Is All Edema Lymphedema?

John Fuller Beckwith3/14/2024

A few years ago several clinicians deeply involved in the shared world of wound and lymphedema treatment presented an article and webinar proposing an alteration in the basic understanding of the pathophysiology of edema.

In “All Edema is Lymphedema: Progressing Lymphedema and Wound Management to an Integrated Model of Care,” (and subsequent online webinar) the authors engaged in an intellectual exercise whose conclusion is not supported by the facts. In the abstract the stated purpose of the article was simply to highlight an interdependence between the venous, lymphatic and integumentary systems. Certainly there is agreement that the wound management field could benefit from seeing the importance of the lymphatic system vis a vis the venous and integumentary systems. However, the conclusion arrived at ultimately went far beyond that. The statement, “...edematous conditions that are not swiftly addressed may progress to lymphatic dysfunction, integumentary dysfunction, ulcerations and ultimately lymphedema,” is true. Yet this true statement also notes a distinction between edematous conditions and lymphedema, and is therefore contradicted by the supposed conclusion of the article, that, “…all edema is lymphedema.”

In discussing the revisions to the Starling Equation as defined by Levick, the authors neglect to put filtration at the blood capillary level in the context of the much more voluminous exchange occurring due to diffusion. The authors state: “…it was realized that nearly 100% of all fluid and proteins moving from the blood capillaries into the interstitial space is subsequently absorbed by the lymphatic capillaries alone.” Diffusion is responsible for 240 liters of fluid per minute in the body, whereas filtration accounts for 20 ml, a massive volume difference of more than ten thousand-fold between these two forces. Diffusion contributes to the interstitial fluid content. One must account for the diffusion volume when considering how much of the interstitial fluid is absorbed by the lymphatic capillaries and what percentage of interstitial fluid is absorbed via diffusion at the venous end of the blood capillary. How can it be true that 100% of interstitial fluid is absorbed by the lymphatic capillaries? It follows therefore that it is not true, as the articles states, that, “...interstitial fluid is synonymous with initial lymph.” To make this statement denies the presence of diffusion and venous return.

Levick’s revised Starling principle is a step forward, but a step that still rests on the foundation of what Starling developed. Starling has not been ‘debunked,’ as some attempt to assert. Nor has a more refined understanding of microcirculation led to fully discarding of the old understanding. To paraphrase Foeldi, "...the Starling equation is extremely valuable, not for calculations, but because it readily shows that, per unit of time, the volume of net ultrafiltrate will increase..." if hydrostatic pressure increases, oncotic pressure decreases, if interstitial pressure decreases and if osmotic pressure of interstitial proteins increases. It can’t be denied that these elemental factors still matter. Otherwise, we would not have our understanding of edema related to hypoproteinemia or the positive impact of effective, skilled compression.

Many of us in this community are pleased to see the lymphatic system getting new attention from the American medical community. This is belated, but is as it should be. The authors make lengthy statements about “new” understanding of the microcirculation, and even in the Methods section state their material is sourced from articles in the years 2010 to 2021. Yet they also make important use of much older, crucial literature including from 1994, and quoting Foeldi when it is convenient. Let’s remember the Europeans have already plowed and cultivated this field. So much of the material presented in this article as the, “new microcirculation paradigm,” is material that has been presented in basic lymphology for more than two or three decades. I learned about the microscopic lymph connection to the ECM ( extracellular matrix) and pre-lymphatic channels 25 years ago and learned that lymph physiology degrades very early in the progression of venous insufficiency, thereby contributing to the development of venous ulcers. Again, this is not a new paradigm.

The article also states the well-known fact that all edemas present with exceeding of maximum lymph capacity, therefore all edemas represent an insufficiency of lymphatic transport. This is true. However, they make the leap that all edemas are therefore lymphedema, or as they say at one point, “…all edema resides on the lymphedema continuum…” To accurately correct that statement, and of crucial importance, it should be re-stated as: all edemas reside on the continuum of lymphatic insufficiency with lymphedema at one end of that continuum. There is little attention given to the difference between a dynamic insufficiency vs. a mechanical insufficiency, as when they conflate the two, "...resulting in a transient lymphedema or lymphatic insufficiency..." To trust this so-called new paradigm, we have to now discard the distinction between a dynamic insufficiency and mechanical insufficiency. This doesn’t even wade into the more nuanced understanding of a combined or safety-valve insufficiency of the lymph system. If you purport to be an expert in lymphedema and understand basic physiology of lymph function, then you must be able to place the safety-valve function of the lymph system in its proper place in the discussion, and thereby discuss safety-valve insufficiency.

Lymphedema requires a different treatment than other edemas. To label all edemas lymphedema creates the very real risk of treating any edema with the wrong intervention. And days or weeks or even months treating in the wrong way could have permanent detrimental effects. In a seminal article in the Lancet in 1989 Dr. Foldi explained why diuretics were not only wrong for the treatment of lymphedema but could lead to harm. If, as the authors say all edemas are lymphedema, then are diuretics wrong for all edemas? If diuretics are appropriate for some edemas but not for lymphedema, then it follows that not all edemas are lymphedema. Failure to recognize the distinctions between different edemas can lead to inappropriate treatment approaches. Lymphedema is a distinction with a difference.

I have a concern that if this concept becomes the accepted standard I, as a lymphedema specialist, may be asked to help resolve a chronic edema due to hypoalbuminemia, or ascites, or cardiac edema, or medication-induced edema. By overgeneralizing the conditions that a lymphedema specialist can treat, this devalues lymphedema treatment for those patients for whom CDT is the optimal treatment.

As a lymphedema specialist of more than two decades experience and much of that treating wounds with some form of chronic edema, I fully empathize with the view that the wound healing field does not give enough credit or attention to the role of the lymphatic system in skin health and wound healing. Over the course of 15 years I presented at multiple regional and national wound conferences, developed and presented continuing education on lymphedema for wound specialists and contributed a section in a lymphedema textbook on the importance of MLD to wound healing. All with a focus on the centrality of lymphatic pathophysiology to wound development. While there were a tiny few who recognized the value, I would say that in the wound healing community there is a deep resistance to fully appreciating the importance of lymph function to skin healing. So I can see the motivation and need for much of what this article presents. However, it is a bridge too far to try to define all edemas as lymphedema since it is an over broad assertion and can lead to misdiagnosis and delay in obtaining the correct treatment.