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Luc Téot - Skin Necrosis

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Luc Téot Skin Necrosis

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In recent years, wound care has gained increasing recognition as a distinct medical specialty. An understanding of the complex mechanisms involved in wound healing facilitates efficient assessment and treatment of patients with wounds, and skin necrosis can be considered the starting point in the entire healing process. This book is the first to discuss skin necrosis as a symptom related to a broad range of pathologies. Richly illustrated, it primarily provides therapeutic strategies and treatment algorithms for different clinical contexts. All chapters were written by renowned specialists in their respected fields and include detailed sample cases and essential take-home messages. In light of the highly interdisciplinary nature of wound management, Skin Necrosis offers an invaluable resource for wound care practitioners and health care professionals across the fields of surgery, dermatology, internal medicine, and nursing.

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Part I
Definitions, Vascular and Imaging Investigations in Skin Necrosis
Springer-Verlag Wien 2015
Luc Tot , Sylvie Meaume , Sadanori Akita , William J. Ennis and Veronique del Marmol (eds.) Skin Necrosis 10.1007/978-3-7091-1241-0_1
1. Dry Necrosis, Wet Necrosis: When to Debride, When Not to Debride
Luc Tot 1 and S. Fluieraru 1
(1)
Wound Healing Unit, Department of Surgery, Montpellier University Hospital, Montpellier, France
Luc Tot
Email:
1.1
1.2
1.3
1.4
1.5
1.6
1.1 Introduction
Skin necrosis is a result of several factors.
Ischaemia of a skin territory leads to venous congestion, which blocks microcirculation. The damage caused may remain reversible for a few hours, but 6 h or more of ischaemia lead to an irreversible situation and tissue loss. Several factors contribute to ischaemia. The most common is thrombosis of small arterioles, which progress, together with regional inflammatory processes, to devascularisation of a defined anatomical territory (angiosome). During the spreading of infections, necrosis is linked to the destructive effect of germs, which induce tissue damage by simple germ proliferation or induce vessel thrombosis. The germs may also secrete toxins, which are diffused inside the arteriolar and capillary vascular systems. This leads to rapid obstruction of the vessels by chemical intimal and subintimal lesions, causing necrosis of large territories involving not only the skin but also the underlying muscles, tendons and bones.
1.2 The Skin Necrotic Process
Subdermal necrosis may be induced by excessive pressure, leading to a mechanical crush. This is the most common factor in pressure ulcers and diabetic foot ulcers. In this situation, successive stages of skin necrosis can be observeda situation reflected in the non-blanching stage 1 pressure ulcer following the National Pressure Ulcer Advisory Panel (NPUAP) classification, which probably corresponds to a prenecrotic stage. This is also observed in extravasation injuries [].
Epidermal-dermal necrosis may rapidly appear at the skin surface. However, in some areas, such as the foot or when the depth of keratinized epidermis is thick, the necrotic tissue may resemble a subepidermal collection. This is partly because of the Tyndall effecta light scattering observed when particles are present in colloid suspension, with blue light being much more strongly affected than red light.
When mature, this subdermal necrosis is easily confused with a deep hematoma. This situation is often observed on the heel.
The time to complete the necrosis may vary from 6 h to 23 days, depending on the state of vascularisation of the limb. It may be more progressive, such as observed during terminal limb ischaemia or during angiodermatitis. Microvascular impairment, autoimmune vasculitis, macroangiopathy and venous blockade are the most frequent causes, together with infection and microarterial emboli.
Dermal necrosis may be accompanied by fasciitis, especially during a severe infection such as necrotising fasciitis, where the presence of germs secreting highly active toxins quickly involves all surrounding tissues and creates a regional progressive necrosis, a spreading infection rapidly leading to a septicaemic life-threatening shock. The proliferation of germs is facilitated at the level of fatty tissue, such as in Fournier gangrene involving the perineal area and progressing very quickly under the skin.
Others toxins and venoms may be secreted by a series of different animals (snails, mosquitoes) and may create an intense local inflammatory process leading to localised skin necrosis combined with an extensive subepidermal tissue degradation [].
1.3 Wet Necrosis
Necrotic tissue and the normal skin with which it is in contact are both adherent to each other for a period of time of around 1 week. Separation starts with a fissure occurring between normal and necrotic tissues, initiated by a difference in mechanical resistance and elasticity. This dissociation creates the elimination fold, allowing the germs to penetrate deeply and to destroy the mechanical links between dead and living tissues. These germs proliferate in the subdermal fatty tissues. In large burns the dissemination of germs all over the involved area are the main cause of death.
In some situations the necrotic tissue presents as wet, usually when necrosis is covered with damp dressings, allowing anaerobes to develop. This wet necrosis is often seen on the heel or other parts of the foot, the perineum, places and where maceration usually occur. Wet skin necrosis is considered to be at high risk of local infection, and should be quickly removed.
1.4 Debridement
  1. Evidence-based medicine
    When analysing the literature from an evidence-based point of view, the Cochrane review considers that debridement has not yet demonstrated its efficacy. Nevertheless, most of the practitioners and paramedics involved in wound healing recognise the beneficial effect of debridement.
    Skin necrosis is not infected for the first few days, but becomes heavily colonised when the edges are dissociated from the healthy skin. The time effect depends on a number of factors, grouped under the name of comorbidity markers. These markers may define the capacity of the patient to heal. Some of them, such as ankle brachial pressure index, albuminaemia, glycated haemoglobin and blood pressure measurement are easily collected. Others, such as inflammatory markers or evolution with time of the wound healing process (surrogate end point) should be accurately determined.
  2. Indications and contra-indications of debridement
    Debridement is indicated when the limb is vascularised enough to prevent renecrosis on the edges of the wound. During the post operative period, when the skin flap becomes necrotic, a surgical revision removing the necrotic areas is required. However, lower limbs presenting an ABPI (ankle brachial pressure index) lower than 0.5 should not be debrided. When the ABPI is over 0.5, the debridement should follow an algorithm depending on multiple factors such as accessibility to surgery, availability of expertise in the use of advanced dressings such as hydrogels, hydrobalance or new debriders. Wet to dry techniques are not recommended any more.
    In the presence of spreading extended necrotic areas, an adapted debridement should be quickly proposed. In necrotising fasciitis, extravasation injuries, haematomas or Fournier gangrene, a large and extensive surgical debridement, including the edges of undermined cavities, is needed and should be considered as an emergency. The immediate post-debridement period should consider the need for repetitive debridement procedures when infection is still present. New debriders such as Versajet or Coblation WoundWand are useful in destroying local germs and preventing biofilm formation.
    In the case of necrotising angiodermatitis, pain and skin necrosis may need surgical debridement and rapid skin grafting using pinch grafts to stop pain.
    Pressure ulcers are common causes of necrosis, particularly in the perineal area and over the heel. On the perineal area, undermining is frequently observed, as a consequence of the shearing forces exerted on the skin. The skin is more mechanically resistant than the underlying structure, a relatively small opening covering a large undermined area being frequently observed. In this situation, all hidden cavities need to be opened to expose living edges. The granulation tissue and retraction is more rapidly obtained. Excision of the cover (decap surgery) by surgical means is an option, but simple incisions along the undermined area are more easily realised by non-surgeons (Figs. ). On the heel, a vascular assessment is mandatory (pedal pulse absence is the first sign, and should indicate ABPI and Doppler ultrasound, and in case of arteriopathy a vascular surgery consultation is needed) before any mechanical debridement to prevent renecrosis of the edges. An ABPI below 0.5 is a contraindication to debride. Poor vascularisation, end of life and palliative situations are contraindications to surgical debridement.
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