The leg ulcer is a very common problem whose social and economic burden is considerable. Considered by many patients as inevitable, it is currently available therapies effective can in most cases be used in ambulatory. Thus, healing can often be obtained provided that employ a diagnostic and therapeutic approach using the most rigorous collaboration between various actors whether medical (general practitioner, dermatologist, angiologist, vascular surgeon, endocrinologist, internist, etc.) and paramedics (nursing (e) s, physiotherapists etc.).

A) the pathophysiological mechanisms
The leg ulcer (UJ) is a loss of substance relevant to chronic skin epidermis, dermis and hypodermis possibly more or less extensive and often sitting on the lower third of the leg. The back of the foot and the proximal region of the leg are often less affected except in certain special circumstances etiological.



This loss is usually ischemic in nature, often triggered by an episode of local trauma more or less important but very often put forward by the patient.
The ischemic tissue appears across the microcirculation but in fact most often the result of various vascular lesions, often macroscopic. The pathological mechanisms vary according to etiology, and is usually divided into three main etiological in leg ulcers of vascular origin that we repeat constitute the vast majority of leg ulcers:
The most numerous are undoubtedly the UJ original vein, it would call more “varicose ulcer” because the presence of varices is neither consistent nor always in the foreground when they are actually present. In this group, the pathophysiologic mechanism is essentially the venous pressure in the subcutaneous venous system of lower limbs due to the presence of varicose veins isolated with only superficial venous disease (varicose pure, essential, often familial, probably genetic) or d ‘ syndrome postphlebitic avalvulation with deep residual and / or persistent obstruction with deep venous and superficial. This disease postphlebitic can cause varicose veins “secondary” in general not systematized in a territory saphenous precise, instead of essential varicose veins are generally much more systematic. In all these cases, the venous causes biochemical changes and hemodynamic stasis with vascular free radical production, appearance of leukocyte and fibrin sleeve around the small vessels, which impairs gas exchange and nutrition between the vessels and cells, leading to progressive ischemia and the disappearance of most superficial cells. Ulcers resulting from this mechanism are usually located on the half infsrieure leg do little or no pain and did not tendency to dig deep.



However, venous ulcers can become very old and even extended circumferential. Other trophic may join such a lipodermatosclerosis by fibrotic changes of chronic panniculitis periulcereuse with aspect gaiter sclerodermiforme surmounted by swelling overlying. This aspect “leg” is primarily a disease of UJ on postphlebitic. Finally, venous ulcers can often be a consequence of venous angiodysplasia or more complex, often with hypoplastic deep veins and superficial varicose veins as in Klippel-Trenaunay, then with ulcers sometimes unusually early childhood.
The UJ arteries are most often linked to a macro-chronic obliterative arteriopathy of the lower limbs of atheromatous origin or tobacco plays an important etiological role. In this case, chronic ischemia is global, affecting both the muscle compartment (with claudication exercise) that skin. The emergence of a UJ is often delayed except in certain etiologies such as Buerger’s disease, and is classified artery in stage IV. These arterial UJ are often painful or very painful digging leading to denudation or necrosis of muscle-tendon, and reach above the back foot before expecting any leg. The addition of a diabetic microangiopathy much accelerates the onset of these disorders and trophic changes in symptomatology as the pain is so often absent or moderate, and ulcers often predominate then the extremity of the limb. It should be noted that the plantar ulcers in principle out of context even expanded the UJ vascular origin since they are largely original neurotrophic.
The original UJ capillaries, also called necrotizing angiodermatitis are associated with obliteration of arterioles often acute subcutaneous, most often in a poorly controlled diabetes, an atheromatous or arteriolosclerosis in a hypertensive ( Martorell acute ulcer). Ischemia is especially felt when the cutaneous region most badly vascularized leg, the union lower third-middle third of the lateral leg. The appearance is characteristic of a necrotic lesion ESTABLISH fast, very painful, often surrounded by an area of livedo necrotizing inflammatory changes. The lesion may spread rapidly, but generally remains superficial. In a non-negligible number of cases no obvious cause is found and it must then search for evidence for a systemic vasculitis.
This classification has the merit of simplicity but, in many cases, the UJ is said to cause “mixed” factors involving arterial and venous or arterial and arteriolar entangled to be taken into account during treatment.
To these three broad categories of UJ, add a number of much rarer causes that need to be thinking in the absence of good cause vascular net:
ulcers by vasculitis of small vessels and middle class, such as leukocytoclastic vasculitis, PAN, Wegener’s disease and inflammatory arteritis of large vessels.
ulcers by primary lymphedema, a rare circumstance (in contrast with the incidence of lymphedema secondary to venous insufficiency, realizing a true veno-lymphatic insufficiency for some authors).
ulcers by micro-occlusive disease causes a wide range, including clotting disorders, congenital or acquired, or cryoproteines through the myelo-proliferative syndromes.
ulcers of congenital hemolytic anemia.
ulcers within the context of rare genetic diseases such as Werner’s syndrome, prolidase deficiency, Klinefelter’s syndrome.
neoplastic ulcers: carcinoma, melanoma, lymphoma, other more rare tumors, sometimes very misleading.
infectious ulcers: ecthyma, anthrax, abscesses, leishmaniasis, opportunistic infections in immuno-compromised, treponematoses, tuberculosis.
ulcers cause “skin”: pyoderma gangrenosum, Halogenid

B) BALANCE OF A LEG ULCER
It will guide the establishment of a prognosis and appropriate therapeutic strategy. This balance is mainly clinical but also build on some paraclinical explorations oriented. It will cover the ulcer itself, its complications and his or her cause (s).
1) Assessment of the ulcer
reconstruction of “history ulcerative” date of onset, course, treatments already tested how effectively, there EARLIER ulcers and how they have been healed.
topography, extension, shape, depth, bottom side (granulation, fibrin, necrotic) and banks (sclerotic or not, purpuric, necrotic) or of ulcer (s).
character or not painful lesions, evaluation of this pain on a visual analogue scale and evolution of pain during the day.
assessing the impact on quality of life, daily activities and work.
2) Research complications

Infectious potentially menacing: finding evidence for a local infection (ulcer pain and purulent discharge; erysipelas peri-ulcer), regional (lymphadenopathy, lymphangitis), seeking neighborhood associated infections including intertrigo interorteil; learn on immunization status against tetanus, no systematic bacteriological sampling but depending on the situation in case of suspicion of superinfection.
trophic: local (hypermite chronic sclérodermiforme acute or thrust) and regional (stiffness of the ankle); clinical assessment sometimes supplemented by radio standard leg to objectify a subcutaneous calcification.
assessing the importance of lymphedema associated with finding a Stemmer sign (inability to pinch the skin on the back of the second toe) and an appearance of “orange peel” or already “up sparkling.
search for a contact dermatitis peri-ulcer priori linked to topical use, possibly to be confirmed by patch testing with a special battery.
neoplastic in the presence of a budding suspect with biopsy in doubt.
haemorrhage including rupture of varicose sub-colitis.
3) Find the cause
examination and clinical examination including complete search of arterial risk factors and signs for a more or less arterial diffuse thrombophlebitis of old (alleged but not always possible given the particular surgical history), varices (family history , reviewing stand, functional signs); making TA; diabetes research associate.
vascular suitable paraclinical examinations, mainly venous Doppler and / or arterial with precise mapping of venous leak points and their significance (focusing particularly on the butts of internal and external saphenous veins and perforators that connect to the network system saphenous vein through the deep fascia), the avalvulations, varicose veins, estimation of a veno-obstructive residual venous pressure measurement, mapping of arterial stenosis, measurement of arterial pressure index; angiography if surgery is planned on a arteriopathy; venography, however, is very rarely necessary except in rare cases surgery or a restuarant avalvulation deep is envisaged study lymphatic rarely necessary because in general do not lead on any specific treatment.
more specific tests if a rare cause is suspected: bacteriological sampling particular, parasitological, mycological, serology, immune balance, biopsy for histology and immunofluorescence, coagulation etc..
4) Evaluation of the patient
assessment of motivations face treatment necessarily long, its potential for monitoring according to his means of travel, the socio-economic and hygiene in which he lives his type of social care.
This assessment can be performed as an outpatient or during a hospitalization days will help develop a general therapeutic approach addressing both the ulcer itself and his or her cause (s). Indeed, it is totally unrealistic and unnecessarily costly to try to heal a leg ulcer or if the conditions that have led to its appearance are not controlled as much as it can, and etiologic treatment must be conducted if possible at the same time as the ulcer itself. This treatment will etiological faster healing of the ulcer itself and above will prevent or at least delay recurrence, which in some cases are unfortunately unavoidable due to a vascular site very difficult to treat. Must imperatively describe precisely these points to the patient to achieve full cooperation, crucial point for a treatment that is necessarily long, sometimes tedious and unrewarding at least initially. This is one more reason to offer the patient a day hospitalization initial structure more conducive to a discussion in depth than mere consultation necessarily shorter.
Finally, this review will help to establish, to some extent, the prognosis of the ulcer. The prognosis in terms of possibilities of complete healing or not both in terms of recurrence to predict, depends largely on 4 factors: the size of the ulcer, the patient’s age, can effectively treat circulatory disorders Underlying and patient compliance vis-a-vis the overall treatment plan. A pure venous ulcer in a patient 50 years motivated effectively operable is in fact totally different in their prognosis of ulcer complicating post-phlebitis syndrome in a patient with poorly motivated than 75 years in which only the elastic is possible but very little followed! However, it must in all cases clearly explain to the patient often discouraged a leg ulcer is not inevitable even if it evolves over several years, and the vast majority of them can actually be healed, sometimes simply by correcting some mistakes in strategy.

C) therapeutic care
It must therefore necessarily be in parallel on the causes of the ulcer and the ulcer itself.

1) The etiological treatment
It is of course guided by the assessment made in advance, and focuses on the vascular conditions loco-regionales. It must address all components pathological highlighted by this review.
a) Component veno-venous or lymphatic
It is the most common but often the most neglected in favor of the blood component, then it is very often the main factor. Therapeutic measures depend on the results of the review:

surgery whenever possible to treat superficial venous insufficiency: saphenous stripping full or partial use various means (stripper classic cryoéveinage, called ambulatory phlebectomy using hooks Miller), ligation of perforating or lacrosse incontinence, ambulatory phlebectomy varices developed on perforating isolated destruction of abnormal superficial network is inconceivable that in the absence of significant obstruction of the deep network, it is imperative to check in all cases and particularly in post-disease phlebitic and angiodysplasia. This surgery is primarily intended for varicose veins called essential, less often varices secondary to post-phlebitis syndrome or within the framework of angiodysplasia. Nevertheless, we must discuss in all cases. Deep vein surgery is indicated much more rare and difficult practice is for highly selected cases of avalvulation deep or deep venous hypoplasia in young patients when the consequences are trophic catastophe.
Sclerotherapy by direct injection of a chemical irritant, when surgery is impossible (varicose post phlebitic poorly systematized refusal operative patient … very old) or in addition to surgery on residual perforating, including perforating sub – ulcerative satellites after saphenous vein (Cockett perforating); those sclerosis may have to be repeated to obtain a complete result. Significant progress has been represented by the practice of ultrasound-controlled sclerosis, particularly in the treatment of incontinence butts.
Elastic restraint is necessary in almost all cases, even transiently after surgery well conducted, the more it can be conceived only after verification of the permeability of the deep venous system but also the arterial system while the latter is is rather theoretical. It must adapt to each case and make clear the order type of tape, or sticky bottom, the diameter, the force of restraint (low medium high very high) and take the time to explain to the patient the purpose and handling these materials. In general, the bottom is rather a bit less efficient in theory that the tapes, but are generally better used. It is sometimes the only feasible therapeutic option, particularly in post-phlebitis syndrome with predominant deep reflux, and one must still explain clearly that it is a share capital of treatment.
The veinotonic may improve symptoms (heaviness, swelling Vesper) of venous insufficiency but usually not enough to ensure a truly effective treatment and prolonged abnormal circulatory conditions in case of trophic disorders, however, this is an extra non-negligible in certain circumstances. Spa treatments require the same comments.
The lymphatic insufficiency with lymphedema, usually associated with venous insufficiency is best treated by an elastic restraint measures associated with lymphatic drainage performed by a specialized physiotherapist. The compression methods automatic sequential segments of members have proved disappointing.
b) Component arterial and arteriolar

Again, arterial gesture to discuss in all cases for infringement of large trunks because the most effective, generally guided by the data of arteriography and may be a bypass surgery or gesture more limited type of endarterectomy or angioplasty.
Control in all cases of various vascular risk factors including restoration imperative for a good balance of diabetes and / or correct RT in cases of necrotizing or angiodermatitis these measures are only effective to stop the progression lesions and allow the healing that is still long to get
The use of vasodilators orally or by IV, though efficiency discussed, is generally recommended. A special case is represented by Ilomédine (Iloprost *), the vasodilator prostacyclin analogue and particularly suited to trophic disorders of Buerger’s disease and diabetic angiopathy.

Be Sociable, Share!