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Wound Series Part 4: Lymphedema: The Basics

1.5 Contact Hours
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This course will be updated or discontinued on or before Thursday, December 4, 2025

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≥ 92% of participants will know key differences between lymphedema and lipedema, how to accurately stage lymphedema, and the main tenants of lymphedema management.


After completing this activity, the participants will be able to me the following:

  1. Define lymphedema and the pathophysiology of lymphedema.
  2. Describe the difference between lymphedema and lipedema.
  3. Describe at least two common signs and symptoms of lymphedema and identify one screening technique for lymphedema.
  4. Classify the stages and progression of lymphedema.
  5. List at least one diagnostic tool to diagnose lymphedema.
  6. Describe how and when to refer a patient to a certified lymphedema therapist.
  7. Identify at least two common treatments for lymphedema.
CEUFast Inc. and the course planners for this educational activity do not have any relevant financial relationship(s) to disclose with ineligible companies whose primary business is producing, marketing, selling, re-selling, or distributing healthcare products used by or on patients.

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Wound Series Part 4: Lymphedema: The Basics
To earn of certificate of completion you have one of two options:
  1. Take test and pass with a score of at least 80%
  2. Reflect on practice impact by completing self-reflection, self-assessment and course evaluation.
    (NOTE: Some approval agencies and organizations require you to take a test and self reflection is NOT an option.)
Author:    Linda J. Cowan (PHD, ARNP, FNP-BC, CWS)

Lymphedema Overview

Lymphedema is a chronic, debilitating, and distressing condition affecting an estimated 35 million individuals in the United States and over 140,200 million people worldwide (O’Donnell et al., 2020). Lymphedema is “the abnormal accumulation of interstitial fluid and fibroadipose tissues resulting from injury, infection, or congenital abnormalities of the lymphatic system” (Mahera, 2023).

In the past, Starling’s Law, introduced by Earnest Henry Starling (1866-1927), described a reabsorption process in the microcirculation where it was believed that most (90%) of the fluid leaking into the interstitial spaces of the lower extremities from venous insufficiency, would enter into the venous end of the capillaries (such as when compression was applied) and end up back in the blood circulation, while 10% of this interstitial fluid would be returned to the blood circulation via the lymphatic system. However, newer evidence suggests that 0% of interstitial fluid is reabsorbed back into the venous end of the capillaries, and 100% of the interstitial fluid load is managed by the lymphatic system (Hettrick & Ehmann, 2019). Bjork (2018) reported, “It has been established that the endothelial glycocalyx layer (EGL) controls the movement of proteins and fluid across the blood capillary wall. Despite prevailing principles regarding Starling’s Law, it is now understood that there is no reabsorption of fluid back into the venous side of blood capillaries. Rather, there is only diminishing net filtration across the capillary bed, and fluid and blood proteins are removed from tissues via reabsorption through lymphatic capillaries alone. Consequently, a new paradigm emerged indicating that all edemas are on a lymphedema continuum.” The revision of Starling’s Principle with a clearer understanding of the endothelial glycocalyx layer (EGL) resulted in a new model of microcirculation based on evidence reported by Levit and Michel in 2010. (Hettrick & Aviles, 2022).

The new evidence demonstrated that the lymphatics manage 100% of interstitial fluid edema and has led to the term “phlebolymphedema,” which has been defined as edema “due to insufficiency of the venous or/and lymphatic system, in combination with possible systemic contributors, leading to accumulation of interstitial protein-rich fluid in the interstitial space” (Ostler, 2018).

Regardless of where it originates, when interstitial body fluids (containing foreign debris, proteins, white blood cells, and microorganisms) leave the interstitial spaces and enter the lymphatic system, it is called lymphatic (or lymph) fluid. This course will focus on the management of lymphedema in general. Still, it is important to recognize that managing all edema (such as what is classified as venous insufficiency) will benefit from considering evidence-based treatment methodologies aimed at improving lymphatic drainage since “all edema is on a lymphedema continuum” (Hettrick & Aviles, 2022).

It is also important to note that this course is not meant to be a “how to” course on performing lymphedema therapy. Nor is the goal of this educational program to make the reader a lymphedema specialist or therapist, but rather to provide the reader with an overview of the problem of lymphedema and become familiar with diagnostic, differential, and treatment options.

The lymphatic circulatory system has been thought to be similar to the cardiovascular circulatory system, with lymph vessels and channels and two types of capillaries. However, it does not have the benefit of cardiac muscle contractions to pump lymph fluid along, and there is not a continuous string of vessels that connect directly. Therefore, it is described as a relatively passive system of fluid movement. In general, contracting and relaxing muscles in the area of the lymphatic vessel help move the fluid through the system. In cases where the lymphatic system is overloaded, the lymphatic system is damaged, or both, it needs the assistance of manual massage, mechanical pumps, compression sleeves, stiff compression wraps, and bandaging systems to assist with lymphatic absorption, capillary filtration, shifting fluid into non-compressed regions and to improve lymph management. In addition, it is now known that “the integumentary and lymphatic systems are interdependent.” Hettrick & Aviles (2022) report, “When initial lymph fills the interstitial space, elastic fibers are stretched, thereby expanding the lumen of the lymphatic capillary and opening the overlapping flaps to allow lymph to enter the capillary plexus. Thus, lymphatics must act as a mechanical extension of the interstitium to function (Bjork, 2018; Hettrick & Aviles, 2022).

Lymph vessels are typically larger than capillaries but smaller than veins. Most of the larger lymph vessels have one-way valves to keep the flow of lymph fluid uni-directional – toward the heart and preventing back-flow or clotting. The lymph system also has hundreds of lymph nodes that serve as filters for the lymphatic fluid (Lawenda et al., 2009). There are two separate systems of lymph drainage within the body: those found within the subcutaneous tissues, which drain lymph fluid that has diffused through capillaries from the superficial tissues and skin of the body, and those that drain lymph fluid diffused from tissues within the deeper spaces and structures of the body such as the head, neck, and thorax. The fluid movement through the lymphatic drainage system occurs partly by muscles contracting and increasing pressure against other structures, effectively “squeezing” the fluid from one place to another.

The deeper lymphatics drain the deep tissues, such as muscle, and follow a pathway similar to the cardiovascular blood vessels. Superficial lymphatics are in the subcutaneous fatty layer of the body and drain the subcutaneous tissues and skin.  The deeper lymphatic system connects with the more superficial lymphatic system through perforating vessels, which pass through the fascia (fibrous layer covering muscle)( NLN, n.d.).  However, these vessels do not connect directly and have open spaces between them. The lymph fluid (containing proteins, cellular debris, and fluids that have escaped from cells, tissues, and semi-permeable blood vessels) passes from the intercellular spaces of tissues into the lymphatic vessels, where they are directed to lymph nodes – the filters of the body. The lymph vessels return the filtered lymph fluid to the venous system. The smallest lymph vessels, which are blind at one end and collect lymph fluid in tissues and organs, are also known as lymph capillaries. However, they are different from those found in the venous-arterial circulatory system.

Clinical Pearl
Adult humans typically have about 800 lymph nodes throughout their body: Extremities, head & neck, axilla, thorax, abdomen, and groin. Lymph nodes are typically smaller than 1-2 cm in size. The lymph node is composed of 4 parts from inner to outer structure: Medulla (center most), Cortex, Subscapular Sinus, and Capsule (outer most). (Bujoreanu et al, 2023). Lymphedema may occur in any part of the body, and is not limited to the extremities (Bryant & Nix, 2023).

For more than 100 years, it was thought that the lymphatic channels did not cross the midline of the body, yet research initiated back in the 1950s after the development of lymphoscintigraphy and confirmed by Fife et al. (2014) suggests this is not the case. Fife et al. demonstrated with fluoroscopy and radio-opaque tracers that Lymphatic fluid was seen to cross the body's midline (head, neck, chest, and trunk) during lymph massage. This information is important when identifying sentinel lymph nodes to dissect in cancer cases and for manual lymphatic massage techniques (Uren et al., 2003).

Etiological Factors of Lymphedema

According to Breslin et al. (2018), “The lymphatic system maintains extracellular fluid homeostasis favorable for optimal tissue function, removing substances that arise due to metabolism or cell death, and optimizing immunity against bacteria, viruses, parasites, and other antigens.” A severe medical problem may occur in any part of the body when lymph fluid does not drain through the lymphatic system adequately.  Lymphedema is caused when there is an excessive build-up of interstitial fluid in any part of the body due to a pathological disruption in the lymphatic drainage system (Lu et al., 2009; Rabe et al., 2018; Hettrick & Aviles, 2022). This may occur when lymph nodes are removed, lymphatic vessels are deformed, injured, or chronically over-taxed (such as chronic venous insufficiency or CVI), or lymphatic vessels/nodes are blocked (such as parasites or tumors). Lymphedema from lymph node removal, lymphatic vessel injury, or lymphatic vessels/node blockages (such as by parasites or tumors) are often unilateral in presentation.

Lymphedema may appear at any age and may be sudden (such as after surgery) or progressive and worsen over time (such as when due to parasitic filariasis) (Rabe et al., 2018). Lymphedema may be mild and hardly noticeable to the patient or clinician, or it may be severe and extremely debilitating (some lower extremities have been reported to get so large that they exceed the size of the rest of the body) and may become life-threatening. Over time, if left untreated, lymphedema may result in further lymph vessel damage, chronic inflammation, and what is often referred to as fibrotic changes or irreversible hardening of the skin(Hettrick & Aviles, 2022; Rabe et al., 2018; Vojackova et al., 2012). It has been suggested that the prolonged sequestering of accumulated lymph fluid leads to the cross-linking of proteins and other components of the fluid, leading to the fibrotic changes that, if untreated, make movement and reduction of the built-up fluid increasingly difficult to achieve.

photo of unilateral lymphedema

 Image 1: unilateral lymphedema

photo of gbilateral lymphedema on legs

 Image 2: bilateral lymphedema


Lymphedema should not be confused with lipedema. Lipedema (may also be called lipoedema or lipodema) is actually a fatty tissue disorder caused by an abnormal deposition of adipose tissue with hypertrophic or hyperplastic fat cells that trap fluid in tissue (Fife et al., 2010; Kruppa et al., 2020). This typically occurs symmetrically in the lower extremities above the ankle but may also occur in the upper portion of the upper extremities. One of the easiest ways to clinically differentiate lipedema from lymphedema is that the feet are spared in lipedema and will appear relatively normal in shape compared to the often puffy “box foot” of someone with lymphedema.

graphic showing lipedema on the leg

Image 3: lipedema

Lipedema may be hereditary and occurs almost exclusively in women over the age of puberty, which has led to theories that estrogen and progesterone may play a role in the development of this problem. One German study suggested that 11% of the general female population have lipedema, and up to 17% of women with lymphedema also have lipedema (Foldi, 2006; Herbst, 2021). Persons with lipedema typically have minimal pitting edema and a negative Stemmer sign (screening test for lymphedema; see clinical pearl box below). In addition, persons with lipedema have pain or tenderness with pressure to the affected tissue and may experience easy bruising (Kruppa et al., 2020). They also may experience persistent enlargement despite limb elevation or weight loss. To complicate matters, persons with lipedema may experience secondary lymphedema due to damaged blood vessels and tissue (altering lymphatic flow) over time (Herbst, 2023). Unfortunately, persons with lipedema or lymphedema are often underdiagnosed, misdiagnosed, or just dismissed as being obese (Fife et al., 2010).  The inclusion of lipedema into the Internal Classification of Disease in 2018, however, will help to increase awareness and research into the diagnosis and management of lipedema (Forner-Cordero et al., 2021).


There are two main types of lymphedema: primary and secondary lymphedema. Primary lymphedema is typically congenital or due to a genetic lymphatic system disorder and is more common in women. Secondary lymphedema is much more common than primary lymphedema and is an acquired impairment of the lymphatic system, typically due to infection, trauma, or as a complication of medical treatment, especially surgery, and radiation, and may also result from damage to lymphatic vessels due to chronic venous insufficiency(Vojackova et al., 2012; Smith, 2023). Cancer involving lymphoid tissue is known as lymphoma. Lymphoma will not be discussed in depth in this module.

Multiple types of cancer and cancer treatment are responsible for a large number of the estimated 3 to 5 million cases of lymphedema in the United States (Lawenda et al., 2009). For instance, after breast cancer surgery and treatment, women have a 10-30% risk of developing lymphedema of the upper extremity on the side of surgery/radiation. It has been reported that the risk of developing lymphedema after any type of cancer is 15.5%. This risk is lifelong. The National Cancer Institute’s (NCI) PDQ cancer information summary about breast cancer (2023) prevention states, “In a survey conducted in 2006 and 2010, 6,593 cancer survivors were asked to identify ongoing concerns. Approximately 20% of respondents reported concerns related to lymphedema. Of these individuals, 50% to 60% reported receiving care for lymphedema.” The NCI also reports a lymphedema point prevalence of 37% in women survivors of ovarian cancer, 33% in women survivors of endometrial cancer, and 31% in women survivors of colorectal cancers.  Additionally, a randomized clinical trial in “women with breast cancer demonstrated 42% of subjects had lymphedema at 18 months after surgery.” (NIH, 2023).

Clinical Pearl: Primary Lymphedema types
Traditionally, Primary Lymphedema can be either congenital or hereditary. The individual with congenital or hereditary developmental abnormalities (dysplasia of the lymphatic system) may not present with symptoms until years after birth. The age of the presenting symptoms determine how it is classified:
  • Type I – Congenital Lymphedema: clinically evident at birth or within the first 2 years of life.
  • Type II - Lymphedema Praecox: most common type of hereditary lymphedema - becomes clinically evident between ages of 2 and 35 years (most often in females and most commonly arising during puberty or pregnancy).
  • Type III – Lymphedema Tarda: Clinical signs of lymphedema develop after age 35, and is relatively rare.  (Zuther, 2009; NORD, 2022).

Lymphedema Classification System

Most classification systems recognize primary or secondary lymphedema as “classifications” of the disease. The most widely accepted staging system for lymphedema is a three-stage scale system (Stage 0 or 1a through 3) proposed by the International Society of Lymphology (ISL). This staging system is traditionally only used for lymphedema of the limbs (arms and legs). Information for the following lymphedema staging table resource is based on the 2016 Consensus Document of the International Society of Lymphology and Bryant & Nix (2023). This 2016 International Society of Lymphology (ISL) Consensus Document is the latest revision of the 1995 Document for the Evaluation and Management of Peripheral Lymphedema (ISL Executive Committee, 2016).

Table 1: Common Lymphedema Staging
STAGE 0 (or 1a)
  • Also known as the latent or preclinical stage (“subclinical condition”).
  • At this stage, the patient is at risk of developing lymphedema.
  • “Swelling is not yet evident despite impaired lymph transport, subtle alterations in tissue fluid or composition, and changes in subjective symptoms.”
  • This stage may be present for months or years before “overt edema” occurs or any more serious signs appear.
Bioimpedance spectroscopy or tissue dielectric constant analysis can assess early fluid changes. Studies indicated through bioimpedance, it is possible to identify changes in the “at-risk” limb before they become visible. When changes develop, if specialized treatment is started immediately, it may be possible to prevent the development of further stages of lymphedema. Bioimpedance is a non-invasive method of determining the composition of body tissues to evaluate the presence of body fluids such as lymphedema. Such measurements have been used to establish a baseline at the time of certain cancer treatments.
  • Stage I lymphedema is an early accumulation of fluid that is relatively high in protein content.
  • There is visible swelling with protein-rich lymph. However, there is no palpable fibrosis.
  • This swelling can be temporarily reduced by limb elevation (reversible pitting edema that begins distally).
  • Negative or borderline Stemmer sign.
  • The swollen tissues are soft, and pitting edema is present.
  • An increase in various types of proliferating cells may also be seen.
Lymphedema treatment should be begun as soon as signs are detected early. Waiting for the swelling to increase or for an infection to develop only makes the condition more difficult to treat. Prompt treatment of this stage can often control the condition and may prevent it from becoming more severe.
  • Stage II lymphedema is an increase in swelling and a change in the tissues. (Minimally pitting or non-pitting (brawny) edema).
  • Elevation of the limb will not reduce the swelling.
  • Positive Stemmer sign.
  • Hyperkeratosis (thickening of skin).
  • The tissues become increasingly firm due to fibrosis. Fibrosis is the formation of fine scar-like structures within the tissues that cause them to harden.
  • Papillomatosis of skin (rough cobblestone appearance and texture).
  • Pressure against the limb produces only a slight indentation or no indentation. Later in stage II, the limb may not pit at all.
  • The tissue changes at this stage increase the risks of even greater swelling, fibrosis, infections, and skin problems.
Stage II lymphedema can usually be improved with intense treatment.
  • Stage III lymphedema, which is also known as lymphatic elephantiasis (massive enlargement and disfigurement of limb).
  • It is a condition in which the tissue becomes extremely swollen and thickened due to a blockage in the lymph flow, chronic fluid buildup in tissues, and loss of elastic skin components.
  • The tissues become increasingly fibrotic (hardened). Pressure does not produce any pitting.
  • Normal elasticity is lost, and the skin hangs in folds.
  • The skin may change color.
  • Papillomas are small solid benign tumors that project above the surrounding tissue and may develop.
  • Hyperkeratosis is an increase in the thickness of the outer layer of the skin, can develop.
  • These skin texture changes are disfiguring and can limit mobility.
  • Infections become more common because of increased risks of breaks in the skin. These infections include fungal infections and open wounds within the skin folds.
  • Skin ulceration.
With intense therapy, Stage III lymphedema can be improved and potentially be prevented from becoming worse; however, it is rarely reversed to an earlier stage.

More research is needed in this area. Experts in the 2016 ISL consensus document stated, “These Stages only refer to the physical condition of the extremities. A more detailed and inclusive classification needs to be formulated with an improved understanding of the pathogenic mechanisms of lymphedema (e.g., nature and degree of lymphangiodysplasia, lymph flow perturbations, and nodal dysfunction as defined by anatomic features and physiologic imaging and testing) and underlying genetic disturbances, which are gradually being elucidated” (ISL Executive Committee, 2016). Research is also warranted to examine lymphedema's impact on socioeconomic status and quality of life (QoL).

Eberhardt & Raffetto, 2005 described a “CEAP” Classification of Chronic Venous Disease. Still, it does not include lymphedema, even though they recognize that chronic venous insufficiency may lead to the development of lymphedema. (Lee et al., 2013). The acronym CEAP was developed to stratify patients into categories based on the presentation of their venous disease and symptoms.

  • “C” represented Clinical presentations
  • “E” represented Etiological considerations and diagnostic results
  • “A” represented Anatomical locations and manifestations
  • “P” Pathophysiologic events and skin/tissue changes leading to skin ulceration or other complications

Initially, these classifications used a complex and detailed scoring system, which many clinicians felt was too cumbersome, so a 6-stage classification was developed under the CEAP umbrella:

  • CEAP 1 = Reticular and spider veins (cosmetic problem, no need to refer)
  • CEAP 2 =Varicose veins only (recommend routine referral to a vein specialist for duplex & photoplethysmography assessment)
  • CEAP 3 = Varicose veins + leg swelling (recommend quick referral to a vein specialist for duplex ultrasound & photoplethysmography assessment)
  • CEAP 4 = Varicose veins + evidence of venous stasis skin changes (recommend quick referral to a vein specialist for duplex ultrasound & photoplethysmography assessment)
  • CEAP 5 = Varicose veins + history of healed venous stasis ulceration (recommend quick referral to a vein specialist for duplex ultrasound & photoplethysmography assessment)
  • CEAP 6 = Varicose veins and open venous ulceration (recommend urgent referral to a vein specialist for duplex ultrasound & photoplethysmography assessment and refer to a wound care center or wound specialist for wound assessment and management).

Gasbarro et al. (2009) adopted the acronym C.E.A.P. (used for venous disease) and added an “L” (CEAP-L) to be more specific to Lymphedema. Gasbarro et al. designed the CEAP-L “based on the most objective sign in these patients” (edema). They subdivided the edema into five different classifications or levels that are dependent on the clinical manifestations noted by the clinician. “The etiological aspect considers two types of alterations of the lymphatic system: congenital and acquired. The anatomic is aimed to locate the anatomical structures involved. Pathophysiological conditions are gathered into five groups: agenesia or hypoplasia, hyperplasia, reflux, overload, obstruction.” While these classification and staging systems are promising (and better than nothing), the most important factor in treating lymphedema is identifying it in patients first and as early as possible. Winiwarter described the development of lymphedema in the scientific literature as early as 1892 (Wittlinger et al., 2011). Yet, Poage et al. (2008) suggest that only about 36% of individuals with lymphedema will seek treatment in the early stages, even after cancer surgery, when they are told it may be a complication. Unfortunately, there is not much information about how many cases of lymphedema are misdiagnosed, but it is clear that earlier intervention and patient education and support are needed.

Diagnosing Lymphedema

As with any disease or condition, diagnosis of lymphedema begins with a thorough history and physical examination. If secondary lymphedema is suspected after trauma or surgical excision of lymph nodes or following procedures such as revascularization or knee replacement surgery, imaging diagnostic tests may be minimized or deemed unnecessary. However, a simple screening test using Stemmer’s sign is recommended to evaluate a patient with an unknown etiology of edema suspicious of lymphedema. See the clinical pearl box below.  Early detection (sometimes even before physical signs or symptoms) may be accomplished using bioimpedance spectroscopy (BIS), where an electrical current is passed through an extremity and impedance is measured. Reduced impedance is suggestive of lymphedema. BIS may also be used to monitor treatment effectiveness (Warren et al., 2007; Bryant & Nix, 2023). Diagnostic tests may also include MRI, CT scan, and Doppler ultrasound, which may help identify where there is a potential lymphatic system blockage (such as a tumor growth). Lymph fluid analysis is also sometimes conducted (protein content between 1.0 and 5.5 g/dl usually indicates lymphedema).Another diagnostic test (the gold standard) provides actual visualization of lymphatic vessels by lymphoscintigraphy (a radionuclide imaging test showing the movement of a radioactive dye through the lymphatic system). Genetic testing may be recommended in patients with primary lymphedema (Bryant & Nix, 2023).

There are four stages of lymphedema (3 numbered stages):

  • Stage 0 (or pre-stage): a latency stage where edema is absent and physical symptoms are mild and reversible.
  • Stage 1: The condition may be controlled if treatment is started promptly.
  • Stage 2: Edema can be improved, but some tissue changes are likely irreversible.
  • Stage 3: Symptoms may be improved, but tissue damage is extensive and irreversible. (Poage, E. (2008); ISL, 2016). [See Table 1 in the previous section)].
  • Chronic lymphedema has no cure (Bryant & Nix, 2023; Hettrick & Aviles, 2022).
Clinical Pearl

Checking for Stemmer’s sign as a screening for lymphedema. It is diagnostic for lymphedema if you cannot pinch the skin on the anterior surface of the base of the second toe (or the base of the second finger on the dorsal aspect of the hand for the upper extremity). If you can gently pinch and lift this skin, it is negative. If you cannot due to thickened skin, it is positive. New evidence suggests this sign can be done over any body part, looking for a “Bjork Bow-Tie” sign (Hettrick, H., & Bjork, R., 2018).

positive stemmers

Image 4: Stemmers sign

Implications of Lymphedema: Chronic Wounds

Lymphedema creates a management challenge for the clinician trying to manage a patient with a chronic or complex wound. In a chronic, non-healing, or slowly healing leg ulcer, all edema is on a lymphedema continuum, and lymphedema is often overlooked (Hettrick & Aviles, 2022). Likewise, cellulitis may be blamed for edema related to lymphedema. To complicate matters, cellulitis, lymphedema, and venous insufficiency may also occur concurrently, making diagnosis of one or all three problems difficult. The important things to remember is to conduct a thorough assessment (physical examination and history), including palpation of the skin in the affected area and the contralateral side/extremity (look for Stemmer’s sign as a screening tool if applicable) (Bryant & Nix, 2023). Mentally list lymphedema in your differentials any time you have a non-healing wound with any edema or surrounding tissue changes present and/or suspicious history (such as previous serious injury to nearby soft tissue or cancer surgery). Venous insufficiency often presents as dependent edema of both lower extremities from feet to knees, which is diminished with leg elevation. However, with lymphedema of a lower extremity, the edema usually involves the entire leg from the toes to the groin and may not be relieved by elevation (Bryant & Nix, 2023). Studies show, however, that compression stockings effectively reduce swelling and prevent ulceration recurrence (HQO, 2019). Although chronic venous insufficiency may contribute to lymphedema and be complicated by the presence of lymphedema, common swelling of both lower extremities below the knees in a hypertensive patient that worsens with salt intake and improves with feet elevation, with negative Stemmer's sign, would lend itself more to a diagnosis of venous insufficiency versus lymphedema. If lymphedema is suspected, additional diagnostic tests may be warranted. Nevertheless, one of the key goals in treating a chronic wound complicated by lymphedema should include fluid management / promoting lymphatic flow in the affected extremity/area (Bryant & Nix, 2023).

Treatment and Management of Lymphedema

The main tenets of lymphedema management revolve around fluid management. Treatment approaches may include Complete Decongestive Therapy (CDT) as the gold standard, compression bandaging, Manual Lymph Drainage (MLD), Skin and nail care, exercise, patient education, and in some cases, surgery(Vojackova et al., 2012; Lawenda et al., 2009; ISL, 2016; Hettrick & Aviles, 2022, Bryant & Nix, 2023).

According to Hettrick & Aviles (2022), Phase 1 of treatment is typically carried out by “a certified lymphedema therapist until a plateau in fluid reduction has been achieved, and Phase 2 is the maintenance phase carried out by the patient for life-long management of lymphedema.” Lifelong management may include compression, MLD, skin and nail care, ongoing patient education, support, encouragement, and regular condition monitoring.

Preoperative reduction of poorly controlled lymphedema is considered helpful in promoting successful incision healing. Reconstructive surgeries such as lymphatic transplant, debulking, or bypass procedures may be considered in extreme cases; however, healing is often difficult and does not eliminate the need for lifelong maintenance treatment and control with appropriate compression garments.


Compression therapy for the management of lymphedema is a non-invasive treatment option that is readily available and widely practiced. Compression therapy typically seeks to counteract gravity and decrease edema. This occurs when a bandage or bandaging system (multilayer compression) applies pressure on the outside surface of the skin and limb. The pressure is transmitted to the internal tissues. Pressure to those deformable internal structures (blood vessels and lymphatic vessels, fluid in the tissue, tissue components) fluctuates with limb movement and muscle contraction when all deformable structures are compressed against bone and the non-movable external bandaging system. The amount of compression impacts the effect of the therapy on the fluid shifts within the lymphatic system (Partsch, 2014; Hettrick and Ehmann, 2019; Bryant & Nix, 2023). This is the main reason short-stretch bandages (with limited ability to stretch) and inelastic wraps are superior to long-stretch bandages (like ace wraps). Interface pressures differ when compression is applied while the patient is at rest versus walking with the compression in place. Studies suggest the goal of compression therapy should be to reach the maximum amount of recommended interface pressure when the patient is walking while maintaining the amount of interface pressure that is not painful or occlusive to the patient at rest. For this reason, multilayer bandaging systems may offer superior advantages because the combined layers provide dynamic properties when applied correctly.

Differences between short-stretch and long-stretch bandaging systems

When considering treatment options for lymphedema, it is important to know the differences between short-stretch and long-stretch bandaging systems. Short stretch bandaging systems provide a firm “wall” for muscles to push against during bodily movement – this compresses or “massages” the tissue where lymphedema is present and helps to move the lymph fluid and prevent the accumulation of lymph in the affected area(s). Ace bandages are long stretch bandages that are not appropriate for lymphedema compression treatment in most cases.

Short stretches are bandages that stretch to less than 100% of their original length; in other words, they have minimal extensibility and produce high working pressure but low resting pressure.

Long stretch are bandages that stretch to more than 100% of their original length and have maximal extensibility because they contain elastic fibers that can stretch and return to almost their original size. They produce low working pressures but high resting pressures (which is why they may be more painful at rest). Examples of these include Ace, SetoPress, and SurePress.

Inelastic bandages and wraps: Plain rolled gauze (such as Kerlix) and rolled gauze impregnated with zinc oxide or calamine.

Many prepackaged multi-layer systems exist, and experienced clinicians may apply their combination to achieve desired working interface pressures. Examples of common multi-layer systems:

  • Two-layer (short stretch combined with long stretch) or a short stretch layer applied over an absorptive wadding layer such as orthopedic wool; three layers (zinc or calamine impregnated gauze applied first, covered with cotton or orthopedic wool layer and short stretch or inelastic wrap)
  • four-layer (first layer: wadding bandage, layer 2: short stretch, layer 3: long stretch, top layer:  flexible, cohesive, long stretch bandage)

Studies suggest interface pressures fluctuate widely when different individuals apply the same bandaging system. These studies also demonstrated the different (2-layer, short stretch, and four-layer) bandaging systems produced varied interface pressures when patients were supine, sitting, standing still, and walking, and the tolerability of the tested bandages was different  (Dale et al., 2004; Hanna et al., 2008; Junger et al., 2009; Partsch, 2014).

photo of compression bandaging in progress

Image 5: Compression bandages in progress

photo of compression stockings

Image 6: Compression stocking

The bottom line is that science suggests that while no one best product exists, more than one layer may be needed to achieve therapeutic outcomes. Clinicians may have to try different types of products to find the one that is right for that individual patient: the compression bandage system that the patient tolerates at rest while still achieving the highest therapeutic interface pressure while walking (working interface pressure). Compression is a continuum; treatments may need to change as the patient’s needs and mobility may change. Compression may need to start light and work up as the patient tolerates, but should not exceed arterial capillary closing pressures at rest – arterial blood flow to lower extremities should be assessed before compression therapy is initiated (Hettrick & Ehmann, 2019; Bryant & Nix, 2023).

It is important to note that some insurance companies may not approve compression therapy on a non-ulcerated, contralateral extremity, so verifying coverage limitations is important.

Potentially Useful Resources

  • Queensland Health Lymphoedema Clinical Practice Guideline 2014: The use of compression in the management of adults with lymphedema. Available here.
  • Circle of Hope Lymphedema Foundation
  • Lymphedema Treatment Act (LTA) – Helpful site related to Federal treatment mandates for insurance coverage of medical supplies to treat lymphedema to improve insurance coverage for the medically necessary compression supplies

Manual Lymphatic Therapy (MLT) or Manual Lymph Drainage (MLD)

Several schools and programs exist to teach this (such as the DR. Vodder School International). Developed in 1932 in France, MLD as we know it today is essentially a “light skin” technique (they don’t like to refer to it as “massage” because massage is typically a deeper tissue/muscle technique). This technique of MLD involved gently stretching and twisting the skin in a “light skin touch” in precise directions to stimulate the movement of lymph fluid out of the tissue and into the superficial lymph channels or “collectors” and back into the vascular circulation.

Skincare is key to successful lymphedema management (Bryant & Nix, 2023). According to Nowicki & Siviour (2013), edematous stretching of the skin can lead to a reduced flow of nutrients to the skin with associated dryness due to reduced oil secretion, leading to cracking and fungal or bacterial infection. Changes in the skin associated with chronic lymphedema are described as hyperkeratosis, typified by a thick build-up of scale and plaques, lymphangioma appearing as blisters caused by dilated lymph vessels and papillomatosis which presents with a ‘cobblestone’ appearance. Cleansing and moisturizing the skin daily is important to promote moisture retention and prevent cracking. However, the use of soap, which is typically alkaline, is discouraged because of the potential to disrupt the skin’s protective natural ‘acid mantle.’ Soap substitutes are preferred and may be combined with bath oils. Atraumatic removal of hyperkeratotic build-up should be considered to facilitate the action of topical moisturizers. One method involves using a microfiber pad with microscopic “hooks” built into the microfiber pad to painlessly remove dead tissue by mechanical debridement. Moisturizers should be placed after bathing and before applying compression wraps or removing knit compression garments.

Overall, it is not certain if MLD adds to the effectiveness of the treatment or prevention of lymphedema. This may result from many factors, including the pace of the MLD, pressure applied, timing of MLD, patient demographics, and specifics of the patient's disease process (Liang et al., 2020).


Exercise may also be recommended as part of the treatment for lymphedema because exercise can help move the lymphatic fluid through lymph channels through muscle contractions acting as a “pump,” especially if compression garments are worn (Bryant & Nix, 2023). There are also quilted garments specially designed to fit any body part, with integrated channels to facilitate lymph flow that can be worn at night to help maintain control. In contrast, standard compression garments are removed for sleep. A quick internet search for “nighttime compression garments for lymphedema” will bring up many brands (e.g., Reid Sleeves ® and Jovi Paks ®). Adjunctive therapies such as Jovi Paks and Reid Sleeves (these are just two examples; the author has no bias towards these products and makes no recommendations for any one product over another) or other types of padded compression modalities are good options for caregivers to know about as they can be sometimes better tolerated than wraps or knit garments; some patients will use these when the swelling has become too painful or becomes temporarily out of control. See more descriptions of potential compression garments available here.

When and where to refer patients for therapy (and other resources)

Any patient with suspected lymphedema, especially when the referring provider is not a specialist in lymphedema management, should be referred to a certified lymphedema therapist (CLT) or clinic (Bryant & Nix, 2023). These specialists are critical in providing a comprehensive lymphedema management plan and should be incorporated as early in the diagnosis as possible. This plan likely includes some form of manual lymphedema drainage therapy (also called decongestive therapy). In most cases, lymphedema is a life-long condition. In most management plans, manual lymphedema therapy is typically combined with compression garments, and sometimes, at-home manual lymphedema therapy is taught to a caregiver or achieved with the use of lymphedema pumps (which use segmented/sequential gentle pulsing massage to move lymph fluid toward the body’s central venous circulatory system).

Highly trained individuals best accomplish manual lymphatic drainage therapy, and they can determine an appropriate treatment plan, and provide proper patient education for self-management. Unfortunately, certified lymphedema therapists may not be available in every part of the United States, but hopefully, this is changing. Physicians, nurses, nurse practitioners, physician assistants, physical therapists, physical therapist assistants, occupational therapists, occupational therapist assistants, athletic trainers, and massage therapists may receive specialized training to become a Certified Lymphedema Therapist (CLT) or CWLT (Certified Wound and Lymphedema Therapist).

  • The National Lymphedema Network (NLN) website lists several lymphedema training programs and many resources available.
  • To see the Lymphedema Treatment Act Public Service Announcement that includes several patients’ stories with physicians’, therapist’s and legislators’ comments, published April 23, 2015 (13 min YouTube video).
  • Lymphoedema Support Network website (2023). (See also their news site).
  • 2022 Guidelines on the Management of Cellulitis in Lymphoedema.
  • Lymphology Association of North America (LANA) website.
  • Academy of Lymphatic Studies (AOLS) website.

Case Study

Mrs. S is a 52-year-old,  5' 4",  220lbs Hispanic female with dark skin tones. Past medical history includes a history of 4 pregnancies with three vaginal deliveries, hypertension, chronic venous leg ulcers, and moderately well-controlled diabetes type II. She presents to your wound clinic with a recurrence of her right lower leg ulcer just above the medial ankle. You are the clinic wound care clinician; this is the first time you have seen this client. Mrs. S. states she is not experiencing any pain, does not smoke, rarely uses alcohol, denies using other un-prescribed substances, and complains that she is tired of this ulcer reappearing every few months. She feels self-conscious with bandages on her lower legs all the time, and they fall “a lot.”

The medical record review shows routine labs conducted three months ago were mostly within normal limits with a hemoglobin A1c of 7.5 (a test that measures the level of hemoglobin A1c in the blood to determine the average blood sugar concentrations for the preceding two to three months). Ten months ago, she also had a normal ABI (ankle-brachial index) of 0.8 to assess her arterial perfusion.

You move on to conduct a focused examination of the lower extremities. You remove ace wraps from both legs, which she says she applies daily. However, she has prescription compression stockings (30-40 mm hg, firm compression), which are about ten months old; she says “are all stretched out” as far as they will go (she admits to putting them in the washer and dryer sometimes more than once a week). You also remove a hydrocolloid dressing from over the right leg wound; you note there is some swelling of both lower extremities, but the right lower extremity appears slightly more edematous than the left. Her dorsalis pedis and posterior tibial pulses are fairly strong, (3+) bilaterally, and you note there was 2+ pitting in the right foot evidence when you were pressing on the dorsal pedis pulse in the right foot (and 1+ noted in the left foot).

There is a shallow 2.5cm diameter ulcer with irregular margins located over the medial right ankle above the malleolus, which you expected to see as it is consistent with a classic venous ulcer. Mrs. S. complains that it “itches” a lot around the lower edge of the wound, especially at night. While there is slight maceration and very slight peri-wound redness extending 0.5 cm from the inferior wound edge, the bed is pink, moist, and otherwise unremarkable.

You also notice something else. The toes of the right foot look like stacked inner tubes, and when you attempt to pinch the skin at the base of the 2nd toe, you cannot do so. This positive Stemmers sign suggests a lymphedema component previously not identified in the patient's chart. You continue your exam to gather more clinical clues.

Even though Mrs. S. has been wearing her stockings, both feet and lower legs are edematous, and the skin is taut. The dorsum of the right foot appears more “puffy” than the left, giving the contour of her foot a 'box-like' appearance- another indication of lymphedema. Although it is sometimes difficult to discern hemosiderin staining of the gaiter region in people with darker skin, you palpate it and feel a woody, non-compressible quality to the tissues consistent with venous insufficiency. However, you continue palpating proximally and note that the calf areas are also firm or what is often described as 'fibrotic,' and this clue is suggestive of lymphedema. The thigh and inguinal areas are spared.

You ask Mrs. S. if she has ever heard the diagnosis of 'lymphedema,' and she says she has never heard of that before. You explain that longstanding venous insufficiency can be associated with secondary lymphedema, which can make it more difficult to manage but, once properly identified and treated, can end the cycle of re-ulceration or at least minimize recurrence.

You decide that this case could likely be managed in the clinic without referral to a lymphedema specialist since there is not one in the local area, and many will not be treated while there is still an active wound. Nevertheless, you talk to Mrs. S about a potential future referral to a lymphedema therapist as an option, should it become necessary.

Since Mrs. S’s lower extremity pulses are palpable and her ABI was 0.8, you anticipate compression can be applied at higher levels to reach therapeutic benefits and get the edema under better control while addressing the wound. Over the next few weeks, you evaluate the compression options and, after talking to Mrs. S., decide to go with multi-layer compression (absorptive contact/base layer, covered with short stretch bandage and a more elastic top layer) on both legs, verifying the amount of compression at rest, standing and walking the first time it is applied (with a pressure monitor explicitly made for this purpose). Your goal is to reach pressures between 40 mm Hg and 60 mm Hg when walking at the strongest contraction of the calf muscle. You also evaluate Mrs. S’s compression tolerance to ensure she has no discomfort from the compression at rest and her pulses are still palpable (and toenails have good capillary refill) when the legs are elevated and at rest with the bandages intact. You also choose a more breathable, antimicrobial fiber absorptive cover dressing over the wound before applying compression bandages. You schedule twice-weekly visits in your clinic to re-evaluate her progress the first two weeks, to re-measure her legs, order her new compression stockings every six months, and give Mrs. S. instructions to hand wash and air dry to maintain elasticity longer.

You encourage Mrs. S. to limit her salt intake, continue efforts with weight loss (maintaining adequate low-fat protein intake), and consider starting a walking exercise program. You proceed to monitor progress with evidence-based wound care for the open ulcer. Serial circumferential measurements of both lower extremities are taken at each visit, along with wound(s) measurements, and Mrs. S. is delighted to see the measurements steadily decrease.

Finally, the ulcer is closed, and you start the next phase of combined lymphedema/venous insufficiency treatment: maintenance. If there is a short gap of time to await new compression stockings, you realize that if you discontinue compression therapy while the custom stockings are being made, there is a good chance of the ulcer reappearing. Since no reimbursement exists for continued compression wrapping on intact legs, you place two layers of tubular compression material over each leg and instruct her to remove the second layer at night to avoid compromising the circulation and replace both layers during the day.

Mrs. S. returns to the clinic in about three weeks with her new stockings (ordered in a darker brown color to blend with the patient’s natural skin tones better). Her legs have increased slightly in circumference, but thankfully, the ulcer has not reopened. You start her on daily wear of her new stockings with instructions to apply them first thing in the morning when she wakes up before she can walk around and remove them at night just before retiring to bed. You reinforce washing them by hand at night, air drying them overnight for wear the next day, and schedule a return visit in 2 weeks. If possible, you may consider two pairs of stockings – the patient can alternate washing one pair and wearing the other.

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Implicit Bias Statement

CEUFast, Inc. is committed to furthering diversity, equity, and inclusion (DEI). While reflecting on this course content, CEUFast, Inc. would like you to consider your individual perspective and question your own biases. Remember, implicit bias is a form of bias that impacts our practice as healthcare professionals. Implicit bias occurs when we have automatic prejudices, judgments, and/or a general attitude towards a person or a group of people based on associated stereotypes we have formed over time. These automatic thoughts occur without our conscious knowledge and without our intentional desire to discriminate. The concern with implicit bias is that this can impact our actions and decisions with our workplace leadership, colleagues, and even our patients. While it is our universal goal to treat everyone equally, our implicit biases can influence our interactions, assessments, communication, prioritization, and decision-making concerning patients, which can ultimately adversely impact health outcomes. It is important to keep this in mind in order to intentionally work to self-identify our own risk areas where our implicit biases might influence our behaviors. Together, we can cease perpetuating stereotypes and remind each other to remain mindful to help avoid reacting according to biases that are contrary to our conscious beliefs and values.


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