Eczema herpeticum is also known as Kaposi varicelliform eruption. It is a skin infection caused by Herpes simplex virus (HSV) type I and II. It most commonly develops in individuals who already have atopic dermatitis/eczema. Eczema herpeticum can cause an acute exacerbation of eczema. It is usually very painful and young children can be unwell with fever and swollen lymph nodes. Eczema herpeticum can become infected with bacteria, commonly Staphylococcus or Streptococcus. Secondary bacterial infection can lead to impetigo or cellulitis. It can cause herpetic keratitis if the eyes are infected by HSV from the surrounding lesions, which if left untreated, can lead to blindness. Eczema herpeticum is considered as one of the few dermatological emergencies. Prompt treatment with antiviral medication (eg, aciclovir, valaciclovir) should eliminate the need for hospital admission.


Infantile haemangiomas (IH) are the most common benign vascular skin tumour in children. They are caused by proliferating vascular endothelial cells. They usually appear shortly after birth (rarely at birth), and grow rapidly in the first 6 months. Most IH stop growing by 6-9 months. They involute over years. Most IH do not require treatment as they usually involute with time. Depending on the location, size, and presence of ulceration, some require treatment. Treatment with beta blockers (oral propranolol) has now replaced oral corticosteroids as the gold standard treatment for complicated or ulcerated IH. The earlier treatment is commenced, the more effective it is likely to be in preventing further growth. Other treatment options include:


A linear epidermal naevus. It is an overgrowth of the epidermis and usually presents at birth or during early childhood. It is mostly flat and hyperpigmented, but there is slight thickening and scale around the ankle. Epidermal naevi present as streaks and swirls of thickened (verrucous, hyperkeratotic, or velvety) skin along the lines of Blaschko, usually with hyperpigmentation and sometimes with adnexal involvement.They are usually unilateral, and only rarely generalised, when they may be associated with skeletal abnormalities (epidermal naevus syndrome). In infancy, epidermal naevi can present as flat tan or brown marks, but as the child ages, they become thickened and verrucous. Most epidermal naevi do not require treatment. Topical calcipotriolmay reduce the thickness of the verrucous lesions. Verrucous epidermal naevi can be treated with an ablative laserwith good long-term aesthetic results.


Subcutaneous fat necrosis of the newborn. This is an uncommon panniculitis of neonates. It usually occurs in the first days of life. There has often been fetal distress in labour and it may be associated with therapeutic hypothermia for hypoxic ischaemic encephalopathy. It can be painful. It usually, ultimately, self-resolves. It is associated with symptomatic hypercalcemia (irritability, constipation, poor weight gain, and arrhythmia) as frequently as in 50% of cases. A baby with subcutaneous fat necrosis should have their blood calcium checked periodically for the first few months of life. Hypercalcaemia can be treated with low calcium milk feeds, increasing fluid intake, frusemide, or bisphosphonates. Sclerema neonatorum is an extremely rare disorder which was described in premature or debilitated children who developed a diffuse board-like stiffness due to generalized fat necrosis.

This condition usually appears in the first days after birth and is usually fatal. Read more on subcutaneous fat necrosis of the newborn.


This is nipple eczema. It is a localised dermatitis involving the nipple and areola. This is frequently bilateral and fluctuates in severity. Lichenification due to scratching can be conspicuous, as can hyperpigmentation, particularly in skin of colour. It improves in response to topical steroids and can deteriorate rapidly when irritated by scratching, soaps, shower gels, and detergents. Nipple eczema is a common local manifestation of atopic dermatitis but can occur in isolation. Patients should avoid any precipitating irritants and allergens. Regular emollients and topical corticosteroids are the mainstay of treatment. Moderate potency topical steroids are usually very effective, followed by low potency topical steroids as maintenance therapy if necessary.Topical coal tar preparations are an effective old fashioned remedy. Sometimes, use of a potent topical steroid with hydrocolloid dressing occlusion for a few days will break the itch-scratch cycle that perpetuates the problem.


This is a granuloma resulting from a dental sinus. They arise when there is longstanding dental abscess or necrosis of a tooth. When a dental sinus connects with the skin rather than the intraoral mucosa, they characteristically occur along the border of the mandible, but may also arise around the maxilla. The tethering of the skin around the sinus opening is a feature and may be appreciated either visually or on palpation. The teeth adjacent to the sinus should be inspected for signs of previous fillings, caries, and local tenderness on tapping. Radiology is the most important investigation and will show bone loss around the root tip of the affected tooth. MRI or CT may be required. Occasionally insertion of a radio-opaque probe into the sinus may be needed to identify the affected tooth. Removal of the affected tooth, retained root or necrotic material is required and the sinus should heal readily thereafter.


There are superficial erosions over the scalp surmounted with thick pus. There are also several actinic keratoses. The picture is typical of erosive pustular dermatosis of the scalp. It is seen mostly in older bald men with sun damaged scalps. It has also been reported on the lower leg, a heavily sun exposed site particularly in women. Removing the overlying crusts and using a potent topical steroid and antibiotic combination cream can be very gratifying. Areas that do not heal should be re-evaluated and possibly biopsied to exclude squamous cell carcinoma.


There is a slightly scaly net-like (reticulate) eruption on the abdomen. The features are typical of confluent and reticulated papillomatosis. It is frequently misdiagnosed as pityriasis versicolor, but mycology is negative and oral azoles are not as effective as tetracycline antibiotics. Recent evidence suggests it is due to infection with a Gram-positive actinomycete called Dietzia papillomatosis. It usually responds to a course of tetracyclines. For more information, see the topic page on confluent and reticulated papillomatosis.


There is striking telangiectasia over the light-exposed area of her upper chest. The likely cause is amlodipine-induced phototelangiectasia. Telangiectasia in light-exposed areas has been reported with nifedipine and diltiazem, although it has had a more common association with amlodipine. In some cases, its resolution has been noted after substitution of the calcium channel antagonist with a different class of antihypertensive.


This is typical of a phytophotodermatitis, a rash that results from a phototoxic plant sap coming into contact with the skin, and subsequent light exposure. It results in redness and sometimes blistering of the exposed skin. He has used a strimmer, or string weeder, and has been working with his top off! The strimmer has spattered phototoxic sap over his trunk. His face was unaffected because he had correctly used a face mask as personal protection. With photoprotection, the rash will heal, but will leave marked post-inflammatory pigmentation which may last for several months.


The recurrent development of redness and blistering in exactly the same place on the skin is very suggestive of a fixed eruption, most commonly caused by drugs. Occasionally they can be caused by foodstuffs, preservatives and other food and beverage additives. Lesions may be solitary or multiple. Uncommon sites to develop fixed eruptions are the lids, lips, palms, soles, and genitalia. They frequently arise within minutes or hours after exposure to the offending agent, once sensitisation has occurred. When they resolve, they commonly leave areas of hyperpigmentation. The likely cause in this case is the antibiotic used to treat her urinary tract infections. Avoiding the offending drug, and similar potentially cross reacting drugs, is the most important aspect of treatment. If there is a blister, then this can be aspirated leaving the roof intact as a biological dressing. A potent topical steroidcan then be applied until the inflammation resolves.


He has streaked erythema where there has been accidental skin exposure to his faeces. Sadly, his opiates have constipated him, and this has been treated with co-danthrusate (dantron and docusate), an anthralin-like agent that acts as a stimulant laxative. It is metabolised in the gut to anthralin, and when there is accidental contact with faeces and the skin, it produces an irritant dermatitis. It may oxidise to a purple-brown colour just as anthralin (dithranol) does in the treatment of psoriasis. The co-danthrusate should be stopped and substituted with a different aperient; the erythema can be treated with a short course of a potent topical steroid.


These acute haemorrhagic lesions are the early stages of coumarin necrosis. Shortly after initiation of a coumarin, there may be a temporary state of thrombophilia, as coumarin reduces the effect of both natural anticoagulants and coagulants. The former (Proteins C and S) have shorter half-lives than the coagulants, hence the early temporary thrombophilic state before anticoagulation is effected. The same situation may occur with longstanding coumarin use if control has been erratic. It is more likely to develop if heparin is not used in the early initiation of coumarins, or if the coumarin loading dose is too high. Lesions tend to occur on the fatter areas of the body such as the thighs and breasts. The coumarins should be stopped and heparin initiated. The condition does not occur with newer oral anticoagulants. Ulceration is likely to happen; surgical debridement may be required.


These are typical syringomas (syringomata)in the most frequently encountered location. They occasionally develop in the bathing trunk area and on the upper trunk. They are benign tumours of the sweat duct; they may be familial. Unlike xanthelasma, which tend to produce plaques, syringomas remain as discrete papules. There are no easy treatments. Light electrocautery can help as may laser, but all modalities may scar, and recurrent lesions are common.


The eruption shows the classical wood graining with redness and scale of erythema gyratum repens. The erythema slowly spreads in a gyrate fashion, leaving scale on the trailing edge of the advancing edge. The term repens probably best translates as creeping. 80% of cases are associated with an underlying malignancy; often affecting the lung, oesophagus, breast, and stomach. Full clinical investigation and meticulous history taking should be performed. This includes probing for symptoms of an underlying cancer, tumour markers, mammography, and PET CT scanning.


The forefoot is dry, red and fissured; the typical features of juvenile plantar dermatosis. It occurs more commonly in boys with an average age of onset of 8. It is more common in atopic children. It is thought to be due to impervious occlusive footwear, and exacerbated by friction. In a small proportion of children, it is due to an allergic footwear dermatitis, identified by patch testing. Avoiding synthetic socks, and wearing two pairs of cotton or wool socks may help. Emollients or humectantssuch as urea cream may help. Applying steroid impregnated tape over fissures or using paste bandages accelerates healing. Topical steroidointments are sometimes useful.


There is wrinkling and rippling of the central portion of the nail plate, also there is loss of the cuticle at the proximal nail fold. This is a habit-tic nail deformity. It is caused by frequent subconscious picking of the proximal nail fold either from the adjacent or the contralateral index finger. The repetitive pushing back of the cuticle results in minor trauma to the nail matrix; secondary rippled central dystrophy subsequently develops. The affected patient is often unaware of the habit but is often appreciated by spouses or other family members. Applying a hydrocolloid dressingaround the nail including the proximal nail fold can break the habit, allowing the nail to regrow normally.


This is the early vesicular phase of incontinentia pigmenti, an inherited condition which affects the skin, eyes, teeth, and central nervous system. It is inherited as a sex-linked dominant condition on the X chromosome. It is usually incompatible with life in utero in males, and therefore manifests only in females. Early in life, the rash is vesicular with eosinophil-filled vesicles. Later, lesions become warty (verrucous phase), before becoming hyperpigmented. In all phases, the rash follows the lines of Blaschko. Read more on Incontinentia pigmenti


There is a rippled hyperpigmented maculopapular eruption on the neck. These features are typical of macular amyloidosis, a reaction that is thought to result from perpetual scratching of the affected areas. It is common in both men and women of Asian heritage. Histopathologically, amyloid deposits are seen within a skin biopsy; furthermore, macular amyloid is not associated with systemic disease as opposed to systemic AL amyloid that is associated with plasma cell dyscrasias.


The groove has been caused by pressure from a myxoid cyst (digital mucous cyst) which overlies the nail matrix. Pressure applied to the nail matrix from any cause will result in either a line or groove in the nail plate distally. The discharge of clear, sticky, mucoid material is typical of intermittent rupture of the false cyst. The diagnosis is usually made clinically, but the presence of a pseudocyst can be confirmed by high resolution MRI scanning of the affected digit. Treatment is difficult and is frequently advocated by recurrence. Under a digital block, the proximal nail fold can be reflected back, the cyst identified, and its communication with the synovium ligated. More proximal digital myxoid cysts can be treated by repetitive puncture and expression of the contents, injection of sclerosants, or surgery.


There is roughness of the nail plates (trachyonychia) affecting all finger and toenails. With repeatedly negative mycology, and absent skin problems elsewhere, the likely diagnosis is twenty-nail dystrophy. This may be associated with previous, concurrent, or the ultimate development of alopecia areata or lichen planus. Evidence of these conditions should be sought in the scalp, mouth, and elsewhere on the skin. Less convincing associations are with psoriasis and eczema. The condition is difficult to treat, but may undergo spontaneous resolution. For more information, see twenty-nail dystrophy.


The eruption has a violaceous hue, and the area covered by his hat and shirt (below the collar line) is spared. These features together suggest a photolichenoid eruption. Biopsy will show epidermal hyperkeratosis, hypergranulosis, basal cell liquefactive degeneration, and a dense upper dermal band-like lymphocytic infiltrate. For more information see lichenoid drug eruption pathology. Photolichenoid eruptions are usually due to medication, and quinine is a well-known cause. Some HIV medications, thiazide diuretics, and docetaxel are other incriminated drugs. Stop suspect medicines (eg, quinine) and use a sunscreen with a good UVA spectrum of protection, as well as other general sun protection measures. A potent topical steroid will need to be used for a short period of time to suppress the lichenoid reaction.


This is scleroedema (U.S. scleredema), not to be confused with scleroderma. It occurs as a result of the accumulation of mucin in the dermis. It may be associated with a paraprotein, diabetes, and can occur acutely after a respiratory infection. Less robust associations include Sjogren syndrome, rheumatoid arthritis, hyperparathyroidism, and HIV infection. Testing for associated biochemical abnormalities (paraprotein, immunoglobulins, HbA1c) should be conducted. Skin biopsy will show accumulation of dermal mucin.


The nail plates are yellow in colour, and have excessive transverse and longitudinal curvature. These features are typical of yellow nail syndrome, and patients usually describe the need to only infrequently cut their nails as the nail growth rate is substantially slower than normal. It is most commonly associated with lymphoedema, pleural effusions, and bronchiectasis. The cause is unknown; there is limited evidence that it may improve with oral or topical vitamin E supplements, and the antifungal agents. Oral itraconazole and fluconazole are oral antifungal agents. It has been noted that they appear to speed up the rate of growth of nails, which may be of benefit in yellow nail syndrome even though it is not caused by fungal infection.


A papulosquamous eruption with lesions on the palms and soles should always raise suspicion of secondary syphilis. This should initiate questioning regarding sexual contacts, and recent history of genital, oral, or perianal primary syphilis lesions (chancres). There may be scars at the site of a recent chancre, and mucosal lesions of secondary syphilis (snail track ulcers and condylomata lata). Other sexually transmitted disease lesions should be sought eg, warts, mollusca. The VDRL test will always be positive in secondary syphilis unless there is co-infection with HIV. Treponema pallidum PCR testing may be positive from mucosal lesions. Referral to STD services is mandatory to both contact trace and identify co-infection with other sexually transmitted diseases. The syphilis infection will be treated with intramuscular penicillinaccording to local guidelines.


The subtle but slowly spreading red ring is characteristic of erythema migrans, the early cutaneous manifestation of Lyme disease. Inoculation occurs after a bitefrom an infected tick. The rash often starts days after inoculation of the skin with a causative bacterium, Borrelia burgdorferi, and slowly spreads over a number of weeks. It is usually the case that the tick needs to feed from the human victim for at least 24-hours in order for infection to occur. A significant proportion of those infected have no recollection of the tick attachment. Early associated symptoms include fever, chills, muscle and joint aches, swollen lymph nodes, and erythema migrans (in about 80%). Late symptoms include arthritis, carditis and arrhythmias, neuritis, and encephalitis. Late skin manifestations include acrodermatitis chronica atrophicans and lymphocytoma cutis. Children under the age of nine should be treated with amoxicillinor azithromycinif they have non-focal symptoms. The presence of carditis or central nervous system disease would require intravenous treatment.


This is periocular dermatitis; it often coexists with perioral dermatitis. It produces small red papules and occasionally pustules firstly at the lower lateral lid, then may spread around the entire periocular skin. It is often sore rather than itchy. It is quite distinct from other causes of periocular eczema, such as atopic, seborrhoeic, or contact eczema. Many cases of perioral and periocular dermatitis (periorificial dermatitis) are due to either intentional or inadvertent topical steroid exposure to the affected sites. Back spray from the nasal steroid aerosol onto the periocular skin has caused this young womans problem. Treatment involves improvement of spray technique to prevent accidental exposure or withdrawal of topical steroids. Oral tetracyclines are very effective and may be needed for a few months; repeat courses may be given should it recur. Other oral antibiotics such as macrolides and metronidazole are effective. Topical therapies such as metronidazole, clindamycin, and calcineurin antagonists have been used but are often not tolerated.


The image shows monomorphic papules over the interscapular area. There are no comedones, and there is no variety in the size and shape of lesions as one sees in acne. These features all suggest Malassezia (pityrosporum) folliculitis. The condition results from the overgrowth of pityrosporum yeasts within the hair follicles. Humidity, heat, seborrhoea, immunosuppression, and HIV contribute to the overgrowth of the yeasts. The back is the most frequently affected area; it can also occur on the chest. It is often associated with seborrhoeic dermatitis in other sites. Routine bacteriology from affected follicles is negative as the causative yeasts require very specialised culture media to grow them. They are most easily visualised on biopsy. Topical antifungals such as selenium sulfide shampoo, or azoles such as econazole lotion or ketoconazole shampoo, can be helpful both in initial treatment and recurrence prevention. Oral fluconazole or itraconazole are sometimes more convenient to use.


Linear IgA bullous dermatosis. There are blisters arranged in a ring  the so-called string of pearls sign, which is most often seen in this condition. Perilesional immunofluorescence will show a linear band of IgA at the dermoepidermal junction, in contrast to the granular deposits of IgA seen in dermatitis herpetiformis. The blisters are sub-epidermal. As opposed to dermatitis herpetiformis, linear IgA disease is not associated with gluten enteropathy. Linear IgA disease may be associated with solid cancers and lymphomas, inflammatory bowel disease, and rheumatoid disease. Several drugs have been implicated in initiating this condition. Treatment of this condition involves the use of potent topical steroids, but oral steroids combined with oral dapsone are usually required.


This is dissecting cellulitis of the scalp, also known as perifolliculitis capitis abscedens et suffodiens and Hoffman disease. It produces nodules, cysts, and discharging scalp lesions with eventual patchy scarring hair loss (alopecia). It may be associated with severe acne(including acne conglobata) and hidradenitis suppurativa, collectively called the follicular occlusion triad. More recently, pilonidal sinus diseasehas been added to this list (follicular occlusion tetrad). Therapy is difficult. It involves considering the following:


There is a well-circumscribed plaque on a sun exposed area. Centrally, there is some atrophy. There is some scaling and follicular plugging. The lesion is red. Coupled with the pathology, the features suggest discoid lupus erythematosus (DLE). The patient requires routine haematology, lupus serology, and urinalysis. If she is a smoker, this should be strongly discouraged. Treatment strategies include:


The photograph shows a well circumscribed scaly patch of erythema as well as early atrophy. Coupled with history of the patch of alopecia, discoid lupus erythematosus is the most likely diagnosis. Skin biopsy is required for diagnostic confirmation; it can be expected to show hyperkeratosis and follicular plugging. There may be epidermal atrophy, and patchy basal cell keratinocyte degeneration. PAS stainingmay show thickening of the basement membrane. In the dermis, there will be dense perivascular and periadnexal chronic lymphocytic inflammation. Topical treatments will include photo protection with sunscreens. Super potent topical steroids, which are usually avoided on the face, can be accurately applied to the lesions. Additional benefit is sometimes shown by combining the use of topical steroids with topical tacrolimus. Intralesional steroids may be useful for recalcitrant disease. Antimalarials, such as mepacrine (quinacrine) or hydroxychloroquine are indicated. If the condition is progressive despite the above, immunosuppression with either methotrexate or azathioprine may be offered as progressive disease will result in permanent scarring and hair loss.


This man has dermatitis herpetiformis. This is an immunobullous disorder associated with gluten sensitivity. The vesicles and blisters that arise in this condition are small (2 to 4 mm) and because the condition is so itchy, they are often excoriated so that intact blisters are seen only infrequently. The clue to the diagnosis is often from the rash distribution. It affects symmetrically the elbows and knees, sacrum, interscapular area, scalp, and beard area. Itch is usually severe. It is slightly more common in atopic individuals. The diagnostic test is direct immunofluorescence from a perilesional skin biopsy. Granular IgA deposits are seen at the dermo-epidermal junction. It is positive in 80% of sufferers on the first biopsy, 95% with the second biopsy, and close to 100% on the third biopsy so repeat investigation may be needed if clinical suspicion persists. Coeliac serology may be positive. Gluten-sensitive enteropathy is always present but may be asymptomatic and may be unassociated with biochemical evidence of malabsorption. However, ironor folic acid deficiency may be identified. There is a known association with haemochromatosis. Treatment requires a rigorous gluten-free diet; this may take two years to be fully effective. It can reduce the incidence of small-bowel lymphoma that can complicate the enteropathy. Oral dapsone usually results in the welcome and rapid relief of itch. The dose can be reduced to the lowest that maintains symptom relief.


This is a cutaneous calculus, or subepidermal calcified nodule, a lesion caused by the accumulation of calcium in the upper dermis. They have a cream white colour, are usually solitary, often appear filiform, and most commonly occur in children on the head and neck, especially the ear. It is thought that they usually arise in a pre-existing skin lesion, possibly a viral wart. They are usually not associated with disorders of calcium metabolism. They respond well to curettage or shave excision, and usually do not recur.


This is coumarin necrosis. It most frequently occurs shortly after the introduction of a coumarin anticoagulant (eg, warfarin). Natural anticoagulants reduce in concentration before natural pro-coagulants, so that there is the potential for a short period of relative thrombophilia and this can result in dermal vessel thrombosis andsubsequent skin necrosis. Dermal vessel thrombosis and skin necrosis has been reported in persons with protein S and C deficiency. It is occasionally seen later during anticoagulant treatment particularly if there has been erratic warfarin control. It can be managed by initiation of heparin, withdrawal of warfarin, and then the use of a new oral anticoagulant which directly inhibits either thrombin or factor Xa. Established necrosis may require devitalised tissue debridement.


Purpura can be seen affecting the upper and lower lids of both eyes. It is quite common for lid purpura to be precipitated after bouts of coughing. In the absence of any clotting or platelet problems, systemic amyloidosis should be considered. The presence of amyloid in the upper dermis disrupts the integrity of the support around small blood vessels making them susceptible to rupturing, and this accounts for the physical signs. Amyloid deposits under the flexor retinaculum of the wrists has produced carpal tunnel syndrome which is quite common in systemic amyloid. Systemic AL amyloid is usually associated with a plasma cell dyscrasia, so serum electrophoresis, estimation of immunoglobulins, and detection of Bence Jones proteins should be undertaken. Skin biopsies from affected skin may show amorphous upper dermal accumulation of amyloid protein.