► Box 15.1 Features of serious causes of rash
Bacterial infections causing a rash
Viral infections causing a rash
►► Call for senior help early if patient unwell or deteriorating.
• 15L/min O2 if short of breath, O2 sats <94%, or unwell
• Monitor pulse, BP, put on defibrillator ECG leads if unwell
• Obtain a full set of observations including temp, BP, and RR
• Take history if possible/check notes/ask ward staff
• Examine patient: skin examination and condensed CVS, RS, abdo
• Establish likely causes and rule out serious causes
• Look for the findings listed in Box 15.1 which may aid diagnosis.
► Box 15.1 Features of serious causes of rash
Fig. 15.1 Meningococcal septicaemia in a young infant with purpura.
Reproduced from Lewis-Jones, S. Paediatric Dermatology 2010, with permission from Oxford University Press.
► Worrying features RR >30, sats <92%, wheeze, systolic <100mmHg, confusion, tachy/bradycardia, rapidly changing, painful, blistering, or non-blanching rash.
Think about ► Life-threatening Meningococcal septicaemia (Fig. 15.1), necrotizing fasciitis, toxic epidermal necrolysis, Stevens–Johnson syndrome, urticaria (anaphylaxis), staphylococcal scalded skin syndrome; Other acute Cellulitis, viral exanthem (eg chickenpox, measles), shingles, erythema nodosum, erythema multiforme, vasculitis (eg Henoch–Schönlein purpura). Chronic Psoriasis, dermatitis (eg atopic, contact), vasculitis, erythema ab igne, bullous disease (eg bullous pemphigoid and pemphigus vulgaris).
Ask about Speed of onset, distribution of rash, pain, associated symptoms, exacerbating and relieving factors, family history; PMH Previous skin disease, joint/GI disease, immunosuppression, weight loss; DH Allergies, new medication, vaccinations, previous drugs to treat skin disease; SH Occupation, exposure to irritants, pets, exposure to others with illness/skin disease.
Obs Temp, RR, BP, CRT, HR, O2 sats.
Look at Hands and nails for pitting, Janeway lesions or Osler’s nodes, splinter haemorrhages, and then examine affected area and fully expose rest of patient. Try to form a description of the lesions based upon size, shape, colour, palpability, blisters, and associated features (
pp. 140–141). Also examine the scalp, genitals, and mouth. Other examination as dictated by history.
Investigations Blds If suspect infection or systemic disease; FBC, CRP, ESR, U+E; blood cultures. Further investigation—Table 15.1.
Table 15.1 Investigating cutaneous eruptions
| Test | Use | Example |
| Skin swab | Viral PCR | Herpes simplex |
| Blood test | Autoantibodies | Systemic lupus erythematosus |
| Serology | Guttate psoriasis | |
| Nail clippings | Fungal culture | Onychomycosis |
| Patch testing | Allergy testing | Nickel allergy |
| Skin biopsy | Culture | Mycobacteria/fungi |
| Histology | TEN/SJS | |
| Immunofluorescence | Pemphigus/pemphigoid | |
| Skin scrapings | Fungal culture | Tinea |
| Microscopy | Scabies | |
| Skin swab | Bacterial culture | Impetigo |
| Wood’s light | Fungal fluorescence | Erythrasma (skin folds) |
Superficial epidermal infection typically seen around children’s faces.
Symptoms Weeping, spreading erythema, highly contagious.
Signs Erythema with yellow crust, serous discharge; occasionally blisters.
Investigations Skin swabs Show Staphylococcus aureus in >90% of cases, but group A streptococci (S. pyogenes) can be found.
Treatment Treatment of localized disease can be achieved with topical fusidic acid/8h for 1wk. More extensive impetigo may require oral antibiotics, eg flucloxacillin 1g/6h PO (for staphylococci) and phenoxymethylpenicillin 500mg/6h PO (for streptococci). Ensure close contacts are examined and treated if necessary; encourage good hand hygiene and avoidance of sharing towels.
Epidermal streptococcal infection with involvement of cutaneous lymphatics.
Results in painful, well-demarcated erythema (±lymphadenopathy); typically seen on face or legs.
Treatment As for cellulitis.
Non-necrotizing infection of the dermis.
Symptoms Hot, usually tender area of erythema, usually on leg or face; may be spreading; history of trauma to skin (insect bite, cannula site) or tinea pedis. May have systemic effects: fever, anorexia, N+V, diarrhoea.
Signs Warm spreading erythema (outline area with marker to observe response to treatment), ±mild oedema, break in the skin, serous discharge, can develop blisters, lymphadenopathy in draining nodes, ↑temp, ↑ HR, ↑ RR.
Investigations blds ↑ WCC and neutrophils, ↑ CRP/ESR; blood cultures if pyrexial; D-dimer likely to be raised in infection so not useful in differentiating cellulitis from DVT; Skin swabs Not usually helpful, but check multisite MRSA swab USS To exclude DVT (depending on Wells’ score p. 464) or ruptured Baker’s cyst.
Treatment Check local guidelines; likely organisms include S. aureus (may be MRSA) or group A streptococci:
• If patient is systemically well and has no other significant comorbidities, oral antibiotics (flucloxacillin 1g/6h PO; if MRSA suspected or proven doxycycline 200mg STAT then 100mg/24h PO)
• If signs of systemic upset (↑temp, ↑ HR, ↑ RR) or coexisting disease (DM, IHD, PVD), admit for short-course IV antibiotics (flucloxacillin 1g/6h IV; if MRSA suspected or proven vancomycin 1g/12h IV)
• ►► Necrotizing fasciitis ( p. 427.) Very unwell, ‘out-of-proportion skin pain’, rapidly spreading. Request senior help immediately
• ►► Orbital cellulitis Painful or restricted eye movement, proptosis or visual disturbance.
Box 15.2 Erythematous cannula sites
Cannulae should be dated and resited every 72h. If a cannula site is red and inflamed or pus is present, remove cannula, and clean and dress the site. Give flucloxacillin 1g/6h PO or clarithromycin 500mg/12h PO (if penicillin allergic) for 5d. Discuss with microbiology if MRSA+ve.
►► Necrotizing fasciitis ( OHAM4 p. 473.)
Symptoms Rapidly spreading painful erythema (pain disproportionate to rash) with features of sepsis, fever, unwell, ↓ GCS; may occur at break in skin or operation site but often no apparent trauma.
Signs Rapidly spreading blanching erythema (outline area with marker to observe rate of spreading), blisters, ±oedema, lymphadenopathy in draining nodes, sometimes crepitus over tissues, ↑temp, ↑ HR, ↑ RR, ↓ BP.
Investigations blds ↑ WCC and neutrophils, ↑ CRP/ESR, ↑lactate; Blood cultures and skin swabs/tissue aspiration May identify infective organism(s) but do not withhold treatment to do tests if patient is systemically unwell; X-ray May reveal gas in subcutaneous tissues of affected area.
Treatment ►► This is a surgical emergency.
• Seek senior help immediately (the moment you suspect, not once you have watched the fasciitis evolve and confirm your suspicions)
• Surgical debridement is the most important measure, consult senior surgeon without delay
• Likely to need combination of IV benzylpenicillin, gentamicin, clindamycin, and metronidazole. Seek urgent microbiology advice.
Pathogens These may be a mixture of aerobic and anaerobic organisms seen following abdominal surgery or in diabetics (type 1), a group A streptococcus (type 2), or clostridia (type 3—gas gangrene).
Outcome This depends upon speed of identification and initiation of treatment, as well as comorbidity and the site affected. Extensive tissue loss from surgery and necrosis is common; overall mortality is ~25%.
►► Meningococcal septicaemia ( OHCM10 p. 822.)
Symptoms Fever, non-blanching (purpuric) rash (note, early rash may blanch), joint and muscle ache, malaise; meningitis frequently occurs, reflected by headache, neck stiffness and photophobia.
Signs ↑temp, ↑ HR, ↑ RR, cap refill >2s, ↓ BP, non-blanching petechial or purpuric rash; meningism/photophobia if meningitis also present ( p. 364).
Investigations blds ↑ WCC and neutrophils, ↑ CRP/ESR, meningococcal PCR, deranged clotting if severe sepsis (DIC); Blood cultures. Do not withhold antibiotics before taking these if patient is unwell.
Treatment ►► This is a medical emergency.
• Airway, Breathing (give O2), Circulation (obtain IV access)
• Seek help immediately—contact your seniors as soon as you suspect
• If patient is in shock (systolic BP <100), involve ICU team urgently
• 0.9% saline 1L STAT IV and goal-directed fluid resuscitation ( p. 495)
Pathogen Neisseria meningitides, a Gram-negative diplococcus; since the introduction of a vaccine for serogroup C, serogroup B accounts for the majority of infections seen in Europe and North America.
Outcome This depends upon speed of identification and initiation of treatment. Mortality for meningococcal septicaemia is about 10% in the developed world. Complications in survivors include neurological deficits (eg cognitive impairment, deafness), limb amputation, renal failure, and adrenal failure (Waterhouse–Friderichsen syndrome).
Chickenpox (varicella zoster virus—VZV) ( OHCM10 p. 404.)
Symptoms These begin with fever and malaise 14–21d after exposure to VZV. The typical rash then develops: flat lesions initially, evolving to itchy scabs. Older children and adults are at risk for the development of pneumonitis or encephalitis, manifesting as breathlessness or altered mental function.
Signs ↑temp, ↑ HR, and presence of evolving rash; macules, papules, vesicles, pustules, scabs, in centripetal distribution (spreading out from the trunk). ↑ RR and ↓ O2 sats suggest respiratory involvement. Altered personality, ↓ GCS, or ataxia suggests CNS involvement.
Investigations Not usually undertaken but vesicular fluid can be examined under electron microscopy or sent for viral PCR; Serology Viral antibody titres can be monitored but this is seldom necessary; CXR may show diffuse consolidation in varicella pneumonitis; CT brain to exclude other causes of neurology in presumed varicella encephalitis.
Treatment Symptomatic with antipyretics and topical antihistamines. Antiviral therapy is usually given to patients >16yr (aciclovir 800mg/5h PO). In the immunocompromised or those with rare complications (pneumonitis, encephalitis), use aciclovir 10mg/kg/8h IV. Consider ICU admission for respiratory support in pneumonitis.
Pregnancy Primary VZV infection during the 1st 20wk of pregnancy is associated with 1–2% risk of foetal anomalies and spontaneous abortion; infection within 5 days of delivery is also associated with a risk of neonatal VZV infection. Women without a clear history of chickenpox should have viral specific IgG titres checked and if negative, should be offered VZV vaccination before becoming pregnant. The vaccine cannot be used in pregnancy, when primary infection may require zoster immune globulin (ZIG) to prevent the onset of disease, and oral aciclovir if the disease develops—discuss with microbiology.
Chickenpox Uncommonly affects an individual more than once. Shingles Reactivation of chicken pox virus; the virus lies dormant in the dorsal root/cranial nerve ganglia. Non-immune individuals Can catch chickenpox from patients who have either chickenpox or shingles; the infectious period runs from 48h prior to onset of the rash until all lesions crust over.
Symptoms Initially focal pain, followed by classical blistering rash in a dermatomal distribution (will not cross the midline), ±malaise. If multidermatomal, consider if patient immunocompromised.
Signs Erythematous papules, evolving into vesicles with pustules which crust over after ~7d. Usually thoracic or lumbar dermatome.
Investigations Clinical diagnosis, but vesicular fluid can be examined under electron microscopy or sent for viral PCR.
Treatment Antiviral therapy limits post-herpetic neuralgia and period of infectivity if started within 72h (valaciclovir 1g TDS 7 days PO); parenteral antivirals can be considered in immunocompromised (aciclovir 10mg/kg/8h IV). Treat pain with paracetamol, NSAIDs, and amitriptyline 25mg/24h PO.
• Herpes zoster ophthalmicus Involvement of the ophthalmic branch of the trigeminal nerve (CN Va); may lead to sight threatening keratitis; apply 3% aciclovir ointment to eye/5h and seek ophthalmic opinion
• Ramsay–Hunt syndrome ( OHCM10 p501.) Facial pain, vesicles in external auditory canal and ipsilateral facial palsy; complete recovery in <50%.
Symptoms Prodrome of fever, coryza, and cough; rash spreading from face and neck to trunk and limbs.
Signs ↑temp, ↑HR, conjunctivitis, pathognomonic grey ‘Koplik’ spots (rare to see!) on buccal mucosa seen ~2d prior to maculopapular rash.
Investigations None required routinely; measles serology in critically ill.
Treatment Supportive care; vitamin A supplements if malnourished; complications include pneumonitis, pneumonia, encephalitis; subacute sclerosing panencephalitis is a degenerative disease appearing ~10yr post infection.
Symptoms Rash with fever and coryza; adults may experience arthralgia.
Signs Discrete macular rash spreading from face to trunk and limbs; features of concurrent illness/infection (↑temp, ↑ HR, etc); tender lymphadenopathy.
Investigations None routine; blds ↑viral specific IgM during infection.
Treatment Supportive care; primary infection during 1st trimester of pregnancy carries ~90% foetal anomalies (eg deafness, cataracts).
Symptoms Rash associated with prodromal symptoms of viral illness (fever, myalgia, arthralgia, headache); may or may not be itchy.
Signs Widespread maculopapular rash; features of concurrent illness/infection (↑temp, ↑ HR, pharyngitis, etc). Rash associated with numerous viruses (echovirus, parvovirus, EBV, measles) so not diagnostic.
Investigations None required routinely; discuss with virology if unwell.
Treatment Simple analgesia; resolves over ~7d.
Symptoms Non-itchy rash on cheeks, which feel burning hot; later spreads to trunk and limbs; headache; otherwise well; usually in children.
Signs Erythematous rash on cheeks, and reticulate erythema (net-like rash) on proximal limbs then trunk; caused by parvovirus B19.
Investigations None required routinely.
Treatment Rash will subside over 7–10d; treat concurrent symptoms.
Symptoms Small painful vesicles usually around mouth or in genital area.
Signs Vesicles or pustules around mouth (usually HSV1) or in genital area (usually HSV2). Often resolve, but then return months or years later.
Investigations Not usually but vesicular fluid can be sent for viral PCR.
Treatment This consists of aciclovir 200mg/5h or 400mg/8h PO for primary HSV infections and painful genital infections. Treat facial and genital ‘cold sores’ with aciclovir 5% to affected area/4h topically.
Symptoms Small, non-itchy spots, occurring on trunk and limbs in childhood (skin contact) and around groin in early adulthood (sexual transmission); highly contagious.
Signs Small translucent papules (1–3mm), which look fluid-filled, but are actually solid, often with the central depression (punctum). Caused by a poxvirus, and usually resolve spontaneously after 6–12mth.
Investigations None routine; screen for other STDs in adults ( p. 479).
Treatment None required, 5% potassium hydroxide can be used in older children or adults.
Dermatophytes These are pathogenic fungi, causing a range of diseases.
Tinea corporis (‘ringworm’): mildly itchy, asymmetrical rash which spreads with a slightly raised, scaly edge, often leaving a clear centre.
Tinea faciei Dermatophyte infection of the face.
Tinea cruris Ringworm in the groin, though this lesion is often red and more plaque-like with a well demarked border.
Tinea pedis ‘Athlete’s foot’, is usually found in the webspaces of the toes, resulting in itchy skin which is fissured and macerated. If found elsewhere on the foot it is often more diffuse and scaly, but just as itchy. Pustules can occur.
Treatment Treatment of small focal areas of tinea can be achieved with topical antifungals (terbinafine, clotrimazole, miconazole, etc); more widespread infections require oral therapy (terbinafine, itraconazole).
Candida albicans Candida is a yeast, and thrives in warm moist areas, in children’s nappies (nappy rash), in body folds (intertrigo), and also in interdigital webspaces, mimicking tinea pedis.
The rash is erythematous with a ragged, peeling edge which may contains small pustules. The mouth and genital tract can also be affected and present with small white plaques/white discharge. Swab to confirm.
Treatment Remove predisposing factors (ensure skin remains clean and dry) and topical antifungal creams (clotrimazole); use drops (eg nystatin) or pessaries (eg clotrimazole) for oral and genital tract infections respectively; resistant infections may require oral therapy (eg fluconazole).
Scabies This is an intensely itchy rash, often worse at night, caused by the scabies mite, Sarcoptes scabiei.
Commoner in children and with social overcrowding (highly contagious). The rash is papular and found in the interdigital webspaces of the hands and feet, ankles, wrists, genitals, axillae, and umbilicus. Linear skin burrows are pathognomonic but not always present. Investigation: microscopic examination of skin scrapings/dermoscopy looking for mites.
Treatment Permethrin/malathion: is only successful if the whole body is treated, if all close contacts are treated and if bedding and clothing are washed. Itching may last up to 4wk after treatment. Severe infection may require PO treatment.
Lice These are blood-sucking parasites. Head lice (Pediculosis capitis) are commonest in children, spread by direct contact and can result in scalp excoriation. The presence of eggs (‘nits’) in the hair confirms the diagnosis. Body lice (Pediculosis corporis) are associated with poverty and not often seen in the developed world; excoriations on the skin are often the only sign. Pubic lice (Phthiriasis pubis or ‘crabs’) are transmitted by sexual contact and commonly affect coarse pubic hairs, but also leg, body, and facial hair.
Treatment Malathion/permethrin (resistance common). Close contacts should also be treated; clothing and bedding should be thoroughly washed on high temperatures.
OHCS10 p. 596.)Dermatitis (eczema) Found in ~10% of the population in various forms:1
• Atopic Onset usually in childhood; associated with asthma and allergies
• Contact Type IV hypersensitivity (delayed); may blister
• Venous eczema Seen in lower limbs of older patients with venous stasis
• Seborrhoeic Greasy scaling of scalp/central face, associated with reaction to skin yeast.
Symptoms These include itchy, dry skin, or patches of infected skin.
Signs Ill-defined erythematous patches with excoriations. Typically affect the flexures of the elbow, knees, and around the neck; vesicles and serous weeping (infected). Superimposed bacterial or viral infections are common. Chronic lichenification and hyperpigmentation can develop.
Treatment This is multifactorial and depends on underlying cause. Attempt identification and avoidance of known irritants/allergens. In atopic eczema, triple therapy with topical steroids ( p. 180), topical emollients, and bath oil and soap substitutes form the mainstay; step 4 treatments such as UVB/PUVA, ciclosporin, methotrexate, azathioprine may be prescribed by a dermatologist (Fig. 15.2). Treat bacterial superinfection promptly, eg flucloxacillin 1g/6h PO.
Fig. 15.2 Step-wise management of atopic eczema. † Calcineurin inhibitors include pimecrolimus (Elidel®) and tacrolimus (Protopic®).
Reproduced from J Allergy Clin Immunol, 118, Akdis, C.A. et al., Diagnosis and treatment of atopic dermatitis in children and adults, 152–69. © 2006, with permission from Elsevier. Available free at 
www.jacionline.org
Psoriasis Inflammation of the dermis, with epidermal hyperproliferation.2
Occurs in ~2% of the population, with peak incidences in the early 20s then again in the 50s. Exacerbations can be precipitated by infections, drugs (eg lithium, β-blockers), UV light, alcohol, and stress.
Symptoms Itchy, dry patches of skin which can bleed when scratched.
Signs Chronic plaque psoriasis Well-defined pink/red scaly plaques, especially on the extensor surfaces of elbows and knees, lower back and scalp; nail pitting is common; Pustular psoriasis can be generalized (emergency) Affects palms and soles; Guttate psoriasis Occurs acutely, often 2–3wk after a streptococcal throat infection, causing numerous small pink papules/plaques on the trunk; Flexural psoriasis Tends to occur in later life, and forms in flexures Treatment Symptom-led and largely topical; emollients, mild to moderate topical steroids, vitamin D analogues, retinoids and purified coal tar are common topical treatments. Specialist use of UVB/PUVA, methotrexate, ciclosporin, anti-TNF therapy, and use of other biologic therapies may be considered, especially if associated psoriatic arthritis ( p. 470).
(hives or ‘nettle rash’). Characterized by the formation of intensely pruritic papules or plaques (‘weal’) which are pale initially but become erythematous with a surrounding rim of pale skin or erythema (‘flare’). Acute (<6 weeks): common in response to certain topical chemicals (eg nettle sting) but also in response to systemic drugs (sometimes part of anaphylaxis) or antigens (eg blood transfusion) or virus. Chronic (>6 weeks)—well patient, fluctuating urticarial rash, cause often unknown. Treat with antihistamines.
Erythema nodosum Characterized by tender, erythematous nodules or plaques, typically on the shins. Commoner causes: infections (streptococcal (commonest), Mycoplasma pneumoniae, TB, and EBV), sarcoidosis, inflammatory bowel disease, autoimmune disorders, pregnancy and drugs (sulfonamides and the oral contraceptive pill) ( OHCS10 p. 588).
Erythema multiforme This is a hypersensitivity rash and has two subtypes. Erythema multiforme minor Produces ‘target’ lesions, with a red centre, a clear circular area, and an outer red ring. Erythema multiforme major A similar rash with involvement of one or more mucous membranes (classically the mouth). Often no precipitant is identified (~50%) but associations are recognized with several infections (eg HSV, adenovirus, Mycoplasma pneumonia) and drugs (eg sulfonamides, NSAIDs, penicillins) ( OHCS10 p. 588).
SJS and ►► TEN These represent different extents of severe, life-threatening skin inflammation that is usually drug induced. Widespread blisters, with skin shedding, erythematous macules, and mucosal erosions affect <10% body surface area (SJS) or >30% (TEN) with an overlap diagnosis in between. There is a significant mortality and senior help should be sought immediately, with close attention to skin care, fluid replacement, and prevention of superinfection ( OHCS10 p. 601).
Pemphigus and pemphigoid These are rare primary blistering diseases. Pemphigus causes superficial blisters and often involves the mucous membranes of the mouth; the blisters are delicate and burst easily, so areas of raw skin are often more noticeable than blisters. Pemphigoid causes tense blisters in older patients, and seldom affects the mouth. Both are autoimmune and require dermatology input. Can be life-threatening ( OHCS10 p. 602).
Pyoderma gangrenosum This presents with painful nodules or pustules which often ulcerate, leaving an undermined ulcer with a dusky purple edge. Associated with inflammatory bowel disease, primary biliary cirrhosis, and rheumatoid arthritis among others, the exact cause remains unclear. Needs urgent dermatology assessment ( OHCS10 p. 588).
Henoch–Schönlein purpura Largely self-limiting small vessel vasculitis typically seen following a simple upper respiratory tract infections in childhood. Petechiae and purpura develop on the legs and buttocks. May have associated abdominal pain, arthralgia, and oedema ( OHCS10 p. 197). Must check renal function and dip urine.
Granuloma annulare Common, benign inflammatory disorder of unclear aetiology, characterized by clusters of firm papules appearing on the hands, feet, or trunk which later merge into a ring. Associations include T1DM, but most cases appear in well patients ( OHCS10 p. 586).
Table 15.2 Common skin manifestations in systemic disease
| Diabetes mellitus ( pp. 334–336) |
Candidiasis, necrobiosis lipoidica (yellow maculopapular lesions on the shins, can ulcerate), skin infections (cellulitis) |
| Coeliac disease ( p. 314) |
Dermatitis herpetiformis (intensely itchy papules and vesicles on knees, elbows, back and buttocks) |
| IBD( p. 315) |
Erythema nodosum, pyoderma gangrenosum |
| Rheumatoid arthritis ( p. 468) |
Rheumatoid nodules (firm nodules either loose or attached to deep structures over extensor surfaces, classically the elbows), vasculitis, pyoderma gangrenosum |
| SLE ( p. 471) |
Facial butterfly rash, photosensitivity, red scaly rashes, diffuse alopecia (hair loss) |
| Hyperthyroidism ( p. 340) |
Pre-tibial myxoedema (non-pitting plaques and nodules, classically on the shins), clubbing, alopecia |
| Hypothyroidism ( pp. 340–341) |
Sparse coarse hair, dry skin, asteatotic eczema (pruritic, dry, cracked skin) |
| Neoplasia | Acanthosis nigricans (velvety, brown pigmented plaques, often around the neck), dermatomyositis, ichthyosis (scaly skin), pruritus |
| Drug eruptions ( OHCS10 p. 601) |
Maculopapular rash (±fever and eosinophilia); urticaria; erythema multiforme, SJS/TEN |
| Vasculitis | Palpable purpuric rash typically on shins; wide range of other pathologies including telangiectasia, urticaria, ulcers ( p. 607 for autoantibodies in diagnosis) |
( |
Infections (oropharyngeal candida, facial/genital molluscum contagiosum, herpes simplex, varicella zoster p. 428); seborrhoeic dermatitis or psoriasis ( p. 431); Kaposi sarcoma (enlarging purple patches or plaques seen on feet, arms, legs or oral mucosa) |
► Worrying features Weight loss, night sweats, hard irregular lump, ↑size.
Think about ► Serious Skin cancer, sarcoma, lymphoma, TB; Common Lipoma, epidermoid cyst, abscess, boil, carbuncle, ganglion, fibroma, lymph node, naevi, skin tags, keratocanthoma, keloid scarring.
Ask about Location, speed, and duration of onset, change with time, pain, other lumps, trauma, bites, infections, skin changes, systemic symptoms (eg weight loss, vomiting, fever); PMH Previous lumps, cancer, radiotherapy; immunosuppression SH Foreign travel, sun exposure, occupation; FH Skin cancer.
Look for Site, size, shape, consistency (hard, firm, soft, fluctuant), tenderness, temperature, surface, association with skin (moves with skin—intradermal, skin moves over it—subcutaneous), overlying skin (colour, punctum, ulcerated), edges, mobility/tethering, pulsatility, transillumination, relationship to nearby structures, lymphadenopathy, splenomegaly.
Investigations blds Consider FBC, U+E, LFT, CRP, ESR; Imaging CXR, USS, CT/MRI; Biopsy FNA, punch biopsy, excision biopsy.
Lipoma Common, benign tumour of mature fat cells.
Symptoms Single or multiple, non-painful, can cause pressure effects, common on the trunk and neck, never found on palms/soles of feet.
Signs Smooth, well-defined, soft, subcutaneous, mobile, no skin changes.
Management Lipoma can be surgically excised if causing distress.
Epidermoid cyst Proliferation of epidermal cells within dermis.
Symptoms Single or multiple, painful if infected, common on the trunk, neck and face, almost never found on palms/soles of feet.
Signs Firm, well-defined, intradermal, mobile; overlying punctum is common; may discharge white/cheesy material; can become inflamed.
No treatment. Consider flucloxacillin 500mg/6h PO if inflamed/tender, may also require incision and drainage; surgical excision once non-inflamed.
Ganglion cyst Cystic lesion of joint or synovial sheath of tendon.
Symptoms Single, non-painful; 80% occur at wrist.
Signs Smooth, well-defined, subcutaneous, transilluminable.
Management Conservative; can be aspirated or excised, but ~40% recur.
Fibroma Benign tumour of connective tissue; can occur in any organ.
Symptoms and signs These vary according to tissue affected, usually slow growing with no overlying skin changes.
Management Biopsy/imaging if any doubt; excision often possible.
Sarcoma Rare, but devastating malignant tumour of connective tissue.
Symptoms Single, painful, progressive enlargement, weight loss.
Signs Firm/hard, tethered, regional lymphadenopathy.
Management Combination of surgery, radiotherapy and chemotherapy.
Melanocytic naevi (moles) Benign proliferation of melanocytes.
► Worrying signs ↑size, change in pigmentation, irregular outline, bleeding, itching, inflammation (may suggest transformation to melanoma p. 436).
Symptoms and signs Most common are acquired naevi that develop during childhood as small, flat pigmented areas and may progress to pale, raised, fleshy naevi with age; congenital melanocytic naevi are larger, present from birth and carry a higher risk of transformation to melanoma.
Management Refer to specialist if worrying signs are present.
► Worrying signs Non-tender, >3wk, >1cm, hard, irregular surface, tethering, weight loss, night sweats, fatigue, absence of infection.
Causes Isolated Local/regional infection; Multiple p. 410.
Symptoms Lump usually in the neck, axilla, or groin.
Signs Firm, subcutaneous; usually mobile, well-defined, smooth surface.
Management Enlarged lymph nodes can often be treated by ‘watchful waiting’; however, biopsy or image if worrying signs are present.
Abscess Accumulation of pus within cavity due to infection or foreign body.
Symptoms Typically single, painful, onset over days, may be febrile.
Signs Fluctuant, well defined, under the skin; tender, inflamed (red, hot); may spontaneously discharge; common on neck, axilla, groin, perineum.
Management Incision and drainage ±antibiotics eg flucloxacillin 1g/6h PO.
Boil (furuncle) Abscess forming in inflamed hair follicle, typically with S. aureus infection.
Symptoms Single, painful, common on neck, axilla, groin, perineum.
Signs Red, tender, hot, central punctum, may discharge pus.
Management Often discharges spontaneously, otherwise treat as abscess; multiple furuncles may coalesce into a carbuncle which requires drainage and extended antibiotic therapy.
Warts Benign proliferation of epidermis associated with infection with human papillomavirus (HPV); can occur in various sites.
Common warts These are papular lesions with a rough surface with black dots within them, often on hands and feet. Spread is by direct contact.
Plantar warts (veruccas) These are usually flat or inward growing with black dots (‘heads’). Often painful if over pressure areas.
Plane warts These are small, flesh-coloured, flat-topped lesions usually on the face or backs of the hands without black dots.
Anogenital warts These are transmitted sexually and associated with different HPV subtypes from non-genital warts; subtypes 16 and 18 are strongly associated with cervical carcinoma, so ensure recent cervical smear in any ♀ with genital warts (or in ♀ partner, of any affected individual); subtype 16 is strongly associated with anal cancer.
Treating warts This is often difficult. Topical keratolytic agents (such as salicylic acid or trichloroacetic acid) is usually 1st-line treatment, and cryotherapy (freezing) is undertaken by many general practitioners as well as in dermatology clinics. Non-genital warts often resolve spontaneously over ~2–3yr.
Actinic keratosis Scaly lesions seen on sun-exposed skin (fair skinned). Can progress to skin cancer; usually treated topically.
Basal-cell carcinoma (BCC)
Commonest form of skin cancer, accounting for ~75% of diagnoses.
Risk factors Exposure to UV light (sunlight and sunbeds), PMH or FH of BCC, exposure to arsenic.
Appearance Slow growing lesion on sun-exposed skin; most are nodular (waxy appearance, rolled pearly edges, and central ulceration—‘rodent ulcer’ typically found on face); other variants include superficial (flat, red, scaly patches—found on trunk) and pigmented.
Investigation Biopsy and histology if large, followed by surgical excision; usually fully excised initially if small and sent for histological analysis.
Treatment Excision (including Mohs’ surgery), topical chemotherapy, radiotherapy, cryosurgery.
Prognosis BCC very rarely metastasize but can cause local tissue destruction (eg ear, lip) and very infrequently cause death.
Mohs’ surgery This involves surgical removal of the obvious tumour and a thin layer of tissue from the site. This layer is frozen and stained then examined under a microscope. If there are tumour cells present, a further (deeper) layer of tissue is removed, and the process is repeated until the area is tumour-free. This procedure minimizes the need for large skin excisions, while ensuring the entire tumour is removed.
Squamous-cell carcinomas (SCC)
These account for~ 20% of cutaneous malignancies.
Risk factors Exposure to UV light (sunlight and sunbeds) or to industrial carcinogens (eg arsenic, tar), chronic ulcer inflammation, immunosuppression, premalignant conditions (eg Bowen’s disease, actinic keratosis).
Appearance Variable; typically fleshy plaque or papule arising on sun-exposed skin (~70% on head and neck), often with bleeding, scaling, or ulceration; other forms include Marjolin ulcer New area of induration at edge of leg ulcer; Keratoacanthoma A rapidly growing nodule with central ulceration that usually spontaneously regresses and is considered by most as a variant of SCC.
Investigation Usually none, may be biopsied.
Treatment Surgical excision; topical chemotherapy, photodynamic therapy and immunomodulators used if unsuitable for surgery.
Prognosis If localized disease, excision gives 95% cure rate but SCC can metastasize rapidly via local lymph nodes with poor outcome.
Malignant melanoma See Box 15.3.
Box 15.3 Malignant melanoma
Accounts for ~4% of all skin cancers, but majority of skin cancer deaths.
Risk factors Pale-skin, sun exposure, sunburn, multiple/congenital naevi.
Symptoms/signs A new, or changing mole, as assessed by ABCDE criteria:3 Asymmetry, Border irregularity, Colour variation, Diameter increasing or >6mm, Evolving over time.
Management Surgical excision, ±lymph node removal, ±chemotherapy.
Prognosis This depends upon completeness of excision, lymph node involvement, presence of ulceration and tumour thickness; these are combined to give a stage (stage I: 5yr survival 85–99%; stage IV: 10%).
► Worrying features >50yr, fixed, hard, enlarging lesion with skin tethering, breast eczema, new nipple inversion, or bloody nipple discharge; PMH or FH breast cancer.
Think about ► Serious Breast cancer; Common Fibroadenoma, fibroadenosis, abscess, isolated cyst, seroma, trauma (fat necrosis).
Ask about Onset, duration, change with menstrual cycle, pain, trauma, skin changes, nipple changes, nipple discharge; PMH Previous lumps, breast cancer, breastfeeding, pregnancy; DH OCP, HRT; FH Breast cancer.
Look for p. 143 for breast examination.
Management Breast lumps require a triple assessment of clinical examination, imaging (mammography ±USS) and histology (FNA) or core biopsy); these should be offered via a ‘1-stop’ breast clinic.
Symptoms and signs Young women (<40yr) with highly mobile, non-tender, well-defined, and small lump (breast mouse), otherwise well.
Management Refer to breast surgeon; usually not excised unless >40yr, suspicious USS appearance or >4cm.
Symptoms and signs 35–50yr, single or multiple, painful, and tender lumps, size and pain vary with menstrual cycle.
Management Refer to breast surgeon; often assessed with USS and aspiration, but may require mammography and excision.
Risk factors Breastfeeding, DM, smoking, steroids, trauma.
Symptoms and signs Single, red, hot, tender lump, fluctuant, may discharge pus from the nipple, fever.
Management Refer to surgeon for incision and drainage with antibiotics.
Breast seromas Collections of serous fluid; post breast surgery.
Seromas may discharge fluid, non-tender, fluctuant.
Management Refer to surgeon for percutaneous drainage.
Breast cancer Most common non-skin cancer in UK; women aged 50–70yr are offered 3yrly screening mammography; overall 5yr survival is 80%.4
Risk factors Age, family history, oestrogen exposure (early menarche, late menopause, nulliparity, obesity), previous breast cancer.
Symptoms Breast lump, nipple inversion or bloody discharge, skin changes, weight loss, bone pain.
Signs Palpable, non-tender mass (often hard, poorly defined), skin dimpling, peau d’orange (prominent pores), nipple eczema (Paget’s), lymphadenopathy.
Investigations Mammography ± USS For women <35yr with dense breasts); Biopsy/FNA For histological evidence of cancer; Staging May require LFT, Ca2+, USS liver ±axilla, CT, bone scan.
Treatment Depends on tumour stage/grade, tumour markers, and the patient’s wishes. Options; combinations of surgery, chemotherapy, radiotherapy, hormonal modulation, and monoclonal antibodies.
Complications Metastases (bones, lung, liver, brain), recurrence, lymphoedema, seroma, cosmetic appearance, psychological.
Loss of epithelial integrity with failure to heal.
Think about Venous insufficiency, peripheral vascular disease, neuropathic (eg DM), pressure ulcers, trauma, infection, pyoderma gangrenosum ( p. 432), vasculitides, skin cancer, steroids.
Ask about Onset, duration, pain, trauma, claudication;
PMH Peripheral vascular disease, ↑ BP, CVA, MI, angina, varicose veins, DVT, DM;
DH Steroids;
SH Smoking, alcohol.
Look for Number, site, size, base, edge, depth, shape, colour, oedema, eczema, vascular disease (peripheral pulses, hair loss, cold), neuropathy (sensation), infection (discharge, lymphadenopathy).
Investigations blds FBC, CRP, HbA1c; consider ESR, complement, RhF, ANA, ANCA; Ankle–brachial pressure index (ABPI p. 462) ±duplex USS or CT angiogram If ABPI abnormal; Wound swab (±X-ray/MRI if osteomyelitis suspected); Biopsy Atypical areas. See Table 15.3.
Table 15.3 Clinical assessment of leg ulcers
| Venous (~80%) | Arterial (~10%) | Neuropathic (~10%) | |
| History | Obesity, immobility, varicose veins, DVT | Intermittent claudication, HTN, DM, IHD, smoker | Numbness, DM, family history |
| Leg | Pigmented, varicose veins, swollen, hot | Shiny, hairless, cold | Joint destruction |
| Site | Medial aspect of legs | Lateral malleolus, toes, dorsum of foot | Heel, metatarsal head, pressure points |
| Size | Can be very large | Usually small | Usually small |
| Base | Usually superficial with sloughy exudate | Deep with a dark, dry base, few signs of healing | Can be very deep (extend to bone) |
| Edge | Irregular, areas of repeated healing and exacerbation | Well defined, often circular | Surrounded by thickened skin |
| Sensation | Painful | Painful | Relatively painless |
Management Ensure good nutrition and treat the cause, where possible. Healing often takes weeks to months and is commonly managed by community nurses, with ulcer clinic visits where appropriate:
• Venous Provided ABPI is >0.8 apply compression bandaging with absorbable dressings to dry out the slough. Emollients and steroid creams also help; may need debridement/grafting
• Arterial Avoid compression bandages (unless under expert guidance); address vascular risk factors and refer to a vascular surgeon for consideration for bypass or angioplasty
• Neuropathic Careful footcare to avoid repeated injury, often needs surgical debridement and antibiotics; osteomyelitis is common; assess for and treat coexistent vascular disease; specialist diabetic foot team if DM
• Infection Ulcers usually have bacteria present; infection or cellulitis should be suspected if there is pus, excessive pain, surrounding erythema, or pyrexia. Swab the ulcer and treat as for cellulitis, if clinical signs of infection ( pp. 426–427). Organisms may be colonizing the wound but not causing infection; be guided by the clinical picture rather than the swab results.
No improvement Consider other diagnoses (including TB and cancer) or dermatitis from therapeutic agents. Ensure swabs sent; discuss with dermatology and consider biopsy. May need curettage or skin grafting.
►► Call for senior help or speak to on-call ophthalmologist urgently if patient has new-onset ↓visual acuity (VA) in affected eye. See Fig. 15.3.
Fig. 15.3 Determining the likely cause of the acute red eye. (Red arrows indicate topics that are discussed in more detail in the text.)
►► Keratitis ( OHCS10 p. 432.)
Corneal infection or inflammation; may ulcerate.
Symptoms Pain, photophobia, reduced vision, and foreign body sensation, commonly in contact lens wearer or patients with dry eyes, blepharitis, or autoimmune disorders.
Signs Conjunctival redness (can be sectoral rather than diffuse as is often the case in conjunctivitis). Fluorescein with a blue light may show punctate epithelial erosions, a white patch (corneal infiltrate/ulcer), epithelial defect, corneal haze (oedema), or hypopyon (pus in the anterior chamber).
Management Refer urgently for ophthalmologist, if ulceration present or suspected. They may undertake corneal swabs/scrapes to establish the cause. Antibiotic eyedrops or systemic immunosuppression may be used.
►► Episcleritis and scleritis ( OHCS10 p. 432.)
Inflammation of white outer coating; often underlying autoimmune disorder.
Symptoms Pain and tenderness—often mild in episcleritis but severe in scleritis (wakes patient from sleep), occasionally with photophobia and reduced vision.
Signs Mild localized redness (often involving just one sector, but occasionally diffuse); normal visual acuity; otherwise normal examination in episcleritis. In scleritis the globe may be tender to touch and there may be ↓visual acuity.
Management Urgent ophthalmology review to consider scleritis.
Likely ophthalmic management Topical steroids or non-steroidal agents for episcleritis, potentially oral immunosuppressants for scleritis.
►► Acute anterior uveitis (iritis) ( OHCS10 p. 432.)
Inflammation of pigmented parts of eye; associated with systemic disease (eg IBD, arthropathies, sarcoid); pain on pupil constriction.
Symptoms Blurred vision, photophobia, and pain.
Signs Red eye, ↓visual acuity, cornea usually clear, pupil may be irregular and small, ±hypopyon (pus in the anterior chamber).
Management Refer urgently to ophthalmologist.
Likely ophthalmic management Intensive topical steroids, dilating agents.
►► Acute angle closure glaucoma ( OHCS10 p. 433.)
↑Intraocular pressure due to blockage of anterior chamber drainage.
Symptoms Aching eye pain (usually unilateral and severe), often associated with N+V; blurred vision and haloes around lights are common.
Signs Red eye, ↓visual acuity, hazy cornea (if severe); pupil often mid-dilated, can be unreactive to light and oval shaped (rugby ball-like); globe tender and firm to touch. ↑intraocular pressure; usually >40 mmHg.
Management Emergency referral to ophthalmologist; anti-emetics and IV opioids may be needed for symptoms but should not delay referral.
Likely ophthalmic management Constrict the pupil (miosis) with pilocarpine drops, and reduce aqueous formation with acetazolamide PO/IV. Mannitol IV is also sometimes used to reduce intraocular pressure. Definitive care achieved with peripheral iridectomy to allow constant drainage of aqueous even when pupil dilated.
Symptoms Sudden-onset discomfort/FB sensation; lacrimation and redness; occurs, eg while hammering or chiselling without eye protection or following minor trauma to the eye. A contact lens may sometimes have been ‘lost’ and cause FB sensation.
Signs Red, watering eye; FB may be visible. Always evert both top and bottom lids to check for FBs here as well; visual acuity is usually reduced. Fluorescein with a blue light may show corneal ulceration/abrasion(s).
Treatment Often the eye needs anaesthetizing with topical local anaesthetic (proxymetacaine, tetracaine, or oxybuprocaine) to allow examination and treatment. Gently pick up FB with cotton bud, or irrigate lavishly with sterile 0.9% saline. Re-examine eye afterwards to ensure all FBs have gone. Protect the eye with an eye shield until local anaesthetic has worn off and give chloramphenicol eye drops 0.5% 4h topical or ointment 1% 6h topical for 3d. If unable to remove FB or evidence of corneal abrasion, speak to senior, or on-call ophthalmologist.
Symptoms Eye discharge, ±FB sensation, itch, concurrent cold, hayfever.
Signs Red eye, discharge, normal visual acuity, clear cornea. See Table 15.4 for causes.
Treatment Conjunctivitis can be highly contagious so care should be taken with hand-washing.
Bacterial Topical antibiotics (eg chloramphenicol drops 0.5%) to both eyes every 2h while awake for 2d, then 6h for 1wk; Viral May need topical antibiotics to prevent secondary infections, but usually self-limiting; Allergic Identify allergen if possible and encourage avoidance; topical antihistamine, (eg azelastine), or mast-cell inhibitors (cromoglicate) may offer relief; artificial tears (eg Viscotears®) may help if dry eyes are a problem.
Table 15.4 Determining the cause of a conjunctivitis
| Bacterial | Viral | Allergic | |
| Discharge | Sticky, pus-like | Watery | Watery |
| Itch | +/– | +/– | ++++ |
| Recurrent | +/– | +/– | Often seasonal |
| Contagious | Yes | Yes | No |
| Uni- or bilateral | One, then both | One, then both | Both |
| Other symptoms | Often none | Common cold | Hay fever |
Symptoms Often an incidental finding by the patient and usually benign; can sometimes initially cause mild FB sensation. There should be no pain, photophobia, or altered vision.
Signs Diffuse area of bright red blood under conjunctiva, very different to inflamed blood vessels seen in other causes red eye; normal VA.
Treatment Check BP, and if recurrent check FBC and clotting; may need eye protection (eg tape at night) if swollen and unable to close readily; discuss with ophthalmologist only if recurrent or severe.
► Worrying features Severe deficit, additional neurology, scalp pain.
Think about Retinal vein occlusion, retinal artery occlusion, giant-cell arteritis, retinal detachment, arteriosclerotic ischaemic optic neuropathy, vitreous haemorrhage; angle closure glaucoma.
Ask about Loss of vision; often painless.
Look for ↓visual acuity or no vision in affected eye, relative afferent pupillary defect (suggests optic nerve dysfunction); abnormal fundoscopy. Check for other neurological signs, for scalp pain/tenderness, and ECG for AF.
Management Immediate referral to on-call ophthalmologist.
►► Giant-cell (temporal) arteritis ( p. 365); ↓visual acuity in affected eye, typically with temporal headache/pain, high ESR. May be optic neuropathy, retinal artery occlusion, or extra-ocular muscle palsy.
►► Retinal artery occlusion ( OHCS10 p. 437.)
Symptoms Sudden, painless, and severe loss of vision.
Signs Relative afferent pupillary defect; pale retina with ‘cherry spot’ macula.
Risk factors For vascular disease (DM, smoker, ↑lipids, IHD).
Treatment If seen within 1h of onset, you may attempt to dislodge the embolus by pressing hard on the globe, then suddenly releasing; most damage will be irreversible.
►► Retinal vein occlusion ( OHCS10 p. 438.)
Symptoms Sudden, painless, and severe loss of vision; may be segmental.
Signs Relative afferent pupillary defect; engorged, red retina in affected area.
Risk factors These include age, chronic glaucoma, HTN, polycythaemia.
Treatment Supportive; laser photocoagulation and intravitreal steroids/anti-VEGF can prevent neovascularization and treat macula oedema.
►► Vitreous haemorrhage ( OHCS10 p. 438.)
Symptoms Sudden painless loss of vision; floaters.
Signs Relative afferent pupillary defect; loss of red reflex; unable to see retina.
Risk factors DM (proliferative retinopathy), coagulopathy, trauma.
Treatment Haemorrhage should resolve spontaneously; prevent further episodes by laser photocoagulation of peripheral retina; vitrectomy if persistent.
Optic neuritis This is often associated with a sub-acute, unilateral loss of vision, with aching, pain on eye movements, and loss of colour vision. Relative afferent pupillary defect; optic nerve usually appears normal when inflammation is retrobulbar
Causes These include demyelinating disease (may be a first presentation of MS).
Treatment Supportive, with resolution occurring over a few weeks.
Think about Refractive error, cataracts, macular degeneration, chronic glaucoma, diabetic retinopathy, optic atrophy, drug toxicity, optic neuroma; inherited disease.
Ask about Painless loss of vision, symptoms of underlying disease.
Look for ↓visual acuity or no vision in affected eye, pupil unresponsive to light or relative afferent pupillary defect (suggest optic nerve disorder), abnormal cornea, lens, retina, or optic disc on fundoscopy.
Management This needs full ophthalmic assessment. If in-patient, try and arrange for review before discharge, or refer as an out-patient. (See also Box 15.4.)
Causes Age-related,DM, steroids, trauma, eye surgery; congenital.
Symptoms Blurred vision (bilateral), poor distance judgement (unilateral).
Signs ↓visual acuity, cataract visible in lens; retina and red reflex visible unless cataract is dense.
Treatment Cataract surgery is performed on a single eye at a time if the cataract(s) are interfering with lifestyle (eg reading or driving). They are usually done as a day-case procedure under local anaesthetic; the lens is removed (phaecoemulsion) and an artificial lens implanted.
Age-related macular degeneration ( OHCS10 p. 440.)
Causes Ageing, smoking.
Symptoms Deterioration of central vision.
Signs ↓visual acuity, but normal visual fields; normal disc, but macula often pigmented or bleeding upon fundoscopy.
Treatment This is aimed at reducing further visual loss; ‘wet’ (neovascular) forms can be treated with intravitreal anti-VEGF injections.
Chronic (open angle) glaucoma This results in peripheral visual field loss in those with ↑intraocular pressure (IOP).
Signs Cupping and atrophy of the optic disc.
Treatment This aims to ↓IOP by ↓aqueous formation (topical β-blockers eg timolol, or carbonic anhydrase inhibitors eg dorzolamide) or ↑reabsorption (prostaglandin drops, eg latanoprost); surgery involves trabeculectomy (allows aqueous drainage into subconjunctiva).
Box 15.4 Registration of visual impairment
A consultant ophthalmologist can apply on behalf of a patient to register as blind or partially sighted; this is a voluntary not a statutory process. Registration entitles the individual to some tax allowances, benefits, and some concessions for public transport and other public facilities. Generally acuity <3/60 (after correction) qualifies as ‘blind’, while corrected vision <6/60 qualifies as ‘partially sighted’; restriction of visual fields or loss of central vision may also qualify.
The Royal National Institute of Blind People advise on benefit entitlements, aids for the house, and independent living, and for guide dogs:
Royal National Institute of Blind People
105 Judd Street, London, WC1H 9NE
0303 123 9999 www.rnib.org.uk
Causes Neurological Meningitis, subarachnoid haemorrhage, migraine, encephalitis, hangover; Ophthalmic Glaucoma, scleritis, keratitis and corneal injury, iritis, cataracts.
Symptoms Bright light causes discomfort or exacerbates pain (especially painful having fundoscopy performed).
Signs Dislike of light; intolerant of fundoscopy. Check for signs of meningism ( p. 364) and for focal neurology; perform full eye examination.
Treatment Treat for likely cause(s); ► seek senior help urgently.
Causes Extra-ocular muscle palsy, cranial nerve palsy, myasthenia gravis, orbital fracture, multiple sclerosis.
Symptoms Double vision which is corrected by closing one eye or at extremes of gaze is called binocular diplopia; monocular diplopia is rarer and is not corrected by closing one eye, being caused by a structural abnormality within the eye.
Signs Double vision usually relieved by occluding vision in one eye (the outer image will disappear when the affected eye is covered), loss of conjugate gaze, ↓ ROM of eye when testing all movements in turn, fatigability of muscles, other evidence of associated disease (MS, CVA, etc).
Treatment Discuss with senior; refer to neurologist/ophthalmologist.
Causes Glaucoma, severe cataracts, alcohol consumption, retinitis pigmentosa, migraine.
Symptoms Loss of peripheral vision with preservation of central vision, as though looking through a tunnel.
Signs Check for visual field defect, ↓visual acuity, cataracts, or abnormal retina; check BP and blood glucose.
Treatment Treat the cause.
Causes Glaucoma, cataracts, post-corrective surgery, idiopathic.
Symptoms Haloes and glare from lights, often more obvious at night.
Signs Look for ↓visual acuity, cataracts.
Treatment Treat the cause.
Causes Retinal detachment, vitreous detachment, migraine, idiopathic (non-sinister).
Symptoms Dark flecks or webs which drift about in the line of vision; flashing lights, usually in the periphery of vision even when eye closed.
Signs Often very few signs if non-sinister cause; ↓visual acuity, visual field, or abnormal fundoscopy may feature in retinal or vitreous detachment.
Treatment Often not necessary. If lots of new floaters have appeared quickly or there are associated flashing lights, haloes or newly impaired visual acuity refer urgently to ophthalmologist.
1 NICE childhood eczema guidelines available at guidance.nice.org.uk/CG57
2 NICE psoriasis guidelines available at guidance.nice.org.uk/CG153
3 Abbasi NR, et al. JAMA 2004;292:2771 available free at jama.ama-assn.org
4 NICE guidelines available at guidance.nice.org.uk/CG80 and guidance.nice.org.uk/CG81