in the lower extremities. With rest, pressures return to normal in approximately 30 seconds. In diseased veins, ambulation decreases venous pressures by only 20%. When ambulation is stopped, pressure in the vein lumen increases slowly, returning to normal over a period of minutes (see Image 2). Venous hypertension in diseased veins is thought to cause CVI by the following sequence of events. Increased venous pressure transcends the venules to the capillaries, impeding flow. Low-flow states within the capillaries cause leukocyte trapping. Trapped leukocytes release proteolytic enzymes and oxygen free radicals, which damage capillary basement membranes. Plasma proteins, such as fibrinogen, leak into the surrounding tissues, forming a fibrin cuff. Interstitial fibrin and resultant edema decrease oxygen delivery to the tissues, resulting in local hypoxia. Inflammation and tissue loss result. ClinicalClinical manifestations include the following:
INDICATIONSSection 3 of 12
Surgical treatment is reserved for those with discomfort or ulcers refractory to medical management. Indications for vein ligation: This technique is reserved for cases of CVI that include reflux in the saphenous system causing severe symptoms. For this reason, a diagnosis of reflux must be established preoperatively, usually with photoplethysmography or duplex imaging. RELEVANT ANATOMYSection 4 of 12
The venous network in the lower extremities commonly affected by CVI is divided into 3 systems. The first is superficial veins, which include the lesser and greater saphenous veins and their tributaries (see Image 7). The second is deep veins, which include the anterior tibial, posterior tibial, peroneal, popliteal, deep femoral, superficial femoral, and iliac veins. The third is perforating or communicating veins (see Images 8 and 9). CONTRAINDICATIONSSection 5 of 12
In patients with symptomatic greater saphenous varicosities, the presence of an occluded deep system must be ruled out. Deep occlusion is an absolute contraindication to vein ligation. Obtaining venographic studies of the deep venous system prior to superficial vein ligation is imperative. WORKUPSection 6 of 12
Imaging Studies
Other Tests
TREATMENTSection 7 of 12
Medical therapyNonsurgical treatments for CVI include the following: Leg elevation By keeping the legs elevated, venous flow is augmented by gravity, lowering venous pressures and ameliorating edema. While sitting, the legs should be above the thighs. Supine, the legs should be above the level of the heart. Compression stockings First described by Jobst in 1940, compression stockings produce graded pressures from the foot to the knee or thigh to decrease edema and minimize venous hypertension. Unna boots First described by Unna in 1854, the Unna boot now is the mainstay of treatment for people with venous ulcers. Unna boots are rolled bandages that contain a combination of calamine lotion, glycerin, zinc oxide, and gelatin. Injection sclerotherapy Injection of sclerosing agent directly into veins usually is reserved for telangiectatic lesions rather than CVI. Phlebotonics have not been proven to be beneficial for CVI. Surgical therapyApproximately 8% of patients require surgical intervention for CVI. Surgical treatment is reserved for those with discomfort or ulcers refractory to medical management. Below are several conditions and the surgical options considered appropriate for each. Chronic venous insufficiency resulting from superficial vein disorders Vein ligation is the treatment of choice for superficial vein disorders. Historically, the entire greater saphenous vein system was removed; this has been replaced by the stab evulsion technique. Several 2- to 3-mm incisions are made overlying the greater saphenous at various levels. The vein is dissected from the underlying tissues and any perforators are ligated. A small hook or blunt needle is used to extract as much of the vein as possible. Typically, stab evulsion is limited to areas above the knee in the greater saphenous system to avoid damage to the saphenous nerve or sural nerve. This technique is reserved for CVI in which reflux in the saphenous system occurs and causes severe symptoms. For this reason, a diagnosis (usually accomplished with photoplethysmography or duplex imaging of reflux) must be established preoperatively. Hematoma, sural or saphenous nerve damage, and infection are possible complications of vein ligation. Chronic venous insufficiency resulting from deep vein disorders The decision to operate on a patient with venous obstruction in the deep veins should be made only after a careful assessment of symptom severity and direct measurement of both arm and foot venous pressures. Venography alone is not sufficient because many patients with occlusive disease have extensive collateral circulation, rendering them less symptomatic. Clot lysis (eg, tissue plasminogen activator [TPA], urokinase) and thrombectomy have been tried but have largely been abandoned owing to extremely high recurrence rates. For iliofemoral disease, the operation of choice is a saphenous vein crossover graft. In the procedure, the contralateral saphenous vein is mobilized and divided at its distal end. It then is tunneled suprapubically and anastomosed to the femoral vein on the diseased side. The result is the diversion of venous blood through the graft and into the intact contralateral venous system (see Image 4). Because of a relatively high failure rate of 20%, ringed polytetrafluoroethylene (PTFE) grafts are used. The long-term patency is unknown. Superficial femoral vein occlusion Described by Warren in 1954 and Husni in 1983, the Husni bypass (as it has come to be called) is used to treat occlusion of the superficial femoral vein. The ipsilateral greater saphenous vein is harvested and used as an in situ popliteal-femoral vein bypass. This surgery is performed infrequently due to the high failure rate (approximately 40%). Deep vein incompetence Valvuloplasty is reserved for patients with a congenital absence of functional valves. A venotomy is performed, and the valve cusps are plicated. To ensure an adequate result, plicating 20-25% of each cusp is recommended. The addition of a PTFE sleeve around the operative site is used routinely to maintain valve integrity. When combined with the ligation of perforating veins, valvuloplasty has a superior outcome in 80% of cases after 5 years. With vein segment transposition, a vein with normal function in close proximity to the diseased vessel is identified. The incompetent vein then is dissected, mobilized, and transposed on to the normal vein distal to a functional valve. With vein valve transplantation, a valve-containing segment of a competent axillary or brachial vein is mobilized and inserted into either the popliteal or the femoral systems. The incompetent segment of the leg vein is excised and replaced with the transplant segment. Allograft or cadaveric vein transplants are being tested, with long-term results pending. Preoperative detailsBoth invasive and noninvasive studies are conducted. Invasive studies Contrast venography is the criterion standard for assessing venous reflux, vein abnormalities, and the presence of valves. Ambulatory venous pressure is measured by placing a catheter in a vein on the dorsum of the foot during exercise. Noninvasive studies Commonly, both Doppler bidirectional-flow studies and Doppler color-flow studies are used to assess venous flow, its direction, and the presence of thrombus. Photoplethysmography uses infrared light to assess capillary filling during exercise. Increased capillary filling is indicative of venous reflux and, consequently, incompetent veins. Outflow plethysmography involves placing and subsequently releasing a tourniquet on the lower extremity; the veins should quickly return to baseline pressures, and failure to do so indicates reflux. Intraoperative detailsCareful monitoring of a patient's cardiac status and vital signs is extremely important. In addition, periodic monitoring of hemoglobin and hematocrit levels yields essential intraoperative data. Postoperative detailsAnticoagulation with heparin (or low molecular weight heparin) in the immediate postoperative period and long-term prophylaxis with Coumadin are recommended. Follow-upPatients should be observed frequently for wound infection after discharge, beginning 1 week postoperatively. Sutures or staples typically stay in 2-4 weeks, depending on the health of the skin at the operative site. For excellent patient education resources, visit eMedicine's Circulatory Problems Center. Also, see eMedicine's patient education article Varicose Veins. OUTCOME AND PROGNOSISSection 8 of 12
Hematoma, sural or saphenous nerve damage, and infection are possible complications of lower-extremity vein ligation. Clot lysis (eg, TPA, urokinase) and thrombectomy have been tried but generally have been abandoned due to extremely high recurrence rates. For iliofemoral disease, the operation of choice is a saphenous vein crossover graft. Due to a relatively high failure rate of 20%, ringed PTFE grafts are being used. The long-term patency is unknown. The Husni bypass for superficial femoral vein occlusion is performed infrequently due to the high failure rate (approximately 40%). Surgery for CVI resulting from deep vein incompetence includes valvuloplasty and allograft or cadaveric vein transplant. Valvuloplasty for patients with congenital absence of functional valves, when combined with the ligation of perforating veins, has a superior outcome in 80% of cases after 5 years. Allograft or cadaveric vein transplants are being tested, with long-term results pending. Tsai et al examined the National Inpatient Sample from 1988-2000 and found that mean hospital charges were $13,900 and did not change over the time period examined. They also found that deep venous thrombosis affected 1.3% of patients and amputation was necessary in 1.2%, with an overall mortality of 1.6%. FUTURE AND CONTROVERSIESSection 9 of 12
Subfascial endoscopic perforator surgery (SEPS) is gaining in popularity as a means of treating CVI. Endoscopic techniques are used to find and ligate perforating veins. Preliminary reports are encouraging. The 1997 North American Subfascial Endoscopic Perforator Surgery Registry showed that after SEPS, the average healing time for ulcers was 42 days, with a recurrence rate of 3%. Ulcers treated with SEPS heal 4 times faster than ulcers treated conventionally. In addition, morbidity of SEPS is significantly lower than traditional operations. Long-term results are pending. ACKNOWLEDGMENTSSection 10 of 12
The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Yale D Podnos, MD, MPH to the development and writing of this article. MULTIMEDIASection 11 of 12
REFERENCESSection 12 of 12
Chronic Venous Insufficiency excerpt Article Last Updated: Oct 5, 2006 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
