Venous and lymphatic diseases Opportunities for improved care
By Paul Hannah
Lymphatic
and venous disease share many commonalities, but there could be a lot more communication between lymphologists and phlebologists. Both professions are frustrated with the lack of understanding in the medical community of venous and lymphatic issues.
Venous disease is common, and for the most part curable, at least in the medium term. Varicose veins occur in about 30% of the population, of which only half are symptomatic, with such complaints as postural heaviness and swelling, relieved by rest and elevation. Venous ulcers occur in about 1% of the population, with another 1% having a healed ulcer. This number increases to 5% of Australians over 65 years of age.
New research continues to identify multiple genetic markers of venous disease, such as the FOX2 gene. The pathological mechanisms of venous disease remain elusive, but multiple lines of evidence point to a diffuse, chronic, inflammatory process with valve damage, venous reflux and venous hypertension leading to leucocyte and protein migration into the extracellular space. The end result of this is a disordered extracellular matrix and abnormal collagen and elastin. Initial phlebo-oedema from venous hypertension gradually blends into phlebolymphedema as the subcutaneous lymphatics become damaged in this process, resulting in skin damage called lipodermatosclerosis. The older theory of proximal valve failure, for example, at the saphenofemoral junction, leading to descending progressive valve failure and distal venous hypertension, has been replaced with a realisation that a diffuse process is damaging the valves of the veins. Sequential examination with ultrasound has
shown that the progression of reflux is more likely to be from distally below the knee to proximally, with time. Asymptomatic children and young adults can be shown to have some refluxing valves, the extent of which usually progresses with the decades. Heredity is the single biggest risk factor for varicose veins, with pregnancy next, and prolonged standing a distant third.
Deep venous disease (below the superficial fascia) is uncommon and usually the result of deep vein thrombosis (DVT). If the clot does not dissolve quickly, it can damage the deep valves resulting in deep venous reflux or deep vein
obstruction. Such post-thrombotic syndrome can usually only be treated by lifelong compression and, rarely, stents for stenosis. Artificial valve replacement has proved elusive so far. Congenital absence of valves is seen in the rare lymphedema-distichiasis syndrome. Superficial (above the fascia) venous disease is easily diagnosed by its clinical appearance and the ultrasound presence of reflux (abnormal distal flow due to incompetent valves) during Valsalva or following a distal calf squeeze to augment venous return. These scans must be done while standing or at least with some body
Dr. Paul Hannah, Phlebologist has had a career divided between Family Practice, Emergency Physician and Phlebologist. He is currently National Director of Training of the Australian College of Phlebology and is actively involved in Medical student and GP education about venous and lymphatic diseases.
tilt. DVT scans on the other hand are performed supine and the veins are compressed with the probe to see if there is a clot within them. A reflux of greater than 0.5 seconds is typically used to diagnose venous incompetence. The presence of chronic distal venous hypertension leads to progressive skin changes from the appearance of ankle telangiectases and venous eczema, through gravitational edema, then to the pigmentation of haemosiderin due to red cell extravasation and pale dermal infarcts called atrophie blanche. The typical pre-ulcerous changes of lipodermatosclerosis, or tight in-drawn hardened skin, are due to progressive fibrosis within the subcutaneous layer. Any minor trauma at this stage cannot be repaired and will lead to an ulcer. Venous ulcers are not usually as painful as arterial ulcers, and often wetter. They are typically found on the medial (great saphenous territory) or lateral ankle (short saphenous territory). Venous ulcers need all the usual wound care and debridement; however, healing will be expedited if the causative venous hypertension is controlled by treating the reflux. Traditional venous surgery was painful and had a five-year recurrence rate around 30%. All relevant worldwide vascular authorities these days recommend other methods of treatment, usually thermal ablation with laser or radiofrequency, but other options are available, such as adhesive superglue and ultrasound guided sclerotherapy.
What does the lymphatic therapist need to know about venous disease? Patients do not come to us with diagnostic labels and, especially in the elderly, often have multiple pathologies. In someone with bilateral swollen legs, one needs to consider cardiac failure, liver and kidney disease, and drug side effects (especially calcium antagonists and steroids). With unilateral
swelling, venous disease is more common than primary lymphedema, although the history or presence of varicose veins will differentiate these often. Ask about previous DVTs and consider proximal obstruction causing either venous edema or lymphedema. Proximal obstruction typically involves the nodes in the case of lymphedema but could be due to pelvic masses, anatomical compression (e.g. May-Thurner syndrome) or lymph nodes, in the case of venous obstruction. Stemmer’s sign may be positive in phlebolymphedema and may be negative if there are multiple pathologies, such as venous hypertension, as well as lymphedema. Treatment of these other pathologies, such as heart failure and venous disease, will make the lymphatic therapists’ job a lot easier. If you see patients who may have venous disease, consider the following. Firstly, do not just rely upon the diagnoses of the referring doctor. Venous disease, in particular, is under-appreciated or even worse, ignored, by the medical profession. Learn to look for the typical symptoms (gravitational
heaviness and swelling) and signs (eczema, pigmentation, lipodermatosclerosis, ulcers) of venous disease. If in doubt, an ultrasound scan looking for reflux is a simple test. Cardiac, renal and hepatic disease are mostly selfevident from the history.
Venous disease is usually easily treatable and will significantly reduce the fluid burden on any lymphedema or lipedema present.
Ultrasound machines are typically very expensive, but we are witnessing a revolution in technology with clever probes that plug into your smart phone or Ipad. I predict the current generation of doctors will be the last to not routinely use this ‘stethoscope of the 21st century’. Although complex to become a master of this technology, the basics are not difficult to learn. For instance, a GP can learn
to do a basic DVT scan in 30 minutes with 90% accuracy. I envisage that a lymphatic therapist could quickly ‘exclude significant venous reflux’ with some training, and professional sonographers would only be needed to elucidate subtle reflux and look for other pathologies, such as proximal obstruction and pelvic venous disease. Indeed, this is how I work with my current sonographers—their skills are at another level beyond mine, but I can make quick and convenient diagnoses by myself without fuss. My sonographers create beautiful venous ‘road maps’ with complex connections and diameters duly recorded. In summary, lymphologists already have the knowledge base to easily understand phlebology. They need to accustom themselves to the visual signs of venous disease and know that venous disease is usually easily treatable and will significantly reduce the fluid burden on any lymphedema or lipedema present. LP
Reprinted with permission from Lymph Exchange (Feb 2020), a publication of the Australasian Lymphology Association.
