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K. Ellermann, H. Röthel
A wound healing by second intention is defined as chronic if it does not show any healing tendency under appropriate causal and local therapy within 8 weeks. Chronic wounds can develop from acute injuries at any time as a result of unrecognised persistent infections or inadequate primary treatment. In most cases, however, chronic lesions are the end stage of progressive tissue breakdown owing to venous, arterial, or metabolic vascular disease, pressure sore, radiation damage, or tumors. |
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General
treatment principles |
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As might be expected from the predisposing factors, patients with chronic wounds are mainly older people and with an ageing population, the incidence of chronic healing failure is likely to considerably increase. The treatment of chronic ulcerations necessitates a comprehensive therapeutic approach and is generally restricted by the fact, that the interrelated processes leading to the observed dysregulated cell activities are not yet fully understood. Nevertheless, the current knowledge of the pathophysiology of wound failure offers promising opportunities for successful therapeutic strategies in chronic wound treatment. A number of impairing factors of endogenous and exogenous origin have been identified and can be compensated or eliminated via proper wound therapy. Based on these findings, a number of general and specific treatment principles for chronic wounds have been established and will be presented below, together with the causative factors for the most common chronic ulcerations of the skin. |
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GENERAL TREATMENT PRINCIPLES |
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Irrespective of the type of ulceration, the pathophysiological mechanisms producing a chronic development of wound healing are altogether very similar. Although the observed deficiencies in nutrient delivery and metabolite removal are due to the most different vascular diseases, they finally all lead to tissue hypoxia and ischemia resulting in devitalisation of the affected cells with eventual formation of necroses. Once established, this situation implies, that the repairing efforts of the cells involved in wound healing, intended to produce complete cure of the ulceration, have to be initiated in a skin region that is extremely metabolically disturbed. Improvement in timely fashion is, therefore, not to be expected without therapeutic intervention. Wound healing can only be initiated and completed under the following two conditions:
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Casual therapy |
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The common techniques used for interventional causal therapy such as vascular surgery, compression treatment, recanalisation of constricted vessels via dilatative techniques, optimal control of the patient’s diabetes, pressure relief etc. will be discussed below together with the description of the respective ulcus type. |
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Wound cleansing |
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The appropriate choice of wound toilet in chronic ulcera is sharp surgical débridement, as this is the most rapid and most effective technique of removing everything from the wound that may impede healing: necrotic tissue, that is no longer supplied with blood and constitutes a dangerous site of infection, as well as other inhibitory factors including toxic debris from tissue and bacteria. With surgical débridement, the vascular situation can be immediately improved and the risk of infections is securely contained. A physiological wound milieu is generated, that encourages the restart of wound healing under improved conditions. Wound cleansing may be accompanied by profuse bleeding which, in turn, leads to the release of numerous cytokines that have considerable influence on the initial processes of wound repair. When the specific situation of the patient does not allow for surgical débridement, satisfactory results can also be achieved with the alternative techniques of enzymatic débridement using proteolytic substances and/or moist wound treatment that causes softening and eventual detachment of necroses. Both these alternatives may also be indicated as additional measures during surgical intervention, to facilitate the removal of thin, superficial necrotic layers that are particularly resistant to mechanical excision. Unfortunately, it often turns out that initial débridement is not sufficient to produce complete wound healing, as the underlying deep vascular disturbances are frequently persistent. New necroses and fibrinous coats may arise, necessitating repeated procedures of subtle débridement, cautious revivification of the wound, and removal of fibrin cuffs, as well as continuos uptake of large quantities of germ-laden and excess exudates from the wound. An adequate control of the latter problem can be ensured with the technique of moist wound treatment. Depending on the condition of the wound, irrigations with Ringer’s solution or sterile water may be advisable to support the wound-healing effects of moist therapy. In the treatment of chronic wounds, it is a frequently observed practice, that attempts are made to accelerate the courses of wound cleansing and wound healing with doubtful polypragmasy. It must, the cytotoxicity and other side effects of the materials used in the respective regimes. Disinfectants, ointments containing antibiotics, dyes, coloured solutions, metalliferous pastes, etc. all possess a certain potential to impair wound healing. The local damage of these substances may be of little importance in short-term use, but not so during long-term treatment. They then can significantly delay wound repair due to their unwanted side effects and considerably diminish the patient’s quality of life, apart from the fact that they can trigger contact allergies, as well as the development of resistance. |
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Wound conditioning |
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If surgical débridement cannot be followed by immediate restorative plastic surgery using the diverse methods of flapping or skin grafting, conditioning of the wound surface is paramount. Wound conditioning means well-directed promotion of granulation until the dermal defect is nearly filled to reach skin level. A healthy granulating wound bed is a prerequisite for wound closure via spontaneous epithelialisation or covering with skin grafts. To encourage the synthesis of granulation tissue, the ulceration needs to be maintained under permanently moist conditions. This prevents cell death owing to desiccation and generates a favourable microclimate for the cells to fully develop their important proliferative activities. |
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Wound closure
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Epithelialisation is the last step in wound repair that brings about complete closure of the lesion. Chronic wounds, however, show especially bad epithelialisation tendencies. Migration of the epithelial cells at the edges of the wound is extremely restricted as Seiler et al. could demonstrate for decubital ulcera in 1989. The rate of cellular growth in the damaged skin area was only 2 to 7 per cent as compared to normal control skin, that showed growth rates of approx. 80 per cent. Toady's standard for wound management during epithelialisation is a moist, absolutely atraumatic therapy. Every desiccation or traumatisation of the epithelial cover during dressing changes causes cell loss and further delays wound healing due to additional minimization of the already limited population of regenerative cells. The treatment of extended superficial ulcerations displays particular problems. In this situation, epithelialisation is considerably slowed down, as it can only start from the wound margins, and the exposed granulation tissue may thus, be subjected to ageing and fibrotic transformation, eventually resulting in complete standstill of the re-epithelialisation process. Large ulcerations with healthy, clean granulation are, therefore, the main indication for wound covering with skin grafts. |
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THE ULCUS CRURIS VENOSUM
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Alterations of the venous system and venous disease belong to the most widespread health problems. For Germany, an estimate of approximately 2 million individuals affected with venous ulceration of the lower leg is recorded. Many among these patients have a history of decades of inadequate and frustrating therapeutic attempts. Ulcus cruris venosum is the most critical metabolic disturbance owing to chronic venous insufficiency in the cutis and subcutis. When venous return is impeded (venous insufficiency), less blood is forced from the deep veins towards the heart and the venous pressure cannot be sufficiently decreased. The venous overload thus created causes progressive development of venous decompensation, finally effecting the capillaries of the terminal vascular bed. The low pressure values necessary for normal metabolic activities are increased, the blood flow in the vascular system, however, is slowed down or even stopped. Metabolism in the cutis and subcutis is impaired. In the long run, even the lymphatic system is affected by this circulatory disturbance, as the compensation of interstitial liquid increase by enhanced uptake into the lymphatics can only be ensured in the initial phase of the morbid process. The first sign of venous insufficiency is the formation of oedema, which in return causes an additional local, partly oncotic pressure increase accompanied by fluid accumulation, thus further intensifying the underlying metabolic problems. Oedema formation is followed by several perivascular activities including fibrosis, degeneration and inflammation along with trophic alterations of the skin. Additional obliterative inflammatory processes in the small veins and arteries eventually lead to the development of ulcus cruris, the now clearly apparent sign of decompensated venous hypertension, that first presents in areas with unfavourable venous hemodynamics. The different clinical pictures of venous disease are determined by the severity, localisation, and history of the venous condition, as well as the degree and duration of stress acting on the venous system of the legs. They are all summarized under the generic term chronic venous insufficiency (CVI) and can generally be graded into three stages according to the severity of the dermal lesion. A stage I CVI is characterized by vein dilation along the sides of the foot with concomitant formation of oedema in the ankle region, stage II already involves hyper- and depigmentation of the skin, dermatoliposklerosis, or even atrophie blanche together with marked oedema formation on the lower legs. Stage III is the florid or healed ulcus cruris venosum that is preferentially located in the perimalleolar region (Bisgaard region), but can also be found at other sites of the low leg. A CVI can arise from primary varicosis, when dilation of the vessel lumen and damage to the valves of the superficial veins eventually affect the perforating and subfascial veins, or may be the result of a postthrombotic syndrom. Postthrombotic syndrom (PTS) is the most frequent cause of ulcus cruris venosus (ulcus cruris postthromboticum). Therapeutic measures concentrate on the following strategies: The CVI inducing the chronic skin alteration has to be improved to the greatest possible extend via causal therapy. The ulcer can only heal when the oedema disappears and venous blood flow has again reached a compensated state. A number of different invasive techniques, e.g. sclerotherapy and/or operation are available for that purpose. The subsequent therapeutic regime should always even after surgical intervention at the venous system include an appropriate basic compression treatment. Local wound management involves careful wound toilet with sharp débridement followed by efficient wound cleansing, as well as wound conditioning and eventual reepithelialisation of the lesion with the help of moist wound dressings. Certain obstinate, therapy-resistant ulcerations do not heal until after surgical intervention for venous insufficiency. Useful methods known to have high rates of therapeutic response are the paratibial fasciotomy according to Hach, as well as its more advanced variant, the endoscopic ligation of the perforators according to Hauer. The ulcus cruris venosum is usually accompanied by eczema. This may be due to bacteria and fungi that colonise the damaged skin area (microbial eczema) or indicate a contact allergy to topically applied drugs. Wound care under these conditions should follow the general principles of eczema therapy: The acute, oozing, and irritated eczema requires moist wound treatment and the subcutaneous or chronic eczema demands a more differentiated therapy, using exclusively substances and ointment bases that are free from allergens. |
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THE ULCUS CRURIS ARTERIOSUM |
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An arterial ulcer is always a sign of tissue hypoxia at rest owing to peripheral arterial occlusive disease (PAOD). As a general rule, there is anamnestic evidence of cardiovascular risk factors such as smoking, hypertension, disturbed fat metabolism, hyperuricemia, or diabetes mellitus. The arterial ulcus can be described as the visible regional manifestation of the end stage of a chronic-progressive vascular condition that has been developing for decades. The obliterative processes are, however, not restricted to the periphery. Additional renal, cardial, and cerebral dysfunctions may be determined due to the generally impeded arterial supply. Every leg ulcer that is not located at the typical sites for venous ulcerations is very likely to be arterial in origin. Missing pulses in the hollow of the knee and on the back of the foot, reduced walking range as defined by intermittent claudication, a cool, pale extremity, toenails showing yellow hue and disturbed growth, a soft, doughy oedema (toxin formation!), as well as possible gangrenous alterations at the tip of the toe facilitate a prima vista diagnosis. The ulceration can usually be detected at sites that, while standing or walking, are exposed to increased pressure (heels, balls of the foot, anterior ridge of the tibia) or shear (above the heel tendon). As patients with arterial ulcer are at increased risk of limb amputation, immediate hospitalisation is compelling. The therapeutic aims and methods for arterial ulcerations will be discussed below in context with the angiopathic gangrene. |
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THE DIABETIC ULCUS
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Today, diabetes mellitus belongs to the most frequently occuring diseases in man. In Germany, an estimated number of at least 4 million patients are currently treated for diagnosed diabetes. Diabetes mellitus is a systemic disease known to be encumbered with a high risk for acute and chronic complications. The acute risks are associated with diabetic coma, chronic risks, on the other hand, are the result of the dreaded late symptoms. With a possible latency of many years, the chronic secondary damages become especially expressed at blood sugar levels that do not cause diabetic coma, nor noticeably impair the patient’s general condition. Among the secondary complications of diabetes, the “diabetic foot syndrom” is particularly problematic. The slowly progressing changes at the feet remain mostly unnoticed and are often painless due to concomitant neuropathy. With additional wounding, the foot is in acute danger and may cause serious problems: A patient with a diabetic foot is at extreme risk of limb amputation. A diabetic lesion is developed owing to neuropathic and angiopathic processes, the situation is particularly problematic if the ulceration is of mixed pathology. The definite diagnosis of the wound including exact verification of its original cause is, therefore, indispensable for a promising therapeutic strategy. The diagnosis has to consider the symptoms of angiopathy and neuropathy, the aetiology of the lesion (anamnesis, injury, infection, lesion of the bone, mycosis, other late effects), as well as the metabolic situation (blood sugar, HbA1c) and inflammatory parameters (leucocytes, C-reactive protein, fibrinogen, erythrocyte sedimen-tation rate = ESR). In order to establish a reliable treatment regime, diabetic foot ulcera should be assigned to one of the following groups:
The treatment of diabetic ulcerations requires patience and experience. The main aim of all efforts is the prevention of limb amputation and the achievement of complete cure of the lesion. The hastened removal of a limb is often the beginning of a disastrous development in the patient’s history. It is now generally accepted, that in most cases, an emergency amputation is not indicated and that there is usually enough time for a detailed diagnosis, which should, however, be accompanied by initiating cosequent control of diabetes and possible infections. |
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Causal therapy |
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The basic measure in the treatment of all diabetic lesions and the best therapy for neuropathy is optimal blood sugar control. The management of the circulatory disturbance with invasive techniques (e.g. PTA = percutaneous transluminal angioplasty, rotary angioplasty, laser angioplasty, PTFE bypass etc.) or conservative measures (heparin-isation, local lysis with urokinase, prostaglandin infusion etc.) requires collaboration of experienced internal specialists, interventional radiologists, and vascular surgeons. |
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Treatment of infection |
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Another problem of prime import-ance in the treatment of diabetic ulcerations is their extremely high susceptibility to infection. In angiopathy, there are only very few lesions that do not show signs of an infected surrounding. The diabetic foot of mixed angiopathic and neuropathic genesis and the neuropathic ulceration may, as a general rule, always be regarded as infected. The chances for spreading are especially high owing to the differentiated structure of the connective tissue in the foot region. A consequent systemic therapy with antibiotics has, therefore, almost always proven effective. |
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Local therapy of neuropathic ulcus |
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For the local therapy of neuropathic ulcerations the following therapeutic principles have been established:
In spite of all difficulties, a neuropathic lesion always implies a good prognosis, so that it is initially advisable to confine to conservative methods, in accordance with the surgical principles of local wound bed hygiene. Major surgery and amputations are never the treatment of choice. |
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Local therapy of angiopathic gangrene |
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A gangrene accompanying arterial occlosive disease necessitates a differentiated approach that depends mainly on the general condition of the vessels and the results of revascularisation. Treatment of this type of diabetic foot ulceration less frequently occurs without amputation. The options for wound toilet are necrectomy, excision of the necrosed part along the lines of demarcation with mainly subsequent secondary healing, or amputation with classic incision followed by primary wound healing. Chosing the appropriate therapeutic strategy requires clinical experience. The decision should be made after thorough consideration and must not be rushed, for example, during night-duty. The main aim should always be the preservation of extremeties. If necrectomy is sufficient, it should always be regarded as the treatment of choice. Even if wound healing by secondary intention may possibly last for months, the results are still most convincing. Unlike the neuropathic foot, an angiopathic ulceration may be exposed to strain on condition of effective pro-phylaxis against infections and in the absence of necroses. A vascular training may support the effects of revascularisation and wound healing. An amputation along the lines of demarcation is always necessary when the necrotic area involves bony structures of the foot. The term demarcation describes the formation of clearly apparent border lines between dead (black) and viable tissue. The time for amputation should not be set before extensive demarcation of the lesion has been achieved. Operations that interfere with inflamed tissue often produce secondary necroses owing to wound oedema formation at insufficient blood supply. When determining the type of incision, the possibilities for subsequent provision of prosthetic devices and footwear should always have priority. An amputation at a high level, as a rule, facilitates more rapid wound healing, but at the same time causes greater problems and discomfort for the patient in terms of limb fitting. One-sided amputations do not seldom produce overstrain of the remaining limb with concomitant malperfusion, again carrying a high risk of wounding. |
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A decubital ulcer is defined as a skin ulceration resulting from continuos action of local interface pressure between the patient and a support surface. The pressure load produces compression of the capillaries, so that the affected cutaneous region can no longer be sufficiently perfused and supplied with oxygen. The now restricted circulation induces the accumulation of toxic metabolic products in the tissue followed by increased permeability of the capillaries, vascular dilation, oedema formation, and cellular infiltration. In the beginning, the inflammatory reactions described are accompanied by hyperaemia with increasing capillary pressure, so that the toxic metabolites are still removed, and the cutaneous cells can still regenerate on condition that the compressed area is completely off-weighted. If the pressure effecting the skin region is persistent, however, an increased hypoxia leads to irreversible decay of the skin cells with subsequent formation of necroses. The injury passes different developmental stages depending on the level and duration of the compression, which implies for everyday practice, that an immediate pressure relief can always prevent aggravation of the present situation. Decubital ulcera may in principle arise on any part of the body. The highest risk is given, however, when the interface pressure acts on a skin area overlying a bony prominence, that has only little subcutaneous fatty tissue to cushion against this force. Classic localisations are, therefore, the sacral region, the heel, the ischium, the greater trochanter, and the sides of the ankles. Approx. 95 per cent of all decubital ulcers are located on these sites. Apart from the interface pressure load that acts directly on a skin area, a risk may also arise from shearing, which forces the cutaneous layers to shift against each other, and thus eventually causes indirect compression of the blood vessels. The treatment of decubitus is based on three therapeutic pillars: The primary precept of pressure sore treatment is the restoration of blood supply in the damaged skin area by means of complete off-weighting. Without pressure relief, healing cannot proceed and all other measures are senseless. Off-weighting needs to be ensured during the whole duration of decubitus treatment. Any strain – even if it lasts for only a few minutes – causes additional damage and may produce set-backs in the healing course. Local wound therapy consists in thorough débridement, possibly via surgical techniques, as well as in continuous wound cleansing using hydroactive wound dressings, wound conditioning with formation of granulation tissue and eventual epithelialisation, which may also be supported by means of moist wound treatment. As a third measure, adjuvant therapies are indicated that may improve the general condition of the patient, as well as his nutritional situation or contribute to the alleviation of pain. Cachexia, together with protein deficiency conditions inhibitory to wound healing, are often noticed especially in the elderly, so that for these patients an adequate food uptake with increased protein, and sufficient vitamin and mineral content has to be assured. |
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THE
CHRONIC POST
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Chronic posttraumatic wounds result from inadequate primary treatment of a trauma or from complications during primary treatment that are not eliminated in the immediately following therapeutic phase. Typical causes for the chronic course of a posttraumatic wound are soft-tissue contusion, skin avulsion, skin necrosis, osteitis, implant infection, endoprosthesis infection, joint infection, or deep soft-tissue infection. In many cases, the disadvantageous development is due to initial under-estimation of the soft-tissue injuries that accompanies the primary trauma. A particular problematic condition among the primary traumas is the open fraction: Here, contaminations may produce soft-tissue and bone infections that often run serious courses. The unstable scar that can be found after secondary healing or split-thickness grafting of skin areas exposed to mechanical stress is a special form of a chronic posttraumatic wound. Although soft-tissue integrity is not interrupted during scar formation, recurrent ulcerations with corresponding risk of infections occur on repeated occasions, eventually necessitating the reconstruction of the affected soft-tissue area. The aim of all measures in the treatment of a chronic posttraumatic wound is the achievement of a stable soft-tissue cover. The first step in this approach is again débridement, and thus the removal of all necroses and infection sites from the wound. Under certain circumstances, it may be impossible to consider functional structures as tendons, fasciae, or also nerves and blood vessels. A soft-tissue situation has to be generated, that enables covering of the defect without risk of continued necroses, and thus of persisting infections. The future reconstructive procedures already need to be considered during operative débridement. An early decision must be made on whether defects of soft-tissue and bones will be closed in a one stage procedure, or whether certain reconstructive measures may be postponed to be performed later, under conditions of completely cured soft-tissue. The time factor must not be neglected. Exposed bones and tendons after débridement may dry out or acquire secondary infections. As a general rule, the definite soft-tissue cover should occur two days after the first débridement, during a planed “second look”. Wound closure requires reconstructive plastic surgery, ranging from simple skin-grafting (on healthy granulating wounds, when no unprotected functional structures are involved and no regions exposed to mechanical stress are affected) to free microsurgical flapping. |
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The treatment with ionising radiation leads to inevitable damage of the skin and underlying tissue. The secondary injuries may not always be visible at the macroscopic level, however, early detectable signs of chronic radiolesion are telangiectasias, that can be regarded as the regeneration products of destroyed capillaries. After radiation, the cutis and subcutis are only insufficiently perfused and show a tendency for secondary atrophy. The skin becomes thinner and firmly attached to the underlying structures due to the loss of subcutaneous fat tissue. This is accompanied by general tissue fibrosis, as well as direct damage to the cells including chromosomal changes. Local lymphatic oedema, an increased hyalinisation at the expense of elastic fibres, and thrombosis of the small arteries and veins eventually cause local malnutrition, and thus the formation of badly healing ulcerations. In the worst case, these ulcerations may undergo malignant transformation with a latency of 4 to 40 years. When an initially stable radioderm suddenly becomes unstable, this may be due to recidivation of the primary tumor or new malignant growth. Cutaneous metastases prefer to nest in irradiated areas of the skin. Further causal factors for a corresponding development are traumas such as injections, biopsies, and insect bites or chemical influences, such as a local therapy, continued local irritation, or an occupational exposure to irritating chemicals. Chronic damages may also occur owing to skin infection, osteomyelitis, and non-infective skin diseases, such as varicosis and congestive dermatitis, as well as to internal diseases as diabetes mellitus or arteriosclerosis. Indications for a surgical intervention are the resection of local recidivations, the resection of an unstable scar, or the resection of skin damaged by radiation in order to alleviate pain, simplify patient care, and improve the patient’s quality of life. Surgical treatment of radiolesions initially requires a radical débridement with thorough histologic examination of the operative specimen, as well as the edges and depth of the wound. This may possibly also include the resection of bones, the sternum, or the whole chest wall. In particular, the treatment of osteo-radionecroses cannot produce satisfactory results without proper, extensive wound toilet. As direct wound closure is, as a rule, not advisable and split skin grafting is often also not sufficient, best cover of the frequently large defects is in most cases achieved with a well vascularised (musculo-)cutaneous flap. It is generally to be mentioned, that conservative treatment of radiation injuries is often pursued for too long, so that an eventual application of surgical techniques occurs at a very late stage. It should be taken more frequently into consideration that ulcera in irradiated regions can, as a rule, not be cured with conservative therapeutic measures, and that chronic ulcerations may easily become a source for secondary malignant growth. Apart from the fact that it can reduce patient misery, an early surgical intervention often also helps to prevent complex defect reconstruction. |
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The growth of benign or malignant tumors under or in the skin leads to the destruction of tissue continuity, which, after months or years of the growing process, may possibly result in the formation of open ulcerations. If the stage, extent of spread, and location of the wound allows, a radical operation is preferred as the most reliable way to combat the tumor. Thus, the lesions caused by the tumor are converted into surgical wounds and can be treated and closed accordingly. Depending on the extent of tumor surgery, the defect may after wound conditioning need to be closed by transplantation. If in a terminal stage the treatment of the tumor can only be palliative, the same applies to wound management. In this case, wound dressings serve the primary function of easing pain, absorbing malodours and maintaining the wound in a tolerable state for as long as possible. |
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Dr. rer
nat. Kerstin Ellermann |
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