Understanding CVI: Causes, Symptoms, and Treatment for Venous Ulcers

mdavis107
Oct 26, 2020
5 min read

Updated: May 8

Understanding Chronic Venous Insufficiency (CVI) and Valve Failure

Chronic venous insufficiency (CVI) occurs when the valves in leg veins become damaged or fail, leading to blood pooling in the lower extremities. This condition disrupts the normal return of blood to the heart and creates a buildup of pressure in the veins over time.

Reduced efficiency of venous return leads to chronically elevated pressure in the affected peripheral veins. This helps explain why deep vein thrombosis (DVT) is one of the most important contributing factors in the development of CVI. Over time, this insufficiency can give rise to varicose veins and venous leg ulcers.

The Role of Damaged Valves and Venous Hypertension

Venous valves help keep blood flowing toward the heart. When they fail, backward flow (reflux) occurs, increasing venous pressure—also known as venous hypertension. Over time, this high pressure further damages the venous system, resulting in chronic symptoms like swelling, pain, skin changes, and eventually ulceration.

The Impact of Venous Pressure on Tissue Health and Healing

As venous pressure builds, it disrupts healthy circulation and causes a cascade of tissue damage. Blood flow slows, oxygen delivery drops, and waste products accumulate—conditions that undermine wound healing and cellular health.

Capillary Pressure and Oxygen Exchange

Increased pressure in the veins raises hydrostatic pressure in nearby capillaries. This backlog in the capillaries slows arterial inflow, reducing the delivery of oxygen and nutrients while also impairing the removal of waste products such as carbon dioxide and nitrates. As a result, tissue becomes increasingly hypoxic, which impairs healing and promotes chronic inflammation.

Edema and Tissue Viability

Increased pressure also reduces the reabsorption of tissue fluid at the capillary level, leading to a buildup of fluid known as edema. The buildup of tissue fluid (edema) further complicates circulation. Edema increases the distance oxygen and nutrients must travel to reach cells and hampers the removal of metabolic waste. This prolonged imbalance can lead to cell death and wound breakdown.

Fibrin Cuff Formation and Cell Death

With prolonged venous hypertension, capillary dilation stretches the vessel walls and widens the gaps between endothelial cells. This increased permeability allows larger plasma proteins like fibrinogen to migrate from the blood into surrounding tissues. Once there, fibrinogen converts to fibrin, forming "fibrin cuffs" around capillaries. These cuffs act as physical barriers to oxygen and nutrient exchange—further reducing tissue viability and contributing to ulcer formation.

Types of Chronic Leg Ulcers: Venous, Arterial, Diabetic & Mixed

Chronic leg ulcers are classified based on their underlying cause. Venous ulcers result from CVI and are the most common type. Arterial ulcers occur due to inadequate arterial supply, often from peripheral artery disease. Diabetic ulcers may result from neuropathy, ischemia, or a combination. Rheumatic ulcers, while less common, can occur as a complication of rheumatoid vasculitis. Mixed ulcers have both venous and arterial features and are more complex to treat.

It is important to identify the type of ulcer accurately before treatment. In purely venous ulcers, arterial blood supply is typically normal, and the ankle-brachial index (ABI) is greater than 0.9—an indicator that compression therapy is safe. However, if a patient has arterial insufficiency or a low ABI (e.g., <0.5), compression therapy should be avoided, as it can worsen ischemia. Mixed ulcers, which involve both arterial and venous compromise, require careful clinical judgment and customized care plans.

Recognizing Venous Ulcer Characteristics

Venous ulcers are typically shallow with irregular edges and may leak fluid. The surrounding skin often shows signs of hemosiderin staining (a rusty discoloration from red blood cell breakdown). Edema is common, and these wounds are frequently painful, especially when the leg is dependent.

Why ABI Testing Is Critical Before Compression Therapy

Before starting compression therapy, it’s essential to rule out significant arterial disease. The ankle-brachial index (ABI) test measures blood pressure at the ankle compared to the arm and helps determine if compression is safe. An ABI greater than 0.9 generally indicates that compression is appropriate.

How Compression Therapy Supports Venous Ulcer Healing

Compression therapy is the cornerstone of venous ulcer treatment. It reduces venous pressure, supports calf muscle pumping, and promotes blood return to the heart. This not only accelerates healing but also reduces the chance of ulcer recurrence.

Elastic vs. Inelastic Compression

Elastic compression (such as multi-layer bandages or compression stockings) maintains continuous pressure and can be used for both ambulatory and non-ambulatory patients, including those with less than 45 degrees of ankle mobility.

Inelastic compression (like an Unna boot) is only effective for actively ambulating patients, as it supports the calf muscle pump during walking and requires at least 45 degrees of ankle mobility.

When Compression Should Be Avoided

While compression therapy is essential for venous ulcer management, it must be used cautiously. If improperly applied, any form of compression—elastic or inelastic—may cause adverse effects such as skin damage, pressure injury, or impaired circulation.

Compression therapy should be avoided in patients with an ankle-brachial index (ABI) below 0.5, signs of critical limb ischemia, or those with untreated arterial ulcers. In these cases, compression can worsen arterial flow and increase the risk of tissue breakdown. Additionally, tubular sleeves should never be used as compression therapy, as they can reverse the pressure gradient by providing more pressure at the knee than at the ankle—further compromising venous return.

Proper assessment, including vascular studies and clinical judgment, is vital before initiating compression.

Strategic Solutions for Managing CVI in Clinical Settings

Shared Health Services (SHS) partners with hospitals and physician practices to strengthen wound care program performance and support the clinical and operational demands of managing patients with chronic venous insufficiency (CVI). Our approach helps wound care teams align care delivery with best practices while addressing cost control, clinical quality, and regulatory compliance.

Whether your team needs support launching a new wound care service line or enhancing an existing one, SHS delivers tailored solutions—from compression therapy protocols and staff education to audit-ready documentation strategies.

Ready to explore how we can help your organization achieve sustainable wound care outcomes? Contact us today to schedule a conversation with our team.

References

Bryant, R. A., & Nix, D. P. (Eds.). (2012). Acute & chronic wounds: current management concepts (4th ed.). St. Louis: Mosby.
Campbell, J. (2006). Campbell’s pathophysiology notes. Carlisle: Lorimer, UK.
Krasner, D. L. (Ed.). (2014). Chronic wound care: the essentials. A clinical source book for healthcare professionals. Wayne: HMP.
Gloviczki, P. (Ed.). (2009). Handbook of venous disorders: Guidelines of the American Venous Forum. Hodder: Hachette UK.
Partsch, H., Rabe, E., & Stemmer, R. (Eds.). (2000). Compression therapy of the extremities. Phlébologiques Françaises: Paris, FR.