between people Can develop glaucoma with \200\230normal pressure-normal tension glaucoma \200\231 (may be high for that person/other factors such as ischaemia may be relev ant). More common in older patients. Fluctuating BP may be contributory Can have \200\230high \200\231 pressures without glaucoma \200\224 \200\230ocular hyperten sion \200\231 \200 Symptoms depend on rate and degree of rise in pressure. Generally asymptomatic unless advanced or acute Primary ( \200\230chronic \200\231) open-angle glaucoma \200 Most common \200 Failure o f out \202 ow of aqueous causes slow rise in pressure, allowing adaptation, so subtle symptoms No pain, corneal cloudiness, or haloes \200 Slow loss of visual \201 eld, typically in an arc shape ( \200\230arcuate scotoma \200\231) with preservation of central vision (macul a has more nerve cells so is relatively protected). Progresses to tunnel vision, and then b lindness Risk factors \200 Age (1 % in 5th decade, rising to 10 % in 9th decade) \200 African Ca ribbean origin (four times risk) \200 Blood relatives with glaucoma Screening \200 Targ et those at higher risk \200 Combination of ophthalmoscopy (looking for disc \200\230cup ping \200\231), automated perimetry testing (for minor \201 eld defects) and tonometry (for intraocular p ressure) is best \200 Most cases picked up by optometrists \200 Encourage regular eye t ests, and include careful fundoscopy in physical examination GLAUCOMA 575 Treatment \200 Topical treatments (eye drops): B -blockers, eg timolol (decrease aqueous secretion. Can cause systemic B -blockade); prostaglandin analogs eg latanoprost (improve d rainage, may darken iris); A -agonists (decrease aqueous production); carbonic anhydrase in hibitors, eg dorzolamide (decrease aqueous secretion); parasympathomimetics, eg pilocarpine (constrict pupil so will reduce visual \201 eld \200\224 not commonly used) Oral treatments: carbonic anhydrase inhibitors, eg acetazolamide very powerful, with many s ide effects including electrolyte imbalance and paraesthesia of extremities Surgical treatment: trabeculectomy \200\224 operation to improve aqueous out \202 ow. Arg on laser trabeculoplasty (applied to the trabecular meshwork) may be effective. Cyclodiode laser to the ciliary body (decreases production) is used in refractory cases Support group: International Glaucoma Association ( M www.iga.org.uk ) Acute angle closure glaucoma 2Emergency sight-threatening condition \200\224 requires urge nt referral and treatment. \200 Apposition of lens to the back of the iris prevents out \202 ow of aqueous with a rapid rise in pressure Causes red, painful eye with vomiting, blurred vision, and haloes around lights (due to corneal oedema) May be precipitated by pupil dilation, eg at dusk. Pupil constricts when asleep so episodes at night may be aborted by sleep \200 Very rarely can be precipitated by anticholinergic drugs \200 More common in older patients, women, and longsighted indiv iduals \200\224 beware of the vomiting older woman with a red eye On examination cornea is usually cloudy and visual acuity signi \201 cantly reduced (eg counting \201 ngers) Treat urgently with iv acetazolamide, topical glaucoma treatment, and laser iridotomy to re store \202 ow. Treat other eye prophylactically with laser iridotomy to prevent pupillary block 576 CHAPTER 22 Eyes Age-related macular degeneration Age-related macular degeneration (AMD) is the most common cause of adult blind registrations in UK and USA. 2New treatments for early stages make det ection crucial. De \201 nition As it sounds \200\224 age-related degenerative changes affecting the macul a (central part of the retina responsible for clear central vision). Two types: 90 % dry with gradual onset of symptoms (drusen and atrophy of the retinal pigment epithelium) 10 % wet , where symptoms relate to leaking vessels causing distortion or sudden loss of ce ntral vision due to sub-macular hemorrhage (choroidal neovascularization \200\224 new vess els can leak, bleed, and scar causing visual loss in a few months) Prevalence \200 Increases with age \200 25 \200\22330 million worldwide \200 Up to 30 % of > 75s may have early disease, and 7 % late disease Risk factors \200 Cause unknown \200 Age, smoking, family history are strongly associat ed \200 Female sex, Caucasian race, hypertension, blue eyes, other ocular conditions (len s opacities, aphakia) and low dietary antioxidants Symptoms \200 Asymptomatic in early stages, progressing to loss of central vision \200 May also have decreased contrast and color detection, \202 ashing lights and hallucinations Distortion of straight lines is a feature of wet AMD \200 Peripheral vision is normal in absence of other pathology Detection \200 Regular ocular examination \200 Use of Amsler grid in high risk patients (Fig. 22.1 ) Prognosis \200 Dry AMD progresses slowly and rarely causes blindness \200 Wet AMD may p rogress rapidly (blind in under 3 months) and accounts for 90 % of AMD blind registrations. Sudden onset of distortion of central vision should prompt urgent referral Bilateral disease \200\224 42 % with wet AMD will develop this within 5 years AGE-RELATED MACULAR DEGENERATION 577 Prevention \200 Smoking is the most important modi \201 able risk factor \200 A diet r ich in fruit and vegetables reduces risk \200 A combination of B -carotene, vitamins C an d E, and zinc is effective in preventing severe visual loss in established moderate-severe AMD A multicentre study showed that antioxidant vitamins halted progression of dry AMD in around 30 % of patients Management \200 Appropriate for subset of wet AMD only \200 Halts progression so early treatment is desirable \200 Fluorescein angiography should be done within a few days of o nset of symptoms to determine the type and location of neovascular areas Treatment options for neovascular AMD include: \200 Photodynamic therapy \200\224 this t argets sub-foveal neovascular areas (whilst preserving normal retina) by using photosensiti ve drug (vertepor \201 n) along with a non-thermal activating laser. Used in early disease , this therapy can slow or halt progression Anti-angiogenic therapy \200\224 eg ranibizumab \200\224 a recombinant, humanized, monocl onal antibody that neutralizes all active forms of vascular endothelial growth factor A. NI CE recommends its use for wet AMD under certain conditions (eg no permanent damage to the c entral fovea). The cost of ranibizumab beyond 14 injections in the treated eye is met by th e manufacturer Laser photocoagulation is sometimes used for extra-foveal lesions 578 CHAPTER 22 Eyes HOW TO Use an Amsler grid to detect macular pathology Fig. 22.1 Amsler grid. \200 Test one eye at a time \200 Usual reading glasses should be worn, and the grid held at comfortable reading distance Ask the patient to look at the central spot, and not to look away \200 Assess the followi ng: Can all four corners of the grid be seen? \200 Are any of the lines missing, wavy, blurre d, or distorted? \200 Do all of the boxes appear the same size and shape? \200 Any abno rmalities may indicate macular pathology and should prompt referral to an ophthalmologist THE EYE AND SYSTEMIC DISEASE 579 The eye and systemic disease Two of the top four causes for blind registration are due to s ystemic disease \200\224 diabetes and vascular disease. Eye disease develops as a late com plication of prolonged poor control in both cases, and the important message is to strive t o prevent these problems in the \201 rst place. Diabetes Causes retinopathy, cataracts, and \200\230microvascular \200\231 cranial nerve p alsies. Retinopathy \200 Associated with increasing duration of diabetes \200\224 at 20 years, 8 0 % will have some retinopathy All patients with diabetes require dilated annual screening (either photographic, or by app ropriately trained professional). Direct ophthalmoscopy alone is inadequate Appearance: microaneurysms, hemorrhages, (background retinopathy) progressing to cotton wool spots, blot hemorrhages and tortuous vessels (pre-p roliferative retinopathy) then new vessels (proliferative retinopathy). Exudates and macula r oedema are indicators of maculopathy Early detection of problems (especially when near the macula) should prompt referral to an ophthalmologist. Sight-threatening retinopathy requires laser treatment to limit progressio n 2A diabetic person diagnosed at age 70 may well live 20 years, so tight control is desirabl e. Meticulous control of diabetes and hypertension has been shown to reduce all complicatio ns including retinopathy. Vascular disease \200 Affects the eye directly with hypertensive retinopathy, and more indirectly when cerebrovascular disease impacts on vision. Associated with \200\230microva scular \200\231 cranial nerve palsies Early detection and control of risk factors for vascular disease will ameliorate this problem (see b \200\230HOW TO Protect your patient from another stro ke \200\231, p.195). Tight blood pressure control, smoking cessation, lipid lowering, diabe tic control, and appropriate anti-platelet use should all be targeted at the older age grou p as aggressively as the younger patients There is little in the way of treatment for the disease once it is established Appearance: silver wiring, arteriovenous nipping, and arteriolar narrowing progressing to exudates, cotton wool spots, hemorrhages and papilloedema Giant cell arteritis See b \200\230Giant cell arteritis \200\231, p.474. 580 CHAPTER 22 Eyes Drugs and the eye Many drugs that are frequently used in the older patient can cause ocular side effects. Older people are more vulnerable to developing side effects, but are least l ikely to report them (attributing it to part of getting older). Direct toxicity \200 Chloroquine and hydroxychloroquine (used in treatment of rheumatoid arthritis and other connective tissue diseases as well as malaria) cause a toxic maculopathy in large prolonged doses Phenothiazines used for a long time (to treat psychosis) may cause retinal damage Tamoxifen (for breast cancer treatment) may cause maculopathy \200 Amiodarone (for arrhyt hmias) may cause cataracts \200 Ethambutol (anti-tuberculous) can cause optic neuritis an d red/green color blindness Altering accommodation Causes blurred vision \200 Antihistamines \200 Some antihyperten sives Decreasing pupil size Causes less light accommodation. \200 Opiates \200 Miotic drops u sed for glaucoma Steroids \200 Oral steroids over time can cause cataracts \200 Topical and oral steroid s may raise the intraocular pressure This page intentionally left blank 582 CHAPTER 22 Eyes Eyelid disorders Eyelids provide physical protection to the eyes and ensure normal tear \201 lm and drainage. Disorders are common in older people, are often uncomfortable and yet are under-recognized and under-treated. Entropion In-turning of the (usually) lower lid. Occurs as orbicularis muscle weakens with age (or with conjunctival scarring distorting the lid). Lashes irritate the eye and may abr ade the cornea, causing red eye. Lubricants and taping of the eye may relieve symptoms. Sur gery (under local anesthesia) pro- vides de \201 nitive correction. Ectropion Eversion of the eyelid. Occurs with orbicularis weakness, scarring of the periorb ital skin or seventh nerve palsy. Distortion prevents correct drainage of tears and correct tear \201 lm, leading to watery eye with con- junctival dryness. Treat with ointment to protect conjunctiva. Surgery (local anesthesia) corrects. Ptosis Drooping of upper eyelid. When severe can cover pupil and impair vision. Causes: apo neurotic (defects in levator aponeurosis), mechanical (lid lesion, lid oedema), neurologica l (third nerve palsy \200\224 look for pupil and eye movement problems, Horner \200\231s s yndrome), myogenic (congenital levator dystrophy, muscular dystrophies, myasthenia gravis, chronic progressive external ophthalmoplegia). 2Do not ignore ptosis in older people \200 \224 it may not be longstanding; look for signs of underlying disease. Dry eyes Common in older people as tear secretion diminishes. Eyes feel gritty, but are not red. Diuretics may exacerbate. Most common cause is blepharitis (in \202 amed lid margins with blocked meibomian gland ori \201 ces and crusting); usually worse in those with rosa cea, eczema, and psoriasis. Treat blepharitis with hot compresses (5min bd), lid massage (upwards towards lid margin lo wer lid, downwards towards lid margin upper lid, eyelid cleaning targeting the base of eyel ashes at the lid margin (warm water baby shampoo on a cotton wool bud). Antibiotic ointm ent not usually required unless staphylococcal infection suspected. Treat dry eyes with art i \201 cial tears or ointment (gives considerable relief). EYELID DISORDERS 583 Eyelid tumors Most common (90 % ) is basal cell carcinoma. Slow growing, non-metas- tasisin g but locally invasive. Often ignored by patient. More common in fairer skins after chronic sun exposure. Waxy nodule with telangiectatic vessels on surface and pearly rolled border (rodent ulcer) is usual appear- ance. Treatment is with surgical excision (Moh \200\231s mi crographic surgery preserves most tissue and may be appropriate in some) or radiotherapy. Varicella zoster infection Facial shingles. Involvement of the ophthalmic division of the t rigeminal nerve will cause vesicles and crusting periorbitally (see b \200\230Varicella zo ster infection \200\231, p.624). This page intentionally left blank 585 Chapter 23 Skin The ageing skin 586 Photoageing 588 Cellulitis 589 Other bacterial skin infections 590 Fung al skin infections 591 Chronic venous insuf \201 ciency 592 Leg ulcers 593 Management of v enous leg ulcers 594 Pruritus 596 Pruritic conditions 598 HOW TO Recognize and manage scabies 599 Blistering diseases 600 Skin cancers and pre-cancers 602 Other skin lesions 604 586 CHAPTER 23 Skin The ageing skin Skin changes with age are universal, but many changes we associate with age ing are actually due to cumulative sun exposure (photoageing), and could be largely prevent ed by protecting the skin from the sun (compare an older person \200\231s facial skin to th eir buttock skin). Intrinsic ageing does occur, however (Table 23.1 ), and there are several skin diseases tha t are age related (eg pruritus, pemphigoid, lichen sclerosus). Hair changes \200 50 % of the over 50s will have gray hair, as melanocyte numbers drop \200 Male pattern baldness (affecting the vertex and temples) starts in the late teens and progresses \200\224 80 % of male pensioners are balding Women may be affected after the menopause, but it is rarely as severe \200 Diffuse hair l oss occurs in both sexes with advancing age (consider checking for iron de \201 ciency, th yroid dysfunction, renal impairment, hypoproteinaemia, in \202 ammatory skin conditions, u se of antimetabolite drugs, etc.) As hair follicles age, their function may be disrupted, leading to longer, tougher hairs gr owing in eyebrows, ears, and noses, in both sexes \200 Postmenopausal hormone changes may cause women to develop hair in the beard area and upper lip THE AGEING SKIN 587 Table 23.1 Age-related changes and their clinical implications Age-related change Clinical implications Increased tendency to blistering Epidermis thins, with \202 attening of the dermo-epidermal junction, limiting transfer of nutrients and making separation of layers easier Increased skin tearing Slower cell turnover Slower healing of wounds Less melanocyte activity, with slower DNA repair Increased photosensitivity, with increased tendency to skin malignancy Altered epidermal protein binding Dry, rough, and \202 aky skin more common Abnormal skin barrier, so more prone to irritant contact dermatitis Altered connective tissue structure and function Reduced elasticity and strength of skin Decreased blood \202 ow through dermal vascular beds Skin appears cooler and paler Thermoregulation is less ef \201 cient Hair and gland growth and function slows Thermoregulation is less ef \201 cient Subcutaneous fat decreases in volume and is distributed differently (eg more abdominal fat) Protection against pressure injury lessens Number of cutaneous nerve endings decreases Cutaneous sensation blunts (eg \201 ne touch, temperature, proprioception) Pain threshold increases Fewer cutaneous glands Thermoregulation is less ef \201 cient Nail bed function decreases Nails become thick, dry, brittle and yellow, with longitudinal ridges The immune functioning of the skin decreases Increased propensity to skin infections and malignancies 588 CHAPTER 23 Skin Photoageing The dermis thickens with tangled elastic \201 bres; the epidermis is variable in thickness with regions of both hypertrophy and atrophy \200\224 leading to considerabl e skin changes: \200 The skin becomes wrinkled (coarse and \201 ne), rough, yellowed, a nd irregularly pigmented \200\224 these changes are all exacerbated by smoking \200 The ski n may develop actinic (solar) elastosis \200\224 thickened, yellow skin with rhomboid pattern and senile comedones Actinic (solar) purpura is a non-palpable rash often on the forearms, due to red cell extra vasation from sun-damaged vessels (the platelet count is normal) Lesions include brown macules, multiple telangiectasia, actinic (solar) keratoses (scaly, r ough hyperkeratotic areas on sun-exposed skin), as well as a tendency to skin tumors Prevention is better than cure for these changes, but topical retinoids may reduce the appe arance of wrinkles and pigment, and certain plastic surgery techniques are employed (eg che mical peels and injections of collagen and botulinum toxin). Sun protection \200 Avoid unnecessary sun exposure \200 Stay out of the sun during the hottest time of the day (11am \200\2233pm) \200 Wear appropriate factor sun screen (incre asing sun protection factor for fairer skins) Areas that are often forgotten include balding heads (wear a hat) and the tops of ears (apply sun screen) Photosensitizing drugs Several drugs may interact with ultraviolet (UV) or visible light to cause adverse cutaneous effects. These may be phototoxic or photoallergic reactions. Possi ble agents include: \200 Amiodarone \200 Phenothiazines \200 Diuretics (including bum etanide and furosemide) \200 Antibiotics eg tetracyclines (especially doxycycline), isoni azid, cipro \202 oxacin Quinine \200 Procainamide \200 Hydralazine CELLULITIS 589 Cellulitis Deep infection of the skin and subcutaneous tissues with oedema, often on the lo wer leg. More common with increasing age, immunocompromise (eg diabetes) and with a predisp osing skin condition (leg ulcer, pressure sore, lymphoedema, toe web intertrigo, traumatic wounds, etc.). Organisms Usually Streptococcus (group A, commonly Strep. pyogenes ) and/or sta- phylococcu s. With open wounds (eg leg ulcers, pressure sores) and lym- phoedema colonization is broad er so infecting organisms may be more diverse, including highly resistant bacteria, eg MRSA (see b \200\230Disease caused by MRSA \200\231, p.612). Clinical features \200 Red, hot, tender, raised area with poorly demarcated margins \200 Portal of entry for bacteria often evident (eg trauma) \200 Systemic upset may follow ( fever, malaise) \200 May present non-speci \201 cally, so always examine the whole skin \200 Spread can cause lymphangitis with tender nodes in the inguinal region \200 Risk o f bacteraemia (up to 80 % in nursing home residents with pressure sores; treat aggressively as mortality is as much as 50 % ) Investigations \200 FBC: elevated white cell count in around 50 % \200 Blood cultures: take in all before antibiotics (positive in 25 % ) \200 Local culture: eg wound swab, inj ection and aspiration of saline in the dermis, skin biopsy. Rarely needed as empirical trea tment often works Treatment \200 If the cellulitis is mild, and the patient well, then oral therapy can be used to start. Oral options include phenoxymethylpenicillin + \202 ucloxacillin, erythrom ycin alone or co-amoxiclav Draw around the cellulitis with a water-resistant pen to allow accurate subsequent assessments and arrange early review (at 24 \200\22348hr) \200 Elevate the lim b: oedema with blistering may cause ulceration \200 If more extensive, with systemic upse t, lymphangitis or worsening on oral therapy, then hospital admission for rest, elevation a nd parenteral therapy is needed Options include benzylpenicillin + \202 ucloxacillin or co-amoxiclav for 48hr (or until t he erythema starts to recede), then an oral course \200 Total treatment may be needed for up to 14 days but treat each case individually If cellulitis complicates ulcers, pressure sores or lymphoedema then broader spectrum antibiotics are needed at outset Look for and treat toe web intertrigo in all (with topical antifungals) \200 Cellulitis c an be painful: ensure that the patient has adequate analgesia \200 Older patients will of ten become dehydrated with bacteraemia: assess clinically (pulse, blood pressure, general c ondition) and biochemically (urea, creatinine, and electrolytes) giving intravenous \202 uids in the acute phase if needed 590 CHAPTER 23 Skin Other bacterial skin infections Erysipelas \200 Type of cellulitis that is common in olde r patients \200 Strep. pyogenes infection of the dermis and hypodermis \200 Occurs on f ace (bridge of nose and across cheeks), and less commonly on legs, arms and trunk Flu-like prodrome \200 Well-demarcated edge with erythema, oedema, and pain \200 Progre sses to vesicles that rupture and crust \200 Portal of entry may be unclear, especially w ith facial erysipelas \200 Bacteraemia in 55 % ; mortality of 10 % without treatment \200 Requires parenteral therapy unless very mild \200\224 48hr of iv benzylpenicillin followed by 12 days or oral phenoxymethylpenicillin Recurs in 30 % at some point Necrotizing fasciitis \200 Rare and serious infection \200 Affects soft tissues (usuall y arm/leg); spreads rapidly along fascial planes \200 Commonly due to Strep. pyogenes , b ut polymicrobial infection also occurs (eg S taphylococci , Pseudomonas , Bacteroides , dip htheroids, coliforms) Patient feels and looks unwell with a high fever \200 Area of swelling, redness, and tend erness enlarges rapidly and becomes purple and discolored. Haemorrhagic bullae develop foll owed by necrosis Prompt parenteral antibiotics and early surgical debridement essential 2Key to management i s early recognition. Review a patient with cellulitis frequently if they are unwell, lookin g for rapid spread. Intertrigo \200 Common complaint, almost exclusively in older patients, when there is super \201 cial in \202 ammation of skin surfaces that are in contact, eg \202 exures of limbs, groins, axillae, submammary Due to friction in a continually warm, moist environment \200 May be underlying skin dise ase (eg seborrhoeic dermatitis, seborrhoeic eczema, irritant contact eczema (urine, feces), psoriasis) Secondary infection with yeast is common Treatment \200 Improve hygiene \200 Wash carefully and always dry the skin thoroughly \200 Use talcum powder to keep areas dry \200 Apply topical antifungal (eg clotrimazole cream plus 1 % hydrocortisone cream) Separate skin surfaces where possible FUNGAL SKIN INFECTIONS 591 Fungal skin infections There are two main groups of fungi that cause infection in humans. D ermatophytes, eg Tinea species ( \200\230ringworm \200\231) \200 Infect the feet, groin, body, hands, nails, and scalp \200 Suspect if there is a distinct edge to an itchy lesion \200 Con \201 rm diagnosis with skin scrapings, or trial treatment \200 Topical imida zoles, eg clotrimazole (Canesten cream) are effective. Terbina \201 ne is more effective, but more expensive Oral terbina \201 ne will work for more resistant infection but should only be used if topical treatment fails and the diagnosis con \201 rmed Yeasts, eg Candida albicans ( \200\230thrush \200\231) \200 Normal commensal of mouth and gastrointestinal tract \200 Produces infection in certain circumstances, eg moist skin f olds, poor hygiene, diabetes, and use of broad-spectrum antibiotics \200\224 many of these commonly occurring in older patients Common sites include genital (associated with catheter use, see b \200\230Vulval disorders \200\231, p.526), intertrigo (see b \200\230Intertrigo \200\231, p.590), around the nail (chronic paronychia) and oral thrush (especially if dentures \201 t poorly, see b \200\230The elderly mouth \200\231, p.354) Topical imidazoles, eg clotrimazole are effective for skin infection. Preparations that include hydrocortisone will also reduce in \202 ammation and help to bre ak the itch/scratch cycle Nystatin, amphotericin, or miconazole lozenges, suspension, or gel can be used for oral infection More widespread infection (eg oesophageal candidiasis) or those with severe immunode \201 ciency may require systemic therapy \200\224 \202 uconazole 50 \200\223100mg daily is ef fective Seborrhoeic dermatitis \200 Chronic in \202 ammatory condition with erythematous scaly e ruptions \200 Possibly due to a hypersensitivity to Pityrosporum \200\224 a yeast skin commensal Classic distribution \200\224 face (eyebrows, eyelids, nasolabial folds, postauricular, beard area), scalp (dandruff), central chest, central back and in older pati ents only, \202 exural (axillae, groins, submammary) May cause otitis externa or blepharitis \200 Increased prevalence and severity in older p atients, exacerbated by poor skin care Associated with parkinsonism and HIV \200 Scalp is treated with ketoconazole shampoo \200 Elsewhere, use ketoconazole shampoo as a wash and apply miconazole combined with 1 % hydrocortisone cream Blepharitis is treated with warm compresses, cleaning eyelids with cotton buds and diluted baby shampoo, and steroid eye cream Dif \201 cult to treat \200\224 recurrence is common, and repeated treatments are often required. Aim to control, not cure 592 CHAPTER 23 Skin Chronic venous insuf \201 ciency Common, ranging from minor cosmetic problems to debilitat ing leg ulcers. More common after phlebitis or DVT (25 % with a history of DVT will develop venous insuf \201 ciency at 20 years, 4 % will eventually develop leg ulcers), after leg injury, in obese patients, and with advancing age. Probably more common in women, although female longevity may account for apparent difference. Pathogenesis Due to failure of the venous pump in the legs. Commonly caused by deep vein oc clusion (although only half will show signs of this on venography). Retrograde blood \202 ow in the deep veins, valvular incompetence, and pro- gressive pericapillary \201 brin d eposition also contribute to the process. Clinical changes Varicose veins \200 Initially there may be no symptoms, just venous dila tion (starts with submalleolar venous \202 ares and progresses to dilated, tortuous, palp able varicose veins) Problems may include itch, ache, thrombophlebitis, or bleeding from varicosities. Treatment at this stage is largely cosmetic and includes surgical stripping of super \201 cial vein s (not where there is a history of deep vein occlusion). Ache may be relieved by use of sup port hosiery Oedema \200 May initially be unilateral and wax and wane with position (classically occurring at the end of a day of standing up) A feeling of leg heaviness is common \200 Low-dose thiazide diuretics (eg bendro \202 um ethiazide 2.5mg od) may help, but as the patient is not \202 uid overloaded, beware of vo lume depletion Skin changes \200 Haemosiderin pigmentation due to red cell extravasation \200 Telangie ctasia \200 Lacy white scars \200 Eczematous changes with itchy, weepy skin exacerbated by many topical treatments \200\224 improve with topical steroid application \200 Lipod ermatosclerosis occurs when \201 brosis of the tissues leads to induration. May become ci rcumferential and girdle the lower leg causing an inverted champagne bottle appearance Venous ulcers Venous ulcers arise in the context of these skin changes, often precipi- tate d by minor trauma. LEG ULCERS 593 Leg ulcers Common condition, af \202 icting 1 % of adult population at any time. 50 % are venous ulcers, 10 % arterial, 25 % mixed venous and arterial, and the remainder due to othe r causes (diabetes, infection, malignancy, blood dis- orders, vasculitis, drug eruptions, e tc.). Associated with high morbidity and healthcare expenditure. Clinical features of common ulcers Venous ulcers \200 Occur on the medial ankle, along th e course of the saphenous vein \200 Shallow and tender with irregular edges that are not undermined \200 The base is usually red, but may be sloughy \200 Associated skin featur es of chronic venous insuf \201 ciency Arterial ulcers \200 Occur at sites of trauma or pressure \200\224 commonly the malleoli, toes, ball of foot, heel and base of \201 fth metatarsal Deep, punched out, and painful with regular edges \200 Associated features of peripheral arterial disease (decreased pulses, slow capillary re \201 ll, pale, cool, hairless skin, see b \200\230Peripheral vascular d isease \200\231, p.304) Diabetic ulcers \200 Occur at pressure points \200 Painless (due to diabetic neuropathy ) \200 Often infected with undermined edges Malignant ulcers \200 Painless with a raise d edge \200 Be suspicious if an ulcer fails to heal, or has an atypical appearance A general approach to leg ulcers \200 Establish cause \200\224 usually possible on clini cal grounds. May need to consider Doppler ultrasound (looking for deep venous occlusion, va lvular incompetence and venous pressures), ABPI (diagnoses arterial disease, see b \200 \230HOW TO Measure ABPI \200\231, p.305), biopsy (looking for malignancy, or for tiss ue culture if infection suspected) or blood tests (FBC, glucose, ESR, CRP, autoantibody scr een) Treat cause where possible, eg compression bandaging for venous disease, revascularization for arterial disease Keep ulcer clean and avoid irritant topical applications. Many available products will cause a contact dermatitis. Keep it simple Ensure there is adequate pain relief \200 Re-evaluate regularly. If the ulcer is not heal ing then reassess the original diagnosis Avoid antibiotics unless there is cellulitis or osteomyelitis. Colonization is inevitable, and swabs usually unhelpful Do a patch test in any patient with a longstanding ulcer to exclude an allergic contact dermatitis 594 CHAPTER 23 Skin Management of venous leg ulcers Chronic and debilitating condition, with serious psychologi cal and social implications. Median duration is 9 months, although 25 % will still be prese nt at 5 years. Correctly treated, 70 % can be healed within 3 months, but 75 % are recurren t. General measures \200 Encourage mobility \200\224 this strengthens the muscle pump and h elps prevent deep vein occlusion. If bed-bound, then exercises such as toe and ankle wiggling an d quadriceps movements can help Stop smoking Limb elevation \200 Raising the legs above the level of the heart improves venous return, reduces oedema, and assists healing of venous ulcers Unfortunately, this is rarely practical \200\224 many older patients cannot tolerate such a position owing to comorbidity (cardiac failure, COPD, arthritic hips, obesi ty, etc.) and even if they can, it is dif \201 cult to sustain Balance bene \201 ts against risks of immobility and complications (thrombosis, deconditioning) \200\224 usually only used for very resistant ulcers when adm ission to hospital may be required Elevating the foot of the bed mattress at night is helpful (easiest with electronic hospita l beds, otherwise use a wedge under the mattress) \200 During the day, sitting with the f eet on a stool is better than nothing, although it fails to raise the legs high enough Elevation should not be used when peripheral arterial disease predominates \200\224 \201 rst check pedal pulses and ABPI (see b \200\230HOW TO Measure ABPI \200\231, p.305) Ulcer care \200 Clean the ulcer by irrigation with saline \200 Debridement of dead tiss ue may improve healing (no trial evidence): Scalpel (local anesthetic cream may make this less uncomfortable) \200 Maggots (consume o nly dead tissue, leaving behind the healthy) \200 Facilitating the body \200\231s own sys tem by creating a moist environment \200 Chemical agents are not recommended (as they als o harm healing tissue) No single wound dressing has been shown to improve healing \200 An ideal dressing keeps t he wound moist with exudate, but not macerated, at an ideal temperature and pH for healing without irritants, excessive slough, or infection Simple, low-adherent, and low-cost dressings are the mainstay \200 Impregnated dressings (eg with antiseptic, antibiotic, debriding enzymes, growth factors or silver sulfadiazine) can cause contact allergic or irritant derm atitis (up to 85 % of patients), worsening the ulcer, so avoid in routine use Occlusive or semi occlusive dressings can aid with pain relief \200 Gel and hydrocolloid dressings can be useful to remove exudates \200 Metronidazole or charcoal dressings can b e used for odor control MANAGEMENT OF VENOUS LEG ULCERS 595 Compression bandaging \200 Mainstay of treatment for venous ulcers \200\224 when correct ly applied, leads to healing for 70 % in 3 months Ensure that the ABPI is > 0.8 (see b \200\230HOW TO Measure ABPI \200\231, p.305) When mixed etiology ulcers are present, some compression is often required, but this has to be carefully moderated to compensate for the arterial insuf \201 ciency Provides an active counter-pressure to venous blood pressure, and enhances the function of the muscle pump Graduated four-layer compression from the ankle to the knee (wool bandage, crepe bandage, elasticated bandage and \201 nally a self-adhesive elasticated ba ndage Should be comfortable, allow the patient to continue with daily life (eg wear shoes as usua l) and last a week (unless highly exudative) Should be applied by an experienced practitioner, as incorrect bandaging can cause more harm than good Intermittent pneumatic compression therapy may be useful for patients for whom standard com pression stockings may be ineffective or not tolerated (eg morbid obesity, severe oedema) Oral agents \200 Aspirin . May improve ulcer healing time \200 Diuretics . Short course s may reduce oedema \200 Antibiotics . Most ulcers are permanently colonized (commonly staphylococci, streptococci, E. coli , Proteus , and Pseudomonas ) and routine use of oral antibiotics will only promote resistance. Wound swabs will only grow these colonizing organ isms and are not indicated. Treat with systemic antibiotics only if there is evidence of sp reading infection (rapidly increasing size, increased pain, surrounding erythema, tracking up lymphatics system, or systemic upset) Other agents . eg pentoxifylline. May have a role in ulcer management but evidence is not robust Surgery \200 Skin grafts may be helpful. Pinch or punch skin grafts may stimulate healing Surgical correction of deep vein incompetence is considered where bandaging has failed. Involves ligation of super \201 cial veins and valvuloplasty Further reading Royal College of Nursing guidelines (in conjunction with NICE) . Online: M www.rcn.org.uk . Simon DA , Freak L ,; Kinsella A , et al . ( 2004 ). Clinical review: Mana gement of venous leg ulcers . BMJ 328 : 1358 \200\223 62 . 596 CHAPTER 23 Skin Pruritus Intense itching. Common condition in older patients, often causing consid- erable distress. Threshold for itch affected by neurological and psycholog- ical factors \200\224 exacerbated by social isolation, sensory impairment (blind, deaf) and depression. Often ig nored, yet simple measures can make a big difference. Causes Often associated with dry skin (xerosis), common with ageing, and fre- quently worst on lower legs, forearms and hands. Skin is dry, scaly, and may develop in \202 amed \201 ssures when severe (asteatotic dermatitis). Contact dermatitis may show few skin changes if mild, yet cause trouble- some itching. Limi ted to areas exposed to allergen (eg under clothing if due to washing power). Systemic disease causes up to half of pruritus in the elderly, including: Liver failure (may be mild jaundice \200\224 itch caused by bile salts) \200 Chronic ren al failure \200 Iron de \201 ciency \200\224 even before anemic \200 Hematological di sorders (lymphoma, polycythaemia \200\224 itch may be exacerbated by water) Infections (including fungal infection, scabies and lice infestations, gastrointestinal parasite infections) Metabolic disorders including: thyroid disease (affects 10 % of hyperthyroid patients, and many hypothyroid patients because of dry skin); diabetes mellitu s Malignancy Many drugs can cause a pruritic rash as an adverse drug reaction (usually allerg ic) but some cause itch without a rash (eg morphine, allopurinol and benzodiazepines) or be cause of cholestasis. Assessment \200 History should include full systems enquiry looking for underlying diseas e, drug history and speci \201 c enquiries about possible irritants (eg biological washing powder, new bath products). Ask if anyone else is itching Examination should include inspection of all skin and thorough general examination (looking for eg burrows or other signs of scabies, lymphadenopathy, hep atosplenomegaly, thyroid enlargement, etc.) \200 Investigations should include: FBC, iron and ferritin, ESR, U,C + E, LFTs, TFTs, and blood glucose. May include other tests, guided by history, eg stool examination for ova, cysts, and parasites, abdominal ultrasound if or ganomegaly felt, etc. PRURITUS 597 Treatment \200 Treat the underlying cause wherever possible \200 Iron supplements if st ores low (even if FBC normal) \200 Stop any drugs that may be causing or exacerbating the condition \200 Apply emollients \200\224 light preparations such as aqueous cream can h elp itch even if the skin does not appear dry, and may be mixed with 0.5 % menthol, which h as a cooling and antiseptic action. Greasier preparations, eg 50:50 liquid paraf \201 n, w hite soft paraf \201 n are useful when the dryness is more severe Urea-containing emollients are used where the skin is scaly, and are often useful in the el derly (eg Balneum plus, E45 itch relief cream, etc.) Avoid excessive bathing \200\224 no more than daily; avoid hot water and prolonged soaking Use preparations such as aqueous cream or emulsifying ointments instead of soap. Emollient bath additives can be added to the water. Brand names such as Oilatum and E45 are sol d as both ointments and bath oils, and there are many others available Avoid exacerbating factors, such as heat (especially hot baths), alcohol, hot drinks and vasodilating drugs Wear loose, cotton clothing \200 Keep nails short to limit skin damage from scratching \200 Consider short-term bandaging where excoriation severe to allow healing Antihistamines may be useful \200\224 sedating preparations such as hydroxyzine hydrochloride, 25mg at night can help sleep. Non-sedating agents can be used du ring the day (eg chlorphenamine, cetirizine, loratadine)