The structure of the skin was sonographically evaluated since the mid of ’80 by Ultra High Frequency (UHFP) probes. These instruments were very expensive but allowed to evaluate only the cutaneous layers (epidermis and dermis). Recent improvements in ultrasound technology allowed to possibly evaluate the morphology of the cutaneous and subcutaneous layers by the same High Frequency Probes (HFP) used for routine vascular investigations. The epidermis appears as a thin hyperchoic band due to the echoes created between the gel and the skin surface. The papillary dermis (PD) appears as a thin and low-echogenic band parallel to the skin surface, immediately below the hyperechoic epidermis. The reticular dermis (RD) appears as a regular band, with homogenous thickness and echogenicity. The subcutaneous tissue consists of hypoechoic fat lobules separated by echolucent connective trabeculae. In legs with impairment of venous or lymphatic drainage, HFP sonography allows to better define the pathology of the skin changes observed during clinical examination. More importantly, HFP sonography may reveal skin changes not evidenced by clinical examination like dermal edema, dermal thinning or thickening, skin inflammatory infiltration, and other. In legs with venous or lymphatic insufficiency HFP sonography demonstrates different patterns of subcutaneous edema and may reveal skin changes that precede ulcer opening. Finally, HFP sonography may reveal skin lesions related to therapeutic procedures (open or endovascular surgery, sclerotherapy) without the need to perform skin biopsy.
Chronic venous disease (CVD), mainly due to venous reflux or, sometimes, to venous outflow obstruction, produces a microcirculatory overload leading to the impairment of venous drainage. Venous drainage depends primarily on a major hemodynamic parameter called trans-mural pressure (TMP). TMP is increased in patients affected by CVD, leading to impaired tissue drainage, and, consequently, facilitating the beginning of the inflammatory cascade. Increased TMP determines red blood cell extravasation and either dermal hemosiderin deposits or iron laden-phagocytes. Iron deposits are readily visible in the legs of all patients affected by severe CVD. Local iron overload could generate free radicals or activate a proteolytic hyperactivity of metalloproteinases (MMPs) and/or downregulate tissue inhibitors of MMPs. These negative effects are particularly evident in carriers of the common HFE gene's mutations C282Y and H63D, because intracellular iron deposits of mutated macrophages have less stability than those of the wild type, inducing a significant oxidative stress. It has been demonstrated that such genetic variants increase the risk of ulcers and advance the age of ulcer onset, respectively. The iron-dependent vision of inflammation in CVD paves the way to new therapeutic strategies including the deliberate induction of iron deficiency as a treatment modality for non-healing and/or recurrent venous leg ulcers. The inflammatory cascade in CVD shares several aspects with that activated in the course of multiple sclerosis, an inflammatory and neurodegenerative disease of unknown origin in which the impairment of cerebral venous outflow mechanisms has been recently demonstrated.
Background The aim of our study was to comparatively assess volume changes related to daily occupation of the whole leg (WLv), of the lower leg (LLv) and of the upper leg (ULv) in subject with no venous and lymphatic disorders. Method WLv, LLv, and Ulv were evaluated by water displacement volumetry (WDV) in the morning and in the evening in 20 healthy subjects. Results In the legs with occupational edema (OE), WLv increased by 7.07%, LLv by 5.25%, and ULv by 9.80%. In legs without clear OE, WLv increased by 2.41%, LLv by 1.35, and ULv by 3.38%. Conclusions Surprisingly, the increase of ULv was greater than that of LLv. An evening increase in the leg volume also occurred in legs with no clear OE. In our series, a clinically evident OE was related to an increase of the WLv, LLv, and ULv greater than 5.83%, 8.68%, and 1.88%, respectively.
The angiosome is a 3D structure which is perfused by a single perforating artery (arteriosome) and drained by a perforating vein (venosome). The concept of arteriosome is applied in plastic surgery and in the revascularization of ischemic limbs. Each venosome is also drained by longitudinal veins running in the subcutaneous layer. Accordingly, the concept of venosome cannot be applied in the field of the venous disorders of the limbs. The concept of phlebosome consider both paths of venous drainage.
The small saphenous vein in its modal pattern flows into the popliteal vein by means of a terminal arch (sapheno-popliteal junction), and frequently gives off an anastomotic branch, ascending on the medial aspect of the thigh, to the great saphenous vein. This branch has often been termed thigh extension of the small saphenous vein. As resulted in this report from autopsy, the venous extension coursed on the midline of the posterior aspect of the thigh, tributary to the deep femoral vein, and the small saphenous vein presented neither a sapheno-popliteal terminal arch, nor evident intersaphenous anastomoses. As a consequence, the small saphenous vein by means of its prolongation continued directly from the calf into the deep femoral vein. In the human embryo the small saphenous vein appears as direct communication with the posterior cardinal vein, and accompanies the developing ischiatic artery and nerve, as the main vein (ischiatic vein) of the lower limb bud. At the end of development, its proximal part persists as inferior gluteal vein. Comparative anatomy indicates that in animals the small saphenous vein is the only superficial vein well developed and that in humans its termination into the popliteal one might be an adaptation to the elongation and relative rigidity of the lower limb. In the horse a posterior vein of the thigh connects the small saphenous with the ischiatic one, and ascends along the ischiatic nerve to anastomose with the deep femoral vein. It would appear also that in the lower animals the small saphenous vein ascends to a higher level on the posterior aspect of the thigh. Thus, a venous extension like that we observed might be an atavism. Therefore, on the basis of these embryological and phylogenetical data, the Authors hypothesized that a small saphenous vein and a thigh extension of such a feature might be regarded as a unique venous channel, wholly axial throughout its course, formed by the small saphenous vein proper in the leg and by a persistent and functional sciatic (ischiatic) vein, which usually disappears, satellite of the ischiatic nerve, in the thigh.
