Recent Published Articles

Lower Extremity Chronic Venous Disease

Cardiopulmonary Physical Therapy Journal, Sep 2004 by Lampe, Katherine E

ABSTRACT

Purpose: Chronic, systemic venous disease negatively impacts a person physically, emotionally, and financially. Reducing cost of venous disease management and improving quality of care are necessary. This paper provides clinicians with an understanding of lower extremity peripheral vein structure/function, clinical disease manifestations, and ramifications. Summary of Key Points: Lower extremity peripheral veins include the superficial, perforating, and deep systems. Veins typically have 3 layers: tunica intima, media, and adventitia. Systemic vein functions include: conducting deoxygenated blood to the right atrium of the heart, interstitial/extrastitial barrier, circulatory pressures maintenance, bioactive substances production (ie, nitric oxide), blood storage, thrombosis inhibition, and other special local functions. Vein pathology presented includes: valve failure, skeletal and smooth muscle pump failure, vein incompetence, and insufficiency. Various venous tests and measures are discussed. Appropriate interventions are presented for varicose veins, chronic venous insufficiency, and venous wounds. Conclusion: Chronic venous disease of the lower extremity is a common and costly entity. In order for appropriate, effective care to be provided, clinicians need a complete understanding of lower extremity vein anatomy, pathology, as well as issues related to examination/evaluation and interventions.

INTRODUCTION

Systemic veins are often an unappreciated circulatory component. The venous system stores 75% of blood volume, the majority in the small veins and venules.1 However, veins are more than just vessels for blood storage and transportation. Clinicians need an understanding of normal vein structure, function, and clinical ramifications of vein pathology. These often-ignored vascular structures definitely have an impact on patient health and well-being. Venous pathology such as varicose veins, chronic venous insufficiency (CVI), and venous ulcers has implications for patients and the health care system. For example, it is estimated that 25% of people in western countries have varicose veins.25 Chronic venous insufficiency affects around 5% of people in developing countries.6 Furthermore, it is estimated that 1% of the population and 3.5% of those 65 years or older have venous ulcers.7 The cost for treating venous disease is significant. It is estimated that more than $1 billion are spent each year for CVI treatment.8 The total cost of venous wound management is around $2.5 to 3.5 billion per year.9 Also, 2,000,000 workdays are lost per year due to venous wounds.8-10 Obviously, chronic venous disease is a significant health concern. With today's medical costs and reimbursement issues, reducing costs for venous disease and improving quality of care are necessary. Besides the financial impact, chronic venous disease also affects a person physically and emotionally. Due to venous disease consequences, a review of the venous system and pathology is warranted. Consequently, this paper will review lower extremity vein anatomy, histology, physiology, and pathology, as well as present examination, evaluation, and interventions issues.

VEIN ANATOMY, HISTOLOGY, AND PHYSIOLOGICAL FUNCTION

The venous system originates at the capillary bed and ends at the right side of the heart (Table 1). In the capillary bed, venules connect the arterial system to the venous system. Venules are very small in diameter (around 20 micrometers) and oval shaped at rest. When pressures increase, they become more circular. While blood vessels typically have 3 distinct layers, the end venules have only an endothelial layer with a thin layer of collagen fibers (tunica intima). As venules increase in diameter and become visible veins, they have the typical 3 layers mentioned earlier.11 See Table 2 for description of the 3 layers of veins. There are 3 different types of lower extremity veins: superficial, perforating, and deep veins. The superficial veins conduct blood from the skin and subcutaneous tissue. The perforating veins connect the superficial veins to the deep veins that convey blood from the periphery to the heart. One anatomical structure the perforating, superficial, and deep veins have in common is valves. The superficial veins have fewer valves than the deeper veins.13 Vein valves are bicuspid and avascular. They consist of thin sheets of collagen and smooth muscle with an endothelial covering. Valves appear to become less flexible as people age.12 The valves prevent retrograde blood flow, thus allowing veins to overcome gravity effects (Figure 1). The pathophysiology of valve failure will be covered later. The reader is encouraged to consult anatomical and histological references for further information on vein anatomy and histology.

The main, superficial leg veins include the greater (long) saphenous, lesser (small/short) saphenous, and the lateral (subdermic) venous system (Figure 2). These veins are very thin walled and distensible. The superficial veins lie above the main fascial plane and are the primary blood collection system for the lower leg. They lack the extensive fascial restriction experienced by the deep veins. Consequently, superficial veins may undergo dramatic volume changes or distention.12 The superficial venous system has multiple collateral veins with connections between the veins themselves. These veins are called accessory, anastomotic, tributary, or communicating veins. Most collateral veins are not named.12 Consult Table 3 for the anatomical descriptions and common areas of reflux (retrograde blood flow) in the superficial system. The greater saphenous vein, also known as the long saphenous vein, is located on the medial aspect of the lower extremity. The greater saphenous does have some fascial support so it has less potential for distention.12 The lesser (small or short) saphenous vein is on the posterior-lateral lower leg and foot. The lateral venous system (lateral subdermic) above/below the knee is a common area for varicosities during pregnancy and occasionally puberty.12 The superficial veins deliver blood to the deep veins, such as the femoral and popliteal veins (see in the deep system). However, the superficial system also connects to perforating veins.

The lower extremity perforating veins have a very fitting name since they penetrate fascia and connect the superficial venous system to the deep veins. see Table 4 for common perforating veins. Muscle contraction within the confines of fascial planes produce pressure that assists blood movement from perforators into the deep veins (muscle pump). The muscle pump is called into action during prolonged postures. For example, during prolonged standing, the lower extremity venous system fills with blood. This circulatory stagnation triggers leg movement to empty veins via the muscle pump, as well as norepinephrine release causing smooth muscle contraction to limit venous capacitance.12 There are 2 kinds of perforating veins: direct perforators linking superficial to deep veins with no intermediaries and indirect perforators that do the same but through muscular venous channels.12 Perforating veins have thin walls, are small in diameter (1-2 mm), and have valves. The upward, oblique orientation of these veins prevents retrograde blood flow (in this case, blood flow from deep system back to superficial).13 The lower leg and foot have more perforating veins than the upper leg. There are about 8 perforator veins in the lower leg for every inch of thigh (ie, a 15 inch thigh may have around 120 perforating veins in the lower leg).12 Perforating veins are located on the sides of the sartorius/peroneals and between the vastus lateralis and hamstrings.14 Clinically, it is important to know that perforator hypertension can be conveyed back to the superficial veins.

In the legs, deep veins often run parallel to superficial veins. The perforating veins mentioned previously, connect superficial veins to deep veins like slanted rungs of a ladder. The deep veins lie below fascia and are enclosed by more dense tissue. Deep veins may be paired or found in multiples. They are conduits for blood flow return from the lower extremities. See Table 5 for a listing of the deep veins of the lower extremity. The deep veins return lower extremity blood to the right atrium via mechanisms such as: skeletal muscle pump, controlled venous diameter, abdominal-thoracic pressure changes from respiration, high pressure on the arterial side, and the low right atrium pressure that draws blood from the great veins.13,15

A well-known vein function is conveyance of blood to the heart/lungs for gas, nutrient, and waste exchange. Another commonly known vein function is the storage of large blood volume.13,15,16 Uncommon or less known vein functions warrant review. The reader is referred to a paper by Monos and colleagues16 who wrote a comprehensive review of vein function. For example, veins are barriers between intravascular and extravascular tissues. The proximal venules allow movement of interstitial fluids, large molecules, and white blood cells through the venule wall. Vein walls also have cellular functions. White blood cells attach to vein endothelium in order to be available should there be an injury or disease process.16 Veins also are a factor in cardiovascular pressures. In the capillary bed, veins influence arterial output resistance. Vein walls produce nitric oxide that causes vasodilation via decreased vascular tone. Nitric oxide has been linked with monochromatic infrared interventions for diabetic peripheral neuropathy, pain management, and wound healing16-19 Veins also have a role in heart filling pressure. The skeletal muscle pump, venous myogenic response, and venous smooth muscle tone prevent orthostatic hypotension.16 The venules also appear to be a site of angiogenesis. Venous endothelium has a role in lessening platelet aggregation to prevent clot development via the formation of Prostacyclin-PG12. Lastly, veins have other unique, regional functions. For example, facial veins allow for blushing and temperature regulation of the head. Cutaneous veins help regulate body/skin temperature. The internal jugular vein facilitates cranial pressure regulation. Lastly, according to Monos et al,16 the proximal portion of the caval and pulmonary veins may play a role in cardiac pacing. Their tunica media layers have cardiac myocytes that might provide cardiac pacing during some pathological conditions.16 It is clear veins are much more than blood thoroughfares.

PATHOGENESIS OF VENOUS DISEASE

Venous pathology includes valve failure, venous reflux, and venous hypertension, all of which may result in poor venous return. Normally, pressure against valves arises from gravity, the thoraco-lumbar pressures, and increased right atrial pressure with conditions such as congestive heart failure.12 If valve pressure is prolonged, veins may distend causing valves to be in poor position for closure. Poor valve closure allows retrograde blood flow. Valvular dysfunction may also be caused by damage or malformation.12 Valve malfunction allows gravity and rising venous pressure to cause further valve malfunction, more venous hypertension, and distention distally (a vicious cycle).12,20 Valve malfunctions and pressure changes contribute to vein incompetence. This incompetence can be found in superficial, perforating, and deep veins. As mentioned earlier, venous hypertension in the deep veins may cause the perforating veins to increase their pressure and this pressure can be transmitted back to the superficial veins causing distention.12 Perforator vein malfunction may present as skin and tissue problems near the medial ankle, also known as the gaiter region. Vein pathology and malfunction also may result in blood stasis leading to increased risk of deep vein obstruction (ie, deep vein thrombosis-DVT). Even with normal vein anatomy and function, a patient may have poor muscle pump capabilities from atrophy/weakness contributing to poor venous function. Venous pathology may lead to clinical conditions described below.

VARICOSE VEINS AND VENOUS REFLUX

Varicose veins (VV) are dilated, distended veins. Table 6 includes common descriptions of varicose vein types.12 The reader should be cautioned that there is poor agreement on terminology used to discuss the size and classifications of varicose vessels. Often individuals have asymptomatic, cosmetically apparent veins, but some people may develop signs/symptoms. The symptoms/signs of venous disorders can include: burning, swelling, throbbing, cramping, aching, heavy feeling legs, standing fatigue, and cramps at night.12 The Framingham Study examined varicose vein incidence.21 This study followed 5,209 men/women ages 30 to 62 years old for 16 years. The incidence of varicose veins (VV) was higher for women compared to men in all ages except the oldest group aged 80 to 89 years old. Interestingly, age did not clearly affect varicose vein incidence for either gender. Women with VV were more likely to be obese, have lower activity level, present with higher blood pressure, increased age at menopause, and a history of 8 or more hours of sitting or standing a day. Men with VV had low activity level and smoked more. The Edinburgh Vein Study resulted in a number of articles on venous conditions.2,22-25 This study was a cross-sectional survey and testing of men and women from age 18 to 64 years old. One of these articles by Fowkes and colleagues2 examined lifestyle factors and risk for venous reflux. Duplex scans were used to determine venous reflux. They found older men were more likely to have reflux in 1 or more veins. Women were more likely to have only superficial vein reflux (24%) and men were more likely to have only deep vein reflux (32%). They also found that body mass index was higher (indicating obesity) in people with multisegment reflux.22 Overall, the potential risk factors for women to have reflux were: previous pregnancy, low use of oral contraceptives, obesity, and sitting more than 1/2 day at work. For men, height and straining with bowel movement were risk factors.22 Table 7 provides a summary of the most common veins that reflux according to the Edinburgh Study.23 Prevalence of venous reflux appeared to be related to having clinical venous disease.21 Another study by Evans and colleagues24 noted 40% of the males and 32% of females had truncal varices and 80% of all subjects had spider and reticular varices (see Table 6 for definitions of varicose veins by size). In summary, Table 8 presents varicose vein risk factors found in the literature.12,20-27

CHRONIC VENOUS DISORDERS AND WOUNDS

Long-term vein malfunction (ie, VV or vein incompetence) may lead to chronic venous insufficiency (CVI) and venous ulcers. When veins no longer function adequately, poor blood flow can lead to tissue changes in the limb. Venous hypertension coupled with capillary hydrostatic pressure leads to venous congestion and leakage of blood cells, protein, fibrin, and fluid into interstitial space. The result will be edema, pigment changes (hemosiderin staining), lipodermatosclerosis, poor tissue nutrition, and impaired cellular waste removal. These tissue changes predispose the limb to ulcers.12,20,26 It is worth noting not all patients with venous hypertension will develop ulcers and not all patients with venous wounds have venous hypertension.12 Evans et al24 found age adjusted prevalence for CVI was 9% in men and 7% in women and prevalence increased with age,21 while Kistner et al28 found that 90% of people with CVI have superficial reflux and 30% have deep reflux. Additionally, approximately 80% of lower extremity ulcers are due to chronic venous insufficiency.26 Often venous ulcers are found above the medial malleolus where venous hypertension is the greatest. Venous ulcers are typically shallow, irregularly shaped, and contain fibrous slough. The ulcers tend to have moderate to heavy exudate and lower extremity edema. Venous wound pain is often minimal and may be described as dull, achy pain or heaviness in the legs. Pain increases with the dependent position and is relieved with compression and/or elevation. Kistner and colleagues28 have presented the Clinical Signs, Etiology, Anatomy and Pathophysiology (CEAP) Classification to aid in determining the extent of CVI (Table 9). The CEAP classifications assess clinical signs for skin health, vein description, etiology, veins involved (deep, perforator, superficial), and pathophysiology. Wesley and associates29 found that as CEAP scores worsen; there is an increase prevalence and number of incompetent perforating veins with associated reflux. The CVI and venous ulcers are common clinical conditions that health care professionals encounter. It is important that clinicians know how to examine, evaluate, and implement interventions to prevent and treat these conditions.

EXAMINATION AND EVALUATION

Venous examination and evaluation include noninvasive and invasive tests/measures (see Table 10 and 11). It is also advisable to examine patient history for varicose vein risk factors listed in Table 8. McGuckin and associates40 have summarized risk factors involved with venous ulcer development. These risk factors include a history of varicose veins, venous hypertension, deep vein thrombophlebitis, pregnancy, previous vein surgery, lower extremity trauma, obesity, employment/activities requiring lower extremity dependency, and increasing age (more so in males).40 Other risk factors to consider are family history of venous disease and clotting disorders.41 Patient examination must involve inspection of skin quality, color and texture; presence of hair, wounds and scars; signs of venous disease; edema; distended veins, and muscle atrophy. It should be noted that distended veins on the dorsum of the foot, around the ankle, and in the popliteal fossa are normal. Palpate any visible veins; they should collapse easily.12 Further palpation should include peripheral pulses (dorsal pedalis, posterior tibial, popliteal, femoral). Adequate assessment of arterial supply is necessary prior to intervention. Compression is often an aspect of venous wound management and should not be used if the patient has arterial insufficiency. See the article on peripheral arterial disease in this same issue for assessment of arterial supply, specifically the Ankle Brachial Index (ABI) (Cardiopulm Phys Ther J. 2004;15:(3):6-12).

Edema needs adequate assessment with venous disease. Recent soft, pitting edema may indicate trauma, congestive heart or renal failure, early stage venous insufficiency, lymphedema, or result from pregnancy. Tissue that is hard and cannot be pinched may be indurated. Induration is due to distended interstitial tissue from accumulated edema. Brawny edema is related to longstanding venous hypertension and venous insufficiency. When palpated, brawny edema feels taut and hard. Measurements of edema such as limb girth or volumetry are important for objective monitoring and documentation. Lastly, the clinician must rule out the following conditions that may resemble venous disease: hepatic insufficiency (ie, portal hypertension), renal failure, cardiac decompensation (CHF), infection, trauma, and lymphatic disease/dysfunction. Complete and careful examination and evaluation is necessary prior to providing interventions.

INTERVENTIONS

Varicose veins may be treated with sclerotherapy or surgical vein stripping. These procedures may be done in combination as well. The procedures are performed proximally at the main site of hypertension and reflux. If this is not the case, then more varicose veins may appear.1' Vein stripping requires general anesthesia. The involved vessels are removed through small incisions. Sclerotherapy involves injecting the vein with a sclerosing solution while the patient is standing. The chemicals used may include sodium tetradecyl sulfate, polidocanol, variglobin, sclerodex, and hypertonic saline.12 After both procedures, the LE is wrapped for compression and ambulation is encouraged to prevent DVT and clear the chemicals. Contraindications for treating varicose veins may include inability to ambulate after the procedures, history of DVT, arterial insufficiency (compression contraindicated), medication allergies, hypercoagulation (increased risk of DVT), pregnancy (veins may improve afterward), massive obesity (difficult to compress), and poor compliance with compression.12 Removal of varicose veins means the deep veins must now carry more blood and new collateral veins may also form. Venous problems reoccur for some patients. Depending on the vein, there may be 23% to 52% reoccurrence in varicose veins after vein surgery.42-44 Small, superficial varicose veins, ie, spider veins may be removed with laser. Milder varicose veins may be treated with elevation, avoiding prolonged sitting/standing, and support hose use.26

When venous disease becomes chronic, other issues may arise. As presented earlier, as CEAP scores worsen there is an increased risk of venous wounds.27 Skin care and wound prevention become pressing issues. Besides ulcers, other common CVI symptoms include skin changes, itching, leg heaviness, cramps/pain/aching, and swelling.45 Kurz and associates reported information from the Veines International Task Force, a task force of venous experts.47 This evidenced-based review presented information regarding the use of medications for CVI symptoms (see Table 12).47 Medications may be used for leg heaviness, swelling, to increase venous tone, and other overall CVI symptoms.47 Other interventions for CVI circulatory symptoms include: compression with ambulation/exercise/activity (muscle pump), elevation, instructions to not cross legs, and if necessary wound management.10,25 Compression provides better alignment for valves within distended veins. Better valve position aids in prevention of retrograde blood flow. Thus better calf muscle pumping action may occur as well as improved venous return. Compression also will decrease edema and assist with lymph How.12 Different types of compression that can be used are presented in Table 13. Graduated compression needs to be at least 35 mm Hg to be effective for edema, skin changes, and venous ulcer treatment.l71'' Relative contraindications for compression include edema from congestive heart or renal failure, arterial insufficiency, and potential fitting difficulties.12 Information from an ABI test can be used to assess arterial supply (see Cardiopulm Phys Ther J. 2004;15:(3):6-12). Compression may be used with an ABI of 0.9 and higher; compression used with caution for ABIs of 0.7-0.9 and with an ABI of lower than 0.7, compression is contraindicated.26 Patient adherence to compression for CVI may be an issue with CVI and venous wounds.50,52 Erickson and colleagues51 assessed venous wound healing and patient adherence. They retrospectively studied 71 patients between 1981 and 1994 with venous ulcers for healing and adherence. Strict treatment compliance was found in only 45% of the subjects. These compliant patients had significantly better healing rates and less reoccurrence of venous ulcers than those who were non-adherent.51 Edwards52 interviewed patients with venous ulcers and found pain, exudate leakage, skin irritation, poor interactions with health care professionals, and lack of patient understanding of their situation may be factors in reduced adherence. Jull and associates50 found that belief in the necessity for compression garments and garment comfort were significant factors in adherence patients with venous leg ulcers.

McCuckin and Kerstein53 conducted a survey of family physicians in the American Medical Association. They found 96% of the physicians saw patients with venous leg ulcers. The physicians saw an average of 1.5 patients a week with venous ulcers. Compression was prescribed by 96% of these physicians. Eighty-three percent of the physicians referred patients with venous ulcers to other health care professionals (79% to specialists, 47% to home health, and 29% to nursing specialists). It was not apparent if physical therapy was provided as an option for referral on the survey.53 Since venous wounds are a fairly common clinical condition, health care providers need to use appropriate interventions. Venous wound interventions entail appropriate wound bed management and compression to address the edema and venous reflux. Due to the numerous issues involved with wound management, the reader is encouraged to seek other resources devoted to wound care. The Venous Leg Ulcer Guidelines (VLUG) is a good source of information on management of venous ulcers.40 It provides ideas for cost effective, quality interventions for venous ulcers. This resource includes intervention algorithms for the clinician. McGuckin and Williams54 conducted a study with 45 patients with venous ulcers. Using guidelines like the VLUG, they studied wound management using short stretch versus long stretch compression (see Table 13 for compression). They found both short and long stretch compression had similar healing rates-short 91% and long 100%. The slower healing wounds treated with long stretch had more cost associated with them than slow healing wounds treated with short stretch compression. Short stretch compression has high working pressure, which is the pressure resulting from a dressing, bandage, or wrap with muscle contraction.12 Short stretch compression with high working pressure and low resting pressure (bandage pressure when muscle relaxed) aid the deep venous system. An example of a short stretch, single layer compression intervention is Comprilan by Jobst. Long stretch, like graduated compression stockings, have high resting pressures (pressure when muscle relaxed). Long stretch will aid the superficial venous system since there is pressure exerted with the muscle at rest.12 It should be noted that high resting pressure may cause arterial compression, thus arterial status must be assessed with any compression. There are also systematic reviews published by Cochrane Library that pertain to chronic venous disease and ulcers. Nelson and colleagues55 reviewed compression for venous ulcer recurrence prevention. They found not wearing compression was linked with recurrence and also that recurrence may be lower if high compression is used.55 Mani and associates56 reviewed intermittent pneumatic compression and venous disease. The authors had no recommendations and stated further research is needed on the use of intermittent pneumatic compression for venous leg ulcers.56 Lastly, Cullum et al57 found compression increased healing rates versus no compression. They reported that multilayer compression systems were more effective than single layer compression and high compression was more effective than low compression. Other systematic Cochrane Library reviews have examined the use of adjunctive treatments for venous wounds. Electromagnetic therapy, laser, and ultrasound were all found to have no support at this time for healing venous ulcers.58-60 There is however, research support for chronic wound healing and electrical stimulation.61-64 Houghton and colleagues64 recently studied electrical stimulation and chronic wounds. Twenty-seven subjects with 42 wounds (diabetic, arterial, and venous insufficiency) were included in the study. Subjects were randomly assigned to high volt pulsed current (HVPC) and sham HVPC. Ten of the 14 (71.4%) subjects receiving electrical stimulation had venous involvement (7 venous and 3 mixed wounds) and 9 of the 13 (69.2%) of those with the sham HVPC had venous involvement (6 venous and 3 mixed wounds). In general, when looking at all subjects, 45 minutes of high volt pulsed current, 3 times a week for 4 weeks decreased the wound size by half of the initial size. The authors also examined the healing of bilateral venous ulcers (n= 7). For these individuals, one wound was randomly assigned to HVPC and the other wound to the sham HVPC. Of these subjects with bilateral venous wounds, the HVPC wounds were 57% ± 15% of the original size and the sham wounds were 20% ± 18.6% of the original size.64 Lastly, a meta-analysis of 15 studies by Gardner, Frantz, and Schmidt63 supported electrical stimulation for the healing of chronic wounds. Six of the 15 studies had mixed ulcers and only 2 studies examined venous ulcers alone. Overall, electrical stimulation was found to increase the healing of chronic wounds by 144%. In order to provide the best circumstances for management of CVI and venous wound healing, the clinician must manage skin changes, edema, the wound bed, and other symptoms. Venous wound bed management is beyond the scope of this article. The reader is referred to wound management resources for information on interventions such as dressings, topicals, debridement, irrigation, and other modalities or physical agents.

CONCLUSION

In conclusion, the veins are a vital component of the vascular system. Venous literature and texts appear to be less abundant than arterial and yet there are a higher proportion of venous wounds. Compared to arterial content, venous anatomy, physiology, and function do not receive adequate time and attention in health care didactic education. Chronic venous disease of the lower extremity is a common and costly entity. Patients are often concerned about venous symptoms, wound management, and cosmesis. In order for appropriate, effective care to be provided, clinicians need an understanding of lower extremity vein anatomy, pathology, as well as issues related to examination/evaluation and interventions.

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Katherine E. Lampe, MPT, CWS

St. Ambrose University, Physical Therapy Program. Davenport, IA and Staff Physical Therapist, Mercy Rehabilitation, Dubuque/Bellevue, IA

Address correspondence to: Katherine E. Lampe, Physical Therapy Program, 518 West Locust St., Davenport, IA 52803 (563) 333-6415, (lampekatherinee@ambrose.sau.edu).

Copyright Cardiopulmonary Physical Therapy Journal Sep 2004

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