Venous Stasis Ulcers

Introduction

Leg Ulcer Evaluation and Treatment Principles

• Patient and wound assessment
• Pathophysiology of chronic venous insufficiency
• Noninvasive vascular assessment
• Segmental pressure recordings
• Duplex ultrasonography
• Recommendations for treatment (compression)
• Dressing selection and education
• Treatment of mobile and immobile patients
• Outcome analysis

Accurate assessment is the key to effective leg ulcer management. Venous stasis ulcers, ischemia diabetic complications are responsible for over 90% of leg ulcers.

Venous stasis ulcers affect 1 to 2% of the population. The cost of management of leg ulcers has been estimated to be:

• Scandinavia – $25 million (1985 U.S. dollars)
• United Kingdom – $200 Million (1989 U.S. dollars)
• United States – Projected $1 Billion

The impact on quality of life is immeasurable but includes pain, decreased mobility, negative self-image, and feelings of anger, fear, isolation and depression.^1,2

An initial assessment of the patient with an ulcer of the lower extremity must include a detailed patient history, which will provide clues as to the differential diagnosis. Careful physical examination is necessary to evaluate the size and characteristics of the wound and should highlight any associated medical conditions. This should also include evaluation of the patient’s social circumstances as these may impact on both care and healing.³

A Recommended Management Pathway for Leg Ulcers
The International Leg Ulcer Advisory Board comprises some of the most eminent clinicians and researchers in the field from Europe, North America and Australia. The panel designed a recommended management algorithm based on a review of the available literature and expert consensus and also looked at relevant conferences and existing guidelines when making their decision about the algorithm. The International Leg Ulcer Advisory Board Published their review in the Journal of the European Wound Management Association, May 2002.⁴

In order to ensure ease of use and effectiveness, the algorithm has been kept as simple and straightforward as possible. The algorithm can be broken down into four stages: Assessment, Diagnosis, Recommendations for Treatment and Outcomes:

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Review a patient’s history:

• Previous history of deep vein thrombosis or venous ulcer
• History of leg edema
• Cause of the wound such as trauma or pressure
• Treatment history of the wound to date
• Wound duration: acute ( 6 weeks)
• Identification of systemic factors that affect wound healing (medications, acute and chronic illnesses, age etc)
• Nutritional status
• History of travel or known exposure to fungal or parasitic causes

Investigating and obtaining a thorough patient history will help in identifying the correct cause and facilitate management.

Wound Assessment
A complete wound assessment consists of a careful evaluation of the wound and surrounding tissue. Components of the wound assessment include:

• Location of the wound
• Physical characteristics of the wound including size and depth of injury
• Presence of undermining, tunneling, sinus tracts, foreign bodies and exposed bone
• Appearance of the wound bed
• Skin color and condition
• Skin temperature
• Amount and characteristics of exudate
• Presence of local or general edema
• Presence and nature of pain

Venous Insufficiency Arterial Insufficiency Neuropathic History Previous DVT and/or varicosities Decreased mobility Obesity Traumatic injury Family history Previous venous ulcer Pain when extremity is dependent for prolonged periods Decreased pain and swelling with elevation Smoking Diabetes Hypertension Aging Hyperlipidemia H/O arterial disease Intermittent claudication Pain with elevation, improves with dependency Intermittent claudication Previous history of ulceration Loss of protective sensation Peripheral vascular disease Duration of diabetes Poor glycaemic control Impaired functional abilities Paresthesia – insensate Location Gaiter area (lower calf area and above the ankle) Most frequent is medial aspect of lower leg superior to malleolus Generally at the ankle or below Over bony prominence or area exposed to pressure Interdigital spaces Plantar or lateral aspect of the foot Metatarsal heads Site of repetitive pressure and/or friction Appearance Colour: wound base fibrinous or granular Size: shallow in depth, small to large in surface area, irregular margins Drainage: moderate to heavy Oedema: frequently present and often associated with dermatitis Skin temperature: normal Surrounding skin: brown staining called haemosiderosis Colour: wound base pale, may see dry necrotic tissue (eschar) Size: tend to be small round ulcers with smooth wound edges “punched out” Drainage: minimal, unless infected Oedema: generally not present unless co-morbid CHF Skin temperature: decrease, cool and may have dependent rubor and pallor on elevation Surrounding skin: shiny, taut, thin, dry, scaly, no hair on lower extremity, thick brittle toe nails Colour: wound base granular Size: variable, usually small, well defined wound margins but may be large. Drainage: minimal, unless infected Oedema: generally not present Skin temperature: warm Surrounding skin: periwound has thick callous, skin is dry often with fissures May see structural changes and bony deformities Perfusion Palpable pulses ABI > 0.8 Capillary refill normal < 3 seconds Pulses diminished, may only be audible with Doppler or absent ABI 0.7 or lower Capillary refill > 3 seconds Palpable pulses ABI may not be reliable in diabetic patients Capillary refill normal < 3 seconds Treatment Considerations • Improve venous return • Compression therapy • Unna Boot • Multi-Layer Compression Therapy • Tubular compression dressing • Compression stockings • Compression pumps • Leg elevation • Must rule out arterial disease before initiating compression Vascular consult to evaluate potential for revascularisation No smoking Moisturise dry skin, do not apply between toes Avoid trauma Appropriate footwear Moist wound healing, if adequate blood flow to support healing, present High risk for pressure ulcers on heels Pressure relief “off loading” the plantar surface of the foot with appropriate footwear Tight glucose control Aggressive sharp debridement of callous No bathroom surgery Aggressive treatment of infection Routine professional foot care

Pathophysiology of Chronic Venous Insufficiency

Normal Venous Return
Normal venous return is the result of two mechanisms. First the calf pump during ambulation: the calf muscle contracts and compresses the venous compartment, which propels blood in the veins up towards the heart.
The one way valves open when the calf muscle contracts and close when the calf muscle relaxes and this prevents the reflux of blood and distention of the veins.

Pathogenesis of Venous Ulcers

Definition: The basic physiologic abnormality underlying the manifestations of “Chronic Venous Insufficiency” is an elevation of ambulatory venous pressure.

The pathogenesis of venous ulcers is the focus of much research. It is generally agreed that venous hypertension is the fundamental problem. There are several hypotheses that have emerged to explain the formation of venous ulcers. Venous hypertension is often the result of valvular incompetence secondary to Deep Vein Thrombosis. As a DVT forms, the thrombus adheres to the endothelium, contracts and scarring destroys the valves. Recanalization of the vessel leaves high resistance incompetent channels.

It has been suggested that venous hypertension leads to the distention of vessels causing an increased permeability of the vessel wall resulting in the leakage of large molecules or blood components into the skin. It is the presence of these components that interferes with the diffusion of oxygen and the delivery of nutrients to the skin. One hypothesis suggests that it is the presence of fibrin, which forms pericapillary fibrin cuffs, which impedes the diffusion of oxygen and nutrients between the blood vessel and the dermis. This results in anoxia leading to ulceration. While this hypothesis has some merit, a number of flaws have been identified.

Another hypothesis suggests that white blood cells can become entrapped in areas of reduced venous flow adhering to endothelium, causing occlusion of the capillaries and damage to dermal vasculature releasing fluid and inflammatory mediators into the tissue leading to chronic inflammation.

The following animation will assist the learner in understanding venous blood flow and the pathogenesis of ulceration.

Non-Invasive Vascular Assessment An accurate vascular assessment of the extremity is necessary to ensure that the correct etiology of the ulceration has been identified and to exclude those patients with arterial disease for whom compression is dangerous. There are a number of non-invasive methods used to confirm venous disease when a patient presents with suspected venous ulceration. Methods of assessment include:Examination of: Skin color and temperature Areas of dryness and cracking skin Capillary refill time;- this is a simple test that provides information about the extent of ischemic disease, normally color should return in 3-4 seconds. Palpation of peripheral pulses;- there can be significant discrepancies with documentation of pulses when the 1+, 2+, 3+ etc technique is used. It is more reproducible to document palpable or absent. The following system for grading palpable pulses is often used. 0 – Absent 3+ – Normal 1+ – Barely palpable 4+ – Bounding 2+ – Palpable but diminished Doppler Assessment and Ankle Brachial Index The Doppler is a vital tool of assessment when trying to determine the underlying etiology of leg ulcers and determine a course of treatment that will maximize wound healing potential. Predominantly leg ulceration is of venous origin and requires sustained compression to facilitate venous return from the lower extremities. However, before any type of compression management can be considered, a Doppler test should be performed to determine whether there is arterial involvement or whether the ulcer is the direct cause of arterial compromise. The significance of assessing for adequate arterial flow in the affected extremity is of utmost importance as the application of compression to an ulcer of arterial or mixed etiology could further compromise blood flow and result in ischemia. The following exercise will assist the learner in developing the skills necessary to locate pulses and differentiate arterial and venous sounds of the arms and lower extremities. Followed by an explanation of the procedure. Ankle Brachial Index Procedure Recording Ankle Brachial Index (ABI) also known as Ankle Brachial Pressure Index (ABPI) or Resting Pressure Index (RPI) Checks should be made that the patient has rested for the appropriate amount of time (15-20 minutes) Prepare the patient’s arms and legs for access The brachial pressure is first measured in both arms using the Doppler. The Doppler probe should be held at a 45- 60-degree angle to the limb. The electrode gel assists the transmission of the pulse to the probe. Identify the sound of the arterial flow. The artery has a high-pitched sound. If the sound you hear is a gale-like whoosh with ill-defined beats you are listening to venous return and need to change the probe position. For the purpose of this test, systolic pressure only is required. To measure the ankle pressure the correct position of the cuff should be located approximately 5cm above the malleolus. Any wounds which have had their dressings removed need to be covered by a sterile shield to prevent contamination of the wound bed and also to prevent cross contamination of the cuff. Prior to inflating the cuff, the pedal pulses have to be located using the Doppler. There are two main pulses (the dorsalis pedis and the posterior tibial) to identify, from which an arterial sound may be heard. It is quite common in arterial compromise to find foot pulses absent or diminished. The posterior tibial pulse is more reliable than the dorsalis pedis that is congenitally absent in 10% of people: in a further 10% the dorsalis pedis is impalpable. The systolic measurements should be taken on each ankle using different pulse points for greater accuracy. When all the measurements have been taken and recorded the Ankle Brachial Index can be calculated using the highest brachial systolic Doppler recordings and readings from each of the ankles. Note ABI isn’t always reliable in patients with diabetes due to arterial calcification that can lead to falsely high ABI’s. ABI CalculationABI = Ankle Systolic Pressure / Brachial Systolic Pressure Example Ankle systolic pressure = 80 mm Hg Brachial Systolic Pressure = 100 mmHg 80 / 100 = 0.8 ABI Clinical Significance 0.9 – 1.1 normal range for ABI 0.7 – 0.8 mild disease and the patient may begin to experience intermittent claudication or pain with ambulation. 0.4 – 0.6 moderate to severe disease and at this point there is likely to be impaired healing. < 0.4 severe occlusive disease. 1.2 may represent a falsely elevated ABI, which can result in patients with sclerotic vessels for example patients with Diabetes or Renal Failure. The blood vessels become stiff and ridged and are not readily compressible leading to falsely elevated reading. These patients may require further vascular testing to determine adequacy of perfusion. It is important to periodically repeat the ABI to monitor progression of disease. A decrease of more than 0.2 is consistent with a decrease in perfusion and progression of disease.

Segmental Pressure RecordingsIn this examination, systolic pressures are measured sequentially up the leg from ankle to thigh. A pressure difference of greater than 25 mmHg between levels indicates occlusive disease. Duplex Ultrasonography measures blood flow velocity through a vessel and is the primary method of identifying venous obstruction or abnormal venous reflux A number of plethysmographic methods, including air and photo plethysmography, may be used to assess venous function. Other investigations may also take place to exclude disorders such as rheumatoid arthritis, diabetes, renal failure, anemia, tumors and auto-immune disorders. A comprehensive physical exam can provide important information for the differential diagnosis of venous disease. It is essential to determine the adequacy of arterial perfusion because compression therapy is the gold standard of treatment for venous ulcers and high level compression is contraindicated in the presence of arterial disease with an ABI of less than 0.8. Reduced levels of compression are recommended in the case of mixed etiology ulceration with an ABI 0.6 – 0.8 mm Hg. Clinical Features There are a number of clinical signs that are associated with chronic venous insufficiency (CVI) and are helpful in making a differential diagnosis. It is helpful to remember that the clinical presentation is in part the result of the blood components leaking into the interstitial space. Hyperpigmentation CVI leads to distension of the blood capillaries and damage to the endothelium, leading to leakage of red blood cells. The breakdown products of hemoglobin cause dark staining of the skin or hemosiderosis. Lipodermatosclerosis may be described as “woody” induration of the tissues with fat replaced by fibrosis. The leg often assumes an inverted champagne bottle shape. Edema Venous pressures and increased capillary permeability can lead to increased interstitial fluid. Venous disease can also be complicated by poor lymphatic drainage. Characteristically edema associated with CVI may involve the lower leg and foot, is considered pitting edema and will occur in one or both legs depending on the extent of the venous disease. Venous dermatitis and eczematous changes These are often associated with CVI and can be aggravated by wound care products through irritation and allergy. Persistent scratching may cause secondary infections. Ankle flare refers to the collection of small venular channels inferior to the medial malleolous and extending onto the medial surface of the foot. This sign is indicative of CVI. Venous Ulcer Characteristics Location Gaiter area – most frequently above the medial malleolus but can occur anywhere on the leg Size Can be small to circumferential, shallow, with irregular wound margins Wound bed Ruddy color, granulation or fibrinous tissue Drainage Frequently moderate to large Skin Scaling, pruritis, weeping, staining Pain Varies greatly – painless to painful

Recommendations for Treatment

There are fundamental principles for developing a comprehensive management plan for the patient with CVI and /or venous ulcers.

Compression therapy is the gold standard for treatment of venous ulcers. It is extremely difficult for venous ulcers to heal in absence of compression. There are a variety of interventions for providing compression, however not all have the same level of effectiveness.

Sustained compression provides the mainstay of treatment in venous leg ulcers. This should be supported with adjunctive medical and surgical therapy, appropriate dressings and patient education. Sustained compression is provided by multi-layer elastic or inelastic bandage systems. There is now considerable evidence to show that this form of sustained high compression improves ulcer healing and provides quality of life and cost benefits. Multi-layer high compression bandaging improves healing of venous leg ulcers when compared with single layer, low compression bandaging although there is little reliable evidence to date of large randomised controlled trials which directly compare 4-layer compression to 3-layer or 2-layer bandaging.

Multi-layer bandage systems are complemented by reduced compression systems (15-25 mmHg) for those patients who cannot tolerate high compression systems, and compression stockings. Intermittent pneumatic compression (IPC) is a useful adjunct to multi-layer compression and has been shown to improve ulcer-healing rates when used with multi-layer compression.

Compression
The degree of compression produced by any bandage system over time is determined by complex interactions between four principle factors – the physical structure of the elastomeric properties of the bandage, the size and shape of the limb to which it is applied, the skill and technique of the bandager and the nature of any physical activity undertaken by the patient.

Laplace’s Law (Determining Sub-Bandage Pressure) – The pressure generated by a bandage immediately following application is determined principally by the tension of the fabric, the number of layers applied, and the degree of curvature of the limb. P=T/R

P pressure
T tension
R radius

Applied pressure is directly proportional to the tension in a bandage (P increases with T) but inversely proportional (P decreases as R increases) to the radius of the curvature of the limb to which it is applied.

Methods of Compression

• Elastic compression (long-stretch) bandages exert high compression during rest and exercise whereas
• Inelastic (short-stretch) bandages produce passive compression mainly when the calf muscle contracts, increases in volume and creates pressure against the bandage. At rest, inelastic compression bandages exert pressure dependent on the tension used during application.

References

1. Phillips T, Stanton B, Provan A & Lew R. (1994). A study of the impact of leg ulcers on quality of life: Financial, social and psychologic implications. J Am Acad Dermatol;31:49-53
2. Sibbald RG, Williamson D, Filanga V & Cherry G. (2001). Venous Leg Ulcers. In Krasner & Sibbald (Eds) Chronic Wound Care: A clinical source book for healthcare professionals (3rd Ed), (pp. 483-494). Wayne PA: HMP Communications.
3. Franks,P.J., Winterberg, H. Moffatt, C.J. (2002) Health-related quality of life and pressure ulceration assessment in patients treated in the community. Wound Repair and Regeneration, 10(3), 133-40.
4. Stacey M et al. The use of compression therapy in the treatment of venous leg ulcers: a recommended management pathway. EWMA Journal 2002.
5. Fletcher A, Cullum N, Sheldon T. A systematic review of compression treatment for venous leg ulcers. BMJ 1997; 315: 576-80.
6. Margolis DJ, Berlin JA, Strom BL. Risk factors associated with the failure of a venous leg ulcer to heal. Arch Dermatol 1999; 135: 920-926.
7. Moffat CJ, O’Hare L. Ankle pulses are not sufficient to detect impaired arterial circulation in patients with leg ulcers. Journal of Wound Care 1995; 4 (3): 134-138.
8. Nicolaides AN. Investigation of chronic venous insufficiency: a consensus statement. Circulation 2000;102:126-163.
9. Palfreyman SJ, Lochiel R, Michaels JA. A systematic review of compression therapy for venous leg ulcers. Vascular Medicine 1998; 3: 301-313.