Venous wounds are a final consequence of several disease mechanisms, but ultimately result from chronic venous insufficiency (CVI). The reported prevalence of CVI varies from less than 1–40% in females and from less than 1–17% in males.25 The varying prevalence rates may be due to differences in the classification or definition used, the methods of evaluation to determine wound etiology, and the geographic differences of the regions studied. Some of the better-known risk factors for first-time development of a venous wound include family history, physical activity (typically prolonged standing), history of ankle injury or immobility, and history of deep venous thrombosis.26 Venous function is also affected by changes in estrogen and progesterone.27
CVI is a common illness and its most severe complications, namely venous ulcers, are often debilitating and slow-healing; thus there is a significant economic burden associated with the disorder. An estimated $3 billion is spent annually on the care of venous wounds in the United States.28
A review of lower extremity venous anatomy is essential for the understanding of the pathophysiology and treatment of venous disease. The venous system of the leg is comprised of two parallel and connected channels, the deep and superficial systems (FIGURE 4-1).
The superficial veins of the leg originate at dorsal and deep plantar veins of the foot. The dorsal veins empty into the dorsal venous arch, which is continuous with the great and small saphenous veins. The greater saphenous vein (GSV), which runs anterior to the medial malleolus and medial to the knee, is located in the superficial compartment and connects with the common femoral vein at the saphenofemoral junction (SPJ). Before the SPJ, the GSV receives medial and lateral accessory saphenous veins, as well as tributaries from the groin and anterior abdominal wall.
The small saphenous vein originates from the dorsal venous arch at the lateral foot and runs posterior to the lateral malleolus and into the posterior calf. It then penetrates the superficial fascia of the calf and empties into the popliteal vein.
The deep system originates with the digital veins that empty into metatarsal veins comprising the deep venous arch. This continues into the medial and lateral plantar veins, which then empty into the posterior tibial veins. The dorsalis pedis veins on the dorsum of the foot become the anterior tibial veins at the ankle. The paired posterior tibial veins run under the fascia of the deep posterior compartment, join with the paired peroneal and anterior tibial veins, and then join the popliteal vein. There are large venous sinuses within the soleus muscle that empty into the posterior tibial and peroneal veins. The popliteal vein enters a window in the adductor magnus, at which point it becomes the femoral vein (formerly superficial femoral vein). The femoral vein receives venous drainage from the profunda femoris vein, or deep femoral vein and after this, becomes the common femoral vein. At the inguinal ligament, the common femoral vein becomes the external iliac vein.
The superficial venous system connects to the deep system via perforating veins that cross through (perforate) the fascial layers. These perforators run perpendicular to the superficial and deep axial veins. The perforators vary in their anatomy and can enter the veins at various points—the foot, medial and lateral calf, and mid- and distal thigh. The valves in the perforator veins aid in preventing reflux from the deep to the superficial system, particularly during periods of standing and ambulation.
CONCLUSION The patient received a right popliteal to posterior tibial bypass graft with the right greater saphenous vein. Four weeks later he had an amputation of the third toe, which had become well-demarcated at the edges with detached eschar, putting the foot at risk for infection. Subsequently, as is sometimes the case, the adjacent second toe became necrotic and required amputation (FIGURE 4-42). After removal of both toes, healthy granulation formed and negative pressure wound therapy was initiated on the amputation site (FIGURE 4-43).
The heel wound was off-loaded with a foam dressing and protective boots, and the edges were trimmed as the eschar lifted away from new epithelium (FIGURE 4-44). When the entire eschar was loose, an escharotomy was performed and the wound treated with collagen matrix and silicone-backed dressings. Both wounds progressed steadily to full closure and the patient was fitted with diabetic shoes and custom-molded inserts (FIGURE 4-45).
Post-amputation of the toes
Heel wound case study A. The eschar on the patient’s heel is becoming detached at the edges, a sign of adequate perfusion for healing. The eschar was trimmed on a weekly basis and was fully debrided when granulation was visible. Healing was slow, but the wound fully closed. B. The heel wound after four weeks of debridement, moist wound healing, and off-loading.
The wall of a vein is made up of three layers: the intima, media, and adventitia. Vein walls have less smooth muscle and elastin than arteries do. The adventitia of the venous wall contains adrenergic nerve fibers, especially in cutaneous veins. Sympathetic discharge, thermoregulatory centers in the brain, temperature changes, pain, emotional stimuli, and volume changes can alter venous tone. Venous valves prevent retrograde flow (FIGURE 4-46). Valvular incompetence, or failure, leads to reflux and its associated symptoms. Venous valves are most prevalent in the distal lower extremity and decrease moving proximally; thus the superior vena cava (SVC) and inferior vena cava (IVC) do not have valves. Because veins do not have significant amounts of elastin, they can withstand large volume shifts with small changes in pressure. This is why most of the capacitance of the vascular tree is in the venous system. The return of the blood to the heart from the leg is facilitated by the muscle pump function of the calf. The calf muscle compresses the gastrocnemius and soleus sinuses and propels the blood toward the heart.
Anatomy of the veins Venous flow is from the interstitial tissue into the venous capillaries, the venules, and the superficial veins, through the perforators into the deep veins. Retrograde flow is prevented by valves located in all three components of the peripheral venous system.
Venous insufficiency is the result of normal venous failure that occurs through several mechanisms that are classified as primary, secondary, or congenital. Ultimately, CVI causes the higher pressure in the deep venous system to be transmitted to the superficial veins (termed venous hypertension)29 and impaired return of venous blood flow to the heart. The underlying pathology is most commonly due to incompetence of the valves of the deep or superficial venous system. (FIGURE 4-47) In the scenario of venous valvular incompetence, there is inadequate coaptation of the valves; therefore, the valves do not prevent retrograde flow of blood. Other contributing factors include dysfunction of the gastroc-soleus muscle that works as a venous pump to push blood flow from the superficial veins to the deep veins (FIGURE 4-48), inherent vessel factors associated with genetic predisposition, and venous obstruction (ie, deep venous thrombosis or DVT). TABLE 4-6 lists the risk factors for acquiring venous insufficiency.
Incompetent valves Normal venous flow is maintained by a series of valves that function like any valve to prevent backwash. With vein distention (eg, with age) the valves do not meet, termed incompetent valves and chronic venous insuffi ciency results.
Varicose veins The gastrocsoleus muscle group works as a venous pump to facilitate the movement of fluid in the distal lower extremity back toward the heart. The pump is activated during any activity that involves gastrocsoleus contraction, especially during ambulation if the ankle range of motion and muscle strength is sufficient to cause compression of the deep veins. The pump action results in compression of the deep vein during toe push-off gait phase, creating a pressure on the vein sufficient to push the blood out of the vein. (A) The pressure drops to 15–30 mmHg when the muscle relaxes (during swing, heel strike, and midstance phases of gait). This gradient between the deep veins and the superficial veins allows the blood to flow through the perforators and into the deep veins until the next gastrocsoleus contraction, at which point the blood is again forced proximally toward the heart. During the muscle contraction, the proximal valve is open to allow flow of the fluid, and the distal valve is closed to prevent reflux. During the relaxed period, the proximal valve is closed and the distal valve is open, allowing flow through the vein without reflux when the vein is at its largest. If the gastrocsoleus does not function, either from muscle weakness or ankle joint hypomobility, the fluid pools in the deep veins, then in the perforators and superficial veins, and leads to interstitial edema and venous hypertension. Varicose veins are enlarged tortuous veins, the result of chronic fluid back-slow from incompetent valves. Varicosities in the superficial veins are visible through the skin. Patient A has a healed venous ulcer with hemosiderin staining of the gaiter area and varicose veins in the proximal calf. The constriction seen in the lower leg is the result of socks with elastic at the top, which the patient has been wearing instead of the recommended compression garments. Patient B has a congenital condition, Klippel Trenaunay Weber syndrome, with visible varicose veins in the lower thigh.
Table 4-6Risk Factors for Chronic Venous Insufficiency ||Download (.pdf) Table 4-6 Risk Factors for Chronic Venous Insufficiency
▪ Varicose veins
▪ Deep vein thrombosis
▪ Previous vein surgery
▪ Multiple pregnancies
▪ Congestive heart failure
▪ Coronary artery bypass surgery with saphenous vein harvesting
▪ Hip, knee, or ankle trauma
▪ Ankle immobility
▪ Prolonged standing
▪ Family history
▪ Age over 50
In the normal peripheral circulation, blood volume is pumped out of the extremity, and the veins refill from the arterial flow. However, with CVI the veins fill from both arterial flow and retrograde venous flow due to dysfunctional valves, resulting in venous hypertension. Valve failure may be the result of weakness in the vessel wall or valve leaflets (termed primary) or may be secondary to injury, superficial phlebitis, or distention caused by hormonal effects or high pressure (termed secondary).
The most common manifestation of CVI caused by reflux is varicose veins, or veins that are tortuous and distended. (FIGURE 4-49) When the incompetent valves are located at junctions of the deep and superficial systems, the high pressure in the deep system is transmitted to the superficial veins. For this reason, varicose veins often start at the saphenofemoral and saphenopopliteal junctions and in the perforating system.
Post-thrombotic syndrome Patients who have a deep vein thrombosis are at risk for CVI with ulceration. Post-thrombotic syndrome is characterized by the symptoms listed in Table 4-7 and visualized in the right lower extremity of this patient who had a femoral DVT. Initial symptoms included pain distal to the thrombosis, severe edema, and erythema of the lower leg.
Obstruction of the deep veins can also limit the outflow of blood and cause increased venous pressure. The obstruction may occur as a result of an intrinsic process, for example, DVT or venous stenosis. Vascular and integumentary changes that occur after a DVT are termed post-thrombotic syndrome. The DVT results in valve destruction that in turn leads to incompetence and persistent venous hypertension both at rest and during ambulation. Signs and symptoms of post-thrombotic syndrome, also termed post-phlebitic syndrome, are listed in TABLE 4-7 and are illustrated in FIGURE 4-49. The obstruction can also result from extrinsic compression, for example, in May-Thurner syndrome, a condition in which the right common iliac artery overlies and compresses the left common iliac vein. The compression prevents flow from the left lower extremity and results in higher risk for clotting and edema.
Table 4-7Signs and Symptoms of Post-Thrombotic Syndrome ||Download (.pdf) Table 4-7 Signs and Symptoms of Post-Thrombotic Syndrome
▪ Aching or cramping in the extremity
▪ Feeling that the leg is heavy or tired
▪ Itching or tingling
▪ Chronic edema
▪ Varicose veins
▪ Hemosiderin staining of the skin
Normal contraction of the calf muscles during ambulation assists in return of blood to the heart by functioning as a mechanical pump. (FIGURE 4-50) Insufficient contraction of the muscle as a result of muscle weakness or paralysis, joint hypomobility, joint fusion, or gait impairment contributes to ineffective venous emptying and increased venous pressure.
Evaluating for pitting in the areas with minimal soft tissue (eg, the ankle and gaiter area) will help determine if indeed edema is present. However, edema may be camouflaged in patients with gastroc-soleus atrophy because the leg presents with a fairly normal size.
Hemosiderin deposition in the skin The dark staining in the lower leg of a patient with CVI is a result of the autolysis of entrapped red blood cells and the attached hemoglobin molecules. The byproducts of autolysis migrate into the epidermis and produce the discoloration.
The ineffective emptying and increased pressure in large vessel hemodynamics are thought to cause venous microangiopathy, defined as derangements in venous function at the cellular level. As venous pressure is elevated, the microscopic anatomy of the vessel breaks down to allow spillage of serum proteins and red blood cells (RBCs) into the interstitial areas where they are trapped by the interstitial edema. When the RBCs die, the hemoglobin is released into the extracellular spaces where it is phagocytosed by macrophages. The byproducts of lysed hemoglobin cause the dark, brawny discoloration termed hemosiderin staining. (FIGURE 4-50)30
The predominant theories of CVI pathophysiology are (1) fibrin cuff formation, (2) growth factor trapping, and (3) white blood cell trapping. The original theory of the fibrin cuff proposed by Browse and Burnand31 involves leaking of fibrinogen into the pericapillary space, thus creating a “cuff” that forms around the venous capillary. This was speculated to increase the diffusion barrier, restrict the diffusion of oxygen into the subcutaneous tissue and skin, and maintain an inflammatory state. This theory has largely been supplanted by other findings but is still thought to play a role in CVI pathology.
The leukocyte-trapping theory involves the sequestering or trapping of leukocytes in the capillaries or postcapillary venules. Venous hypertension results in decreased flow, which in turn causes the accumulation of white cells in the capillaries. The adhesion of activated white blood cells releases inflammatory mediators and proteolytic enzymes that cause endothelial damage. This process may also increase permeability and contribute to protein leak.32
Finally, trapping of growth factors by fibrin and other macromolecules is thought to occur via the same mechanism as white blood cells. When the growth factors are bound, they are unavailable to facilitate healing.33
As the varicose veins dilate and become tortuous, they may become painful as a result of distention. Patients describe the pain or discomfort of the leg as heaviness, aching, or limb fatigue that is worsened by prolonged standing and relieved by elevation of the extremity. Edema can begin in the foot and ankle and extends up the leg with progressive worsening during the day as the legs are dependent and fluid accumulates. These veins are also prone to superficial thrombophlebitis, as well as occasional bleeding and thinning of the overlying skin.
Skin changes that may also develop include hyperpigmentation in the perimalleolar region from hemosiderin deposition; lipodermatosclerosis with scarring and thickening of the skin secondary to fibrosis in the dermis and subcutaneous fatty tissue; and atrophie blanche, circular whitish and atrophic skin surrounded by dilated capillaries and hyperpigmentation. Brawny edema of the distal calf, “champagne bottle leg,” fibrotic and hypertrophic skin, and hyperpigmentation are also visible signs of CVI. These are further described and illustrated in FIGURES 4-51 to 4-55. Advanced lipodermatosclerosis may involve fibrosis of the Achilles tendon, thus impairing motor function of the extremity. Patients may also develop eczematous dermatitis, cellulitis, and lymphangitis.
Lipodermatosclerosis Lipdermatosclerosis, defined as scarring of the skin and fat, is the result of fibrin leaking into the subcutaneous tissue, causing fat necrosis, thickened smooth skin, subcutaneous immotility, and in severe cases, ulceration. Both lower extremities also have extensive hemosiderosis.
Atrophie blanche Obstruction of the small vessels to the skin results in atrophie blanche, literally white skin, and may be a precursor to ulceration. Wounds that have adjacent atrophie blanche will frequently extend into the white area before full healing can occur.
Brawny edema Brawny, ordinarily defined as strong and firm, in this case refers to the discoloration from hemosiderin. Brawny edema is characterized by firm, discolored skin with non-pitting edema due to the underlying fibrosis of subcutaneous tissue.
Champagne-bottle leg Lipodermatosclerosis of the ankle and gaiter area can prevent flow into that part, resulting in excessive collection of fluid in the calf and the champagne-bottle shape of the leg.
Fibrotic, hypertrophic skin In addition to the fibrosis of the subcutaneous tissue, the epidermis can become thick and scaly. If not managed adequately, the skin under the scales can ulcerate or bacteria can collect and cause cellulitis. The erythema seen in this photo is suggestive of cellulitis.
When evaluating the etiology of edema and ulcerations in CVI, a comprehensive medical and surgical history is crucial, with special attention to family history of varicosities, leg ulceration, thrombotic disorders, previous history of deep venous thrombosis or phlebitis, use of anticoagulation, unexplained transient unilateral edema, or previous venous-related interventions. Although unilateral edema often suggests venous pathology, a variety of other illnesses with a similar presentation need to be excluded.
Generally, edema that occurs below the knee is due to CVI and edema that extends above the knee to the thigh is due to lymphedema, which is discussed in detail in Chapter 5. Unilateral edema is more likely to be caused by CVI, whereas bilateral edema is usually caused by some systemic disorder (eg, renal failure, kidney failure, congestive heart failure) or by medications. If the edema has a sudden onset, is hard and indurated, and does not respond to compression, the concern is obstruction of the pelvic or abdominal lymph nodes, which is most commonly from a malignancy. (FIGURE 4-56) The correct differential diagnosis is imperative for effective interventions.
Lower extremity edema due to lymph node obstruction Sudden onset of hard indurating edema that does not respond to compression is suggestive of abdominal or groin lymph node obstruction, frequently related to metastatic disease.
Additional signs and symptoms that are typical of venous wounds include the following:
■ Location: Venous wounds occur above the medial and lateral malleoli in the distal third of the lower leg, termed the gaiter area. (FIGURE 4-57) If the wound is outside of this area (eg, directly on the malleolus, on the post-malleolar skin, on the calf, or on proximal leg), the origin is probably not venous.
■ History of wound formation: Venous wounds tend to be preceded and surrounded by changes in color and texture of the skin and have a more insidious development. If there are no skin changes and the wound onset was sudden, even in the presence of edema, other causes need to be considered. For example, a traumatic wound, a wound secondary to sickle cell disease, or a surgical incision may cause edema that then impedes wound healing; however, it would not be diagnosed as a venous wound.
■ Wound appearance: Venous wounds tend to have uneven edges, shallow depth, and a fibrotic or granular wound base. (FIGURE 4-58) If the wound has been present for a long period, the edges may be senescent or rolled. There is usually little if any eschar.
■ Periwound skin: Changes in the periwound skin include increased dermal thickness (eg, > 1.985 mm measured with high frequency ultrasound), hemosiderin staining, crusting or scaling, lipodermatosclerosis, varicosities, or atrophie blanche.34
■ Drainage: Just as water flows from a hole in a hose or water pipe, fluid flows from a wound on an edematous extremity. Drainage from a venous wound is usually serous; however, if there is infection present, it may be thick, purulent, and odiferous. If a wound appears venous in all respects but tends to have little or no drainage, there is concern for arterial insufficiency as well.
■ Pain: Venous wounds are not typically painful like ischemic wounds. Wounds that are exquisitely painful to any tactile stimulation are more likely to be vasculitic or arterial (FIGURE 4-59).
Location of a venous wound Venous wounds are located in the medial or lateral gaiter area, defined as the distal third of the lower leg. Wounds outside this area, including over or distal to the ankle, on the calf, or on the anterior shin, are usually caused by some other etiology although chronic edema may impede the healing.
Typical appearance of a venous wound A venous wound typically has serpentine, or uneven, edges; striated granulation or yellow fibrous tissue; serous or serosanguineous drainage; and rolled edges. Wounds with even, punched-out edges should be evaluated for an arterial component.
Vasculitic wounds on patient with systemic lupus erythematosus Vasulitic wounds may be close to the typical location of venous wounds, but as in this photo, can be anywhere on the extremity. If they appear on or distal to the ankle, the wounds are probably not venous in origin, although the vasculitic inflammation may cause edema. In addition, vasculitic wounds are very painful, are usually smaller than most venous wounds, and require treatment of the underlying vasculitis in addition to wound care.
Skin temperature elevated more than 1.1°C or or 3 degrees F is suggestive of infection, along with erythema of the periwound skin, increased drainage with odor, friable granulation tissue, and pain.35 Wounds that fail to improve within 6 weeks after initiation of treatment are very likely not a result of CVI and should be investigated for other diagnsoses. (TABLE 4-8) Studies have also indicated that wounds that decrease by 40% in the first 3 weeks of treatment have higher healing rate.30
Table 4-8Differential Diagnosis of Venous Wounds ||Download (.pdf) Table 4-8 Differential Diagnosis of Venous Wounds
Wounds that fail to heal after six weeks of evidence-based care (compression, moist wound healing, exercise) should be studied further for diagnoses that may appear as venous wounds but are indeed caused by other pathologies:30
▪ Polyarteritis nodosum
▪ Pyoderma gangrenosum
▪ Mycobacterial or fungal infections
▪ Necrobiosis lipoidica diabeticorum
▪ Systemic lupus erythematosus wounds
Classification of Venous Wounds
The International Consensus Committee on Chronic Venous Disease has developed a classification of chronic venous insufficiency, designed to standardize parameters for medical and surgical research. In the CEAP classification, each letter stands for a particular dimension of the disease: C represents the clinical signs, E stands for the etiology, A is for the anatomy involved, and P is the pathophysiology.36–38 Refer to TABLE 4-9 for a complete outline of the CEAP classification with illustrations.
Mrs. VB is a 52-year-old female who has a history of non—healing wounds on the right medial and lateral lower extremity in the gaiter area, of more than one year duration. (FIGURES 4-60, 4-61)
▪ Patient works as a manager for a department store and wants to continue to work while she is being treated.
▪ Pain levels are 6-8/10 almost constantly and 10/10 with any tactile stimulation to the wound bed.
▪ Patient is currently applying Silvadene to the wounds daily and covers them with cotton gauze and pads, anchored with tape.
▪ Patient lives in a one-story home with her husband and two dogs.
▪ Patient reports copious drainage that interferes with her social and professional life, as well as keeping her awake at night.
▪ History of hypertension
▪ History of hysterectomy about 5 years previously; no pregnancies reported
▪ History of obesity
▪ History of deep venous thrombosis in the right femoral vein
▪ History of hypertension
▪ Negative for diabetes, cardiac disease, peripheral arterial disease
What skin changes are observed in the lower extremity?
Describe the tissue in the wound bed.
What other information is needed to determine the cause of the patient’s wounds?
Classify the patient’s venous disease and wounds using the CEAP system.
Which noninvasive tests are indicated for this patient and why? What would you expect to learn about the patient in order to make a diagnosis?
Which invasive tests are indicated and why?
Right lower extremity of case study
Left lower extremity of case study
Table 4-9CEAP Classification of Venous Wounds ||Download (.pdf) Table 4-9 CEAP Classification of Venous Wounds
C represents the clinical signs, E stands for the etiology, A is for the anatomy involved, and P is the pathophysiology.
Clinical signs are identified from the following list, then designated symptomatic or asymptomatic:
0 = No visible or palpable signs of venous disease
1 = Telangiectasia or reticular veins—small dilated veins (0.5–1 mm in diameter) that develop in the superficial skin as a result of venous hypertension
2 = Varicose veins—dilated, tortuous veins in the lower leg that signify the progression of CVI due to venous hypertension
3 = Edema without ulceration
4 = Skin changes ascribed to venous disease (pigmentation, venous eczema, lipodermatosclerosis)
5 = Skin changes as defined above with healed ulceration
6 = Skin changes as defined above with active ulceration
S: symptomatic, including ache, pain, tightness, skin irritation, heaviness, and muscle cramps, and other complaints attributable to venous dysfunction
Etiology is defined as one of the following:
Ec: Congenital (for example, congenital valvular dysfunction)
Ep: Primary, in which venous insufficiency is the primary disease process observed
Es: Secondary, in which another disease process occurring first (for example, acquired lymphatic insufficiency)
En: No venous cause identified
Anatomical class is divided into the following:
Telangiectasia or reticular veins
Long saphenous vein above the knee
Long saphenous vein below the knee
Short saphenous vein
6. Inferior vena cava
7. Common iliac vein
8. Internal iliac vein
9. External iliac vein
10. Pelvic, gonadal, broad ligament, other veins
11. Common femoral vein
12. Deep femoral vein
13. Superficial femoral vein
14. Popliteal vein
15. Crural, anterior tibial, posterior tibial, peroneal veins
16. Muscular, gastrocnemial, soleal veins
Pathophysiology is classified as follows:
Pr: Reflux, usually from incompetent valves
Po: Obstruction, usually from DVT; refers to a total occlusion of one of the veins at any point or more than 50% narrowing of at least half of a vein segment
Pn: No venous pathophysiology identifiable
With the CEAP classification in mind, there are four questions to be addressed during the process of evaluating a patient with a venous wound.
What are the clinical signs present in the lower extremity?
What is the etiology of the venous stasis disease?
Where is the anatomic disease process occurring?
Is the pathology at that anatomical location obstruction or incompetent valves resulting in reflux, or a combination of the two?
In addition, the clinician needs to identify other disease processes, confirm infection, and identify contributing factors that can be addressed in the care plan.
A comprehensive examination of any patient with a wound below the knee, including a venous wound, begins with an assessment of the arterial circulation, as discussed in the section on arterial wounds. A notable sign that arterial insufficiency may be impeding the wound healing is lack of hair growth in the lower half of the leg and foot.30 An ankle-brachial index (a ratio of the blood pressure measured at the ankle and arm) is indicated if there is any sign of diminished flow and results less than 0.8 suggest that the patient should be referred to a vascular specialist.
The venous system is assessed with the patient in both standing and supine positions. Standing increases venous hypertension and dilates the veins, thereby facilitating the examination. Patients with superficial valvular incompetence commonly exhibit palpable great saphenous veins. Palpable cords may also be present. (FIGURE 4-62) Venous stasis dermatitis at the distal ankle can mimic eczema or dermatitis of another cause. For this reason, history and physical findings must be weighed alongside focused vascular studies, both invasive and noninvasive.
Distended saphenous vein Distended veins are visible in the lower leg as a result of superficial valvular incompetence or with compression of the blood pressure cuff around the calf when testing for augmented venous flow.
A thorough wound assessment includes all of the components discussed in Chapter 3, Evaluation of the Patient with a Wound. The clinical findings are used to select interventions, determine outcomes, and measure progress.
Noninvasive Vascular Studies
Venous Duplex Examination
Duplex ultrasound for superficial/deep/perforating vein assessment has largely replaced the Brodie-Trendelenburg and Perthes tests. There are different types of venous ultrasonography, including compression ultrasound (B-mode imaging only), duplex ultrasound (B-mode imaging and Doppler waveform analysis), and color Doppler imaging. Different lower extremity veins are best evaluated with different techniques. Compression ultrasound is typically performed on the proximal deep veins (the common femoral, femoral, and popliteal veins), whereas a combination of duplex ultrasound and color Doppler imaging is used to evaluate the calf and iliac veins.39
Valve reflux is identified with distal augmentation of flow and release, normal deep breathing, and performance of a Valsalva maneuver. Augmentation of flow is achieved by compressing the leg distal to the ultrasound probe in order to exaggerate the natural calf-pump mechanism and increase fluid return. With the patient standing, the probe is used to obtain sample volumes from the femoral and saphenous veins. Sudden release of augmentation allows the assessment of reflux and valvular competence. The small saphenous vein and popliteal veins are then examined. Perforator veins can also be assessed this way.35
In addition, assessment of microcirculation by either transcutaneous oxygen tension can predict wound healing potential as discussed in the section on arterial wounds. Values of more than 30 mmHg in the periwound skin suggest sufficient oxygenation for healing to occur.
Invasive vascular studies include phlebography or venography, ambulatory venous pressure, and intravenous ultrasound. Phlebography uses intravenous contrast and radiography to help distinguish saphenofemoral anatomy and reflux, and thus primary from secondary venous insufficiency. Although its routine use has largely been replaced by venous duplex imaging, phlebography is occasionally performed before deep vein reconstruction or in patients with inconclusive duplex results before other venous surgery.
Approximation of central venous pressure is a screening test to determine if an element of congestive heart failure (CHF) is contributing to lower extremity edema. The hand is held below the heart until the veins are visibly filled. When the hand is elevated slightly above heart level, the veins flatten if there is minimal risk of CHF being present because the fluid can return to the central vascular system. If, however, the veins remain distended, referral to the physician for further medical care is advised before any compression therapy is considered. Prominent jugular venous distention is another visible sign of increased central venous pressure with CHF.
Ambulatory venous pressure is considered the hemodynamic gold standard for the assessment of CVI;40 however, it is seldom used in clinical practice because of its invasive nature, concern about its accuracy, and availability of numerous alternative diagnostic modalities. A needle is inserted into the pedal vein and connected to a pressure transducer; pressure is measured at rest and after exercise, as well as before and after placement of an ankle cuff to distinguish deep from superficial venous disease.
Intravascular ultrasound has gained acceptance in the management of venous disease and is increasingly being used to help guide interventions. A catheter-based ultrasound probe is used to visualize periluminal vessel anatomy to assess for obstructive disease. Intravascular ultrasound may be superior to venography in estimating the morphology and severity of central venous stenosis, especially in the pelvis, and in visualizing the details of intraluminal anatomy.41
Venous ulcer guideline documents based on extensive database searches to review reliable research provide evidence-based standards of care for patients with venous disease. One document is from the Association for the Advancement of Wound Care, which uses the same level of evidence criteria that the National Pressure Ulcer Advisory Panel uses to evaluate interventions for pressure ulcers. (See Chapter 6, Pressure Ulcers.) The Wound Healing Society used a similar method of evaluating the data, but included animal studies to support suggested strategies.42,43 The guidelines published by these two organizations dedicated to providing the best evidence-based care to all patients with wounds are the basis of this discussion on prevention and treatment.
Prevention is predicated on first determining the risk factors of any individual, then providing the education needed to effect lifestyle changes, including causes of skin breakdown, principles of good skin care, smoking cessation, how and why to use compression, and appropriate exercise.30 (TABLE 4-10) Additional strategies are to avoid prolonged standing and sitting, avoid crossing the legs, and wear light compression garments, especially for flying and prolonged standing and sitting. Elevation with the leg higher than the heart is supported for prevention and treatment; however, it is not sufficient in and of itself. Elevation is only a principle to use when sitting or supine, and is not a substitute for compression and exercise.
An engaging way for a patient to perform ankle exercises is to “write” the alphabet with the big toe while sitting on the edge of a chair. This activates the lower leg muscles in all the compartments and mobilizes the ankle joint in all directions.
Table 4-10Exercises for the Patient with Venous Wounds ||Download (.pdf) Table 4-10 Exercises for the Patient with Venous Wounds
Gastrocsoleus stretches to optimize ankle range of motion
Ankle pumps and circumduction
Heel/toe raises in both sitting and standing positions
Ankle rocker board exercises
Step over a 3- to 4-inch obstacle using a heel strike in front, toe push-off in back.
Exaggerated heel/toe sequence during ambulation
Walking or bicycling for fun
Selection of treatment strategies is guided by the disease severity using the CEAP classification system in a stepwise fashion. The mainstay of initial treatment for CVI is non-surgical measures to reduce symptoms, prevent the development of secondary complications, and halt disease progression. The four basic components of wound treatment include compression, treatment of infection, moist wound healing, and exercise to activate and strengthen the venous pump.
Two questions drive the selection of compression for the patient with a venous wound: (1) What needs to be wrapped? and (2) What materials are best for the patient?
An algorithm for the first question is presented in FIGURE 4-63. Bilateral edema can be present as a result of reflux or obstruction; however, systemic diseases that cause edema need to be ruled out and treated. In some cases of CHF, compression is deferred until the patient is stabilized and there is no concern about overloading the heart with fluid from the extremities.
Algorithm for deciding what to wrap when treating a patient with a venous wound Selecting the compression intervention begins with a careful assessment of the edema. If the patient has bilateral lower extremity edema, systemic disorders such as congestive heart failure, kidney failure, or liver disease must be ruled out, as well as carefully reviewing the medications. (See Chapter 5, Lymphedema.) If the patient has acute congestive heart failure, compression may need to be deferred until the patient is diuresed and there is no risk of overloading the heart. Any systemic issue must be addressed in order for local treatment to be effective. If the edema extends above the knee, there is probably secondary lymphedema, which would be treated with manual lymphatic drainage, exercise, and compression applied from toe to upper thigh. If the edema is limited to below the knee, the next step is to evaluate the vascular status to determine the type of material that is best for the individual patient (Used with permission from Rose Hamm.)
An algorithm for selection of materials and wrapping technique based on the lower extremity ABI is presented in FIGURE 4-64. Materials are classified as elastic, non-elastic, rigid, stiff, single-layer, and multilayer, and wrapping can be performed in a spiral or a figure-8 pattern. The principles of compression are based on: (1) there must be a gradient between the pressure at the ankle and the calf to push the fluid cephalad, and the usual differential for a limb with no arterial disease is 40 mmHg at the ankle and 18 mmHg at the calf,44 and (2) LaPlace’s Law, which has been modified to determine the sub-bandage pressure by using the following equation:
Pressure = the sub-bandage pressure, also termed the compression force
T = the tension of the material, determined by the material and how much it is stretched
N = the number of layers of material used
4630 = a constant calculated using the original LaPlace’s Law
C = circumference of the extremity being compressed
Algorithm for selection of appropriate compression therapy Selection of the appropriate compression therapy is based on vascular examination and patient comfort and tolerance. Every garment, compression system, elastic or non-elastic wrap has a tension that determines the amount of pressure when properly applied. Manufacturer’s guidelines should be followed carefully to avoid complications that can occur with inappropriate compression therapy. Compression of any type is generally contraindicated if the ABI is less than 0.5; however, if the patient can tolerate multiple layers of soft gauze wrapping, it may be beneficial in activating the lymphatics as well as anchoring the appropriate primary dressing (Used with permission from Rose Hamm.)
Using the principles in the equation, the sub-bandage pressure can be altered to meet the needs of an individual by changing any of the components of the equations. Some of the more common applications of these principles in the clinical setting include the following:
■ Tension is varied by the kind of material used and how much it is stretched. Stiffer materials provide more pressure, and elastic materials provide more compression as they are stretched. Usually appropriate pressure with elastic materials is calculated on a 50% stretch (eg, the elastic component of a multilayer compression system).
■ The number of layers provided by a wrap depends upon the technique used (eg, a spiral wrap with a 50% overlap will result in 2 layers; a spiral wrap with 66% overlap, 3 layers; and figure-8, 4 layers). If all other factors are equal, a figure-8 wrap will produce two times the compression force of a spiral wrap. (FIGURES 4-65, 4-66)
■ If the extremity has no contour, the compression will be the same throughout the entire length, if the other factors are equivalent. In order to obtain a pressure gradient between the ankle and calf, there must be a circumference differential. If the limb is shaped like a pencil (ie, with no difference in size), extra padding can be placed around the calf to create a cone shape that results in the ankle/calf differential. Also, if the limb is shaped like a champagne bottle, padding can be placed around the ankle to even out the shape and reduce the gradient to 40/18 mmHg. (FIGURES 4-67, 4-68)
■ Wide bandages provide less compression than narrow ones; thus using narrow bandages distally can help create greater pressure around the ankle, and using wider bandages around the calf can help reduce the proximal pressure. This principle is used especially when wrapping toe to thigh for lymphedema. In addition, narrow bandages are easier to apply around the ankle without creating wrinkles that can cause high-pressure spots.
Spiral wrap of the lower extremity A spiral wrap is performed with the bandage kept at a 30–45 degree angle and can have a 50% overlap (providing two layers of compression) or 66% overlap (providing three layers of compression). Consistency of overlap and tension is essential for optimal therapy and requires practice, practice, and more practice for any clinician.
Figure-8 wrap A. Compression of the lower extremity must include the foot and ankle. Two or three wraps around the foot and figure-8 around the ankle are the best techniques to anchor the bandages and prevent wrinkles that can abrade and blister the skin. Tape over the “seams” of the wrap prevent loosening and slippage of the bandages. B. Figure-8 wrap provides four layers of compression and is performed with consistent 50% overlap and a 45-degree angle of the bandages. A consistent chevron appearance on the anterior leg provides feedback to the clinician about the quality of the wrap.
Adding padding to a straight leg The ideal shape of the lower extremity to achieve the pressure differential for fluid return is a cone. If the leg is straight, or a pencil leg, padding around the calf helps to increase the calf circumference and thereby create an ankle/calf pressure gradient.
Adding padding to a “champagne-bottle” ankle Similarly, if the ankle is atrophied and the calf enlarged, like the champagne bottle, padding around the ankle will decrease the pressure gradient so that it is closer to the ideal 40/18 mmHg. This can be accomplished by adding gauze padding, cast padding, or any soft conformable material around the ankle to create the ideal conical shape before applying the elastic layer.
While LaPlace’s Law supplies the science of compression, the art is in the hands of the clinician who is applying the bandages. Absolute and consistent tension on the bandages, meticulous placement for appropriate overlap, and avoidance of wrinkles are necessary for patient comfort and optimal outcomes.
A number of compression garments or systems are available, including graded elastic compressive stockings, zinc oxide paste and gauze boots, multilayered compression systems, layered bandaging using either short-stretch or long-stretch bandages, and garments with adjustable elastic or non-elastic Velcro straps. (FIGURES 4-69–74) Compression stockings are classified according to the amount of pressure provided at the ankle and are prescribed according to symptoms and history of ulceration. (TABLE 4-11)
Graded compression garments A. Slippery toe sock. B. Graded compression garments for the lower extremities are available in knee high (primarily for CVI), thigh high, and panty style (both for lymphedema). There are also several types of donning aides, including the slippery toe sock seen in A and B, as well as a wire cage that is useful for patients who have difficulty reaching the foot.
Zinc oxide paste and gauze boots For many years, the zinc oxide paste and gauze boots (commonly called the Unna boot) were the mainstay of compression for venous insufficiency. The gauze is impregnated with a zinc oxide paste that hardens after application, much like a cast, and forms a rigid compression bandage. A. The boot has been adapted in several ways, including using a hydrocolloid primary dressing over the wound and a self-adhering bandage on the outside. This adaptation was termed the Duke boot. involves leaking of fi brinogen into B. The disadvantage of the zinc paste boots is the inability to contract as the extremity becomes smaller, thus providing less pressure and allowing the leg to telescope inside the bandage.
Multilayer compression systems Multilayer compression systems include the following layers: (1) A soft cotton padding that is wrapped in a spiral. Additional layers can be placed over bony prominences (eg, the shin or ankles) to prevent pressure areas or around the calf or ankle to help shape the extremity. (2) A non-elastic layer that is wrapped in a spiral and provides the first layer of pressure. (3) A long-stretch layer that is wrapped in a figure-8 and provides the majority of the pressure. (4) A self-adhering bandage that anchors the system and prevents slippage. Layer 3 is omitted for modified compression if the ABI is between 0.6 and 0.8. The compression systems are changed every 3 to 7 days, depending on the amount of drainage from the wound and patient tolerance.
Single-layer elastic bandages Single-layer elastic bandages are long-stretch and need to be used with caution. Application with consistent and even compression takes practice. Some brands have guides woven into the bandage to help the clinician monitor the amount of stretch, ergo tension, that is placed on the bandage. Studies have shown that single-layer bandages are not as effective in facilitating wound healing; they may, however, be helpful in reducing edema on extremities without wounds while compression garments are being obtained, provided the patient has adequate arterial flow.
Compression garments The Farrow wrap (FarrowMed, Bryan, Texas) is a compression garment consisting of a foot piece and a series of Velcro bands that extend from the ankle to the upper calf, providing low resting and high working pressures like a short-stretch bandage system. The amount of tension can vary by the amount of stretch placed on each band. The system is beneficial for patients who have difficulty donning elastic garments.
Circ-Aid Circ-Aid (a Medi company) consists of adjustable non-elastic Velcro bands that provide compression at recommended pressures for long-term edema management. These garments are custom fit to each patient and are available in styles for both wound healing and lymphedema.
Table 4-11Classification of Compression Stockings ||Download (.pdf) Table 4-11 Classification of Compression Stockings
|Description ||Amount of Pressure at the Ankle ||Indications for Use |
|Support ||15–20 mmHg ||Early signs of CVI without ulceration, prophylaxis for high risk factors |
|Class I ||20–30 mmHg ||Signs of CVI without ulceration, post-sclerotherapy, prophylaxis for high risk factors, post-healing with inability to don/doff or tolerate higher compression, mild lymphedema |
|Class II ||30–40 mmHg ||Post-ulceration, pronounced varicose disease, moderate lymphedema, post traumatic edema, burn scar management |
|Class III ||40–50 mmHg ||Severe lymphedema, severe CVI, with venous wounds and no arterial disease |
|Class IV ||60+ mmHg ||Severe lymphedema, elephantiasis, severe post thrombotic disease |
A review of the evidence and the abovementioned guidelines provide direction on which compression is the most efficacious in promoting wound healing. For example, elastic compression is more effective than inelastic.30 This may be explained by findings by Partsch et al., who measured sub-bandage pressure of zinc paste bandages immediately and 24 hours after application. They found that the pressure of zinc paste bandages during dorsiflexion dropped from 130–140 mmHg to 40–50 mmHg, suggesting that the effectiveness of a rigid system decreases because the leg reduces in size but the bandage does not.45 Multilayer systems, on the other hand, “give” as the limb reduces in size and sub-bandage pressure remains high. Another difference is that inelastic bandages are more effective if the gastroc-soleus muscle is functioning—the muscle pushes against the rigid bandage with contraction and thereby produces pressure on the veins.46 Elastic bandages provide compression both at rest and during ambulation, regardless of the muscle action, and are thus more effective for patients with a hypomobile or fused ankle or with paralysis. Elastic bandages are contraindicated for patients with arterial insufficiency or post-bypass revascularization.
An extensive Cochrane review concluded that wounds treated with compression heal faster than those treated without compression; multilayer systems facilitate faster healing than single-layer bandages; and multilayer systems with an elastic component were more effective than those without.47
Intermittent pneumatic compression pumps are useful in reducing edema at a first visit before applying a compression bandage, or for patients who do not tolerate other types of compression to use at home, especially after wound healing has occurred.48 More discussion on pumps is included in Chapter 5, Lymphedema.
The benefits of compression therapy have been well-defined, with significant improvement in pain, swelling, skin pigmentation, activity, and well-being as long as a high level of compliance with therapy is maintained. In fact, with a structured regimen of compression therapy 93% of patients with venous ulcers can achieve complete healing at a mean of 5.3 months.49
Evaluating and treating a venous wound for infection or for periwound cellulitis is an integral part of caring for the patient and facilitating wound healing. Edema fluid neutralizes the fatty acids of sebum and inactivates the bactericidal properties of the skin; thus venous wounds are extremely susceptible to developing infection.50
The Wound Healing Society includes the following guidelines for infection control in the treatment of venous ulcers:
■ Debridement of necrotic tissue on a venous wound reduces the bacteria and the risk of infection. Debridement is an integral part of wound bed preparation and facilitates the healing process.
■ If the wound edges do not begin to epithelialize within 2 weeks of initiation of therapy, infection should be ruled out by either a tissue biopsy or quantitative swab culture for both aerobic and anaerobic bacteria.
■ Infection is defined as ≤ 1 × 106 colony forming units (CFUs) per gram of tissue or any level of beta hemolytic streptococci and significantly impedes wound healing.
■ Topical antimicrobial dressings are recommended for any wound with the above levels of bacteria; however, they should be discontinued when bacterial balance is achieved.
■ Systemically administered antibiotics have not been shown to be effective in granulating venous wounds; however, periwound cellulitis should be treated with systemic gram-positive bactericidal antibiotics.49
The amount of drainage and the presence of bacteria are the primary factors to consider when selecting a dressing. Initially, absorbent dressings such as alginates, hydrofibers, hydroactives, and foams are recommended to manage exudate and protect the periwound skin from maceration. As the wound granulates and drainage decreases, advanced dressings such as collagens may facilitate epithelial migration at the edges. Biological dressings or living skin equivalents may facilitate closure once the wound bed is clean and granulated. An extensive Cochrane review concluded that the dressing was not a factor in wound healing, and that indeed compression is the determinant intervention.51
Some oral agents (eg, diosmin, rutoside) in use in Europe have been reported to improve the feeling of heaviness, fatigue, and even edema of CVI, but these agents are not available in the United States. Pentoxifylline, an oral medication that improves the microcirculation and thereby improves healing rates, is supported by both guidelines and a Cochrane review.52 Its benefit may be most noticeable in patients who have combined arterial and venous insufficiency. Additionally, if the wound is failing to show progress, a careful review of the patient’s medications for drugs that may impede wound healing (eg, NSAIDs) is recommended.
Dysfunction in calf and foot muscle pump function play a significant role in the pathophysiology of CVI, and graded exercise programs have been used in an effort to rehabilitate the muscle pump and improve symptoms.27 Just as it is beneficial for prevention, exercise can improve dynamic muscle strength and calf muscle pump function in patients with all levels of CVI from varicose veins to venous ulceration.
Venous wounds that decrease in size > 40% in 4 weeks usually achieve full closure with standard care described above. However, wounds that do not progress at this rate may benefit from adjunctive therapies, including electrical stimulation, non-contact low-frequency ultrasound, bilayered living cellular dressings (eg, Apligraf, Organogenesis, Inc., Canton, MA), and negative pressure wound therapy (for extensive wounds with some depth). Therapies that have not been shown to have statistically significant effects on venous wound healing include hyperbaric oxygen, laser, phototherapy, and whirlpool.30,48
When CVI is refractory to medical and/or local treatment, invasive options are used to both reduce edema and facilitate wound healing. Removal of the saphenous vein with high ligation of the saphenofemoral junction has been the surgical standard for superficial saphenous insufficiency in more severe CEAP classes.53 This procedure plus stripping of the great saphenous vein results in significant improvement in venous hemodynamics, provides symptomatic relief, and assists in ulcer healing.54
Advances in endovascular surgery have led to successful closure of the veins with incompetent valves using either radiofrequency or endovenous laser ablation. Both methods use a duplex-guided percutaneous access to the great or small saphenous vein. A tumescent anesthesia formula is administered along the course of the vein to be treated, which is then visualized with the duplex. Closure of the vein is accomplished with radiofrequency heat or laser.
These procedures are percutaneous, do not require general anesthesia, and are performed on an outpatient basis. Long-term follow-up studies have compared these procedures with conventional surgery and found equivalent efficacy and often reported improved quality of life.55
The decision to recommend surgical intervention is based on the degree of disease according to CEAP classification and the success or failure of non-operative management. Listed below are the predominant surgical interventions and their indications.
Sclerotherapy is a treatment for obliterating telangiectases, reticular veins, varicose veins, and saphenous segments with reflux. Rather than remove the diseased vessel surgically, sclerotherapy obliterates and seals the vessel in situ. Sclerosing, a procedure in which agents are injected into the venous segments by direct visualization or ultrasound guidance, can be used as primary treatment or in conjunction with surgical procedures for the correction of CVI.
Foam sclerotherapy is a relatively new procedure that combines traditional liquid sclerosing agents with gas to create a foam that has more surface area and expands to reach greater areas of the vessel. Emerging data suggest that it is safe and has equivalent healing and success rates with conventional surgery.56
Endovenous Radiofrequency and Laser Ablation
Thermal energy in the form of radiofrequency or laser treatment is used to obliterate veins. This technique is used for saphenous vein reflux as an alternative to stripping and for its tributaries as an alternative to phlebectomy. These catheters generate heat, which causes thermal injury to the vein wall and thereby leads to thrombosis and eventually fibrosis. Several studies comparing endovenous ablation with conventional ligation and stripping found that the short-term efficacy and safety of ablation and surgery are comparable, although the surgical group had increased postoperative pain and bruising.57
Approximately 10–30% of patients with severe CVI have a significant abnormality in venous outflow involving iliac vein segments that contributes to the persistent symptoms.52 Historically, iliac vein stenosis and obstruction causing CVI were treated with surgical procedures such as cross-femoral venous bypass or iliac vein reconstructions with prosthetic material. More recently, endovenous stenting has replaced the traditional bypass. In a large study of patients with CVI and evidence of outflow obstruction, iliac vein stenting resulted in clinical improvement with complete pain relief in 50% of the patients and complete resolution of edema in 33% of the patients.58 The authors also noted that 55% of patients with venous ulcers achieved complete healing.
Open surgical procedures are reserved for patients who do not respond to less invasive treatment (usually with anatomic abnormalities) and form the basis for the endovascular therapies that are becoming widely used as a first line intervention.
Ligation and Stripping and Venous Phlebectomy
Removal of the saphenous vein with high ligation of the saphenofemoral junction was one of the first treatments developed, going back to the mid-1800s or earlier.59 This procedure has been the surgical standard for superficial saphenous insufficiency in CEAP clinical classes 2 to 6. Varicose clusters that communicate with the saphenous vein are often avulsed during the same procedure by phlebectomy.
In a study evaluating patients with venous ulcers and reflux of the superficial and deep venous systems, randomization to surgery (only on the superficial venous segments) plus compression therapy led to a reduction in ulcer recurrence at 12 months when compared with compression alone (12% versus 28%). This supported an additional benefit of correcting the incompetent superficial venous system on prevention of ulcer recurrence.60
Finally, venous valve reconstruction of the deep vein valves has been performed in selected patients with advanced CVI who have recurrent ulceration with severe and disabling symptoms. Venous valvuloplasty has been shown to provide 59% competency and 63% ulcer-free recurrence rates at 30 months.52 A percutaneous valve has also been studied with moderate success, and the creation of a neovalve from the intima and media of the thickened venous wall to fashion a new monocuspid or bicuspid valve has also been undertaken with moderate success in select patients.61
CONCLUSION Mrs. VB responded to standard care of compression, non-adherent dressings, and non-contact low-frequency ultrasound. The small wound on the left leg healed and the patient transitioned to a compression garment on that side. No vascular procedures were indicated due to her initial progress, including a decrease in pain levels to 5-6/10 with treatment.
Ankle exercises were included to increase range of motion and facilitate heel/toe gait sequence with good outcomes; the patient was able to ambulate without gait impairments; however, her work did require prolonged standing.
After 3 months of therapy, the wounds stalled. (FIGURE 4-75) There were no signs of infection but because of the chronicity of the wounds, cultures were obtained and were negative. Negative pressure wound therapy was added to the standard care of selective debridement, absorbent dressings, and multilayer compression. The patient took a 3-week leave of absence from work with little improvement in both tissue quality and wound size. The patient had poor tolerance for negative pressure and requested that it be discontinued after a 3-week trial. The wounds did respond with increased granulation, flatter edges, and less epibole. (FIGURES 4-76, 4-77)
Collagen matrix dressings were added to the plan of care with slight increase in epithelial migration at the edges. At this point, the clinician reviewed again with the patient all of her recent laboratory values and medications. The patient admitted to taking 800 mg of Motrin a day, which she was advised to take for pain. After consulting with her physician, medications were adjusted to a different hypertensive medication given transdermally, and the patient discontinued Motrin with no need for alternative pain meds. Within one week new epidermis was visible at the edges, and the patient made significant and rapid improvement with full closure within three months.
Right lateral lower extremity before use of negative pressure
Right medial lower extremity after use of negative pressure
Right lateral lower extremity after use of negative pressure
In summary, current research suggests that endovenous therapy, RFA, and laser ablation are the gold standard. There is a select role for stripping and ligation but many of the historically used surgical techniques have been discontinued in favor of less invasive, less morbid endovascular techniques that offer equivalent benefit.
Post-healing care to prevent recurrence of venous wounds includes consistent wearing of compression garments, continued exercise, and meticulous skin care. If a patient has a history of ulceration, at least Class II garments are recommended unless the patient is unable to don them or has confirmed PAD that has not been treated by a vascular specialist. There are several donning aids available for patients with other impairments (eg, arthritic hands or total hip replacement), and the patient needs to demonstrate competency in don donning and doffing the garments before being discharged from therapy. Compression garments consisting of either elastic or non-elastic Velcro straps are also available for patients who have difficulty donning stockings. A recommended wearing schedule is to don the garments in the morning immediately upon awakening and before the limb swells, and to remove them at night before showering and providing skin care. The importance of adherence to post-healing protocols cannot be overemphasized to patients who have healed venous wounds.