602 y g o o t a m r e D Fig 1. Pyogenic granuloma. Courtesy of Dr Jonathan Bowling. l Non-scarring alopecia: nutritional (Fe or Zn de \201 ciency); androgenetic ( \200 & \200 ) autoimmune (alopecia areata: smooth round patches of hair loss on scalp; hairs like excl amation marks are a typical feature; often spontaneously regrows; total scalp hair loss = a lopecia totalis; total body hair loss = alopecia universalis \200\224its treatment is diffi cult: consider topical or intralesional steroids, or minoxidil, or dinitrochlorobenzene); telogen ef \202 uvium (shedding of telogen phase hairs after period of stress, eg childbir th, surgery, severe illness). Scarring alopecia: lichen planus; discoid lupus erythematosus; trauma. Blistering disorders Infection (eg herpes); insect bites (eg on legs); drugs (ACEi; furosem ide); dermatitis herpetiformis, (p588); friction; discoid eczema;1 Zn \200\201; autoimmune blistering disorders (ABD), eg pemphigoid \200\224the chief ABD in the elderly \200\224due to IgG autoantibodies to basement membrane (bullous pemphi- goid antigens 1 & 2). Signs: Te nse blisters on an urticated base. Skin biopsy: (+ve immuno \202 uorescence; linear IgG an d C3 along the basement membrane). \201\227: clobetasol cream up to 40g/day is better than oral steroids. 159 Pemphigus aff ects younger people (<40yrs) than pemphigoid and is due t o IgG autoantibodies against desmosomal components (desmoglein 1 & 3). This leads to acanth olysis (keratinocytes separate from each other). Drugs may cause it, eg ACEi, NSAID, phenob arbital, L-dopa. Signs: Flaccid blisters which rupture easily to leave widespread erosions. The oral mucosa is often aff ected early. Skin biopsy: +ve immuno \202 uorescence (interc ellular IgG giving a crazy- paving eff ect). \201\227: prednisolone (60 \200\22380mg/day P O, eg life-long in low doses). IVIs of rituximab and immune globulin may have a dramatic ef f ect. 160 1 Discoid (=nummular, ie coin-shaped) eczema may begin with vesicles. 161 Typical patient: \200 50 \200\22370yrs or \200 20 \200\22330, with somewhat symmetrical round/oval very itchy vesicles, or papular plaques often on legs (or trunk/arm, not face) with well-de \201 ned irregular margins (p587 \201 g 5). They may crust and get infected by staphs bef ore \202 attening into hyperpigmented macules. It recurs at the same sites. Sunlight may improve it. Cause: unknown; patch test +ve in 50% (if +ve, avoid culprits). 162 \200\224: lukewarm baths + moisturizers + steroid ointment (eg high-potency, preceded by a 20min wat er-soak 163) + oral antihistamine. Photosensitivity For classi \201 cation of susceptibility to ultraviolet, see p593. Photos ensitivity denotes conditions triggered by light (eg solar urticaria; poly morphic light er uption). Photoaggravation describes disorders worsened by light but not due to abnormal sen sitivity to light (eg recurrent herpes la- bialis; rosacea). Photosensitivity can occur to visible light, UVA (320 \200\223400nm) or UVB (290 \200\223320nm). \200\207Usually a caref ul history allows accurate diagnosis. \200 A rash every summer, for example, suggests tha t uv has a role. \200 How long does the rash take to appear? Within 30min suggests solar urti- 603 caria; polymorphic light eruption may take days to appear. \200 Itching suggests polymorp hic light eruption or solar urticaria. \200 Face rashes, including the V of the neck, but sparing periorbital skin. \200 The dorsum of the hands and the arms are other typical si tes. \200 As hands are usually relaxed in the semi- \202 exed position, skin around DIP y g o o t a m r e D joins is less aff ected than that around the knuckles and PIP joints. l Is there a family history? If so, refer to genophotodermatologist. Is it xero- derma pigmentosum, Bloom \200\231s syndrome, or Cockayne \200\231s syndrome? \200 Pain ( family history) suggests erythropoietic protoporphyria (sun may hurt so much that a child quickly avoids it, so there is pain but no rash). \200 Was the rash related to starting a drug (eg nalidixic acid)? See below. \200 Are there papules: this suggests polymorphic light eruption. \200 Any blisters or linear marks where plants have scratched the skin (p hyto- photodermatitis from furocoumarins)? Ask about hobbies/work. Polymorphic light eruption: This is a common idiopathic disorder typically aff ecting young women in spring. After light exposure, itchy red papules, vesicles, and plaques develop on exposed sites, often improving over the sum- mer due to a phenomenon called \200\230harde ning \200\231. Smoking and alcohol may trig- ger it. 164 \201\227: Sun-avoidance; sun-prot ection (high factor UVA + UVB sunscreen). Acute attack: potent topical steroids a short course of systemic steroids. Severe cases: desensitization (UVB phototherapy or PUVA therap y). 165 Porphyria cutanea tarda: (The commonest porphyria) The 1 ab nor mality is \200 \201uroporphyrinogen decarboxylase in liver. Causes/triggers: some alleles of haemochromato sis gene; HIV; hepatitis C; alcohol; estrogen, \200\200iron, \200\201ascorbic acid. Signs: Vesicles/bullae in sun-exposed sites, hypertrichosis, hyperpigmen- tation, skin fragility, and scarring (milia). Tests: \200\200LFT; \200\200ferritin; \200\200plasma, fecal & urin ary porphyrins (protect urine from the light and ensure it gets analyzed promptly; phone la b). \201\227: Remove precipitants; sun-avoidance/protection; reg- ular venesection until f erritin in normal range; chloroquine, ascorbic acid. 166,167 Systemic lupus erythematosus: (OHCM p556) Light exposure often triggers erythematous rashes, with systemic \202 are. A variant of lupus, subacute LE, is associated with marked photosensitivity and anti-Ro antib odies. Drugs often cause of photosensitivity, so \200\207look up details of all drugs take n. Frequent off enders: thiazides (sunburn-like or lichenoid rash); tetracyclines/ sulfonam ides (sunburn-like); tricyclics; phenothiazines; NSAIDs; amiodarone (sunburn-like eruptions ). It may take months to settle, after drug withdrawal. Ordinary urticaria Acute: Rash (eg to latex) lasts <6wks. Skin prick or blood RAST tests (p596) may help. Chronic: Idiopathic, but can be auto immune in 45 % of patients (IgG against IgE receptor, 168 causing degranu lation, p610) or seen with collagen, thyroid or sinus disease. Physical urticaria is caused within minutes by an external trigger, eg heat, cold, exercise, or trauma (dermato- graphi sm). Contact urticaria arises eg on contact with food, insect bites, or pet saliva. Urticar ia pigmentosa ( \201 g 1, p610) May be caused by H. pylori. Urticarial vasculitis Cutaneou s lesions resemble urticaria, but histologically show features of a vasculitis. Also: \202 itting arthralgia, GI symptoms obstruc- tive lung disease especially in smokers. If co mplements are low, it may be as- sociated with SLE, Sj gren \200\231s syndrome, or cryoglo bulinaemia. \201\227: Antihistamine, NSAIDs, but some patients may need immunosuppressive therapy. 169 Skin disorders in old age Venous leg ulcers ( \201 g 2) Risk factors: Varicose veins, DVT, venous insuffi ciency, poor calf mus- cle function, arterio-venous \201 stulae, obesity, leg fracture. Venous hypertension from damaged valves of the deep venous system causes su- per \201 cial varicosities and skin changes (lipo- dermatosclerosis, \201 g 2). Minimal trauma typi- cally over the medial malleolus causes ulcers. Management: Graded compression is the main- stay. Do Dopplers \201 rst to exclude arterial disease (ensure the ankle \200\223brachial pressure index is >0.8, OHCM p658). 4-layer compression bandaging is ap- p lied with 40mmHg pressure at the ankle, ta- pering off to 18mmHg below the knee. This re- duces super \201 cial venous pressure. Ulcers heal more quickly with occlusive dressings which absorb exudate and improve comfort. Treat varicose eczema ( \201 g 3) with emollient s and topical steroids. Infection is most chie \202 y caused by Staph aureus, Pseudomonas, and \200 -haemolytic strep. These should be treated empirically (broad-spectrum penicilli n: macrolide or quinolone) until de \201 ni- tive sensitivities are available. Avoid topic al antibiotics as they \200\200 the risk of re- sistance and contact dermatitis. Ulcers wh ich don \200\231t heal on adequate treat- ment for 3 months must be investigated further (e g biopsy for malignancy). Once an ulcer is healed, patients should follow advice aimed at p reventing re- currence: wearing compression stockings, skin care, leg elevation, calf exerc is- es, and suitable diet. Annual recurrence rate: 20%. 170 Asteatotic eczema (eczema craq uel ) Com- moner in the elderly, this particularly aff ects the lower legs with a dry ecze ma which polygonally \201 ssures into a crazy-paving pattern ( \201 g 1). Emol- lients a nd soap substitutes help. 171 1% pimecroli- mus cream may help itch. Rare (paraneoplastic) association: lymphoma (suspect if the eczema is diffi cult to treat). Pruritus is a common complaint in the elderly. Skin causes: Eczema; scab- ies (appearance can be in the elderly) ; pemphigoid/pre-pemphigoid erup- tions; asteatotic eczema; generalized xerosis. Medical ca uses: Anemia; polycythaemia; lymphoma; solid neoplasms; hepatic and renal failure; hypo- an d hyperthyroidism; diabetes (candidiasis). Excluded by blood tests. Pressure sores If made immobile by age, stroke, or cord lesions, uninter- rupted pressure on skin leads to ulcers and extensive, painful, subcutaneous destruction, eg on the sacrum, heel, or greater trocha nter. Protein malnutri- tion and arteriopathy make this more likely, particularly if nursin g is poor. They are a big problem. Cost: > 800 million/yr. 172,173 A full-thickness sacral sore causes much misery and extends hospital stay by months. \200\207This should make pre vention a central preoccupation, not just on long-stay geriatric wards, but in all acute wa rds, where most pressure sores start. Nurse edu- cation, \200\200staff numbers, and nursin g comatose patients prone (with a prone- head support system) may help. 174 Don \200\231t r ely on special mattresses! 175 604 Typical causes \200 Gravity/stasis \200 Neuropathy \200 Vascular: venous 75%; arterial 10%; mixed 15% Trauma Rarer causes \200 Pyoderma gangrenosum (eg with Crohn \200\231s; UC) Sickle-cell disease \200 Vasculitis (SLE, rheumatoid) \200 Vasculitis (eg SLE) \200 C ryoglobulinaemia \200 Malignancy \200 Leishmaniasis y g o o t a m r e D l Fig 1. Eczema craquel . Dr Baron. Staging Stage Stage Stage III: Full thickness skin loss, extending into fat Stage IV: Destr uction of muscle, bone, or tendons Prevalence: 7% of inpatients have pressure sores; >70% are over 70yrs. Up to 85% of paraplegic patients have pressure sores. Complications: Osteom yelitis. I: Non-blanching erythema over intact skin II: Partial thickness skin loss, eg shallow crat er 605 Treatment and prevention of pressure sores \200 Prevent the condition getting worse (see below). \200 Optimize nutrition (get systematic help).176 Insulin if hyperglycaemic. \200 Treat systemic infection with antibiotics (evidence is lacking on whether antimicrobi als are eff ective in the treatment of pressure ulcers.) \200 177 \200 Dress the area. T here is no convincing evidence from randomized trials which favors any one type of dressing. \200 Elevation may increase perfusion around heel pressure sores.178 \200 Debridement of dead or necrotic tissue, or other debris, from the wound. \200 Topical negative pressure treatment. \200 Vascular reconstruction, if need ed, and if practicable. \200 Split thickness skin grafts. \200 Neurosensory myocutaneou s \202 ap surgery. Prevention \200 Find an interested, knowledgeable nurse to educate t he patient. \200 Proper positioning, with regular turning (eg every 2h, p768 \200\223p776 , alternat- ing between supine, and right or left lateral position). Use pillows to sepa- r ate the legs. \200 On ITU, anatomical foam supports do prevent heel pressure ulcers.179 \200 Functional electrical stimulation can prevent sores in paraplegics, by inducing the b uttocks to change shape, and by improving blood \202 ow. A good randomized trial (N=44 pa tients aged 85yrs with hip fracture) showed that a DeCube mattress with removable cubes for provision of rest for pressure points can halve the incidence of pressure sores.180 y g o o t a m r e D l Fig 2. Venous leg ulcer (with eczema). Is there healthy granulation tissue on the ul- cer \202 oor? Remove all that over-ripe cam- embert pus to \201 nd out. Pain is frequent in these patients (who are often obese, so compounding immobility). Dr S Baron. Fig 3. Varicose eczema with hyperpig- mentation and lipodermatosclerosis (an ill-de \201 n ed band causing leg tapering, as if a bottle with a tightish neck were pouring liquid rhuba rb down towards the ankle). Dr J Bowling HIV: infectious and non-infectious skin problems Skin disease is a burdensome stigma for HI V patients and a challenge to us all due to severity and recalcitrance. 181 Skin problems a re markers of HIV progression, so understanding them is vital. 182 They are classi \201 ed as primary (eg seroconver- sion illness) or secondary (eg opportunistic infections that co rrelating with \200\201CD4 levels). The full scope of primary HIV skin disease has yet to be elucidated. \200\207Any new lesion in HIV patients must prompt a hunt for unusual organ isms. With highly active antiretrovirals (HAART, OHCM p415), some are becoming less common. HIV skin pathologies may co-exist with conditions re \202 ecting the same risk exposure ( eg secondary syphilis rash or condylomata lata, or sometimes rare complications, eg chronic annular plaques of nodular tertiary syphilis). 183 Infections HIV +ve people are at \200 \200risk from common pathogens (in their nastier guises, eg MRSA) and commensal organisms t hat don \200\231t normally cause disease. \200 HIV seroconversion causes an acute mononuc leosis-type illness, usually ac- companied by a non-speci \201 c maculopapular eruption af f ecting the upper trunk, associated with lymphadenopathy, malaise, headache, and fever. 606 Thrush may be severe, disseminated, and treatment-resistant, involving the posterior pharyn x and esophagus. \201\227: Topical nystatin; systemic imidazoles. \200 Tinea (eg on head ) is a common and early HIV-related mycosis. 184 \200 Warts are common; oral warts cause cancers (p570); verrucas: Risk \200\200 \211\210 4. \200 Molluscum contagiosum: (eg face ; genitals). \201\227 (diffi cult): cryotherapy, topi- cal retinoids, cautery, or curettag e. \200 \200 : Disseminated cryptococcosis. \200 Malignant syphilis: Multiple cutaneous ulcers and leonine features. 185 \200 Cryptococcosis: Looks like facial molluscum contag iosum. \201\227: Fluconazole. \200 Helminths: Non-blanchable macules; examine sputum, fe ces, etc for eggs. 186 \200 Scabies: Severe variants, eg crusted are more common in advan ced HIV dis- ease. Paradoxically, patients may not complain of severe itch. A widespread sc aly, crusted eruption occurs (highly infectious p608). \201\227: Permethrin lotion. Iverme ctin may also be of bene \201 t (but side eff ects may be serious). y g o o t a m r e D l In \202 ammatory disorders Seborrhoeic dermatitis: (31%) Red scaly patches on hairy areas and naso-labial folds & \202 exures. \201\227: Ketoconazole cream. Others: \200 Oral p igmentation (29%), xerosis/ichthyosis (23%), pyodermas (22%). \200 Psoriasis: Treating HI V will often improve response to standard \200\224 (p594). \200 Eosinophilic folliculiti s: The cause of this intensely itchy rash is unknown \200 : Biopsy. \201\227: 0.1% tacrol imus, topical steroids, UVB therapy, PUVA therapy. 187 \200 Drug reactions are common in HIV (esp. co-trimoxazole \200\231s maculopapular eruptions or erythema multiforme; toxic ep idermal necrolysis; \201 g 2 p601). \200 Pityriasis rubra pilaris is rarely the present ing feature of HIV, eg with palmo- plantar keratoderma, long horny keratotic spiny follicul ar papules coalescing to form orange plaques, eg over ears, limbs, and trunk. 188 Cause: un known. \200 Darier \200\231s disease: (= keratosis follicularis; rare; re \202 ects Ca2+ dysregulation of synthesis, folding, and traffi cking of desmosomal proteins, eg from muta t i- ons in ATP2A2) 189 Signs: many follicular keratotic red-brown papules on scalp, face, retroauricular area, ears, sternum, upper trunk, hands, axillae & groins. 190 HIV & nail ch anges: Onychomycosis (30%; eg Trichophyton rubrum; multiple fungi are often cultured in a s ingle patient); melanonychia (15%); leukonychia (14%); transverse lines (7%), onychoschizia (7%); clubbing (6%). 191 HIV & skin neoplasia Kaposi (BOX), BCC, skin lymphoma, MCC,1 leuk oplakia ( \201 g 2). IR(I)S (Immune reconstitution (in \202 ammatory) syndrome) With anti retro virals, immunity begins to recover, but then responds to previously acquired oppor- t unistic infection with a powerful in \202 ammatory response, paradoxically wors- ening sym ptoms, often involving the skin. You may confuse this with serious HIV progression. IRS is hardly ever fatal. 192,193 607 Herves viruses and HIV Herpes simplex virus infection: This can be increasingly troublesome as HIV progresses. Painful ulcers and erosions develop, eg around mouth and genitals. Any ulcerated or eroded area is HSV until proven otherwise. \201\227: High- dose aciclovir (or al or IV). Aciclovir resistance may develop and foscarnet is an alternative. Start a more h ighly active antiretroviral therapy (HAART). 194 Varicella zoster: This may occur with atyp ical signs. Ulceration and post- herpetic neuralgia may be more frequent and severe. In adv anced disease, disseminated infection occurs. \201\227: High-dose aciclovir (IV if systemi c disease). Kaposi \200\231s sarcoma (KS): Cause: HHV-8 (herpes hominis virus). There is pr oliferation of vascular endothelial & lymphoreticular cells multicentric skin nodules/ p laques ( \201 g 1). 4 types: classic KS (typically on legs), endemic (Af- rican) KS, iatro genic KS, and epidemic AIDS-related KS, often multi-organ (skin is not always involved); 19 5 incidence is falling thanks to HAART (OHCM p415). HHV- 8 sero prevale nce is higher in me n who have sex with men (NB: no spread). 196 Kiss het erosexual transmission (if much saliv a ex- changed) may be important in HIV+ve & \200\223ve men. 197 \201\231 \201\231: Bacill ary angiomatosis (Bartonella species); pyogenic granuloma. \201\227 : (if HIV +ve) HAART; radiotherapy can palliate symptomatic disease (esp. if unable to tolerate chemotherapy, eg liver failure). Local \200\224: intralesional chem- otherapy, cryo, laser, photodynamic tr eatment, and excision. 199 Systemic interferon- \200 or chemotherapy (eg pegylated-liposom al anthracyclines & pa- clitaxel). In resource-limited settings, consider IV vincristine, o ral etoposide or IM bleomycin. 200 HAART does not greatly in \202 uence other HIV malignan cies. 201 y g o o t a m r e D l Fig 1. Kaposi \200\231s sarcoma. Purple macules, papules, nodules, and plaques aff ecting l imbs, and face periorbital purpura/raccoon eyes ( \200 \200 : skull frac- ture, myeloma , amyloidosis, OHCM p355, \201 g 1), and neuroblastoma). 198 Also seen in mucosae, eg ora l, tongue, appendix, prepuce. Dr S Baron. Fig 2. Oral hairy leukoplakia (adherent white plaques) is caused by Epstein \200\223Barr vi rus in oral mucosa. \200\230Corrugated \200\231 would be a better term than \200\230hairy \200\231 as there are no hairs. Associations: HIV (esp. if CD4 <200/mm3); 202 immunosuppre ssives (steroids), eg in transplant pa- tients; lamotrigine. \201\227 (if needed): Topical podophyllum 25% resin + aciclovir 5% may work 203 systemic aciclovir or valaciclovir. 2 04 Other oral signs of HIV: KS, candida, linear gingival erythema, and necrotizing ulcerati ve periodontitis/gingivitis. Prof D. Rosenstein 1 MCC (Merkel cell cancer) is a rare, aggressive neuroendocrine skin malignancy, and positi vely correlates with UV exposure and immunosuppression; see p502. Infestations Scabies (Sarcoptes scabei; \201 g 1) A highly contagious, common disorder pa r- ticularly aff ecting children and young adults. Spread: direct person to person, eg by h olding hands or prolonged hugs. The \200 mite digs a burrow (pathogno- monic sign \200 \224a short, wavy, gray or red line on the skin surface) and lays eggs which hatch as larva e. The itch and subsequent red rash is probably due to allergic sensitivity to the mite or its products. Signs: It presents as very itchy papules, vesicles, pustules, and nodules aff ecting \201 nger-webs (esp. \201 rst), wrist \202 exures, axillae, abdomen (esp. aro und umbilicus and waistband area), but- tocks, and groins (itchy red penile or scrotal papu les are virtually diagnostic). In young infants, palms and soles are characteristically inv olved. The eruption is usually excoriated and becomes eczematized. Mites can sometimes be e x- tracted from burrows and visualized microscopically; eggs can be seen in skin scrapings. Crusted or Norwegian scabies is seen in the elderly or immunocom- promized. They harbor up to 2 million mites and are highly contagious. If it occurs on your ward, get help. Simulta nous mass prophylaxis may reduce the need for ward closures.205 Management: A good explanat ion (verbal + written) will aid concordance between the patient \200\231s and the doctor \200\231s requirements, and will promote the chances of successful cure.206 Permethrin 5% d ermal cream is probably the most eff ective topical agent. It is also drug of choice for pr egnant women. Preparations are applied to all areas of the skin, from the neck down, for 24 h. Areas which are washed during this period (eg hands) should have treatment re-applied. M alathion is a good second choice. Oral ivermectin is also eff ective (200 g/kg stat (may n eed repeating).207 All members of a household should be treated at the same time, even if a symptomatic. The rash and symptom of itch will take a few weeks to settle, occasionally lon ger. A suitable anti-pruritic such as crotamiton cream (Eurax ) (which also has anti-scabe tic activity) can be useful during this period. Example of written advice: \200 Take a wa rm bath and soap the skin all over. \200 Scrub the \201 ngers and nails with a \201 r m brush. Dry your body. \200 Apply permethrin or malathion 0.5% liquid (not if pregnant o r <6 months 608 y g o o t a m r e D l old). Remember to paint all parts, including soles (+head if <2yrs old). Wash off after 24h. If you wash your hands before 24h is up, reapply the liquid to the parts you have washed. Avoid the eyes! Use fresh pillow cases and sheets, if you have any. \200 Treatment may worsen itch for 2 weeks \200\224so use calamine lotion or Eurax . Headlice (Pediculus capitis; \201 g 2) a re common in children; but spread is only by head to head contact. Lice are 3mm long and ha ve legs adapted to cling to hair shafts. Eggs (nits) are bound \201 rmly to the scalp hai rs and when empty ap- pear white. Signs: Itch papular rash on the nape. Neurotoxic agent s: (work in 70% \200\224alcohol based: take great care not to ignite): Malathion, carbaryl , phe- nothrin (repeat after 1 week). Resistance is a problem so many health boards operate treatment by rotation. Non-irritant options: Dimeticone (4%; repeat at 1wk).208 Hot air at temperatures lower than blow-dryers can be eff ective.209 Meticulous combing (see BOX). On ly treat head-to-head contacts (over the past 5wks) if they have lice (say to have a carefu l look). Crab lice (Phthiriasis pubis) Often sexually transmitted and aff ect pubic hairs. Eyebrows, eyelashes, and axillae may also be involved. Management: Topical malathion to all aff ected (or potentially aff ected) areas. Look for evidence of other sexually transmitte d diseases. Treat all sexual contacts. Flea bites (Pulicidae) spread plague, typhus, and ca t-scratch disease. The ani- mal (eg cat or dog) which spreads the \202 ea may not itch or scratch itself. Flea bites cause a papular urticaria in a sensitized individual. Treatment : de- \202 ea pets; de- \202 ea household carpets and soft-furnishings. 609 y g o o t a m r e D l Fig 1. \200\234Doctor, have I caught scabies? \200\235 \200\234Do you recall sharing bedd ing, clothing, or towels with anyone, 4 \200\2236 weeks ago? Have you cuddled a pet? Or bee n to an institution? Is the itching worse at night? \200\235 Look for rows of irregular or s-shaped red furrows in web spaces, axillae, ventral skin on wrist, knee or penis (also pal ms & soles in children). Here is a scabies burrow with a mite just visible (with the eye of faith) beyond the red area. Dr J Bowling. Advice on detection combing for head lice Seeing lice is hard; using a special \201 ne comb (prescribable, or bought at chemist) is 3 \200\2234-fold better than simple measures. 210 Here \200\231s how to do it. \200 Wash hair with ordinary shampoo, rinse, and apply lots of ordinary conditioner. Comb the hair with a normal comb to un- tangle it; then use the \201 ne-toothed comb. Slo t its teeth into the hair roots so they touch the scalp; draw it through to the hair tips. Ensure all hair is combed; check comb for lice after each stroke (use a magnifying glass). If lice seen, clean comb by wiping it on tissue, or rinse it before the next stroke. Combin g takes 1h. NB: nits (empty eggshells) don \200\231t mean live lice, as they can stick to hair even if lice have gone. After all hair combed, rinse out conditioner. \200 Repeat combing every 4 days; only stop when no more lice have been seen for 12 days. 211 Fig 2. Pediculus humanus. Prof S. Upton, Kansas Univ. The \202 ea (as lovers \200\231 go-between) Mark but this \202 ea, and mark in this How little that which thou deny \200\231st me is; Me it suck \200\231d \201 rst, and now sucks thee, And in this \202 ea our two bloods m ingled be; Confess it; this cannot be said A sin, or shame, or loss of maidenhead, Yet this enjoys before it woo, And pamper \200\231d swells with one blood made two, And this, alas, is more than we can do. Oh stay, three lives in one \202 ea spare, Where we almost, nay more than married are: This \202 ea is you and I, and this Our marriage bed, and marriage temple is. John Donne, to his lover, circa 1600. Mast cell disorders Mastocytosis (urticaria pigmentosa) There are too many mast cells in th e skin ( other organs), eg in nests or as a single mastocytoma. These release his- tamine , leukotrienes, and heparin (with systemic eff ects) and proteases (local eff ects). Adults have mutations of the stem cell factor receptor (kit D816V).212 610 Signs: red-brown itchy macules/pap- ules ( \201 g 1) which urticate, ie become more itchy, swollen, red ( weals) if scratched \200\224Darier \200\231s sign. Also: head- Courtesy o f Dr Sue Burge. ache, palpitations, syncope, \202 ushing, wheeze, D&V, hepatosplenomegaly , os- teoporosis, osteosclerosis, anemia, eosinophilia, mast cell leukemia (rare).213 \201 \231 \201\231: Multiorgan multifocal in \201 ltrates of mast cells, plus one of: a) >25% o f mast cells have abnormal morphology b) C-kit mutation at codon 816 c) Mast cells in marro w express CD2 or CD25 d) Serum tryptase \200\200.214 \201\231 \201\231: Sarcoid; histiocyt osis. \201\227: Avoid triggers (eg aspirin, heat, cold). Try antihistamines + disodium cro - moglicate. UVB phototherapy,215 Nd:YAG lasers, interferon, and cladribine may help. D816V kit mutation predicts resistance to imatinib, while the FIP1L1-PDGFRA mutation suggests a good response to low-dose imatinib.216 Fig 1. Mastocytosis. y g o o t a m r e D l Lasers in dermatology Lasers (light ampli \201 cation by stimulated emission of radiation) have an in- creasing role. The destructive energy of lasers can be concentrated in time an d space, and the light \200\231s wavelength can be adjusted to match the target lesion. Ene rgy can be selectively taken up by targets as long as the volume delivered is less than the target \200\231s capacity to absorb it. If this limit is exceeded, unnecessary destruction is caused. Variables to specify \200\224an example from treating keloid scars: wavelength 585nm, pulse duration 0.45msec, spot size 5mm, mean \202 uence per pulse 7Joules/cm2, tre atment interval: 6 weeks. NB: melanin in dark skins may be a problematic competing chromoph ore. Photoacoustic damage by shock waves (intense energy over picoseconds). Photocoagulatio n implies less rapid, and less intense treatment. Selective photothermolysis is somewhere b etween the above 2 categories. It may produce minimum scarring. Examples of laser-treatable skin disorders Tuberous sclerosis: (p638) Angio \201 bromata (misnamed adenoma sebaceum) can cover much of the face. Port wine stain: (OHCM p703) Best treated when young (small, sm ooth lesions). Strawberry naevi: (p602 & \201 g 1 p121) These do not need treatment, unle ss they fail to resolve spontaneously. If they ulcerate, get expert advice. Flat, pigmented lesions: Problematic unless known to be benign. Tattoos: If multicolored, multiple wavelen gths must be used. Scars: Raised, red, nodular keloid scars may appear ugly (and itchy); la sers can help somewhat. Acne scars (atrophic or \200\230ice-pick \200\231). UV phototherap y UVA315 \200\223400nm & UVB290 \200\223315nm stabilizes many skin conditions when topical or systemic agents disappoint. In the neonatal nursery blue light (459 \200\223460nm) reduc es bilirubin levels and prevents kernicterus. Psoralens and UVA (PUVA): see p595. Narrowban d UVB (311nm) can help atopic dermatitis, pso- riasis, vitiligo, morphea, mastocytosis, and lymphocytic in \201 ltrative diseases (mycosis fungoides, alopecia areata and pityriasis lichenoides).217 Protect the eyes. Local delivery of narrowband UVB can be given by excimer laser (308nm). \201\201 611 The skin, identity, and psychodermatoses To construct a coherent identity, we must distingu ish what belongs to the ex- ternal, perceived world from what belongs to our inner world. T he skin marks this boundary and can become the battle- \201 eld where diff erent identitie s \201 ght for dominance (see case report1). In a famous thought-experiment, Arthur Rimba ud spells out the advantages of connecting with universal monstrosi- ties by receiving graf ts of warts to his face, for gleeful cultivation 218 \200\224in order to free himself from not just from his past selves, but from the stability of identity in general and so to beco me strong, aware, and vis ionary. Dermatolo- gists rarely recommend his methods, but unless we develop the \202 exibility to understand this and related points of view,1 our patien ts with self-mutilation and dermatitis artefacta will never be understood by us. y g o o t a m r e D The range of self-destructive skin phenomena: neurosis/obsessiveness, neurotic excoriations (compulsive picking at the skin), and trichotillomania \200\224 and psychosis ( \200\234I make holes in my skin to let the demons out \200\235) and dermati- tis artefacta re \202 ecting diffi culties with the solidity of these patients mental and physical limits. For th ese men and women (not necessarily patients) their real skin is metaphorically linked to th e fantasized mental structure that de- limits individual mental space. They are said (accor ding to the Anzieu moi- peau hypothesis) to show a pathology of action and attack their own skin, paradoxically, to test the solidity and reliability of their own limits. 219 Dermati tis artefacta 3 key signs diff erentiate dermatitis artefacta from other psychodermatoses: 1 Lack of direct suicide ideation. 2 Denial of respon- sibility for the lesions. 3 Resistan ce to the idea that the lesions are important unconscious non-verbal messages (eg dealing w ith emotional deprivation). Associations: Any chronic medical or skin condition, eg acne, a lopecia, leg ulcer (which they may encourage); also psychosocial problems, eg borderline pe rsonality, p366; stress; unemployment; depression; anorexia nervosa (in 33%); chronic pain syndrome; sexual con \202 icts. There is overlap with M nch- hausen \200\231s and other p athomimicry, factious or somatizing syndromes. Epidemiology: Typical age: any, eg as young as 3yrs. 220,221 \200 : \200 \211\2106:1. In con- script armies sex ratios may reverse (t here is usually obvious secondary gain). Signs: Variable (simply showing images can be very misleading). Look for unusual/inexplicable features. Diagnostic work-up: Background: Is th ere borderline personality disorder or anorexia nervosa? Any secondary gain? What does the family think? Is there a spouse? If not, why? (Could the rash be protecting your patient fr om an un- fortunate marriage?) But don \200\231t ask too many questions: you risk only gett ing answers in reply, when what you need is insight. Histology: non-speci \201 c. Self- in jection of foreign matter eg causing abscesses is provable by spectrometry. Treatment: Supp ortive care will only gain traction once issues surrounding emotional deprivation, isolatio n, insecurity and other psychological states are addressed. Don \200\231t just prescribe an tidepressants or antipsychotics and move on. Spend time with your patient and develop a ric h therapeutic alliance. In- clude the family. Avoid addictive drugs. Find a specialist (GP, dermatologist, or psychiatrist) who enjoys a nice juicy holistic challenge of epic ectoder mal proportions and who can roll skin and brain into a single uni \201 ed management plan. Don \200\231t lapse into idle confrontations. If this method is to be tried it must be car efully planned. Acceptance may be a better approach. l 1 14-yr-old girl presented with many large, deep ulcers with unnatural shapes on her left f orearm, leading to a provisional diagnosis of dermatitis artefacta. Psychiatric examination revealed that she had dissocia- tive identity disorder and that mutilations only occurred when one of her identities was assumed. 224 612 9 Anesthesia Pre-operative assessment The history 613 The examination 614 Tests 614 ASA classi \201 cation (American Society of Anesthesiologists) 615 Premedication 616 Equipment and anesthetic agents Inhalational agents 618 Commonly used IV anesthetic agents 620 Other IV anesthetic agents 6 21 The ideal IV anesthetic agent 621 The ideal inhaled anesthetic agent 621 Neuromuscular b lockers 622 Practical conduct of anesthesia Fig 1. Immuno \202 uorescent labeled image of the motor unit including the neuromuscular j unction (NMJ). Axons and nerve terminals (in green) are marked with anti bodies against neu ro \201 lament and synap- tophysin respectively. Acetylcho- line receptors (in red) are la beled with rhodamine- \200 -bungarotoxin. Blockade at the NMJ is just one arm in the triad of: Induction 624 Airway control 624 Mechanical ventilation 625 Intubation 626 Rapid sequence i nduction (RSI) 626 Maintenance of anesthesia 626 End of anesthesia 626 Intubation technique 627 Monitoring during anesthesia 628 Some complications of anesthesia 628 Sedation and rec overy 630 Local and regional anesthesia 632 \200\2235 Pain management 636 Muscle relaxation Hypnosis and Analgesia that is required for eff ective an- aesthesia. See p622 for how we can interpose at this ju nction in the safest possible manner. Image courtesy of Prof. Mendel Rimer, School of Biological Sciences, University of Texas, A ustin. Other relevant pages Pain relief in labor (p66); resuscitation after delivery (p107); neona tal ITU (p108); ventilating neonates (p110); major injury (p724); choosing the correct dose of lidocaine according to body weight (p729); pain relief in children (p719); Bier \200 \231s block (p744). Online resources www.frca.co.uk Introduction Anesthesia evolved from humble origins in 1842 when CW Long gave ether, but he failed to report this landmark in pain relief. Then, in 1844, Horace Wells used nitrous ox ide for tooth extraction (p617), and in 1846 WTG Morton gave the \201 rst surgical anesth etic with ether. It is now a highly sophisticated spe- cialty in its own right. While the t riad of anesthesia (hypnosis, analgesia, and muscle relaxation) remains the fundamental pri nciple behind general anaes- thesia for surgery, the role of the anesthetist has expanded t o encompass not only the provision of ideal operating conditions for surgery, but also inte nsive care, resuscitation, alleviation of acute and chronic pain, obstetric anesthesia and anesthesia for diagnostic procedures. A detailed knowledge of general medicine, physiology, pharmacology, the physical properties of gasses and the workings of the vast array of anes thetic equipment are essential in order to practice well. \200\207We emphasize that this short chapter is no substitute for a specialist text or for experience on the ward and in theater or clinic. The main aim is to en- able understanding of the issues anesthetists face, and to prepare one \200\231s mind for intelligent discuss ions on anesthetic issues. We thank Dr Mike Nathanson \200\224our Specialist Reader for thi s chapter. \200 613 Pre-operative care Aims To ensure that patients: \200 Get the right sur- gery \200 Are happy and pain free \200 Are as \201 t as possible \200 Have individualized decisions on type of anaesthe- sia/analgesia taking into account risks, bene \201 ts, and wishes. T he pre-operative visit Have the symptoms, signs or patient \200\231s wishes changed? If so, inform the surgeon. Assess cardiovascular and respira- tory systems, exercise tolerance, e xisting illnesses, drug therapy, and allergies. Assess past history \200\224see MINIBOX. Fa mily history Ask about malignant hyperthermia (p628); dystrophia myotonica (OHCM p514); por phyria; cholinesterase problems; sickle-cell disease (test if needed). Does the patient hav e any speci \201 c worries? Drugs Ask about allergy to any drug, antiseptic, adhesive band age, & latex. \200 ACE inhibitors: No special action is required if BP & u&E are OK. \200 Antibiotics: Aminoglycosides, colistin, and tetracycline prolong neuromus- Past history screen: \200 MI or IHD \200 Asthma/COPD \200 Hypertension \200 Rheumat ic fever \200 Epilepsy \200 Liver/renal disease \200 Dental problems \200 Neck prob lems \200 GI re \202 ux or vomiting (needing rapid sequence induction \200\224see p626) a i s e h t s e a n A Past anesthesia/ problems (eg intubation diffi culty/PONV) Recent GA? cular blockade, even depolarizing neuromuscular blockers. Anticoagulants: Know the indication. Check the INR and switch warfarin to heparin pre-opera tively, leaving suffi cient time for the INR to drop to <1.5 before surgery. Admit early, a nd discuss the plan of action so that all goes smoothly. Avoid epidural/spinal blocks. Bewa re regional anesthesia. Anticonvulsants: Give the usual dose up to 1h before surgery. Give drugs IV (or by NGT) pos t-op, until able to take oral drugs. Sodium valproate: an IV form is available (give the pa tient \200\231s usual dose). Phenytoin: give IV slowly (<50mg/min). IM phenytoin absorption is unreliable. Beta-blockers: Continue up to and including the day of surgery as this re- duces the likelihood of a labile cardiovascular response. Bronchodilators: Continue and consider supplementing with nebulizers. \200 Contraceptive Pill: See BNF. Stop 4 weeks before major (or leg) surgery, restarting at 2wks post-op if mobile.