Page 12 - VOL 26 N. 72 - 2015

LYMPHATICS AND VEINS: AN INTIMATE RELATIONSHIP
LEE BB, MD, LAREDO J, MD, AND NEVILLE R, MD
Department of Surgery George Washington University, Washington DC, USA
Venous and lymphatic circulation systems are “inseparable” dual outflow systems to transport the used blood out from the tissue. But these two systems function based on totally different venodynamics and lymphodynamics with entirely different rheodynamic characteristics.
“Normal” lymphodynamic is based on self-propelled peristalsis by each unit of “lymphangion” with positive pressure of 50-60mmHg, while venodynamics is purely based on a passive low-pressure system in average pressure of 10mmHg by heart, diaphragm/breathing, and muscle contraction, etc.
However, once this “normal” lymphodynamics based on peristaltic function of lymphangion should be lost by various conditions, the rheological condition of ‘abnormal’ lymphodynamics becomes essentially same as the venodynamics.
Venous and lymphatic systems are such one mutually interdependent system to provide the compensation to each other that the insufficiency or overload to one of two systems, either transient or permanent, allows the other to play an auxiliary role of fluid return through micro- & macro-anastomosis.
But, both systems are “mutually complimentary” ONLY when they are in normal condition/ function. When one of these two systems should fail (e.g. chronic venous hypertension, lymphedema), the homeostasis/balance between two systems is threatened and such mutual interdependence generates a new problem.
Following initially enhanced lymphatic function to compensate for the insufficient venous system, the lymphatics themselves are damaged and a safety valve insufficiency of lymphatic system would result in lymphostasis.
When the venous insufficiency/stasis exceeds this maximum lymphatic compensatory capacity, the imbalance between capillary as well as tissue blood-lymphatic pressure will build up the liquid in the interstitial space together with the concentration of intra- extravascular proteins to lead characteristic fibrosis due to increased interstitial protein concentration.
Hence, a failure of one system gives additional burdening/loading to the other system, and a long term one system failure results in total failure of these ‘inseparable’ dual systems altogether and the insufficiency becomes “phlebolymphatic”, generating a new condition of “combined”.
June 4, 2015 - Auditoire C. Roux
PLENARY SESSION 2
LYMPHATIC MALFORMATIONS AND GENETICS
GENETICS OF LYMPHOEDEMA: ONE SYMPTOM, MANY CAUSES
P. OSTERGAARD
St. George’ s, University of London, UK
We have demonstrated that stringent phenotyping can be helpful in gene identification. Building on 14 years of experience in our Primary Lymphoedema Clinic at St George’s Hospital, London, an updated classification of this condition has been proposed. This new tool has been useful in our research department and we have had success in identifying genes for Primary Lymphoedema using this rigorous phenotyping combined with linkage analysis, Sanger sequencing and/or Whole Exome Sequencing. In this talk, this classification tool will be presented with examples of the various genetic causes of Primary Lymphoedema.
THE EUROPEAN JOURNAL OF LYMPHOLOGY - Vol. XXVI - Nr. 72 - 2015
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