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COMMON DERMATOLOCICAL PRESENTATIONS IN THE ELDERLY Dr Orlagh Mulholland ST5 Dermatology Discuss common skin conditions in Geriatric Dermatology How to recognise Objectives How to manage and treat QuestionsBiology of ageing skin Icthyosis • Characterized by pruritic, dry, cracked, and fissured skin with scaling. • Occurs most often on the legs of elderly patients but may be present on the hands and trunk. • porcelain. These cracks or fissures are present fromcracked epidermal water loss. If the skin splits and cracks deeply enough to disrupt dermal capillaries, bleeding fissures may occur. • Pruritis occurs leading to secondary lesions. Scratching and rubbing activities produce excoriations, an inflammatory response, lichen simplex chronicus, and even oedematous patches. Subsequently, environmental allergens and of allergic and irritant contact dermatitis, as well as infection Treatment Mainstay of Usually petroleum treatment is based e.g SWP/LP, emollients to keep Cetraben Reduce itch barrier function Ointment, Epaderm intact. Ointment Reduce Improve the barrier Prevent entry of transepidermal function irritants, bacteria water lossPruritis • Risk increases with age • Female > Male • Persistant scratching can develop Lichenification or Nodular Prurigo like lesions Localised •Rash •Neuropathic Systemic Causes •Uraemic •Hepatic – cholestasis •Haematological eg PCV •Endocrine – Graves, Diabetes Mellitus •Paraneoplastic eg NHL •Infection – HIV, Hepatitis C Full blood count, Iron, B12 and Folate Creatinine and renal function tests Liver function tests Investigations Thyroid function tests Erythrocyte sedimentation rate Chest radiography HIV serologyManagement • Emollients • Menthol aqueous cream • Antihistamines • Topical steroids/ calcineurin inhibitors• Doxepin • Mirtazepine • Gabapentin • Opioid antagonists • Phototherapy • Behavioural Therapy • ?MethotrexateVenous Eczema • AKA Varicose Eczema, Venous Insufficiency, Stasis Eczema • Who gets venous eczema? • Venous eczema is most often seen in middle-aged and elderly patients — it is reported to affect 20% of those over 70 years. It is associated with: • History of deep venous thrombosis in an affected limb • History of cellulitis in an affected limb • Chronic swelling of the lower leg, aggravated by hot weather and prolonged standing • Varicose veins • Venous leg ulcers• What causes venous eczema? • Fluid collects in the tissues and causes activation of the innate immune response. • Normally during walking the leg muscles pump blood upwards and valves in the veins prevent pooling. A clot in the deep leg veins (deep venous thrombosis or DVT) or varicose veins may damage the valves. As a result back pressure develops and fluid collects in the tissues. • An inflammatory reaction occurs.Clinical Features • Discrete patches or become confluent and circumferential. • Features include: • Itchy red, blistered and crusted plaques; or dry fissured and scaly plaques on one or both lower legs • Orange-brown macular pigmentation due to haemosiderin deposition • Atrophie blanche (white irregular scars surrounded by red spots) • 'Champagne bottle' shape of the lower leg — narrowing at the ankles and induration (lipodermatosclerosis) Venous Eczema and Lipodermatosclerosis Venous Venous Ulcer EczemaComplications Impetiginisation — secondary infection with Staphylococcus aureus resulting in yellowish crusts Cellulitis — infection with Streptococcus pyogenes: there may be redness, swelling, pain, fever, a red streak up the leg and swollen nodes in the groin Secondary eczema — the eczema spreads to other areas on the body ‘id reaction’ Contact allergy to one or more components of the ointments or creams used•TREATMENT • Reduce swelling in the leg • Don't stand for long periods. • Take regular walks. • Elevate feet when sitting: need to be above your hips to drain effectively • Elevate the foot of bed overnight • During the acute phase of eczema, bandaging is important to reduce swelling • When eczema has settled, wear graduated compression socks or stockings long term. Fitted moderate to high compression socks. • Light compression using travel socks may be adequate, and these are easy to put on. They can be bought at pharmacies, travel and sports stores. More compression is obtained by wearing two pairs.•Treat the eczema • Dry up oozing patches with potassium permanganate • Oral antibiotics such as flucloxacillin may be prescribed for a secondary infection. • Apply a prescribed topical steroid: start with a potent steroid cream applied accurately daily to the patches until they have flattened out. After a few days, change to a milder steroid cream until the itchy patches have resolved (maintenance treatment) • Using emollients frequently • Protect skin from injury: this can result in infection or ulceration that may be difficult to healTreatment for varicose veins Seek the opinion of a vascular surgeon regarding varicose veins These can be treated surgically, by endovenous laser, or sclerotherapy. Varicose veins may develop again after an apparently successful operation because venous disease is progressive.How can venous eczema be prevented? Venous eczema cannot be completely prevented but the number and severity of flare- ps can be reduced by the following measures. Avoid prolonged standing or sitting with legs down Wear compression socks or stockings Avoid and treat leg swelling Apply emollients frequently and regularly to dry skin Avoid soap; use water alone or non-soap cleansers when bathing What is the outlook for venous eczema? Venous eczema tends to be a recurring or chronic disorder lifelong. Treat recurrence promptly with topical steroidsULCERS • An ulcer is an area of full-thickness skin breakdown • VENOUS ULCERS A stasis ulcer is the most common cause of chronic full-thickness skin loss on the lower leg. The name implies that the veins are incompetent so that venous blood doesn’t flow properly from the leg back towards the heart. A stasis ulcer is also called a venous leg ulcer, a gravitational ulcer and a varicose ulcer (although the latter is an inappropriate name when varicose veins are not present)• Stasis ulcers affect 1% of the population. A variety of medical problems and lifestyle factors have been linked to their development. These include: • Increasing age • Previous deep venous thrombosis (DVT) • Obesity • Lower limb fracture, surgery or injury • Immobility • High blood pressure • Standing upright for long periods • Multiple previous pregnancies • Varicose veins • Stasis ulcers account for at least 40–50% of chronic lower limb ulcers and contribute to a further 20% of mixed arterial and venous ulcersStasis Ulcers are caused by: Venous Venous insufficiency hypertension OedemaFactors leading to venous insufficiency include: Venous obstruction from DVT or obesity The incompetence of the valves within the blood vessels Impaired venous pump, which requires muscle contractions. When blood is unable to be efficiently returned to the heart: Fluid leaks from the engorged blood vessels into surrounding tissues. The vessel walls become fibrotic (thickened).There is reduced delivery of oxygen and nutrients to the tissues. There is impaired removal of metabolic waste products. The tissues become inflamed. Wound healing is impaired. eventual skin breakdown, especially after an acute injury• What are the clinical features of stasis ulcers? • Being located on the lower legs, commonly the inner ankle or ‘gaiter’ region • Causing minimal pain • A tendency to be shallow, with lots of exudate. • Accompanying features confirming venous disease include: • Ankle swelling • Varicose veins • Red-brown skin discolouration due to haemosiderin deposition resulting from the breakdown of red blood cells • Dermatitis, either blistered and oozy, or dry and scaly, itchy skin • Lipodermatosclerosis (thickened, woody tissues) • Slow-growing, thick toenails.• What are the complications of stasis ulcers? • The main complication of stasis ulcers is an infection. Wound infection can impair the healing process. Bacteria colonise nearly all leg ulcers, but systemic antibiotics are not required unless clinical signs of infection are present. Signs that a stasis ulcer may require treatment with antibiotics include: • Redness and swelling of the skin surrounding the wound • Increasing warmth • Increasing pain • Increasing wound size • Increasing purulent discharge from the wound • Fever • Topical antibiotics are not recommended because they slow the rate of wound healing, despite their bactericidal properties• Stasis ulceration is usually a clinical diagnosis, made on the basis of the patient's history and examination findings, and includes the presence of risk factors for venous stasis, that is, congestion and slowing of venous circulation, and the characteristic features of the wound and surrounding tissues. • Duplex ultrasonography is used to confirm venous obstruction orvalvular incompetence prior to saphenous vein ablation surgery • Concomitant arterial disease is identified using the ankle-brachial index (ABI) • Other investigations to evaluate venous insufficiency and providehaemodynamic information may include: • Intravenous ultrasonography • Ascending or descending venography/phlebography (direct contrast, magnetic resonance) • Venous air plethysmography • Photoplethysmography • Lymphoscintigraphy • Liquid crystal thermography • Ambulatory venous pressure measurements • Arm-foot pressure differential tests • Venous function tests • Haematological studies of the coagulation systemTREATMENT • What is the treatment for stasis ulcers? • The treatment for stasis ulcers aims to address the underlying cause, provide symptomatic relief, and promote wound healing. • General measures • Aim for weight reduction if the individual is overweight. • Advise the individual to increase exercise to aid circulation. • Reduce leg swelling by getting the individual to elevate the leg above the level of the heart as frequently as possible, a minimum of 30 minutes, three times daily. • Compression • Compression is a mainstay of treatment for stasis ulcers. • Compression (eg, four-layer elastic bandaging) helps heal stasis ulcers, limits leg swelling and provides symptomatic relief. • Compression stockings are less effective in the treatment of established ulcers but are useful for wound prevention.• Local wound care • Adequate wound care involves keeping the wound clean and moist with regular dressing changes. • Debridement is used to remove dead tissue along the borders of the wound and excessive slough from the wound bed. • Treat venous eczema with topical steroids and regular emollients. • Medical and surgical treatment • Oral medications that affect blood flow, particularly aspirin, provide some benefit in promoting the healing of stasis ulcers. • Surgical interventions may help stasis leg ulcers heal and prevent their recurrence. • Superficial vein ablation reduces the backflow of blood from deep penetrating veins to superficial leg vessels; see leg vein therapies. • shown improvement with other measures.le, uninfected, large stasis ulcers who have not • In the case of a resistant stasis ulcer, other therapies may be tried, including: • Hyperbaric oxygen therapy • Medications that cause venous constriction, including flavonoids • Medications that affect blood flow, such as pentoxifylline • Therapeutic ultrasound and electromagnetic therapy.• What is the outcome for stasis ulcers? • Stasis leg ulcers are chronic and may persist for a few months to many years. Once they have healed, there is a high likelihood that stasis ulceration will recur, unless the underlying venous insufficiency is effectively treated Arterial Ulcers • An arterial ulcer is an ulcer due toischaemia. Arterial ulcers tend to occur on the lower legs and feet, and may be acute, recurrent or chronic. Ulcers may have multiple contributing factors; these ‘mixed ulcers’ constitute roughly 15% of all leg ulcers. • Who gets arterial ulcers? • Certain lifestyle factors and medical conditions have been associated with the development of arterial ulcers. These include: • Diabetes • Smoking • High blood fat and cholesterol • High blood pressure • Renal failure • Obesity • Rheumatoid arthritis • Clotting and circulation disorders • Other arterial disease, such as heart disease, cerebrovascular disease and peripheral vascular disease.• Arterial ulcers are caused by arterial insufficiency • Most often, an arterial ulcer develops following a minor injury that is slow to heal due to the poor blood supply to the wound. • In severe arterial disease, spontaneous cell death may cause skin breakdown without a precipitating injury. • Alternatively, cholesterol deposits lining the blood vessel walls may break off and become lodged in smaller vessels downstream, causing a sudden and complete blockage in flow; this process is called embolic occlusion.• What are the clinical features of arterial ulcers? • Distinguishing features of arterial ulcers include: • Located on the lower legs and tops of the feet or toes • A tendency to be painful, particularly at night • A symmetrical shape with well defined borders, often described as having a 'punched-out appearance' • Minimal bleeding when touched or knocked • Cool, pale or bluish surrounding skin that appears shiny • Loss of leg hair • Faint or absent ankle pulses. • Other symptoms of arterial insufficiency may also be present, such as: • Cramping pains in the buttocks and back of the legs during exercise, relieved by rest (intermittent claudication); this is due to insufficient oxygen supply to meet the increased needs of exercising muscle • Burning leg or foot pain at rest, which is relieved by lowering the foot and made worse by elevating it.• How are arterial ulcers diagnosed? • The underlying cause for a leg ulcer is diagnosed by taking a thorough patient history and a careful examination. Bedside tests include: • Capillary refill time—A prolonged capillary refill time may indicate arterial insufficiency in a patient with a lower limb ulcer, but it is a non-specific sign • A Buerger test —A positive test suggestive of arterial disease is marked by the patient's foot turning pale when elevated and subsequently becoming bright red when lowered below the bed • Ankle Brachial Pressure Index (ABPI)— this is where a Doppler probe is used to measure the blood pressure in both the ankle and arm. If the ratio of these two values is < 0.9, arterial disease is likely. A value of ≤ 0.5 suggests severe disease • Transcutaneous oximetry — this is a measurement of the skin oxygen content around a wound. Measurements < 40 mmHg indicate vascular insufficiency and < 20 mmHg indicates severe insufficiency• What is the differential diagnosis of an arterial ulcer? • venous disease • Diabetes • pressure injury • skin cancer and rare causes, • vasculitis • pyoderma gangrenosum• What is the treatment for arterial ulcers? • The treatment for arterial ulcers involves addressing the relevant factors contributing to arterial insufficiency and subsequent ulcer development in an individual. This may involve: • Lifestyle changes, such as stopping smoking and change of diet in order to reduce blood lipid and cholesterol levels or control blood sugar • Wound care — keeping the ulcer clean and moist by regularly changing wound dressings and physical or chemical debridement • Treating wound infection — it should be noted that although bacteria colonise nearly all leg ulcers, systemic antibiotics are not required unless clinical signs of infection are present • Topical antiseptics and topical antibiotics have been shown to slow the rate of wound healing despite their bactericidal properties and are not recommended• Surgical intervention • An arterial ulcer can be repaired by skin grafting or by a skin flap to cover the wound. • Surgical revascularisation of a limb aims to restore blood flow either by bypassing or angioplasty (re-opening) of narrowed vessels. This improves the healing of an ischaemic ulcer by restoring oxygen and nutrient supply to the tissue. Pyoderma Gangrenosum Presents as a rapidly enlarging, very painful ulcer. It is one of a group ofautoinflammatory disorders known as neutrophilic dermatoses. • Pyoderma gangrenosum is an uncommon disease that affects males and females of any age but is more common in those aged over 50 years. It is thought to be a reaction to an internal disease or condition. Known associations include: • Inflammatory bowel disease (ulcerative colitis and Crohn disease) • Rheumatoid arthritis • Myeloid blood dyscrasias including leukaemia • Monoclonal gammopathy (usually IgA) • Chronic active hepatitis • Granulomatosis with polyangiitis • PAPA syndrome • Use of levamisole-adulterated cocaine • About half of those affected by pyoderma gangrenosumhave none of the associated risk factors.• What are the clinical features of pyoderma gangrenosum? • Pyoderma gangrenosum usually starts quite suddenly, often at the site of a minor injury. • It may start as a small pustule, red bump or blood-blister. • The skin then breaks down resulting in an ulcer. The ulcer can deepen and widen rapidly. • Characteristically, the edge of the ulcer is purple and undermined. • Pyoderma gangrenosum is usually very painful. • Several ulcers may develop at the same time or over months to years. • Untreated, the ulcers may continue to enlarge, persist unchanged or may slowly heal. Treatment is usually successful in arresting the process, but complete healing may take months. This is particularly true if there is underlying venous disease, another reason for leg ulcers • Deep ulcers heal with scarring, and this is sometimes with a characteristic cribriform pattern. A rare superficial bullous variant of pyoderma gangrenosum may heal without leaving a scar. This may be similar to or confused with another neutrophilic dermatosis, acute febrile neutrophilic dermatosis (Sweet disease).• How is pyoderma gangrenosum diagnosed? • Pyoderma gangrenosum is diagnosed by its characteristic appearance and the severe pain. The pathergy test is usually positive • The wound should be swabbed and cultured for micro-organisms, but these are not the cause of pyoderma gangrenosum • A biopsy may be necessary to rule out other causes of ulceration. Pyoderma gangrenosum causes a neutrophilic inflammatory infiltrate, but this may be absent when on treatment • Mostly, blood tests are not particularly helpful. Some patients may have a positive ANCA• Treatment of pyoderma gangrenosum is mainly medical • The necrotic tissue should be gently removed. Wide surgical debridement should be avoided during the active stage of pyoderma gangrenosum because it may result in enlargement of the ulcer • Small ulcers are often treated with: • Potent topical steroid ointment (Dermovate) • Tacrolimus ointment • Intralesional steroid injections into the ulcer edge• Special dressings such as mepilex border • Oral anti-inflammatory antibiotics such as doxycycline or minocycline • If tolerated, careful compression bandaging to reduce swelling • Systemic treatment for larger ulcers due to pyoderma gangrenosum may include: • Oral prednisone for several weeks or longer, or intermittent intravenous methylprednisolone for 3–5 days • Ciclosporin • Biologic agents: success with infliximab, adalimumab, etanercept and ustekinumab is reported in a small number of cases (used off-label).• Other therapies may include: • Mycophenolate mofetil • Dapsone • Azathioprine • A tetracycline such as minocycline • Potassium iodide solution • Methotrexate • Cyclophosphamide • Chlorambucil • Intravenous immunoglobulins and plasmapheresis. • Expert wound care and pain management are essential. Once the disease is stable and inactive, surgical repair may be considered using a skin flap, skin graft, negative pressure wound therapy, and cultured skin. • Systemic therapy should be tapered slowly over several months.Pressure sores/ulcers • A pressure ulcer is an area of reddened skin that progresses to breakdown of skin and underlying tissue to form an erosion or ulcer, and is due to persistent pressure on the affected area. A pressure ulcer is also known as a bed sore, decubitus ulcer, pressure wound and pressure ulceration. • What causes a pressure ulcer? • A pressure ulcer is caused by a lack of blood flow due to mechanical stress on the skin and tissues over a bony area that has been under pressure for a prolonged period. If the blood supply is cut off to an area of skin for more than 2–3 hours, the skin is deprived of oxygen and begins to die. In addition, when slowly sliding down a bed or chair, friction to the outer skin layer — such as from wrinkled bedding and clothing — contribute to skin injury and ulceration. Excessive exposure to moisture, such as sweat, blood, urine or faeces, also increases the likelihood of developing a pressure ulcer.Most people with a pressure ulcer will feel some pain and itching. However, people who have impaired senses may not feel any pain even with a severe, deep sore.• Who is at risk of a pressure ulcer? • People whom are immobile due to illness or injury are at greatest risk of getting a pressure ulcer. • They may be wheelchair-bound or bedridden, and are unable to change position without assistance. • They may have nerve damage from injury or illness, such as spinabifida, diabetes or stroke, and are unable to sense pain or the signals that normally make people move. • Older people are at greater risk because their skin is thinner and more fragile. • An ulcer may develop underneath a plaster of Paris or fiberglass plaster (plaster ulcer).• Pressure ulcers are classified into stages according to wound severity. • Stage 1 • Skin is unbroken but shows a pink or reddened area • May look like a mild sunburn • Skin may be tender, itchy or painful • Stage 2 • Skin is red, swollen and painful • Blisters may be present • Upper layers of skin begin to die • Stage 3 • Ulcer has broken through the skin and wound extends down to deeper layers of skin tissue • Crater-like ulceration is present • Wound is prone to infection • Stage 4 • Sore extends past the skin and into fat, muscle and bone tissue • Blackened dead tissue called eschar may be seen in deep open wounds• Can pressure ulcers be prevented? • Pressure ulcers can be prevented with intensive nursing care. Measures to prevent pressure ulcers include: • Avoid and correct malnutrition if present (fluid, energy, protein, vitamins and minerals) • Daily inspection of an immobile person's skin to detect early redness • Frequent repositioning (every 2 hours) • Maintaining skin hygiene • Special foam, fibre and gels used as padding materials on chairs and beds to relieve the pressure on bony prominences • Powered alternating-pressure mattresses and overlays. • Prevention of pressure ulcers is the best approach, as an establishedpressure ulcer can be painful and even life threatening, it may also lengthen hospital stay• What is the treatment for a pressure ulcer? • A pressure ulcer can be difficult to treat once it has gone beyond stage 2. In the early stages when the skin is still intact, a pressure ulcer usually heals by itself if the pressure has been removed. Once the skin is broken, the main aim is to prevent infection and protect the sore so that it can heal. Special dressings and honey preparations may be used to help the healing process. Dead tissue may be removed with a scalpel (debridement). • Therapeutic devices used to treat a pressure ulcer include: • Topical negative pressure wound therapy (VAC®) • Hydrotherapy debridement, using saline solution in a syringe or a water pressure jet • Warming therapy, using radiant heat in a moist environment to maintain skin surface temperature of 37–38°C. • Deep pressure ulcers are very difficult to treat and often require surgical treatment to remove dead and decaying tissue. • Healthy skin may be grafted onto the damaged area. • Infection needs treatment with antibiotics • In severe or life-threatening situations, amputation of a limb may be necessary.Bullous Pemphigoid •subepidermal blistering disease.mune, •people over 80 years of age, and mostly affects people over 50. It can occur in younger adults, but bullous pemphigoid in infants and children is rare • The most common drugs associated with bullous pemphigoid are the PD1-inhibitor immunotherapies (such as pembrolizumab, nivolumab) used to treat metastatic melanoma and other cancers • Dipeptidyl peptidase four inhibitors used to treat diabetes (such as sitagliptin, saxagliptin and vildagliptin) • Other cases have been associated with penicillamine, furosemide, captopril, penicillin, sulfasalazine, topical fluorouracilClinical Presentation • Sever itch and (usually) large, tense bullae (fluid-filled blisters), which rupture forming crusted erosions. • Other variable features include: • Nonspecific rash for several weeks before blisters appear • Eczematous areas resembling nummular dermatitis • Urticaria-like red skin • Annular (ring-shaped) lesions • Smaller blisters (vesicles) • Prurigo nodules (pemphigoid nodularis) • Clear or cloudy, yellowish or bloodstained blister fluid • Postinflammatory pigmentation • Milia in healed areas • Bullous pemphigoid may be localised to one area, or widespread on the trunk and proximal limbs. • Frequently it affects the skin around skin folds. • Blisters inside the mouth and in genital sites are uncommon. • Some patients have a diagnosis of bullous pemphigoid made despite not having any bullae (non- ullous pemphigoid). This can affect any body site.•Complications • Bullous pemphigoid can be a serious disease, particularly when widespread or resistant to treatment. Morbidity and mortality result from: • Bacterial staphylococcal and streptococcal skin infection and sepsis • Viral infection with herpes simplex, varicella or herpes zoster • Complications of treatmentManagement • Biopsies for direct immunofluorescence (antibodies along the basement membrane that lies between the epidermis and dermis) • Histology shows a split under the epidermis. A dermal neutrophilic infiltrate is usual but not always present. Eosinophils prominent.• Adequate dressings are key for improvement • Aspirate Bullae keeping roof intact acts as barrier • Topical Dermovate ointment and non adhesive dressing such as Mepitel to eroded areas. • Mesorb • Alternate day dressings • Monitor for signs of infection - if suspected swabs for bacteriology and virology • Monitor for Oral and Occular involvement if occurs requires Oral Surgery and Ophthalmology input immediately.• Oral Prednisolone usually 0.5mg/kg reducing dose • Oral Doxycycline 100mg BD (anti-inflammatory benefit) • Long-term aim to wean off Prednisolone and switch to Steroid sparing agent such as Mycophenolite Mofetil or Azathioprine. • Treatment is usually needed for several years. In many cases, the pemphigoid eventually completely clears up, and the treatment can be stopped. If it recurs, it can be started againOther common skin issues • SEBORRHOEIC DERMATOSIS • A common, chronic or relapsing form of eczema/dermatitis that mainly affects the sebaceous, gland-rich regions of the scalp, face, and trunk . • There are infantile and adult forms ofseborrhoeic dermatitis. It is sometimes associated with psoriasis (sebopsoriasis). Seborrhoeic dermatitis is also known as seborrhoeic eczema. • Dandruff (also called ‘pityriasis capitis’) is an uninflamed form of seborrhoeic dermatitis.• The cause of seborrhoeic dermatitis is not completely understood. It is associated with proliferation of various species of the skin commensal Malassezia, in its yeast (non-pathogenic) form. Its metabolites (such as the fatty acids oleic acid, malssezin, and indole-3-carbaldehyde) may cause an inflammatory reaction. Differences in skin barrier lipid content and function may account for individual presentations.• Adult seborrhoeic dermatitis • Seborrhoeic dermatitis affects scalp, face (creases around the nose, behind ears, within eyebrows) and upper trunk. • Typical features include: • Winter flares, improving in summer following sun exposure • Minimal itch most of the time • Combination oily and dry mid-facial skin • Ill-defined localised scaly patches or diffuse scale in the scalp • Blepharitis: scaly red eyelid margins • Salmon-pink, thin, scaly, and ill-defined plaques in skin folds on both sides of the face • Petal or ring-shaped flaky patches on hair-line and on anterior chest • Rash in armpits, under the breasts, in the groin folds and genital creases • Superficial folliculitis (inflamed hair follicles) on cheeks and upper trunk • Extensive seborrhoeic dermatitis affecting scalp, neck and trunk is sometimes called pityriasiform seborrhoeide.TREATMENT • Treatment of seborrhoeic dermatitis often involves several of the following options. • Keratolytics can be used to remove scale when necessary, eg salicylic acid, lactic acid, urea, propylene glycol • Topical antifungal agents are applied to reducemalassezia eg ketoconazole, or azole antifungals. Try zincpyrithione or selenium sulphidemalassezia are resistant to • Mild topical corticosteroids are prescribed for 1–3 weeks to reduce the inflammation of an acute flare • Topical calcineurin inhibitors (Protopic) are indicated if frequent need for topical steroids. • In resistant cases in adults, oralitraconazole, tetracycline antibiotics or phototherapy may be recommended. Low dose oral isotretinoin has also been shown to be effective for severe or moderate seborrhoeic dermatitis. SCABIES Scabies is a very itchy rash caused by a parasitic mite that burrows in the skin surface. Scabies is nearly always acquired by skin-to-skin contact with someone else with scabies. •The contact may be quite brief such as holding hands with an infested child. •It is sometimes sexually transmitted. •Occasionally scabies is acquired via bedding or furnishingsCLINICAL FEATURES • Scabies causes a very itchy rash. It’s essential to search for burrows carefully in a patient with a severe itch, especially if the rash is mild. Contacts should be examined for burrows, whether or not they are itchy. • Itch • If it is the first episode of scabies, itch arises 4–6 weeks after transmission of a mite • It may occur within a few hours of subsequent infestation. • Itch is characteristically more severe at night, disturbing sleep • It affects the trunk and limbs, sparing the scalp. • Itch is mild or absent in some patients with crusted scabies. • Itch can persist for several weeks after successful treatment to kill the mites.• Burrows • Scabies burrows appear as 0.5–1.5 cm grey irregular tracks in the web spaces between the fingers, on the palms and wrists. They may also be found on or in elbows, nipples, armpits, buttocks, penis, insteps and heels. Dermatoscopic or microscopic examination of the contents of a burrow may reveal mites, eggs or mite faeces (scybala).• Generalised rash • Scabies rash is a hypersensitivity reaction that arises several weeks after initial infestation. It has a varied appearance. • Erythematous papules on the trunk and limbs, often follicular • Diffuse or nummular dermatitis • Urticated erythema • Vesicles on palms and soles • Acropustulosis (sterile pustules on palms and soles) in infants • Papules or nodules in the armpits, groins, buttocks, scrotum and along the shaft of the penis • Rare involvement of face and scalp.TREATMENT • Management of a scabies outbreak involves the identification and treatment of individual patients and household contacts with insecticides. Oral antibiotics are required for secondary infection • Careful attention to instructions is essential if scabies is to be cured • Topical insecticides is applied to the whole body from the scalp to soles. The usual topical treatment is 5% permethrin cream, left on the entire skin for 12 hours. It should be applied under fingernails using a soft brush • Oral ivermectin 200 mcg/kg is convenient, but more expensive than topical permethrin. It may be slightly less effective. Mainly used forNorweigan Scabies or in those unable to use topical treatments• 0.5% aqueous malathion lotion, left on for 24 hours • 25% benzyl benzoate lotion, applied daily for 3 days. This is irritant, and should not be used in children. • 2–10% precipitated sulphur ointment (pregnant) • Treatment should be repeated after 7 days after the first application to catch mites that have newly hatched. • Patients with crusted scabies may need repeated oral and topical treatments over several weeks or longer. • Additional management • Contacts must be identified and treated. In addition: • Bed linen, towels and clothing should be laundered after treatment. • Non-washable items should be sealed in a plastic bag and stored for one week. • Rooms should be thoroughly cleaned with normal household products. Fumigation or specialised cleaning is not required. • Carpeted floors and upholstered furniture should be vacuumed.REFERENCES • www.dermnetnz.org • Oxford Handbook of DermatologyEdition • Rook’s Handbook of Dermatology 9 Edition