Venous leg ulcerI83.0

Substance defect of varying depth in pathologically altered tissue of the lower leg due to chronic venous insufficiency (CVI) with ambulatory venous hypertension which heals with scarring.

If there is no tendency to heal within three months under optimal therapy or if it has not healed within 12 months, it is considered resistant to therapy.

The most frequent form of venous leg ulcer in chronic venous insufficiency due to varicosis ( varicose leg ulcer) or postthrombotic syndrome ( postthrombotic leg ulcer), as blow-out ulcer or as acute phlebitic leg ulcer.

Prevalence: An average prevalence of 0.1-0.3% is reported for florid venous leg ulcer. For the healed venous leg ulcer, the average prevalence is 0.6%. For people in the 8th decade of life it is about 2-3%. With a proportion of 50-80%, venous leg ulcers are the most frequent cause of chronic ulcerations of the lower leg (see also venous diseases).

Insufficiency of the intrafascial, extrafascial and/or transfascial veins leads to ambulatory hypertension of the venous system of the lower extremities, accompanied by venous hypervolemia. Ambulatory venous hypertension is based on the inability to reduce venous pressure in the leg veins by adequately activating venous return. This is followed by disturbances of micro- and macrocirculation with the development of chronic venous insufficiency (CVI) with all its consequences. The cause of venous insufficiency is usually a valve insufficiency, more rarely an obstruction/destruction, e.g. an occlusion due to thrombosis.

Strongly age-dependent occurrence, rarely before the age of 40; increasing with advancing age.

The predilection site is slightly above the inner ankle. Mostly occurring on the distal half of the lower leg and medial (insufficiency of the V.saphena magna) and/or lateral (insufficiency of the V. saphena parva) backdrop of the ankle region. Always epifascially localised; no exposed tendon.

Ulcer of varying size and depth (small defects up to large-area gaiter ulcers), usually only moderately painful, or completely indolent ulcer in pathologically altered tissue of the lower leg with varying degrees of signs of chronic venous insufficiency (CVI), often accompanied by relevant extensive tissue hardening(dermatolipo(faszio)sclerosis). Mostly moist secreting, red ulcerous surface (veno-lymphatic congestion), less frequently with a greasy yellowish coating (see biofilm below), usually not haemorrhagic. The outer border of the ulcer is often raised, arched, red or whitish macerated. Gram-negative bacterial colonization is often detectable (odor). A long-term untreated ulcer can reach a veritable surface area with involvement of the entire inner or outer ankle region. Proximally, a CVI ulcer can extend to the middle of the lower leg in an arched configuration, and in extreme cases can encompass the entire lower leg circumferentially (gaiter ulcer).

• Basic diagnostics: Directional Doppler sonography or duplex sonography of the leg arteries (with measurement of the systolic osseous arterial pressure in correlation to the brachial arteries, if necessary with presentation of the Doppler signal curve) and veins (epifascial, transfascial and subfascial, spontaneous and provoked signals, Valsalva manoeuvre) as well as performance of a functional examination procedure such as light reflection rheography/photoplethysmography (with Tourniquet in the case of pathological values).
• Biopsy in case of therapy-resistant and morphologically unusual ulcerations (e.g. suspected malignancy).
• In case of superinfection smear and antibiogram.
• Extended diagnostics: Colour-coded duplex sonography of the vein and arterial system; ascending press phlebography (possibly in DSA technique), possibly in combination with phlebodynamometry; magnetic resonance tomography; intracompartmental pressure measurement.

The following list refers only to the differential diagnosis of venous leg ulcer. Thus, the frequency information (very frequent, frequent, low frequency, rare, rarity) only applies to this differential diagnosis. For ulcers in other localizations, see below. Ulcer of the skin.

• Arterial (very common):
  • Ulcus cruris arteriosum
  • Ulcus cruris hypertonicum (Martorell).
• Mixed arterial/venous:
  • Ulcus cruris mixtum (very frequent).
• Genetic (common):
  • Factor V deficiency, congenital.
• Vasculitic/vasculopathic (common):
  • Vasculitis allergica
  • Ulcer in livedo racemosa.
  • Cholesterol embolism (in patients with pAVK).
  • Polyarteritis nodosa
  • Pyoderma gangraenosum
  • End(thromb)angiitis obliterans
  • Wegener's granulomatosis
  • Ulcerative concomitant vasculitides in collagenoses (e.g. systemic scleroderma)
• Infectious:
  • Bacterial:
    • Ecthyma (frequent, nursing errors)
    • Ecthyma gangraenosum (Pseudomonas).
  • Mycotic:
    • Mold infections (rare at this site; e.g., disseminated aspergillosis).
    • North American blastomycosis.
  • Other pathogens (rare):
    • Leishmaniasis
    • Dracunculosis
    • Furunculoid myiasis.
• Lymphatic (common):
  • Ulcers associated with chronic lymphedema.
• Panniculitic (rare):
  • Histiocytic cytophagic panniculitis.
• Neuropathic (frequency varies):
  • Neurogenic leg ulcer
  • Malum perforans (localization: pressure sores).
  • Ulcers in syringomyelia
  • Acropathia ulcero-mutilans non-familiaris.
• Trophic (low frequency):
  • Decubital ulcer (e.g. with appropriate foot cuffs).
• Metabolic:
  • Calcinosis cutis ( calciphylaxis)
  • Necrobiosis lipoidica (medium frequency).
• Hematologic/immunologic (important DD):
  • Pyoderma gangraenosum
  • Sickle cell anemia, thalassemia
  • Polycythemia vera
  • Thrombocytosis
• Traumatic:
  • Traumatic leg ulcer (rare).
• Physical/radiation induced (easily elicited by history):
  • 3rd degree burns
  • Radiodermatitis chronica (rare)
  • Radiation ulcer (rare)
  • Current marks (rare)
• Artifactual (component should not be underestimated):
  • e.g. simulations.
• Drug-related:
  • Embolia cutis medicamentosa
  • Hydroxyurea, methotrexate, leflunomide.
• Chemical:
  • Burns e.g. by gentian violet, acids, alkalis (history).
• Neoplastic (rare but important DD; see also ulcus cruris neoplasticum):
  • Ulcerated malignant tumors of the skin
    • Basal cell carcinoma
    • spinocellular carcinoma
    • malignant melanoma (rare)
    • Cutaneous lymphoma (rare)
    • Kaposi's sarcoma (rare)
    • Metastases (rarity)
  • Ulcerated benign tumors of the skin.
• Idiopathic:
  • Livedovasculopathy (moderate frequency).

Remember! 2/3 of all patients with venous leg ulcers have severe pain with a marked reduction in their quality of life. As a result, their mobility is reduced. A pain therapy adapted to the existing pain with the therapeutic goal of a satisfactory pain reduction is recommended.

• The venous leg ulcer is the most severe form of CVI.
• The aim of treatment is to reduce pressure and volume overload in the venous system.
• Compression therapy as an indispensable part of standard therapy. The effects can be achieved either with a phlebological compression bandage (short-stretch bandages) or with a medical compression stocking (MCS). Strong compression (e.g. to reduce oedema) is better achieved with short-stretch bandages! Long-stretch bandages are reserved for special indications. An alternative to compression bandages and compression stockings are segmental-adaptive compression cuffs, which are highly accepted by patients.
• Sclerotherapy: Epifascial veins can be eliminated by sclerotherapy. The sclerotherapy of (periulcerous) varices (so-called "nutritive veins") in combination with compression therapy accelerates the healing of venous ulcerations. Sclerotherapy with foamed sclerosing agents seems to further improve the effectiveness.
• Improvement of mobility: The limitation of the functionality of the muscle-joint pumps of the lower extremities has a significant influence on the development and severity of CVI. Therefore, an improvement of the patient's mobility is essential.

• The role of external therapy of the venous ulcer is often overestimated. It can optimise ulcer healing but cannot replace the main haemodynamic therapeutic approaches such as compression therapy and surgical or sclerosing treatment of venous insufficiency (see also varicosis).
• External therapy includes debridement, exudate management and infection control as essential components and takes into account the stage of wound healing, see also wound treatment.

  Notice! Early performance of epicutaneous tests on ointment bases, ointment supplements, local anaesthetics, antibiotics and disinfectants is highly recommended, as patients with chronic wounds tend to develop contact sensitisation, which leads to relevant disturbances in wound healing!

• Cleaning:
  • Softening of coatings: Superficial coatings can be softened by baths or compresses with additives. Developments of resistance are rarely to be feared here. Hydrogels (see gels, hydrophilic gels) have also proved to be effective, which, in addition to promoting granulation, soften coatings and necroses.
  • Mechanical removal: Firmly adhering necroses can usually only be removed mechanically with the ring curette, the sharp spoon or with tweezers and scissors. Local or surface anaesthesia with lidocaine / prilocaine (e.g. apply EMLA cream 1/2-1 hour before the procedure) may be necessary.
  • Enzymatic cleansing may be helpful in case of minor deposits (collagenase, Iruxol ointment).
• granulation:
  • Superficial ulcers: Hydrocolloid foils (e.g. Varihesive extra thin, Tegasorb, Comfeel, Gothaderm GTH) and hydrogels (Intrasite Gel, Geliperm, Cutinova Gel) have proven effective for clean, non-superinfected ulcers. For less secreting ulcers, wound dressings with a limited fluid absorption capacity such as hydrogels or foils (e.g. Bioclusive, Cutifilm plus, Tegaderm) are also suitable. Synthetic wound dressings such as polyurethane foams are an effective microbial barrier and offer good mechanical and thermal protection. Dressing changes are generally painless and without trauma, so that they are well tolerated by patients.

Notice! Indifferent moist therapy with synthetic wound dressings has proven successful!

• • Deep ulcers: Gels are useful. Alginates (e.g. Algosteril, Tegagel) are well suited for tamponing deep wounds and niches, as they unfold properly with the secreted fluid of the wound. A mechanical freshening of the ulcer base promotes granulation.
  • Secreting ulcers: Wound dressings with a high resorption capacity, e.g. polyurethane foam or alginates, which unfold fully by absorbing the secretion.
  • Pyodermic ulcers: Suitable here are wound dressings with elemental silver and possibly activated carbon, e.g. Actisorb, Actisorb silver, Acticoat, Aquacel AG.
  • Excessive granulation: Excessive granulation may impede wound healing. With sufficient granulation, epithelialisation should therefore be promoted (see below) or the progression of granulation prevented (e.g. pressure dressing). Etching is possible with silver nitrate.
• Epithelisation
  :Most preparations used for granulation, such as hydrocolloid foils, hydrogels, polyurethane foam, also promote epithelisation.
  • For large wound areas, split skin grafts, possibly as mesh graft grafts, are helpful alternatives which can shorten the healing process many times over. Prerequisites are a clean wound bed or previous shave excision of the leg ulcer and the elimination of trophic disorders (e.g. venous stasis). In addition, the transplantation of autologous and/or heterologous keratinocytes in the granulation and epithelialisation phase is considered.
    In the case of large and/or deep ulcerations or excessively long wound healing, primary surgical wound care with necrectomy, incision and subsequent plastic defect covering may be necessary (full skin flap plastics/Reverdin plastics, musculocutaneous flap plastics, etc.).
• Treatment of the periulcerous environment:
  • Cleaning: Careful cleaning with oils, e.g. olive oil.
  • Covering: It is sometimes advisable to cover the ulcer area with zinc paste (Pasta zinci), possibly with antiseptic/antiphlogistic additives (e.g. R014 ) or pure Vaseline to protect against irritation by the ulcer secretion. In the case of heavily weeping ulcers, special wound dressings or calcium alginates (see above) are also used.
  • Desiccation eczema: Iatrogenic dehydration eczema, e.g. after intensive disinfectant moist treatment, is treated with indifferent fatty ointments such as Vaselinum alb., Paraffin. subliq. or R273, R156.

Notice! Compatible bases are consistently maintained in ulcer patients, since each new external agent carries a renewed risk of sensitization! If desired and as far as possible, active ingredients can be incorporated into the compatible base! In most cases, it is possible to dispense with differentiated active ingredients completely.

• • Weeping eczema: In case of accompanying, weeping eczema reactions, carry out a lipid-moist local treatment. Here, combinations of mild glucocorticoids in indifferent fatty bases such as 0.1% triamcinolone cream (e.g. Triamgalen) or 0.25% prednicarbate (e.g. Dermatop ointment/fatty ointment) and moist saline compresses are suitable, if necessary also combinations with disinfecting solutions such as polihexanide (Serasept, Prontoderm) or octenidine (Octenisept).

Remember! In ulcer patients, the use of substances with a high allergenic potential such as certain ointment components (e.g. wool wax alcohol, cetylstearyl alcohol, sorbic acid) should be avoided if possible!

• • Antiseptic ointments can be used such as polyvidon-iodine ointment (e.g. Betaisodona ointment/wound fleece, Braunovidon ointment) and also quinolinol (e.g. Leioderm). Ointments with antibiotic additives should be avoided because of the high risk of sensitization.
• Therapy for signs of inflammation: The ulcer surface is usually contaminated with bacteria. Antibacterial therapy is not indicated until clinical signs of critical colonization or infection are detected. Wound dressings containing elemental silver, antiseptics such as quinolinol (e.g. R042 ), polyvidon iodine, octenidine and polyhexanide as well as systemic antibiosis in the case of more severe signs of inflammation are considered.
  In the case of vasculitic components (petechial haemorrhages), systemic glucocorticoidsmay also be indicated in addition to ulcer cleansing, disinfectant therapy and clarification of the causes of vasculitis.

• The indication for surgical ulcer treatment exists if, after all conservative options have been exhausted, no healing tendency is evident within 3 months or an ulcer has not yet healed after 12 months (DGP guideline).
• The surgical measures include 4 therapeutic approaches:
• Shave therapy (tangential fibrosis and necrectomy as well as defect coverage by means of a mesh graft): surgical method of choice in the case of long-term, therapy-resistant venous leg ulcer.
• Fascicectomy: for very extensive, deep-reaching ulcers involving the tendon apparatus and in the case of transfascial necrosis or in the case of therapy failure after Shave therapy.
• Surgical rehabilitation of epifascial reflux routes.
• Surgery of the deep vein system in special centres.

• The history should be specific to venous disease and other factors that may affect wound healing such as diabetes mellitus, heart failure, polyneuropathy, rheumatic diseases), risk factors such as occupational exposure and sports activities, surgery and trauma to the lower extremities and pelvic girdle region, intermittent claudication.
• In Western countries, topical aminoglycosides, perubalsam, fragrance mix, Amerchol L-101, rosin, and lanolin alcohols represent the most common contact allergens. In addition, applications and possible sensitization to non-prescription "home remedies" should be considered in the history (e.g., tiger balm, Franz brandy, horse ointment).
• General rules of conduct for the ulcer patient: Frequent elevation of the legs. Keep legs elevated at night (approx. 20 cm above body level). Venous exercise is recommended after exclusion of pAVK or a mixed ulcer.

Remember. "LL not SS": lying and walking instead of sitting and standing!

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