Free gastroepiploic lymph nodes and omentum flap for treatment of lower limb ulcers in severe lymphedema: Killing two birds with one stone

Why do the saphenous vein varices arise? According to our concept this is a process of slow deconstruction of the vein wall by inflammation caused by microbes penetrating plantar skin, colonizing deep tissues, entering veins and sticking to valves, as well as, transported to lymphatics, bringing about damage to their wall and evoking immune response in the inguinal lymph nodes. Venous stasis caused by a variety of hemodynamic factors remains secondary to the primary damage of the vein wall. With respect to ulcer, irrespective of the predisposing factors as venous stasis, colonization of the denuded calf surfaces takes place by bacteria drained from foot skin and also those floating down to calf from the perineum. This set of microbes is responsible for progression of ulcer or its delayed healing. In this study, the numerical phenotypes of varicose veins and ulcer granulation tissue bacteria were presented. The dominant strains in the vein walls were Staph. epidermidis and aureus with Enterococci and Pseudomonas frequent in ulcers. High percentage of Staphylococci both in vein walls and ulcer sensitive to antibiotics may suggest that they originated from the microbiome inhabiting leg tissues prior to the development of varices and ulcer.

Download Full-text

Lower limb lymph nodes

10.53347/rid-72926 ◽

2019 ◽

Author(s):

Craig Hacking ◽

Daniel Bell

Keyword(s):

Lymph Nodes ◽

Lower Limb

Download Full-text

Value of one additional injection at the root of the limb in the lymphoscintigraphic evaluation and management of primary and secondary lower-limb lymphedemas

PLoS ONE ◽

10.1371/journal.pone.0253900 ◽

2021 ◽

Vol 16 (7) ◽

pp. e0253900

Author(s):

Pierre Bourgeois ◽

Olivier Leduc

Keyword(s):

Lymph Nodes ◽

Lower Limb ◽

Lymphatic Vessels ◽

Lymphatic Drainage ◽

Nodal Status ◽

Lymphatic Pathways

Introduction The classical lymphoscintigraphic investigations of lower-limb lymphatic edema [LLLE] sometimes reveal either no or few lymph nodes [LNs] at the root of the limb[s] and/or in the abdomen. The aim of the present paper is to report the results of performing one additional injection at the root of the edematous limb[s] to force the visualization of the LNs and/or to demonstrate the collateral lymphatic pathways in such patients. Methods and findings We retrospectively reviewed our database and found 99 patients [44 primary LLLE with 47 limbs injected and 55 with LLLE secondary to treatments for cancer with 64 limbs injected] where such an additional injection had been performed. In the 43 LLLE patients where no LNs were seen at the end of the classical exam [15 primary LLLE and 28 secondary LLLE], the extra injection showed lymphatic drainage toward LN[s] in all except 3 and when at least one LN was seen, the injection showed lymphatic drainage in every case toward the same ipsilateral [inguinal and/or iliac] LNs [as shown by the classical injection] and/or toward additional LNs. In 40.7% of patients, we observed one or more additional lymphatic pathways: prepubic superficial lymphatic vessels [LV] crossing the midline anteriorly toward contralateral inguinal LNs in 21 [18.9%], “posterior” LV [toward contralateral inguinal LNs and/or ipsi- or contralateral lumbo-aortic and/or para-renal LNs] in 14 [12.6%], but deep LV toward the ipsilateral common iliac LNs passing between the gluteal muscles in 32 [28.8%]. Conclusion Our work pinpoints one limitation of classical bipedal radionuclide lymphangiography. In patients with primary and secondary LLLE where inguinal and/or iliac LNs cannot be seen on bipedal radionuclide lymphangiography, this additional injection reveals the true lympho-nodal status and shows unexpected collateral lymphatic pathways in 40% of cases. Such information is of the utmost importance in LLLE management and its acquisition is consequently recommended in these patients.

Download Full-text