Venous insufficiency: Rehabilitation management of venous stasis and postphlebitic syndrome

Author(s): Sikha Guha, MD, Eathar Saad, MD

Originally published:09/20/2014

Last updated:09/20/2014

1. DISEASE/DISORDER:

Definition

Chronic venous disorders (CVDs): a spectrum of morphologic and functional abnormalities of the venous system from telangiectasias to venous ulcers.1

Venous insufficiency: a fixed venous outflow disturbance of the limbs as a result of a malfunctioning venous system.2

Post-thrombotic syndrome (PTS): a complication occurring 1 to 2 years after deep venous thrombosis (DVT) despite optimal anticoagulation therapy.3,4

Epidemiology including risk factors and primary prevention

The prevalence of chronic venous insufficiency ranges from less than 1% to 17% in men and less than 1% to 40% in women based on the different populations studied.5The incidence of PTS is about 50% in the first year, despite optimal anticoagulation.

Severe PTS (ulceration) will affect one third of patients by 6 years.6,7Established risk factors for venous insufficiency include family history, older age, sex, obesity, occupation, and diet.5Risk factors for PTS include incomplete resolution of signs/symptoms 1 month after DVT, DVT of proximal veins, previous ipsilateral venous thrombosis, obesity, and older age. In one study, patients with a subtherapeutic international normalized ratio more than 50% of the time during the initial 3 months of treatment for DVT with vitamin K antagonists had a 3-fold increased risk for developing PTS.

Primary prevention of PTS includes the following:

  1. Thromboprophylaxis to prevent DVT in high-risk hospitalized patients.
  2. Reduce risk of recurrent DVT by appropriate anticoagulation after acute DVT.
  3. Use elastic compression stockings (ECS) with ankle pressure gradient of 30 to 40 mm Hg for at least 2 years if patients have symptomatic, proximal DVT and symptoms of PTS.
  4. Thrombolysis of acute DVT followed by standard anticoagulant therapy.8

Patho-anatomy/physiology

The venous network in the lower extremities is divided into superficial, deep, and perforating veins. The deep veins within the calf muscles are the main conduit for venous blood to return to the heart. The superficial compartment is a low pressure chamber. The deep compartment is a high pressure chamber because of the calf muscle pump. The perforator veins connect the deep and superficial veins. When the calf muscles (muscular systole) contract, the perforator valves close, preventing transmission of high pressure to the superficial veins. When the calf muscles relax (muscular diastole) the pressure in the superficial compartment is higher than the deep veins causing a reversal of blood flow.5

Chronic venous insufficiency (CVI) results from venous hypertension caused by valvular incompetence leading to extravasation of macromolecules and red blood cells, microvascular endothelial cell activation, and leukocyte diapedesis. Alteration of the extracellular matrix produces intense collagen deposition. Microcirculatory changes are mediated by increased levels of transforming growth factor-β1 and its effect on matrix metalloproteins and tissue inhibitors of metalloproteinase production. The presence of mast cells suggests a regulatory role in ulcer formation.9

Pathophysiology of PTS starts with an obstructive thrombus causing damage to the vein wall, initiating an inflammatory response. A phenotypic change of the vascular smooth muscle cell occurs, which promotes collagen and other matrix accumulation, vein wall fibrosis, and stiffness.10

Specific secondary or associated conditions and complications

Of patients with DVT, 5% to 10% develop severe PTS, including ulcers, which is precipitated by trauma to the gaiter area (perimalleolar).8

2. ESSENTIALS OF ASSESSMENT

History

Medical history should include the following:

  1. Family history
  2. Pregnancies
  3. Age
  4. Previous DVT/thrombophlebitis
  5. Medications/oral contraceptives
  6. Smoking
  7. Pain in the limbs/pelvis
  8. Skin changes/ulcers
  9. Edema
  10. Prior treatments/compression therapy11

Physical examination

Examine patients in a warm, well-lit room while standing to allow physiologic distention of the veins.

  1. Note the distribution of abnormal spider veins, telangiectasias, ankle or malleolar flare, size, location, and distribution of varicose veins, skin changes, edema, location of active or healed ulcers, and inflammatory changes
  2. Palpation for venous cords
  3. Measure bilateral calf and ankle circumference at a consistent time of day
  4. Pedal pulses for underlying arterial disease
  5. Ulcer description
  6. Ankle mobility
  7. Auscultation for bruits
  8. Neurologic exam12

Functional assessment

Patients with CVD and venous leg ulcers have poorer quality of life (QOL) in all aspects of daily living compared with the general population. Pain is the main factor that impacts QOL. Other factors are decreased mobility, social and emotional isolation, sleep disorders, depression, feeling of uncleanliness because of the malodorous ulcers, and problems finding appropriate footwear. Loss of employment has a significant social impact.13

Imaging

Duplex scanning is recommended as the first diagnostic test for all patients with suspected CVD.

  1. Air plethysmography (APG) is used for assessing severity of disease. APG can evaluate calf muscle pump function and quantify global venous reflux and outflow obstruction.
  2. Venography is indicated in more complex postthrombotic disease and preoperatively because it provides more detail than duplex ultrasonography.14
  3. A repeat duplex scan is indicated to evaluate recanalization for recurrent DVT and ulcers.

Supplemental assessment tools

The Villalta score is the only scale that is specific for the diagnosis and categorization of PTS. Points are given to the following symptoms: pain, cramps, heaviness, paresthesia, and pruritis. Clinical signs scored are pretibial edema, skin induration, hyperpigmentation, redness, venous ectasia, and pain on calf compression. Points ranging from 0 to 3 for each of these elements are recorded. PTS is diagnosed if the Villalta score is greater than 5 or if an ulcer is present. A score of 5 through 9 signifies mild disease, 10 to 14 signifies moderate disease, and greater than 15 (ulcer) signifies severe disease. The score has also been used on follow-up to assess the effectiveness of treatment.15

Environmental

Environmental and behavioral factors associated with CVI include prolonged sitting and standing at work.12

Social role and social support system

The socioeconomic impact of CVI is significant because it is the seventh leading cause of chronic disability in the United States.9This results in impaired ability to engage in social and occupational activities, reducing QOL and imposing financial constraints. Disability related to venous ulcers leads to loss of productive work hours (estimated at 2 million work days per year). Of workers with venous ulcers, 12.5% will retire prematurely. The financial burden on the health care system is estimated at $2 to $3 billion annually for the treatment of venous ulcers.12

3. REHABILITATION MANAGEMENT AND TREATMENTS

Available or current treatment guidelines

Lifestyle modifications (weight loss, diet, exercise, leg elevation, ECS) are recommended.

Venoactive drugs (diosmin, hesperidin, rutosides, micronized purified flavonoid fraction [MPFF], horse chestnut seed extract) are used for pain and swelling. Pentoxifylline or MPFF accelerate healing of venous ulcers.12

Compression therapy

  1. Graduated ECS with higher pressure at the ankle are the cornerstone of CVD management.
  2. Knee-length stockings are as effective as thigh-length stockings, easier to apply, more comfortable, have better compliance, and are cheaper.16
  3. Stockings with 30 to 40 mm Hg compression pressure are recommended for C5-6 CVI; 20 to 30 mm Hg are recommended for symptomatic varicose veins and mixed venous and arterial disease.
  4. Unna boot (50-60 mm Hg pressure) is used for ambulatory patients unable to tolerate graduated ECS.
  5. Multilayer bandages (40 mm Hg pressure) are more effective in healing ulcers.
  6. Indications for intermittent pneumatic compression are nonambulatory patients, need for higher compression, patients not responding to stockings/wraps, or patients with very large legs who cannot tolerate stockings/wraps.14

Exercise has a role in patients with acute or previous DVT. Early walking and habitual physical activity do not worsen symptoms in DVT and improve calf-muscle pump and QOL.6,7

At different disease stages

The clinical, etiology, anatomy, pathophysiology (CEAP) classification is a useful guide for treatment at different stages of the disease.

  1. In CEAP class 1, patients display spider veins and telangiectasias.
  2. In class 2, patients have varicose veins. They have mild symptoms and no venous insufficiency. No treatment is recommended. For cosmetic concerns, vein stripping, endovenous thermal ablation (EVLA), or foam sclerotherapy may be prescribed, along with ECS of 20 to 30 mm Hg.
  3. CEAP class 3 displays edema. Treatment is similar to CEAP classes 1 and 2.
  4. CEAP class 4a displays edema and early skin changes (eg, pigmentation, eczema). This is indicative of venous reflux, which is sufficiently severe to cause venous hypertension. Daily compression and/or correction of venous hypertension by venous ablation or other techniques are recommended.
  5. CEAP class 4b has severe skin changes, lipodermatosclerosis, significant tissue inflammation, or induration. These patients are at a higher risk to progress to ulceration. They need a corrective venous procedure.
  6. CEAP classes 5 (healed ulcer) and 6 (active ulcer) should undergo correction of venous hypertension to speed the healing of the ulcer and prevent recurrence. The preferred procedure for correction of reflux in the perforator veins is subfascial endoscopic perforator surgery. Newer, less invasive techniques (eg, percutaneous ablation of perforators, EVLA, ultrasound-guided sclerotherapy) are less well studied.14,17

Surgical repair of incompetent valves have resulted in 65% to 80% healing of stasis ulcers at 5 years and some even at 15 to 20 years. Venous stenting is minimally invasive and a much easier procedure. Two thirds of patients with venous stasis ulcers have healed following stent placement. However, a third will have recalcitrant ulcers and require valve reconstruction.9

Lifelong ECS with 30 to 40 mm Hg compression is recommended to prevent recurrence of ulceration.14,17

Coordination of care

Multidisciplinary care of patients with CVD includes medical practitioners, vascular surgeons, dermatologists, wound care specialists, and psychologists. Nursing is the most important discipline; they are the leaders in this field and are responsible for the continuum of care in the home and clinics. Patients treated in nurse-led leg ulcer clinics experienced better QOL.13

Patient & family education

Education should focus on life-long use of ECS, leg elevation, smoking cessation, exercise, avoiding trauma to the legs, weight management, and nutrition.18Home-based exercises to improve calf-muscle pump function is recommended.18It has been suggested that stretching, leg strengthening/flexibility, and walking for 45 to 60 minutes 3 times per week for 6 months improves overall fitness, disease-specific QOL measures, and severity of PTS.19

Emerging/unique Interventions

Commonly used generic QOL measures include the Medical Outcomes Study 36-Item Short-Form Health Survey and visual analog scale. Disease-specific scales include the Venous Insufficiency Epidiomologic and Economic Study of Quality of Life and Charing Cross Venous Ulceration Questionnaire.14

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

  1. Lifestyle modification is important in prevention and mangement of CVI.
  2. Compression therapy is the mainstay of management.

4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE

Cutting edge concepts and practice

  1. The association of circulating biomarkers with CVI.
  2. Use of D-dimer levels to identify patients at risk for DVT recurrence after discontinuing anticoagulation.
  3. Use of statins in the prevention of DVT and PTS.
  4. Prosthetic valves for venous system.10
  5. Recently, a multicenter, randomized, placebo-controlled trial of active versus placebo ECS used for 2 years to prevent PTS after a first proximal DVT found similar cumulative incidences of PTS in both groups and did not support routine use of ECS after DVT.20

5. GAPS IN THE EVIDENCE-BASED KNOWLEDGE

Gaps in the evidence-based knowledge

  1. There is no standard score for the diagnosis of PTS.15
  2. Lack of QOL measures in current disease-specific scales.15
  3. Venoactive drugs have not been studied intensively for the treatment or prevention of PTS.10

REFERENCES

1. Eklöf B, Rutherford RB, Bergan JJ, et al. Revision of the CEAP classification for chronic venous disorders: consensus statement.J Vasc Surg. 2004;40(6):1248-1252.

2. Kasperczak J, Ropacka-Lesiak M, Breborowicz HG. [Definition, classification and diagnosis of chronic venous insufficieny – part II] [Polish].Ginekol Pol.2013;84(1):51-55.

3. Prandoni P, Lensing AW, Cogo A, et al. The long-term clinical course of acute deep venous thrombosis.Ann Intern Med. 1996;125(1):1-7.

4. Kahn SR, Shrier I, Julian JA, et al. Determinants and time course of the post thrombotic syndrome after acute deep venous thrombosis.Ann Intern Med. 2008;149(10):698-707.

5. Beebe-Dimmer JL, Pfeifer JR, Engle JS, Schottenfeld D. The epidemiology of chronic venous insufficiency and varicose veins.Ann Intern Med. 2008;149(10):698-707.

6. Gabriel F, Labois M, Portoles O, et al. Incidence of post-thrombotic syndrome and its association with various risk factors in a cohort of Spanish patients after one year follow-up following acute deep venous thrombosis.Thromb Haemost. 2004;92(2):328-336.

7. Roumen-Klappe EM, Heijer MD, Janssen MC, et al. The post-thrombotic syndrome: incidence and prognostic value of non-invasive venous examinations in a six year follow-up study.Thromb Haemost. 2005;94:825-830.

8. Kahn SR. The post-thrombotic syndrome.Hematology Am Soc Hematol Educ Program. 2010;2010:216-220.

9. Meissner MH, Gloviczki P, Bergan J, et al. Primary chronic venous disorders.J Vasc Surg.2007;46 Suppl S:54S-67S.

10. Henke PK, Camerota AJ. An update on etiology, prevention, and therapy of post thrombotic syndrome.J Vasc Surg. 2011;53(2):500-509.

11. Mowatt-Larssen E, Desai SS, Dua A, et al.Phlebology, Vein Surgery and Ultrasonography: Diagnosis and Management of Venous Disease. Switzerland: Springer; 2014.

12. Eberhardt RT, Raffetto JD. Chronic venous insufficiency.Circulation. 2005;111(18):2398-2409.

13. Gonzalez-Consuegra RV, Verdu J. Quality of life in people with venous leg ulcers: an integrative review.J Adv Nurs. 2011;67(5):926-944.

14. Gloviczki P, Camerota AJ, Dalsing MC, et al. The care of patients with varicose veins and associated chronic venous diseases: clinical practice guidelines of the Society for Vascular Surgery and the American Venous Forum.J Vasc Surg. 2011;53(5 Suppl):2S-48S.

15. Soosainathan A, Moore HM, Gohel MS, Davies AH. Scoring systems for the post thrombotic syndrome.J Vasc Surg. 2013;57(1):254-261.

16. Prandoni P, Kahn SR. Post-thrombotic syndrome: prevalence, prognostication and need for progress.Br J Haematol. 2009;145(3):286-295.

17. Marston WA. Evaluation of varicose veins: what do the clinical signs and symptoms reveal about the underlying disease and need for intervention.Semin Vasc Surg. 2010;23(2):78-84.

18.Wound, Ostomy, and Continence Nurses Society (WOCN). Guidlines for Management of Wounds in Patients With Lower Extremity Venous Disease: WOCN Clinical Practice Guidline Series No. 4. 2011.

19. Kahn SR, Shrier I, Shapiro S, et al. Six-month exercise training program to treat post-thrombotic syndrome: a randomized controlled two-centre trial.CMAJ. 2011;183(1):37-43.

20. Kahn SR, Shapiro S, Wells PS, et al. Compression stockings to prevent post-thrombotic syndrome: a randomized placebo-controlled trial.Lancet. 2014;383(9920):880-888.

Author Disclosures

Sikha Guha, MD
Nothing to Disclose

Eathar Saad, MD
Nothing to Disclose

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