Oxford Handbook of Geriatric Medicine (2 edn)
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The ageing skin
Skin changes with age are universal, but many changes we associate with ageing are actually due to cumulative sun exposure (photoageing), and could be largely prevented by protecting the skin from the sun (compare an older person's facial skin to their buttock skin).
Intrinsic ageing does occur, however (Table 23.1), and there are several skin diseases that are age related (eg pruritus, pemphigoid, lichen sclerosus).
| Age-related change | Clinical implications |
|---|---|
Epidermis thins, with flattening of the dermo-epidermal junction, limiting transfer of nutrients and making separation of layers easier | Increased tendency to blistering 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 flaky 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 flow through dermal vascular beds | Skin appears cooler and paler Thermoregulation is less efficient Hair and gland growth and function slows |
Subcutaneous fat decreases in volume and is distributed differently (eg more abdominal fat) | Thermoregulation is less efficient Protection against pressure injury lessens |
Number of cutaneous nerve endings decreases | Cutaneous sensation blunts (eg fine touch, temperature, proprioception) Pain threshold increases |
Fewer cutaneous glands | Thermoregulation is less efficient |
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 |
| Age-related change | Clinical implications |
|---|---|
Epidermis thins, with flattening of the dermo-epidermal junction, limiting transfer of nutrients and making separation of layers easier | Increased tendency to blistering 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 flaky 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 flow through dermal vascular beds | Skin appears cooler and paler Thermoregulation is less efficient Hair and gland growth and function slows |
Subcutaneous fat decreases in volume and is distributed differently (eg more abdominal fat) | Thermoregulation is less efficient Protection against pressure injury lessens |
Number of cutaneous nerve endings decreases | Cutaneous sensation blunts (eg fine touch, temperature, proprioception) Pain threshold increases |
Fewer cutaneous glands | Thermoregulation is less efficient |
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 |
Hair changes
50% of the over 50s will have grey hair, as melanocyte numbers drop
Male pattern baldness (affecting the vertex and temples) starts in the late teens and progresses—80% of male pensioners are balding
Women may be affected after the menopause, but it is rarely as severe
Diffuse hair loss occurs in both sexes with advancing age (consider checking for iron deficiency, thyroid dysfunction, renal impairment, hypoproteinaemia, inflammatory skin conditions, use of antimetabolite drugs, etc.)
As hair follicles age, their function may be disrupted, leading to longer, tougher hairs growing in eyebrows, ears, and noses, in both sexes
Postmenopausal hormone changes may cause women to develop hair in the beard area and upper lip
Photoageing
The dermis thickens with tangled elastic fibres; the epidermis is variable in thickness with regions of both hypertrophy and atrophy—leading to considerable skin changes:
The skin becomes wrinkled (coarse and fine), rough, yellowed, and irregularly pigmented—these changes are all exacerbated by smoking
The skin may develop actinic (solar) elastosis—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 extravasation from sun-damaged vessels (the platelet count is normal)
Lesions include brown macules, multiple telangiectasia, actinic (solar) keratoses (scaly, rough hyperkeratotic areas on sun-exposed skin), as well as a tendency to skin tumours
Prevention is better than cure for these changes, but topical retinoids may reduce the appearance of wrinkles and pigment, and certain plastic surgery techniques are employed (eg chemical peels and injections of collagen and botulinum toxin).
Sun protection
Avoid unnecessary sun exposure
Stay out of the sun during the hottest time of the day (11am–3pm)
Wear appropriate factor sun screen (increasing 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. Possible agents include:
Amiodarone
Phenothiazines
Diuretics (including bumetanide and furosemide)
Antibiotics eg tetracyclines (especially doxycycline), isoniazid, ciprofloxacin
Quinine
Procainamide
Hydralazine
Cellulitis
Deep infection of the skin and subcutaneous tissues with oedema, often on the lower leg. More common with increasing age, immunocompromise (eg diabetes) and with a predisposing skin condition (leg ulcer, pressure sore, lymphoedema, toe web intertrigo, traumatic wounds, etc.).
Organisms
Usually Streptococcus (group A, commonly Strep. pyogenes) and/or staphylococcus. With open wounds (eg leg ulcers, pressure sores) and lymphoedema colonization is broader so infecting organisms may be more diverse, including highly resistant bacteria, eg MRSA (see 
‘Disease caused by MRSA’, p.612).
Clinical features
Red, hot, tender, raised area with poorly demarcated margins
Portal of entry for bacteria often evident (eg trauma)
Systemic upset may follow (fever, malaise)
May present non-specifically, so always examine the whole skin
Spread can cause lymphangitis with tender nodes in the inguinal region
Risk of bacteraemia (up to 80% in nursing home residents with pressure sores; treat aggressively as mortality is as much as 50%)
Investigations
FBC: elevated white cell count in around 50%
Blood cultures: take in all before antibiotics (positive in 25%)
Local culture: eg wound swab, injection and aspiration of saline in the dermis, skin biopsy. Rarely needed as empirical treatment often works
Treatment
If the cellulitis is mild, and the patient well, then oral therapy can be used to start. Oral options include phenoxymethylpenicillin + flucloxacillin, erythromycin alone or co-amoxiclav
Draw around the cellulitis with a water-resistant pen to allow accurate subsequent assessments and arrange early review (at 24–48hr)
Elevate the limb: oedema with blistering may cause ulceration
If more extensive, with systemic upset, lymphangitis or worsening on oral therapy, then hospital admission for rest, elevation and parenteral therapy is needed
Options include benzylpenicillin + flucloxacillin or co-amoxiclav for 48hr (or until the erythema starts to recede), then an oral course
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)
Cellulitis can be painful: ensure that the patient has adequate analgesia
Older patients will often become dehydrated with bacteraemia: assess clinically (pulse, blood pressure, general condition) and biochemically (urea, creatinine, and electrolytes) giving intravenous fluids in the acute phase if needed
Other bacterial skin infections
Erysipelas
Type of cellulitis that is common in older patients
Strep. pyogenes infection of the dermis and hypodermis
Occurs on face (bridge of nose and across cheeks), and less commonly on legs, arms and trunk
Flu-like prodrome
Well-demarcated edge with erythema, oedema, and pain
Progresses to vesicles that rupture and crust
Portal of entry may be unclear, especially with facial erysipelas
Bacteraemia in 55%; mortality of 10% without treatment
Requires parenteral therapy unless very mild—48hr of iv benzylpenicillin followed by 12 days or oral phenoxymethylpenicillin
Recurs in 30% at some point
Necrotizing fasciitis
Rare and serious infection
Affects soft tissues (usually arm/leg); spreads rapidly along fascial planes
Commonly due to Strep. pyogenes, but polymicrobial infection also occurs (eg Staphylococci, Pseudomonas, Bacteroides, diphtheroids, coliforms)
Patient feels and looks unwell with a high fever
Area of swelling, redness, and tenderness enlarges rapidly and becomes purple and discoloured. Haemorrhagic bullae develop followed by necrosis
Prompt parenteral antibiotics and early surgical debridement essential
▸Key to management is early recognition. Review a patient with cellulitis frequently if they are unwell, looking for rapid spread.
Intertrigo
Common complaint, almost exclusively in older patients, when there is superficial inflammation of skin surfaces that are in contact, eg flexures of limbs, groins, axillae, submammary
Due to friction in a continually warm, moist environment
May be underlying skin disease (eg seborrhoeic dermatitis, seborrhoeic eczema, irritant contact eczema (urine, faeces), psoriasis)
Secondary infection with yeast is common
Treatment
Improve hygiene
Wash carefully and always dry the skin thoroughly
Use talcum powder to keep areas dry
Apply topical antifungal (eg clotrimazole cream plus 1% hydrocortisone cream)
Separate skin surfaces where possible
Fungal skin infections
There are two main groups of fungi that cause infection in humans.
Dermatophytes, eg Tinea species (‘ringworm’)
Infect the feet, groin, body, hands, nails, and scalp
Suspect if there is a distinct edge to an itchy lesion
Confirm diagnosis with skin scrapings, or trial treatment
Topical imidazoles, eg clotrimazole (Canesten® cream) are effective. Terbinafine is more effective, but more expensive
Oral terbinafine will work for more resistant infection but should only be used if topical treatment fails and the diagnosis confirmed
Yeasts, eg Candida albicans (‘thrush’)
Normal commensal of mouth and gastrointestinal tract
Produces infection in certain circumstances, eg moist skin folds, poor hygiene, diabetes, and use of broad-spectrum antibiotics—many of these commonly occurring in older patients
Topical imidazoles, eg clotrimazole are effective for skin infection. Preparations that include hydrocortisone will also reduce inflammation and help to break 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 immunodeficiency may require systemic therapy—fluconazole 50–100mg daily is effective
Seborrhoeic dermatitis
Chronic inflammatory condition with erythematous scaly eruptions
Possibly due to a hypersensitivity to Pityrosporum—a yeast skin commensal
Classic distribution—face (eyebrows, eyelids, nasolabial folds, postauricular, beard area), scalp (dandruff), central chest, central back and in older patients only, flexural (axillae, groins, submammary)
May cause otitis externa or blepharitis
Increased prevalence and severity in older patients, exacerbated by poor skin care
Associated with parkinsonism and HIV
Scalp is treated with ketoconazole shampoo
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
Difficult to treat—recurrence is common, and repeated treatments are often required. Aim to control, not cure
Chronic venous insufficiency
Common, ranging from minor cosmetic problems to debilitating leg ulcers.
More common after phlebitis or DVT (25% with a history of DVT will develop venous insufficiency 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 occlusion (although only half will show signs of this on venography). Retrograde blood flow in the deep veins, valvular incompetence, and progressive pericapillary fibrin deposition also contribute to the process.
Clinical changes
Varicose veins
Initially there may be no symptoms, just venous dilation (starts with submalleolar venous flares and progresses to dilated, tortuous, palpable varicose veins)
Problems may include itch, ache, thrombophlebitis, or bleeding from varicosities. Treatment at this stage is largely cosmetic and includes surgical stripping of superficial veins (not where there is a history of deep vein occlusion). Ache may be relieved by use of support hosiery
Oedema
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
Low-dose thiazide diuretics (eg bendroflumethiazide 2.5mg od) may help, but as the patient is not fluid overloaded, beware of volume depletion
Skin changes
Haemosiderin pigmentation due to red cell extravasation
Telangiectasia
Lacy white scars
Eczematous changes with itchy, weepy skin exacerbated by many topical treatments—improve with topical steroid application
Lipodermatosclerosis occurs when fibrosis of the tissues leads to induration. May become circumferential and girdle the lower leg causing an inverted champagne bottle appearance
Venous ulcers
Venous ulcers arise in the context of these skin changes, often precipitated by minor trauma.
Leg ulcers
Common condition, afflicting 1% of adult population at any time. 50% are venous ulcers, 10% arterial, 25% mixed venous and arterial, and the remainder due to other causes (diabetes, infection, malignancy, blood disorders, vasculitis, drug eruptions, etc.).
Associated with high morbidity and healthcare expenditure.
Clinical features of common ulcers
Venous ulcers
Occur on the medial ankle, along the course of the saphenous vein
Shallow and tender with irregular edges that are not undermined
The base is usually red, but may be sloughy
Associated skin features of chronic venous insufficiency
Arterial ulcers
Occur at sites of trauma or pressure—commonly the malleoli, toes, ball of foot, heel and base of fifth metatarsal
Deep, punched out, and painful with regular edges
Associated features of peripheral arterial disease (decreased pulses, slow capillary refill, pale, cool, hairless skin, see ‘Peripheral vascular disease’, p.304)
Diabetic ulcers
Occur at pressure points
Painless (due to diabetic neuropathy)
Often infected with undermined edges
Malignant ulcers
Painless with a raised edge
Be suspicious if an ulcer fails to heal, or has an atypical appearance
A general approach to leg ulcers
Establish cause—usually possible on clinical grounds. May need to consider Doppler ultrasound (looking for deep venous occlusion, valvular incompetence and venous pressures), ABPI (diagnoses arterial disease, see ‘HOW TO . . . Measure ABPI’, p.305), biopsy (looking for malignancy, or for tissue culture if infection suspected) or blood tests (FBC, glucose, ESR, CRP, autoantibody screen)
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
Re-evaluate regularly. If the ulcer is not healing 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
Management of venous leg ulcers
Chronic and debilitating condition, with serious psychological and social implications. Median duration is 9 months, although 25% will still be present at 5 years. Correctly treated, 70% can be healed within 3 months, but 75% are recurrent.
General measures
Encourage mobility—this strengthens the muscle pump and helps prevent deep vein occlusion. If bed-bound, then exercises such as toe and ankle wiggling and quadriceps movements can help
Stop smoking
Limb elevation
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—many older patients cannot tolerate such a position owing to comorbidity (cardiac failure, COPD, arthritic hips, obesity, etc.) and even if they can, it is difficult to sustain
Balance benefits against risks of immobility and complications (thrombosis, deconditioning)—usually only used for very resistant ulcers when admission to hospital may be required
Elevating the foot of the bed mattress at night is helpful (easiest with electronic hospital beds, otherwise use a wedge under the mattress)
During the day, sitting with the feet 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—first check pedal pulses and ABPI (see ‘HOW TO . . . Measure ABPI’, p.305)
Ulcer care
Clean the ulcer by irrigation with saline
Debridement of dead tissue may improve healing (no trial evidence):
Scalpel (local anaesthetic cream may make this less uncomfortable)
Maggots (consume only dead tissue, leaving behind the healthy)
Facilitating the body's own system by creating a moist environment
Chemical agents are not recommended (as they also harm healing tissue)
No single wound dressing has been shown to improve healing
An ideal dressing keeps the 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
Impregnated dressings (eg with antiseptic, antibiotic, debriding enzymes, growth factors or silver sulfadiazine) can cause contact allergic or irritant dermatitis (up to 85% of patients), worsening the ulcer, so avoid in routine use
Occlusive or semi occlusive dressings can aid with pain relief
Gel and hydrocolloid dressings can be useful to remove exudates
Metronidazole or charcoal dressings can be used for odour control
Compression bandaging
Mainstay of treatment for venous ulcers—when correctly applied, leads to healing for 70% in 3 months
Ensure that the ABPI is >0.8 (see ‘HOW TO . . . Measure ABPI’, p.305)
When mixed aetiology ulcers are present, some compression is often required, but this has to be carefully moderated to compensate for the arterial insufficiency
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 finally a self-adhesive elasticated bandage)
Should be comfortable, allow the patient to continue with daily life (eg wear shoes as usual) 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 compression stockings may be ineffective or not tolerated (eg morbid obesity, severe oedema)
Oral agents
Aspirin. May improve ulcer healing time
Diuretics. Short courses may reduce oedema
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 organisms and are not indicated. Treat with systemic antibiotics only if there is evidence of spreading 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
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 superficial veins and valvuloplasty
Further reading
Pruritus
Intense itching. Common condition in older patients, often causing considerable distress. Threshold for itch affected by neurological and psychological factors—exacerbated by social isolation, sensory impairment (blind, deaf) and depression. Often ignored, yet simple measures can make a big difference.
Causes
Often associated with dry skin (xerosis), common with ageing, and frequently worst on lower legs, forearms and hands. Skin is dry, scaly, and may develop inflamed fissures when severe (asteatotic dermatitis).
Contact dermatitis may show few skin changes if mild, yet cause troublesome itching. Limited 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—itch caused by bile salts)
Chronic renal failure
Iron deficiency—even before anaemic
Haematological disorders (lymphoma, polycythaemia—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 mellitus
Malignancy
Many drugs can cause a pruritic rash as an adverse drug reaction (usually allergic) but some cause itch without a rash (eg morphine, allopurinol and benzodiazepines) or because of cholestasis.
Assessment
History should include full systems enquiry looking for underlying disease, drug history and specific 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, hepatosplenomegaly, thyroid enlargement, etc.)
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 organomegaly felt, etc.
Treatment
Treat the underlying cause wherever possible
Iron supplements if stores low (even if FBC normal)
Stop any drugs that may be causing or exacerbating the condition
Apply emollients—light preparations such as aqueous cream can help itch even if the skin does not appear dry, and may be mixed with 0.5% menthol, which has a cooling and antiseptic action. Greasier preparations, eg 50:50 liquid paraffin, white soft paraffin are useful when the dryness is more severe
Urea-containing emollients are used where the skin is scaly, and are often useful in the elderly (eg Balneum® plus, E45® itch relief cream, etc.)
Avoid excessive bathing—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 sold 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
Keep nails short to limit skin damage from scratching
Consider short-term bandaging where excoriation severe to allow healing
Antihistamines may be useful—sedating preparations such as hydroxyzine hydrochloride, 25mg at night can help sleep. Non-sedating agents can be used during the day (eg chlorphenamine, cetirizine, loratadine)
Colestyramine is used to decrease itch in biliary obstruction and primary biliary cirrhosis
Light therapy (phototherapy) may help—normal sunlight, or a course of UVB therapy can be arranged
Pruritic conditions
Lichen simplex
Local patch of pruritus, which when scratched leads to skin damage with thickening, discolouration, and excoriation
Worse in times of emotional stress
Treat with steroids (topical or intralesional) and avoidance of scratching (bandaging may help). Capsaicin cream may alleviate itching by decreasing substance P levels in the skin
Pruritus ani
Common complaint
Occasionally due to infection (streptococci, candidiasis, threadworms)
Exclude allergic contact dermatitis, seborrhoeic dermatitis, lichen sclerosus (see ‘Vulval disorders’, p.526) or psoriasis
Usually due to soiling of the perianal skin, which is worse with loose stool and difficulty in wiping effectively (eg with arthritis)
Mainstay of treatment is improving hygiene after bowel movement (assist with wiping if physically difficult; consider wiping with a damp cloth, etc)
Use aqueous cream as a soap substitute
Once developed, the itch may be self-perpetuating—break the cycle with steroids ± topical antifungals or antiseptics
Patch test to exclude allergy
▸Thinking of this diagnosis is the first step.
Caused by Sarcoptes scabiei mite
Spread by skin-to-skin contact
Outbreaks can occur within institutions (eg nursing homes, hospital wards)
Occasionally serious, even fatal
Symptoms and signs
Intense itch (worse at night)
Widespread excoriation
Examine the patient carefully for burrows and/or erythematous papules that are found:
Between fingers and toes
On the wrist flexor surface
Around the nipples and umbilicus
In the axillae and groin
Treatment
Isolate the patient in a side room
Barrier nurse (gloves, aprons)
Apply topical pesticidal lotions or creams, eg permethrin, malathion
Apply to the whole body including the scalp, neck, and face. Ensure the interdigital webs are well covered
Treat all household members (or all others in close contact in an institution) simultaneously, including asymptomatic contacts
Wash clothes and bedding
Repeat treatment after a week
Prescribe 30–60g of cream and 100mL of lotion for each application
Applying after a hot bath is no longer recommended
Antibiotics may be needed for secondary infection
Itch may persist for weeks after treatment has eradicated the mite, but should slowly diminish. Topical steroids and sedating antihistamines to aid sleep can be helpful
Persistent itch may indicate treatment failure
Norwegian scabies occurs in immunosuppressed and frail older patients. A heavy load of mites produces hyperkeratotic lesions. Highly contagious. May require additional oral treatment (eg ivermectin—not licensed).
Blistering diseases
There are many disorders causing skin blistering in older people—see Table 23.2 for a differential. Common causes include blistering secondary to cellulitis or rapid onset oedema. Bullous pemphigoid is significant in that it occurs almost exclusively in the elderly population.
| Blistering disorder | Clinical features |
|---|---|
Blisters secondary to cellulitis | Features of cellulitis present (see |
Blisters secondary to oedema | Occurs when onset is rapid, eg heart failure |
Traumatic blisters | Due to friction, pressure, or knocks to skin Localized to site of insult, eg heel blister with ill-fitting shoes |
Pressure blisters | Due to prolonged pressure that causes skin ischaemia Can occur after 2hr of immobility Risk factors include advancing age, immobility, dehydration, extremes of body size May progress to pressure sore (see |
Fixed drug eruption | Itch, erythema, and blistering that appears and reappears at the same site after ingestion of a drug (eg furosemide) Reaction usually within 6hr |
Eczema | Blisters may occur in eczema, especially if there is secondary infection (eg eczema herpeticum, staphylococcal infection) |
Infections | Herpes simplex—usually cause blisters on the face or genitals Herpes zoster—shingles is common in older patients (see Staphylococci and streptococci may cause primary infections (eg impetigo—facial blisters that rupture to leave a yellow crust; erysipelas—well-defined area of redness and swelling that later blisters, usually on face or lower leg) or secondary infection of, eg, a leg ulcer or wound. Either may result in blistering |
Bullous pemphigoid | See |
Pemphigus vulgaris | Serious autoimmune blistering disease Rare disorder, mainly affecting young or middle aged patients Widespread flaccid, superficial blisters that rupture early Patients are systemically unwell |
Dermatitis herpetiformis | Symmetrical extensor surface tense blisters, associated with coeliac disease Rare, with peak incidence in the fourth decade |
| Blistering disorder | Clinical features |
|---|---|
Blisters secondary to cellulitis | Features of cellulitis present (see |
Blisters secondary to oedema | Occurs when onset is rapid, eg heart failure |
Traumatic blisters | Due to friction, pressure, or knocks to skin Localized to site of insult, eg heel blister with ill-fitting shoes |
Pressure blisters | Due to prolonged pressure that causes skin ischaemia Can occur after 2hr of immobility Risk factors include advancing age, immobility, dehydration, extremes of body size May progress to pressure sore (see |
Fixed drug eruption | Itch, erythema, and blistering that appears and reappears at the same site after ingestion of a drug (eg furosemide) Reaction usually within 6hr |
Eczema | Blisters may occur in eczema, especially if there is secondary infection (eg eczema herpeticum, staphylococcal infection) |
Infections | Herpes simplex—usually cause blisters on the face or genitals Herpes zoster—shingles is common in older patients (see Staphylococci and streptococci may cause primary infections (eg impetigo—facial blisters that rupture to leave a yellow crust; erysipelas—well-defined area of redness and swelling that later blisters, usually on face or lower leg) or secondary infection of, eg, a leg ulcer or wound. Either may result in blistering |
Bullous pemphigoid | See |
Pemphigus vulgaris | Serious autoimmune blistering disease Rare disorder, mainly affecting young or middle aged patients Widespread flaccid, superficial blisters that rupture early Patients are systemically unwell |
Dermatitis herpetiformis | Symmetrical extensor surface tense blisters, associated with coeliac disease Rare, with peak incidence in the fourth decade |
Bullous pemphigoid
Chronic autoimmune bullous eruption.
Clinical features
Patient is systemically well
Skin becomes erythematous and itchy
Large, tense blisters then appear, usually on the limbs, trunk, and flexures (rarely mucous membranes)
Blisters then heal without scarring
May appear in normal looking skin, or at the site of previous skin damage (eg ulcer, trauma)
Chronic and recurrent condition
Diagnosis
Confirmed by skin biopsy, that shows linear IgG deposited at the basement membrane
Circulating autoantibody (anti-BPAg1 and anti-BPAg2) is found in the serum of up to half of patients
Treatment
Should be managed by a dermatologist
Responds well to steroids
Mild, local disease can be treated with strong topical steroids
More widespread disease requires oral prednisolone (40–60mg daily initially, reducing fairly rapidly to 10mg within a few weeks)
Topical or intralesional steroids are used for resistant lesions
Remember to monitor for and protect against steroid side effects
Consider steroid-sparing agents for longer treatment courses (eg azathioprine)
Prognosis
50% have self-limiting disease
The majority will be off medication within 2 years
Causes of blistered skin (Table 23.2)
Skin cancers and pre-cancers
All increase in frequency with increasing age and sun exposure. They are most common on sun-exposed areas, especially the head and neck and are diagnosed by biopsy. Any suspicious skin lesion should be referred to a dermatologist for consideration of this after discussion with the patient.
Actinic keratoses
Rough, scaly patches
Vary from skin coloured to red, brown, yellow, and black (often patchy)
Pre-malignant, with a small risk of becoming squamous cell carcinoma over years. Some resolve spontaneously. Treat established lesions
Removal with cryotherapy, topical 5-fluorouracil (5-FU—applied bd for 4–6 weeks, causes erythema, burning, ulceration, and then healing) or topical diclofenac (treat for 60–90 days; therapeutic effect may occur up to 30 days after stopping)
Bowen's disease
Intraepidermal carcinoma, with small risk of transformation into squamous cell carcinoma
Typically occurs on the lower leg of elderly women
Caused by sun exposure, arsenic exposure, or human papilloma virus infection
Pink or reddish scaly plaques with well-defined edges
Histology should be confirmed
Watchful waiting may be appropriate, but most lesions are removed by cryotherapy, topical 5-FU, curettage, or excision
Lentigo maligna
Irregular pigmented macules that can be brown, black, red, or white
Usually over 1cm in size, they occur in areas of sun exposure
1–2% become invasive with time
Excision is required, although watchful waiting may be appropriate if the patient is frail
Basal cell carcinoma
Commonest, accounting for 75% of all skin cancers
Other risk factors include irradiation, arsenic ingestion, or chronic scarring
Slow growing and usually only locally invasive (metastasis virtually unknown), but facial tumours left untreated can cause erosion of cartilage and bone with significant disfigurement
Begins as a pearly papule, that then ulcerates, characteristically with a rolled everted edge and surface telangiectasia (so called rodent ulcer)
Most lesions need excision with a 5mm margin; Moh's microsurgical method involves inspecting histology during the procedure to limit tissue loss; radiotherapy can be used where surgery is not an option, or in cases of recurrence. Intralesional interferon or photodynamic therapies are newer options
Recurrence in 5% at 5 years, so follow-up is required
Squamous cell carcinoma
Second most common skin cancer
Other risk factors include irradiation, chronic ulceration or scarring, smoking, or exposure to industrial carcinogens
5–10% will metastasize, usually to local lymph nodes initially
Begins as an erythematous, indurated area that becomes hyperkeratotic and scaly, and may then ulcerate
Removal is by surgical excision with 5mm margins. Radiotherapy can be used for recurrence, or in older patients if excision would be hard (eg on the face)
▸May develop in the edge of a leg ulcer.
Malignant melanoma
Most lethal of skin tumours, readily metastasizing
Different subtypes include superficial spreading melanoma (most common; plaque with irregular border and uneven pigmentation), nodular melanoma (dark pigmented nodule), lentigo maligna melanoma and acral lentiginous melanoma (pigmented macule in nail beds, palms and soles)
Suspect if a pigmented lesion has changed in size or colour, become irregular in shape, bleeds, itches, or looks inflamed
Early detection is key as the thicker the lesion the worse the outlook and once metastasized, the disease is fatal—older men often ignore suspicious-looking skin lesions
Removal is by surgical excision with wide margins
Other skin lesions
Campbell de Morgan spots
Small bright red papules on the trunk
Benign capillary proliferations
Occur from middle age onwards, almost universal by old age in Caucasians
Skin tags
Pedunculated, benign fibroepithelial polyps
Occur in older patients
Benign, usually multiple, cause unknown
Removal for cosmetic reasons by snipping the stalk with scissors, or cryotherapy (liquid nitrogen)
Seborrhoeic warts
Also called basal cell papilloma
Not infectious
Oval papules (1–6cm diameter) occurring on the face and trunk of older patients
Initially yellow, become darker and more warty in appearance
Seem to be ‘stuck-on’, usually multiple
Removal can be done (usually for cosmetic reasons) by cryotherapy or curettage
Where concerns exist about more serious pathology, excision biopsy is performed
