Have you got skin problems?Is your skin itching, breaking out, covered in a rash, or playing host to strange spots?
To provide even greater transparency and choice, we are working on a number of other cookie-related enhancements. When hospitals fail to turn and reposition their patients, skin breakdown (like pressure sores) develop. Leg ulcers in diabetics are the result of nerve damage and arterial blockage, which reduces sensitivity of leg dermis towards heat, pressure and injury, causing continued damage and subsequently neuropathic ulceration. The positioning of ulcers with associated clinical characterization like callus, edema or decreased pulses, will determine the predominant cause of the leg ulcer. For any lower extremity ulceration, the best treatment remains prevention of ulcer development.
For patients with venous ulcers and arterial occlusive disease, compression therapy can be a hazardous procedure. Diabetic patients with arterial leg ulcer should consult a vascular surgeon to determine the probability for a peripheral revascularization therapy. The arterial ulcers will only recover with sufficient tissue oxygenation that may require a need for partial amputation of the leg. Intensive blood glucose management is must to slow the onset or progression of peripheral neuropathy for diabetic patients. Wound debridement is a process of removing nonviable tissue that if left, within the wound might lead to infection. In case of presence of osteomyelitis along with leg ulceration, the antibiotic therapy with surgical debridement is performed, to remove the infected bone. For diabetic leg ulcers, wound need to be kept moist and clean to prevent infection and promote granulation. If the moisture content of the skin varies significantly from normal values it can result either in dryness and cracking, or excoriation and the development of infection. The term maceration is commonly used to describe changes to the skin resulting from prolonged exposure to water or moisture from sweat, urine or faeces. Unlike 'maceration' the proposed new term can also apply to adverse changes caused by insufficient moisture within a wound or areas of vulnerable tissue.
Local treatment of moisture-related skin damage generally involves the use of dressings with significant fluid handling properties to remove excess fluid from the wound and to provide protection to periwound skin. This article describes the importance of controlling the moisture content of wounds and areas of vulnerable tissue, with particular emphasis on the use of dressings that provide protection to periwound skin, which may be damaged by proteolytic enzymes present in exudate from chronic wounds. The article also proposes a new definition for the 'ideal dressing' in the light of recent developments in the wound management field, which takes account of the requirement to protect vulnerable tissue from secondary damage caused either by insufficient or excessive moisture. It is suggested that the correct application and frequent replacement of appropriate dressings, combined with the use of skin protectants or barrier creams where appropriate, will help prevent periwound damage, reduce the risk of infection and improve patient quality of life. In a clinical context, 'maceration' is commonly used to describe changes in the appearance of the skin, resulting from prolonged exposure to moisture or wound exudate, the causes and treatment of which have been described comprehensively in a series of articles      .
In the present article it is argued that the widespread use of the term 'maceration' can be misleading, and that it is sometimes applied incorrectly, potentially leading to inappropriate treatment in some instances.
The skin, the largest organ in the human body with an area of approximately 1.8m?, plays an important role in fluid regulation. Moisture loss by evaporation (determined by intercellular lipids, which form a barrier to transepidermal water loss (TEWL)). This, in turn, is governed by the presence of intracellular water-soluble hygroscopic substances formed within the corneocytes by degradation of the histidine-rich protein known as filaggrin .
According to Verdier-S?vrain and Bont? , glycerol, a well-known cosmetic ingredient, has been discovered in the stratum corneum as a natural endogenous humectant.
The NMF can be readily released or extracted from the cells of the stratum corneum with water after first treating it with solvents or detergents to extract protective polar lipids such as sphingolipids, which exist in the intercellular spaces . If the fluid regulating ability of the skin is adversely affected, it makes it susceptible to dryness and scaling, particularly if the moisture content of the stratum corneum falls below about 10%. Most people are familiar with the skin changes that occur after spending too much time immersed in a hot bath. Similar changes can also result from simple occlusion, for example by the extended use of rubber or plastic disposable gloves.
In fact it is probable that the skin changes that occur from prolonged immersion in a bath result not just from absorption of water by the outer layers of the stratum corneum, but also by the accumulation of moisture in the deeper layers of the epidermis caused by the skin's inability to transpire excess water away in the form of sweat. These two simple examples clearly illustrate that major changes in the water content of the skin can be influenced by both endogenous and exogenous moisture. Irrespective of the cause, in the two simple examples cited above, the obvious change in the thickness and appearance of the skin is reversible and therefore does not normally represent any serious threat to the individual concerned. However, in the treatment of certain dermatological conditions associated with the formation of dry or cracked skin, such an effect may be clinically desirable. The skin changes described thus far are very different from those often observed around the margin of chronic wounds such as leg ulcers.
In such situations a barrier cream or a dressing that provides an effective seal to the periwound skin is probably indicated to provide a protective function.
A third commonly encountered cause of superficial skin damage is the presence of urine or faeces on the skin surface, the irritant nature of which can also lead to superficial damage (see Figure 3). Obese or neglected children and adults are further subject to intertrigo - chafing or excoriation between moist skin folds or adjacent surfaces.
Where skin is at risk, it is possible to apply topical agents such as zinc paste or modern proprietary skin protectants  that are easier and quicker to apply and remove  and which have the additional advantage of being transparent. Although the presence of liquid (be it urine, sweat or wound exudate) is undoubtedly a major contributory factor in all of these conditions, the skin does not have to be completely macerated in order for the damage to occur, which is why the term 'moisture-related skin changes' may be preferred. In direct contrast, conditions that lead to a depletion of the moisture content of the skin can also produce visible changes of varying severity. If the moisture content of the skin is seriously depleted, to below about 10%, it can result in dryness , leading to chapping or cracking, particularly on the fingertips or knuckles (see Figure 4). If the integrity of the epidermis is seriously compromised by trauma or some metabolic or physiological disorder, the healing rate of the resulting wound will be influenced by the moisture content of the surrounding skin and the local environment. In addition to facilitating healing, a product that maintains a moist environment can also help to prevent secondary damage to a vulnerable area of tissue that occurs as a result of dehydration. Work on burns reviewed by Lawrence  showed that the application of an occlusive dressing will salvage not only dermal tissue but also certain epithelial elements in the zone of stasis surrounding the original injury.
In the intervening period, developments in the wound management field coupled with an increased understanding of the wound healing process, have been such that the list of functions that a dressing may be required to perform have been revisited. These are summarised in Table 1, where they are divided into primary and secondary requirements. Even a cursory review of the performance requirements identified in Table 1 will indicate that it is unlikely that a single dressing or dressing system will possess all of these attributes. A dressing that is ideally suited to the early stages of the treatment of infected, malodorous or necrotic wounds may not be appropriate for the later stages of healing. It will be seen that this definition applies equally to products designed to achieve debridement, combat odour or infection, or promote granulation or epithelialisation.
In the list of dressing functions identified previously, the primary performance requirements that are influenced by the condition of the wound are directly or indirectly related to the management of exudate or TEWL - the principal causes of maceration. In clinical practice, although some dressings such as hydrogels are used to rehydrate eschar in order to promote autolytic debridement, the majority are applied to remove excess wound fluid (exudate) from the immediate vicinity of the wound. With the exception of the vacuum assisted closure technique (VAC? Therapy), in which fluid is actively withdrawn from the vicinity of the wound before it has time to spread onto the surrounding skin, exudate control with many advanced and traditional types of dressings is commonly achieved by one or more different mechanisms. The presence of materials with high absorption retention greatly improves the ability of a dressing to retain liquid under pressure as the fluid is 'locked away' within its structure. It is self-evident that the absorbent capacity of any dressing is finite, limited by size (area) and volume, and although in theory it is possible to increase the absorbent capacity by simply increasing dressing thickness, this impacts negatively upon conformability and patient comfort. A third fluid handling mechanism is therefore often employed, which involves the incorporation of a semipermeable film or foam backing layer into the dressing's structure.
A further important component included in many dressings is a wound contact layer that is designed to reduce the possibility of adherence of the dressing to the surface of a drying wound. Many dressings, as they take up fluid, transport this laterally throughout the absorbent layer, including the inner surface that is in direct contact with the skin. The presence of a suitable wound contact layer can reduce although not eliminate this effect entirely as it forms an interface layer that physically separates the moist dressing surface from the periwound skin. In the case of a chronic wound that contains high concentrations of proteolytic enzymes, this may lead to excoriation of the skin with consequent enlargement of the wound itself.
An alternative method of preventing this problem involves the use of a dressing that forms an adhesive bond or seal with the skin right up to the margin of the wound. A similar sealing effect is achieved in products coated with soft silicone technology in which an absorbent layer of foam, backed with a polyurethane membrane, is coated with a layer of soft silicone that forms a gentle bond or seal between the dressing and the wound in order to ensure that fluid is taken up by the dressing and does not escape on to the surface of the skin.
Such products differ from dressings in which an absorbent pad is located in the centre of a sheet of foam or film coated with adhesive to form an island dressing. A soft silicone dressing was compared with an island dressing in a clinical study involving 38 patients.
It is vital, however, that all dressings used in this way are either sufficiently permeable to moisture vapour or have sufficient fluid affinity to cope with TEWL through the intact skin. Hard data on the effect of moisture-related skin changes on treatment costs are hard to find, and the author is unaware of any dressing studies specifically focused on this area. Given the multiplicity of dressings available and the clinical and financial implications of significant maceration, it might be supposed that the medical literature would contain a wealth of information on the treatment of this condition. The authors also considered the evidence for the use of honey, topical negative pressure therapy, compression therapy and the use of a skin protectant. In the absence of hard evidence from controlled studies, best practice standards based on expert opinion supported by laboratory or other experimental data (where relevant) must be used to guide clinical practice.
For example, despite the lack of published data, many clinicians would accept that the use of compression, which reduces oedema and exudate production, will almost inevitably impact upon maceration. In most instances it is likely that periwound skin damage, regardless of its primary cause, may be prevented by the adoption of simple measures including the application and frequent replacement of appropriate dressings, and the use of skin protectants or barrier creams combined with good nursing practice. Historically, the selection of a dressing was determined by a number of factors, the majority of which were related to the position and nature of the wound, with particular attention paid to the presence of infection, odour and the amount of exudate present.
AcknowledgementThis article was sponsored by an unrestricted educational grant from M?lnlycke Health Care.
Please specify in the message section below which office you would like to be seen at. It has a distinctive anti-inflammatory and healing power with broad spectrum antimicrobial effect. Skin inflammation, changes in texture or colour and spots may be the result of infection, a chronic skin condition, or contact with an allergen or irritant.
It is intended for general information purposes only and does not address individual circumstances. American hospitals recently implemented the chart on the left in an effort to prevent pressure sores. While treatment of hospital bedsores is expensive, it is a requirement to maintain the patient’s health.
Patients with decubitus ulcers are at a higher risk of infection (like sepsis) and disease by way of their open wounds. Leg ulcers are the result of venous insufficiency, peripheral arterial occlusive disease or peripheral neuropathy. Infection of a leg ulcer further increases the risk of severe damages that need to be controlled, through systemic therapy. Edema need to be well managed with help of mechanical therapy, for treating venous insufficiency. Compression stocking increases the healing rate of ulcers and lowers the chances of its recurrence, by reducing venous hypertension, increasing fibrinolysis and improving the microcirculation of the skin.
The therapy may involve less or more invasive vascular procedures that help to elevate the peripheral blood flow. Hence, a vascular surgeon must be consulted for arterial ulcers, to determine the right level of amputation, whenever necessary.
Once ulceration initiates, treatment focuses on debridement (removal of dead or infected tissue), pressure relief and treating the core infection. Platelets get accumulated in the debrided wound, thereby promoting the inflammatory stage of wound healing. Topical growth factors, silver impregnated dressings, negative pressure wound therapy and living skin equivalents are amongst the various adjunctive therapies available at the specialist end that can be employed to treat wound, during leg ulcer care.
However, the widespread use of the term maceration can be misleading and may potentially lead to inappropriate treatments. This encompasses skin changes such as superficial damage including nappy rash and intertrigo, as well as severe excoriation caused by the efflux of proteolytic enzymes from chronic wounds such as leg ulcers.
Sometimes, however, dressings are applied to donate or conserve moisture in order to prevent desiccation and tissue death. It also discusses the importance of preventing excessive moisture loss from certain wound types and describes the way in which dressings can donate or conserve moisture in such situations. The total volume of fluid held in the skin of a 70kg man is about 7 litres, but the moisture content varies throughout its structure. Together these comprise around 30% of the stratum corneum and are known as natural moisturising factor (NMF), consisting of 40% free amino acids, 12% prolidine carboxylic acid, 12% lactate and 7% urea, together with minerals, electrolytes and sugars. Hyaluronan, which is regarded principally as a dermal component, is also present in the epidermis, where it helps to maintain the structure and epidermal barrier function.
It has also been demonstrated that repeated exposure to water can adversely affect the fluid control mechanisms of the skin by depletion of NMF even without prior solvent extraction .
These are characterised by pronounced softening, swelling and wrinkling of the epidermis, which certainly may be described as maceration according to the strict definition of the term. The relatively impermeable nature of these materials prevents normal TEWL, which in turn leads to the accumulation of moisture within the skin and, ultimately, the same softening and wrinkling as described above. In a hot bath, the situation is actually exacerbated by the fact that the capillaries within the skin are dilated as the body attempts to produce increased sweat as part of its normal temperature-regulating process.
However, while in this condition the skin is more susceptible to physical damage, and its protective barrier properties to chemicals and micro-organisms are impaired. In such situations, oily emollients added to the bath, which form a film on the surface of the water, are transferred to the skin as the person rises out of the water. While these skin changes may be partly due to maceration, which predisposes the affected area to traumatic injury (which may also be caused by some types of adhesive dressings), a second and potentially more important factor is the presence within chronic wound fluid of proteolytic enzymes. In one clinical study it was reported that maceration occurred in 55% of ulcers under investigation .
Every year pharmaceutical and cosmetic companies spend millions of pounds in developing and promoting products designed to improve the moisture content of the skin and reduce the appearance of lines and wrinkles.
In extreme cases, total dehydration caused by death of the underlying dermal structures will lead to the formation of a dry black leathery eschar, commonly associated with pressure ulcers (see Figure 5). Too dry and epithelialisation will be delayed, too wet and there is a risk of maceration and infection .
The capacity of deep partial thickness wounds to undergo spontaneous healing depends upon the survival of epidermal cells in hair follicles and sweat glands in the base of the wound; if these are allowed to become dehydrated and devitalised the wound may actually increase in size and convert from a partial-thickness to a full-thickness injury. The use of traditional dry dressings in these situations can result in progressive dehydration of the threatened zone followed by devitalisation and necrosis, with the result that this zone becomes indistinguishable from the original lesion.
Primary requirements are those that are common to most wound management materials; secondary requirements relate to specific types of wounds or wounds in a particular condition or stage in the healing process. For example, sterile maggots represent arguably the most rapid and cost-effective non-surgical method for achieving a clean wound bed, but few would suggest that they should be applied to all types of wounds throughout the entire healing process.
It follows, therefore, that for some wounds, but by no means all, optimal wound management may involve the sequential application of a number of 'ideal dressings' that are selected according to the condition of the wound as it progresses towards healing. Most products possess some absorptive capacity that may be provided by means of absorbent fibres or foam that rapidly take up fluid from the wound surface. This can be particularly important in the case of products made from foam which, although capable of taking up significant volumes of fluid, do not necessarily retain this well under compression.
Such layers permit the loss of fluid by evaporation through the back of the dressing while preventing the ingress or egress of liquid or micro-organisms.
Available in many forms, including perforated plastic films or nets, these layers are most commonly used in dressings that have an absorbent layer made from foam or cellulose fibre. This can increase the moisture content at the skin surface, which in turn may lead to maceration or other moisture-related effects described previously. If the wound is heavily exuding and the absorbent capacity of the dressing is insufficient to cope with all the fluids produced, exudate may accumulate in the defect and then gradually spread across the surface of the skin beneath the wound contact layer. An early example of such a product is the hydrocolloid dressing, which has one surface that is uniformly coated with an adhesive gel-forming mass. In clinical studies such dressings have been shown to facilitate vertical wicking and reduce periwound maceration and pain  . When selecting such a dressing its island area must be larger than the wound itself so that it covers the wound area by some distance and overlaps the surrounding skin. Although healing rates were similar in the two treatment groups, as might be predicted, the incidence of maceration and local skin damage was significantly greater in the group treated with the island dressing .
It is not unreasonable to assume, however, that secondary damage caused in this way will delay healing and extend treatment times - with obvious financial implications for dressing usage, nursing time and, potentially, extended periods of hospitalisation. In fact, in 2007 a systematic review of the literature relating to the management of maceration of the periwound skin  identified nine relevant articles and in only six of these was maceration cited as a primary or secondary outcome variable.
While there was reasonably strong evidence to support the use of skin protectants, the authors found no supporting evidence for the other treatment modalities .
It must also be remembered that absence of evidence of effectiveness is not the same as evidence of ineffectiveness. Similarly the application of topical negative pressure, which continuously removes exudate from the immediate vicinity of a wound, will reduce the possibility of skin damage caused by the spread of irritant wound fluid over the periwound skin.
These simple measures should impact favourably on the patient's quality of life by reducing the pain and some of the inconvenience associated with a heavily exuding wound. Relatively little attention was given to the management of periwound skin or the effect that the choice of dressing system might have on this potentially vulnerable area. The situation has been further improved by the advent of effective skin-friendly adhesive systems which form an effective seal between the dressing and the skin around the wound margin, and which also permit replacement of dressings without the production of the pain or trauma sometimes encountered with traditional adhesive materials . It is not a substitute for professional medical advice, diagnosis or treatment and should not be relied on to make decisions about your health. The pressure sore flow chart diagram offers insight into the steps a hospital nurse or doctor should take to prevent bedsores in hospital patients. Bedsore patients also suffer painful decubitus ulcer wounds which require debridements and surgery. One may also make use of multilayer of compression bandages to effectively reduce the edema.
The dermis contains about 80% water and the stratum corneum about 30%, which is non-uniformly distributed, varying from around 40% in the inner layers to around 10-15% in the outermost horny layer .
For a more comprehensive review of the fluid control mechanisms of the skin, see Agache and Black . A water-transporting protein, aquaporin-3, has additionally been discovered in the viable epidermis. These effects are generally assumed to be caused by absorption of the bath water by the outer layer of the skin. Occluded (macerated) skin has also been shown experimentally to be more sensitive to irritants . This thin oily layer helps to conserve any additional moisture taken up in the stratum corneum during bathing.
These can chemically degrade exposed skin, resulting in a red, weeping surface (see Figure 1). Maceration is a particular problem in diabetic ulcers , which in common with heavily exuding ulcers of all types, require frequent re-dressing to avoid or reduce damage to the surrounding skin   (see Figure 2).
When the occlusive effects of a nappy are not matched by its absorbency, hyperhydration of the stratum corneum occurs that progresses to maceration, increasing the coefficient of friction of the skin and predisposing to epidermal damage caused by rubbing. The prevention of dehydration by the application of a suitable occlusive or semipermeable dressing may limit or prevent these secondary effects. In both groups, the performance requirements have been divided into those which are determined principally by the design and construction of the dressing, over which the clinician has little or no influence, and those in which the ability of the product to perform in the required fashion is also influenced to a significant extent by the nature and condition of the wound. Similarly, a dressing that promotes angiogenesis and the production of granulation tissue may not be equally suitable for the final epithelialisation stage of wound closure.
Depending on the design of the dressing, this is then distributed throughout the body of the absorbent layer, spreading both laterally and vertically towards the outer surface. Unlike the finite absorption capacity, the ability of the dressing to cope with exudate by evaporation is relatively unlimited, and is determined only by the permeability of the membrane relative to the rate of exudate production by the wound. The moist layer forms a pathway along which micro-organisms can migrate, either into or out of the wound.
Provided that the seal remains intact, such a dressing is able to form a very effective protective covering to the healthy skin while absorbing (gelling) exudate in the immediate vicinity of the wound.
However, when using this technique, it is important to consider the moisture vapour permeability of the film component of the dressing system for if this is too low it could actually cause maceration of the periwound skin by preventing TEWL. It was often tacitly accepted that wound fluid would inevitably escape from a heavily exuding leg ulcer on to the surrounding skin under the effects of gravity and there was relatively little that could be done to prevent this, other than to apply large quantities of bulky padding in an attempt to absorb the excess fluid. Prevention and treatment of moisture-associated skin damage (maceration) in the periwound skin. Effect of soaking and natural moisturizing factor on stratum corneum water-handling properties.
The silver-releasing foam dressing, Contreet Foam, promotes faster healing of critically colonised venous leg ulcers: a randomised, controlled trial.
Comparison of two periwound skin protectants in venous leg ulcers: a randomised controlled trial. Formation of the scab and the rate of epithelization of superficial wounds in the skin of the young domestic pig. A note on wound healing under dressings with special reference to perforated-film dressings.
A study to compare a new self-adherent soft silicone dressing with a self-adherent polymer dressing in stage II pressure ulcers.
Yet, while many are minor, they may indicate something more serious, so always seek medical advice for correct diagnosis. Never ignore professional medical advice in seeking treatment because of something you have read on the BootsWebMD Site.
However, once a bedsore deteriorates to a Stage III or Stage 4 decubitus ulcer, it becomes harder to heal. This figure can increase to around 60% when the skin is immersed or exposed to a very wet environment . All these findings have brought new insights into the mechanisms of skin water distribution and barrier function.
The water then permeates the intercellular spaces, crosses cell membranes and swells the corneocytes . When exposed to a warm dry environment the skin returns to normal in minutes and no further treatment is indicated or required. Faecal enzymes (urease, proteases and lipases) also can have a deleterious effect on the skin . And a film dressing that may provide ideal conditions for the final stages in the healing process of an epithelialising wound, will not be suitable for a slough-filled heavily exuding infected leg ulcer.
At this point a second mechanism of action may come into play in which the absorbed fluid comes into contact with gel-forming agents located within or behind the absorbent layer. The relative importance of these fluid handling mechanisms is determined by the structure, composition and physical characteristics of the various components from which the dressing or dressing system is constructed.
If the adhesive seal fails around the wound margin, however, exudate contained within the vicinity of the wound will escape and flood over the skin, leading to maceration or excoriation by the mechanisms described previously. If the skin changes also contribute to the development of infection, there may be additional costs for systemic antimicrobial therapy.
Products made from alginate or carboxymethylcellulose fibre are particularly prone to this problem, especially if they are not used with appropriate secondary dressings .
Blow the whistle, expose the elder neglect, file an administrative report with the hospital and file a decubitus ulcer lawsuit with a decubitus ulcer lawyer. In elderly or immobile patients, maceration secondary to incontinence of urine or faeces is sometimes regarded as a precursor to skin damage caused by pressure and shearing effects, leading to pressure ulcer formation or extension . These gel formers may be derivatives of starch, or superabsorbent polymers that possess a remarkable affinity for liquid.
As in many areas of clinical practice, prevention of moisture-related skin changes is better (and cheaper) than cure.
Debridements and plastic surgery are possible treatment solutions for Stage 4 decubitus ulcers.
Sometimes, as in the case of dressings made from alginate, the absorbent and gel-forming layers are one and the same. Most people recover, but pain, numbness, and itching linger for many and may last for months, years, or the rest of their lives. Speak with a decubitus ulcer lawyer to obtain relevant legal advice specific to your potential case. The hiring of a lawyer is an important decision that should not be based solely upon advertisements.
Hives (urticaria)Hives, a common allergic reaction that looks like welts, are often itchy, stinging, or burning. Severe hives can be associated with difficulty breathing (get immediate medical attention if this occurs). Medication, foods, or food additives, temperature extremes, and infections like a sore throat can cause hives. PsoriasisA non-contagious rash of thick red plaques covered with silvery scales, psoriasis usually affects the scalp, elbows, knees, and lower back. The precise cause of psoriasis is unknown, but the immune system mistakenly attacks skin cells causing new skin cells to develop too quickly. EczemaEczema describes several non-contagious conditions where skin is inflamed, red, dry, and itchy. Stress, irritants (like soaps), allergens, and climate can trigger flare-ups though they’re not eczema's cause, which is unknown.
Treatments include emollient creams and ointments, steroid creams and ointments, antibiotics and antihistamines.
RosaceaOften beginning as a tendency to flush easily, rosacea causes redness on the nose, chin, cheeks, forehead, and can cause eye irritation. If left untreated, bumps and pus-filled pimples can develop, with the nose and oil glands becoming bulbous.
Rosacea treatment includes topical gels, medication, as well as surgery to remove blood vessels or correct nose disfigurement.
Rash from poisonous plantsMost plants in the UK will not give you a rash, but the same is not always true on holiday abroad where you may be in contact with species that don't grow here. For example, in the US, contact with sap from poison ivy, oak, and sumac causes a rash in most people. The typical rash is arranged as a red line on an exposed area, caused by the plant dragging across the skin. The sharp edge of closely shaven hair can curl back and grow into the skin, causing irritation and pimples, and even scarring. To minimise razor bumps, have a hot shower before shaving, shave in the direction of hair growth, and don't stretch the skin while shaving. Skin tagsA skin tag is a small flap of flesh-coloured or slightly darker tissue that hangs off the skin by a connecting stalk.
They’re usually found on the neck, chest, back, armpits, under the breasts or in the groin area. Skin tags are not dangerous and usually don't cause pain unless they become irritated by clothing or nearby skin rubbing against them.
Have a medical check-up for moles that change, have irregular borders, unusual or uneven colour, bleed or itch. Age, sun or liver spots (lentigines)These pesky brown spots are not really caused by ageing, though they do multiply as you age.
They're the result of sun exposure, which is why they tend to appear on areas that get a lot of sun, such as the face, hands, and chest. To rule out serious skin conditions such as melanoma, seek medical advice for correct identification. Pityriasis roseaA harmless rash, pityriasis rosea usually begins with a single, scaly pink patch with a raised border. Days to weeks later, salmon-coloured ovals appear on the arms, legs, back, chest, and abdomen, and sometimes the neck. The rash, whose cause is unknown, usually doesn't itch, and usually goes away within 12 weeks without needing treatment.
MelasmaMelasma (or chloasma) is characterised by brown patches on the cheeks, nose, forehead and chin.
Melasma may go away after pregnancy but, if it persists, can be treated with prescription creams and over-the-counter products. Cold soresSmall, painful, fluid-filled blisters around the mouth or nose, cold sores are caused by the herpes simplex virus.
Antiviral pills or creams can be used as treatment, but seek medical advice immediately if sores contain pus, you have a fever greater than 38C, or if your eyes become irritated. WartsCaused by contact with the contagious human papillomavirus (HPV), warts can spread from person to person or via contact with something used by a person with the virus. You can prevent spreading warts by not picking them, covering them with bandages or plasters, and keeping them dry. Seborrheic keratosisNoncancerous growths that may develop with age, seborrhoeic keratoses can appear anywhere on the body - but particularly on the chest or back - alone, or in groups. They may be dark or multicoloured, and usually have a grainy surface that easily crumbles, though they can be smooth and waxy. Because seborrheic keratoses may be mistaken for moles or skin cancer, seek medical advice for correct diagnosis.
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