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However asthma symptoms rib pain albuterol 100 mcg amex, two recent Swedish studies demonstrated a risk of cardiovascular defects in the neonate in patients taking erythromycin so this treatment should be avoided if possible in the first trimester [8,9]. Oral antihistamines are the treatment of choice; the second generation antihistamines loratadine and cetirizine are safe to use from the second trimester onwards. A study of 38 women presenting with pityriasis rosea in pregnancy showed that nine women had a premature delivery and five miscarried. Treatment is normally conservative as the rash fades rapidly within a few weeks in most cases. Pregnancy and oral contraceptive therapy can also trigger this eruption, which presents with tender erythematous nodules or plaques over the anterior lower legs. In most cases, this is due to an underlying skin disorder such as eczema, urticaria, or one of the specific pregnancyrelated inflammatory dermatoses. However, there is also a small group of women who experience intense pruritus without evident primary cutaneous changes and it is to these patients that the term pruritus gravidarum applies. Pruritus gravidarum is considered to be a mild variant of recurrent intrahepatic cholestasis of pregnancy (see Chapter 83), occurring in 0. Secondary skin lesions develop due to scratching and range from subtle excoriations to severe prurigo nodules as pruritus persists. Disease course and fetal prognosis the prognosis for the mother is generally good. After delivery, pruritus disappears spontaneously within days to weeks, but may recur with subsequent pregnancies and oral contraception [3]. In cases of jaundice and vitamin K deficiency, there is an increased risk for intra and postpartum haemorrhage in both the mother and child [3]. However, more significantly fetal prognosis can be impaired with an increased risk of prematurity, fetal distress and stillbirth [3,4]. Therefore, prompt diagnosis, specific therapy, close obstetric monitoring and maternal counselling are essential. Investigations Liver function tests are usually normal, while alkaline phosphatase may be raised (which is normal for pregnancy due to placental production) [6]. Of note, cholestyramine and other bile acid exchange resins may contribute to malabsorption of vitamin K with possible bleeding complications, and should therefore be avoided [8]. A retrospective study of over 500 pregnant women with pruritus demonstrated considerable overlap in clinical presentation and histopathology between pregnant women with atopic eczema, prurigo of pregnancy and pruritic folliculitis of pregnancy (together accounting for 50% of the patient database) [2,3]. Consequently a new classification of specific dermatoses of pregnancy has emerged: pemphigoid gestationis, polymorphic eruption of pregnancy, intrahepatic cholestasis of pregnancy and atopic eruption of pregnancy [2,3]. Epidemiology Polymorphic eruption of pregnancy is a benign, selflimiting pruritic inflammatory disorder that usually affects primigravidae in the last few weeks of pregnancy or immediately postpartum (15%) [3]. Its incidence is about 1: 160 pregnancies and it is associated with excessive maternal weight gain and multiple pregnancy [3,4]. The main theories proposed focus on abdominal distension and hormonal and immunological factors [3,5]. Although a previous study found no link with high fetal birth weight [3], this has previously been thought to be an association [5]. Hormonal and immunological changes have not definitively been shown to play a role; nor has an association with increased birth weight or male sex of the newborn been confirmed [3,6]. Often the eruption remains on these sites but it can quickly become generalized in severe cases. In contrast to pemphigoid gestationis, umbilical sparing is a characteristic finding. Lesions are selflimiting and the disease tends not to recur; the exception being in a multiple pregnancy, when earlier presentation in pregnancy may occur. Investigations the histopathology of this condition is nonspecific and there are many similarities with the early prebullous phase of pemphigoid gestationis. Most biopsies show epidermal and upper dermal oedema, with a perivascular infiltrate of lymphocytes and histiocytes. There may be a striking number of eosinophils (as there may be in pemphigoid gestationis). Spongiotic vesicles are also seen, as are hyperkeratosis and patchy parakeratosis [2]. Direct immunofluorescence is generally negative, even by immunoelectron microscopy, and this provides the best means of distinguishing this disorder from pemphigoid gestationis should there be any diagnostic doubt [8]. It can also occur in association with trophoblastic tumours (choriocarcinoma, hydatidiform mole). There is also an increased risk of developing other organspecific autoimmune diseases, in particular Graves disease. Management Symptomatic treatment with topical corticosteroids and emollients, with or without antihistamines, is usually sufficient to control pruritus and skin lesions. Most women are relieved to learn that the condition is not serious, that all should be well with them and their baby and that the rash will disappear at, or soon after, delivery [4,5]. Of interest, the primary site of autoimmunity seems not to be the skin, but the placenta, as antibodies bind not only to the basement membrance zone of the epidermis, but also to that of chorionic and amniotic epithelia, both equally of ectodermal origin. Initially, erythematous urticarial papules and plaques typically develop on the abdomen, characteristically involving the periumbilical region, but may spread to the entire skin surface. After delivery, the lesions usually resolve within weeks to months but may recur with menstruation and hormonal contraception. Fetal prognosis is generally good but there is an increase in prematurity and smallfordate babies. It has been shown that this risk correlates with disease severity, as represented by early onset and blister formation, and not with corticosteroid treatment, as has been repeatedly speculated before [3]. In all cases, conservative management is all that is required until maternal antibodies are cleared from the fetal circulation. Pemphgoid gestationis can recur in subsequent pregnancies, and with the use of oral contraceptive therapy. Investigations Histopathological findings from lesional skin depend on the stage and severity of the disease. The prebullous stage is characterized by oedema of the upper and middle dermis accompanied by a predominantly perivascular inflammatory infiltrate, composed of lymphocytes, histiocytes and a variable number of eosinophils. Histopathology of the bullous stage demonstrates subepidermal blistering that, ultrastructurally, is located at the lamina lucida of the dermo-epidermal junction [1]. It usually starts early on in pregnancy, with 75% of cases presenting before the third trimester, and a tendency to recur in subsequent pregnancies [1]. Management Treatment depends on the stage and severity of the disease and aims to control pruritus and to prevent blister formation. Topical corticosteroids with or without oral antihistamines may be sufficient in cases of mild prebullous pemphigoid [1]. All other cases require systemic corticosteroids (prednisolone, usually started at a dose of 0. When the disease improves, the dose can usually be reduced, but should be increased in time to prevent the flare postpartum. Cases unresponsive to systemic corticosteroid treatment may benefit from third line treatments including azathioprine, intravenous immunoglobulins and plasma exchange [6]. After delivery, if necessary, the full range of immunosuppressive treatment may then be administered.

Diseases

• Pili torti onychodysplasia
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• Chromosome 8 Chromosome 9
• Trichodermodysplasia dental alterations
• Fraser syndrome
• Chromosome 18, tetrasomy 18p
• Hypercalcemia, familial benign
• Froster Iskenius Waterson syndrome
• Sclerosing lymphocytic lobulitis

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Spontaneous regression of transplacentally transferred melanoma has been reported [4 hay asthma definition purchase albuterol paypal,5]. Transplacental transmission of acute monocytic leukaemia [6], natural killer cell lymphoma [7] and choriocarcinoma [8] have also been reported. The induration resolves over a period of a week or so, often leaving some residual postinflammatory hyperpigmentation. Neonatal cold injury Neonatal cold injury is a disorder, now rare in developed countries, in which cold exposure of a smallfordates neonate causes hypothermia associated with lethargy and generalized pitting oedema of the skin, clinically and pathologically distinct from sclerema neonatorum. Other factors that appear to have predisposed babies to this complication of cold exposure include intrauterine growth retardation, which results in a relatively thin panniculus, and tight wrappings, which restrict muscular activity. The infant is usually a fullterm neonate, born at home, but small for gestational age. In the great majority of cases, presentation is within the first 4 days of life, and usually during the first 24 h. The skin feels cold, and the baby is usually hypothermic with a low core temperature. Associated noncutaneous features of cold injury are generally present, and may occur in the absence of skin changes. These include immobility, drowsiness, poor feeding, vomiting, oliguria and gastrointestinal bleeding with vomiting of altered blood or melaena. Skin biopsy shows a thin panniculus; otherwise there is little obvious abnormality apart from dilatation of the dermal blood vessels [5]. Profuse exudation of clear fluid from the cut surface at postmortem suggests that the induration is due to oedema. The mortality rate of historical cases was about 25% (usually due to massive pulmonary haemorrhage). Transfer of toxic substances in maternal milk When considering the cause of any rash in a young infant, the possibility that it reflects exposure of the mother to a toxic substance that has been transferred in her milk needs to be borne in mind. A good example is provided by two reports of bromoderma occurring in neonates whose mothers had taken bromide medicinally [1] or had been accidentally exposed in a photographic laboratory [2]. The fat of the newborn appears to be more highly saturated than that of older children and adults, with the effect that it solidifies at a higher temperature [1,2]. Applying ice for 50 s causes panniculitis in all newborn infants, in only 40% of 6monthold infants and almost never in 9monthold infants [3]. Cold panniculitis in infancy has most often followed exposure of the cheeks to: (i) extremely cold air [4]; (ii) ice bags applied as a therapy for supraventricular tachycardia [5,6]; or (iii) frozen lollies (popsicles) [7,8]. Indurated, warm, red, subcutaneous plaques and nodules appear within hours or days of appropriate cold exposure. Skin biopsy is not usually needed but if done early it shows a lymphohistiocytic infiltrate around blood vessels at the junction of the dermis and subcutaneous fat [9]. After a few Subcutaneous fat necrosis of the newborn Definition Subcutaneous fat necrosis of the newborn is an uncommon and transient disorder of neonates in which focal areas of fat necrosis cause nodular skin lesions [1,2]. Age Subcutaneous fat necrosis generally occurs in fullterm or post term infants of normal birth weight during the first 6 weeks of life. The nodules tend to be symmetrically distributed and show a predilection for the buttocks, thighs, shoulders, back, cheeks and arms. Lesions may be single or multiple, rounded or oval, and peasized or many centimetres in diameter. Where calcium deposition is marked, the lesions may take rather longer to resolve. Pathophysiology Clinical variants There have been several reports of the occurrence of lesions analogous to those of subcutaneous fat necrosis of the newborn in children who have had hypothermic cardiac surgery [6,7,8]. The cutaneous application of ice to induce hypothermia, trauma and/or hypoxia may all have contributed. It is noteworthy that these children appear to have developed lesions of subcutaneous fat necrosis rather than cold panniculitis. Lesions appeared between 14 and 30 days later, principally at the sites subjected to the greatest cold exposure. Predisposing factors the precise cause is unestablished, but a variety of insults appear to have contributed in individual cases. The most important predisposing factors appear to be the combination of local tissue hypoxia and cold injury. Pathology Biopsies of the affected subcutaneous tissue show patchy fat necrosis, with a granulomatous inflammatory reaction of foreignbody type, and fibrosis [1,11,12]. Both the fat cells and the giant cells contain needleshaped clefts, which may be radially arranged. Ultrastructural examination has shown parallel aggregations of electronlucent, needleshaped spaces within the adipocytes [11,12]. Similar changes in visceral adipose tissue have been reported in postmortem studies of affected infants [3]. Widespread calcium deposition in internal organs has also been shown in postmortem specimens from hypercalcaemic cases and nephrocalcinosis has been observed in such infants during life [13]. It may be due to increased calcium absorption due to extrarenal production of 1,25dihydroxyvitamin D [17,18], which has been observed in other granulomatous disorders including sarcoidosis. The finding of increased urinary excretion of prostaglandin E1 led to the suggestion that increased bone calcium resorption might be responsible [19]. Transient thrombocytopenia has been reported during the period of initial development of the lesions, possibly due to sequestration of platelets [21]. Plasma lipid abnormalities have been reported in Environmental factors Hypoxia, cold and trauma all seem to play a role. Clinical features Presentation Infants who develop subcutaneous fat necrosis are generally full term or postterm neonates of normal weight [1,2,3,7,8,9]. Nodular thickening of the subcutaneous tissues is usually first detected between the second and 21st days of life. Subcutaneous fat necrosis of the newborn was in the past frequently confused with sclerema neonatorum. If hypercalcaemia is present, its cause requires thorough investigation to exclude disorders such as primary hyperparathyroidism and vitamin D intoxication. Nephrocalcinosis is a common persistent finding even in those children who have undergone treatment for hypercalcaemia, but fortunately renal impairment is very rare. Pathophysiology Predisposing factors Prematurity and smallness for dates appear to be frequent predisposing factors [2]. It has been recorded as already present at birth in infants subjected to placental insufficiency [3]. The disorder does not seem to occur in otherwise healthy infants, and most characteristically develops during the course of one of a wide variety of severe illnesses, particularly serious infections, congenital heart disease and other major developmental defects [2]. A proportion of these infants have been hypothermic, and occasionally sclerema has been described as a complication of neonatal cold injury [4]. Nevertheless, cold does not appear to be an important aetiological factor in the majority of cases. Lipolytic mechanisms are poorly developed in the newborn, particularly in those born preterm [5]. The maturation of these enzyme systems might be further compromised by major infection or hypoxia. It has been suggested that sclerema might reflect defective lipolysis within adipose tissue, which would result in failure of fat mobilization, and an impaired capacity to maintain body temperature. It has been reported that the ratio of saturated to unsaturated fatty acids is relatively high in the adipose tissue of all neonates, and that this ratio was even higher in an infant with sclerema [6].

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Environmental factors Perniosis occurs in susceptible individuals during the autumn or winter in a climate that is both cold and damp asthma humidity buy albuterol on line. Clinical features Introduction and general description Perniosis lesions are cold induced and affect areas of the skin vulnerable to cold exposure, such as the digits, nose and ears. Perniosis develops symmetrically on the acral skin, in particular the fingers and toes, but other body extremities may also be involved including the heels, lower legs, nose and ears. Erythrocyanotic papules, located on the fingers and toes, develop in cold weather and tend to persist, in some cases becoming ulcerated [9]. Perniosis may also complicate haematological malignancy, typically myelodysplastic syndrome and chronic myelomonocytic leukaemia (see Chapter 148). Cyanotic swelling of acral digital skin, particularly the toes, has been reported in these patients [11]. The onset of perniosis may coincide with a blast crisis, which can be demonstrated on skin biopsy by the presence of large, atypical mononuclear cells in the perivascular infiltrate [12]. Pathophysiology In perniosis there is a persistent coldinduced vasoconstriction of the deep cutaneous arterioles with concomitant dilatation of the smaller, superficial vessels. This is in contrast with normal subjects, in whom cold exposure induces cutaneous vasoconstriction succeeded by vasodilatation, a homeostatic mechanism necessary for the maintenance of reperfusion. Investigation of the cutaneous nerves in patients with perniosis demonstrated no quantitative or qualitative difference in immunoreactivity for substance P, neuropeptide Y, calcitonin generelated peptide or vasoactive intestinal peptide compared with controls [6]. However, in the affected skin of patients with acral perniosis, who also had a past history of very low body weight, immunohistochemistry revealed a great increase in nerve bundles in the papillary dermis, some with an abnormal morphology [6]. This indicates that in uncomplicated perniosis the neuronal supply to the microvasculature is normal and suggests that the pathology involves the microvessels themselves. In papular perniosis, crops of small chilblains develop on the sides of the fingers often on a background of acrocyanosis [13]. Clinically, these lesions are composed of clustered papules or plaques, which may ulcerate. Tightfitting trousers, such as riding breeches, have been implicated aetiologically [9]. In chronic perniosis, especially in the presence of arterial disease or prolonged cold exposure, irreversible changes of fibrosis, lymphoedema and hyperkeratosis may occur, altering the physical signs. Pathology the histopathology of perniosis usually demonstrates dermal oedema with superficial and deep dermal inflammation [7]. The mononuclear cell infiltration, mostly T cells, is primarily perivascular but also occurs in a perieccrine distribution [8]. Most patients will experience good disease control when steps are taken to prevent cold exposure. Investigations Investigations should be guided by the clinical presentation of the patient but may include a full blood count and/or blood film, protein electrophoresis, an autoimmune screen, cryoglobulins and cold agglutinins. Investigations were positive in 11/20 tested patients from a Mayo Clinic series [2]. A doubleblind, placebocontrolled study demonstrated the efficacy of nifedipine in clearing existing chilblains and preventing the development of new lesions [14]. Acrocyanosis y Definition Acrocyanosis is a persistent cyanotic or erythrocyanotic mottled discoloration of the hands and, less commonly, feet and face. Introduction and general description Acrocyanosis may be idiopathic or secondary to a number of systemic disorders, including an underlying malignancy (Box 125. Clinical features Idiopathic acrocyanosis usually starts in adolescence and persists into adult life. The changes may be transient after cold exposure but usually persist during the winter and even throughout the summer months. Clinically there is a painless mottled duskiness of both hands in the presence of normal peripheral pulses. Acrocyanosis must be distinguished from the Raynaud phenomenon, which occurs episodically with triphasic colour changes and often involves just a few digits. In cases of acrocyanosis developing for the first time in adult life a secondary cause should be sought (Box 125. Epidemiology Age and sex Presentation is typically in adolescence, with a reported female preponderance [2]. Pathophysiology There is vasospasm of peripheral arterioles, aggravated by cold, and dilatation of the subpapillary venous plexus [3]. The condition is most probably a primary vascular defect since studies have not demonstrated a deficit of neuronal supply to the cutaneous vessels [4]. Differential diagnosis this includes Raynaud phenomenon, arterial occlusion and venous occlusion. However, the usefulness of this technique in distinguishing primary acrocyanosis from connective tissue disease has yet to be firmly established. Prognosis the disorder may persist indefinitely but spontaneous improvement can occur in adolescent patients. Vasodilator therapies, such as the calciumchannel antagonists, do not appear to be beneficial. Treatment of an underlying systemic disorder may improve the appearance in secondary acrocyanosis. Warm clothing, exercise, weight reduction and elastic support hosiery may be helpful. Introduction and general description Erythrocyanosis is a condition that predominately affects the lower legs, distinguishing it from acrocyanosis, which affects peripheral areas such as digits and appendages [1]. Introduction and general description Livedo reticularis is a lacelike pattern on the surface of the skin created by low blood flow within anastomoic areas of the skin. Each cone is supplied by an arteriole, which passes through the dermis perpendicular to the surface. Livedo reticularis may be physiological, idiopathic or secondary to intravascular obstruction or vessel wall disease (Box 125. Age and sex Erythrocyanosis occurs most commonly in adolescent girls and middleaged women. Pathology There is hyperkeratosis, red blood cell aggregates and vessel wall thickening in the deep dermis. If the livedo reticularis is caused by vasculitis, there will be vascular inflammation and arterial obliteration in the deep dermis and the subcutaneous tissue. There is no difference in the histological features between the blanched and erythematous areas [2]. Clinical features Erythrocyanosis is seen on the lower legs of adolescent girls, the thighs and buttocks of overweight boys and the thighs and lower legs of middleaged women. It is characterized by dusky discoloration of the skin and may be accompanied by keratosis pilaris, angiokeratomas and telangiectases. Nodular perniotic lesions occurring after cold exposure may complicate erythrocyanosis. Clinical features Livedo reticularis most commonly occurs on the legs but the arms and trunk may also be affected. Cold usually exacerbates the cyanotic discoloration, while leg elevation tends to decrease the intensity of the colour changes. Diffuse arterial disease or hyperviscosity problems give rise to diffuse livedo reticularis; limited arterial disease leads to patchy mottling. In many cases livedo reticularis forms a complete network, in other cases there is a branching Differential diagnosis Whilst the diagnosis is often clinically apparent, other vascular disorders and livedo reticularis may be considered in the differential. Also known as cutis marmorata, this is a transient cyanotic mottling of the skin that occurs as a physiological response to cold exposure and disappears with warming. It is usually encountered in healthy infants and resolves during the first year of life. Physiological livedo reticularis rarely occurs in adults, but in this situation is often associated with a disorder that causes stasis within blood vessels, for example paralysis. Lesions are usually asymmetrical, typically on a limb, less often involving the torso or head. Usually congenital livedo reticularis occurs in isolation but it may be associated with a variety of other congenital abnormalities.

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Seborrhoeic dermatitis Genital involvement is frequent with this common dermatosis asthma symptoms sneezing generic albuterol 100 mcg online. A good his tory (including family history) and careful examination of other sites typically affected aid the diagnosis. On the scalp, the face, in the flexures and at anogenital sites seborrhoeic dermatitis and psoriasis may be indistinguishable. However, treatments that diminish the Malassezia load and reduce irritation and eczematization can be success fully and safely used long term. These include topical antifungals (such as clioquinol, nystatin and imidazoles) as ointments, creams, lotions or shampoos, and mixtures of the same agents with mild and moderately potent topical corticosteroids used alongside emollients and soap substitutes. Zoon balanitis Introduction and general description An asymptomatic, inflammatory and irritant condition of the glans and mucosal prepuce that is probably overdiagnosed. The evidence suggests that Zoon balanitis is a chronic, reactive, principally irritant dermatosis brought about by a dysfunctional prepuce. There is no evidence of an infectious cause, and immu nohistochemical findings suggest that Zoon balanitis represents a nonspecific polyclonal tissue reaction [9,10], consistent with an irritant dermatosis. Although vegetative and nodular presentations have been recorded, atypical or unusual morphology should be viewed with great suspicion and biopsied [7,8]. Differential diagnosis the differential diagnosis includes lichen sclerosus, erosive lichen planus, psoriasis, seborrhoeic dermatitis, contact dermatitis, fixed drug eruption, secondary syphilis, histoplasmosis [13], erythro plasia of Queyrat [14] and Kaposi sarcoma. A confident clinical diagnosis is not always possible or safe [6,8,15], so a biopsy is advisable, and the pathologist should be asked to look for con comitant disease. In other words, the signs of Zoon balanitis may be sec ondary to underlying preputial disease [8]. Zoon balanitis indicates a dysfunctional foreskin Pathology the classic histology is of epidermal attenuation with absent gran ular and horny layers, and diamond or lozengeshaped basal cell keratinocytes with sparse dyskeratosis and spongiosis. Extravasated erythrocytes, haemosiderin and vascular prolifera tion are also seen. Although Zoon stressed the presence of the plasma cell infiltrate in this condition, the plasma cell numbers can be very variable [7,8,11]. Clinical features the presentation is classically indolent and asymptomatic, although staining of the underclothes with blood has been reported [12]. Most patients diagnosed with Zoons balanoposthitis probably have clinically subtler underlying lichen sclerosus. Case reports concerning the use of topical calcineurin inhibitors have appeared [20,21,22] but these agents should be used with circumspection in the setting of a dysfunctional foreskin and the attendant risk of penis cancer, long term. Again, the pathologist should be asked to examine the whole specimen for signs of another underlying dermatosis. Lichen sclerosus definition and nomenclature Lichen sclerosus is a common inflammatory dermatosis with a predilection for anogenital skin. But the epidemiology and clinical tenor of lichen sclerosus are not those of an infectious or sexually transmit ted disease: it is never seen in sexual partners [9,36]. The presence of the histopathological features of lichen sclerosus in a percentage of acrochordons (skin tags) suggests that occlusion of flaccid skin is a pathogenic factor [37]. Nuclear magnetic resonance spectroscopy of urine has not identified a single culpable chemical constituent of urine [43]. Introduction and general description Lichen sclerosus is a common dermatosis of the penis. The diag nosis and management of lichen sclerosus is a frequent reason for patients to be referred to a male genital dermatology clinic. Sometimes, lichen sclerosus may be difficult to differentiate from lichen planus, and criteria to assist, in the vulva, have been proposed by Fung and LeBoit [47]. In adults, anogenital lichen sclerosus is said to be about 10 times more common in women than men. Clinical features the development of secondary phimosis in schoolage boys is highly suggestive of lichen sclerosus [14]. In the older male, persistent primary phimosis or the secondary development of phimosis in a previously retractable foreskin may be related to lichen sclerosus [9]. Lichen sclerosus of the penis may be asympto matic, but diverse, sometimes vague, symptomatology is usually encountered at rest or during or after sexual congress. Patients may describe itching, burning, bleeding, tearing, splitting, rash, Pathophysiology the aetiopathogenesis of male genital lichen sclerosus has become clearer in recent years. Predomi nant purpura, angiokeratomas, bullae, erosions and ulceration may be encountered. Alternatively, the clinical features may be florid with severe inflammation, gross adhesions, loss of anatomical definition and dissolution or effacement of the normally sharply defined architectural features, especially of the frenulum and the coronal sulcus and rim: pearly penile papules may be destroyed. Posthitis xerotica obliterans refers to chronic damage to the prepuce by lichen sclerosus, whereas balanitis xerotica obliterans properly describes involvement of the glans penis (although the term has been used imprecisely). Balanitis xerotica obliterans can be a consequence of other scarring dermatoses such as lichen planus and cicatricial pemphigoid. The involvement of the anterior urethra can be serious; 29% of patients undergoing urethroplasty for urethral stricture had pathological evidence of lichen sclerosus [25]. Lichen planus, Zoon balanoposthitis, nonspecific balanopost hitis and very rarely mucous membrane pemphigoid are in the differential diagnosis. A biopsy might be performed if there is clinical doubt or if the result might impact on management deci sions. There should be a low threshold for biopsying lesions that are eroded, ulcerated or verrucous. The aims are early diagnosis and effec tive treatment to obtain normalization of sexual function, reverse or check urinary dysfunction and limit urethral disease and reduce, if not abolish, the risk of penis cancer [1,53,54]. There are reports of the efficacy of longterm systemic antibiotic therapy (penicillin and azithromycin) in cases of lichen sclerosus thought to be associated with Borrelia infection [59,60]. The exhibition of topical calcineurin inhibitors is to be deprecated because of the risk of accelerated carcinogenesis [1,53,62,63]. If medical treat ment with ultrapotent topical steroid is not possible or fails, then surgery is indicated. In boys, complete circumcision is the treatment of choice because all affected tissue is removed and any secon dary involvement of the glans probably regresses or resolves [16]; it is the unproven impression that this phenomenon also occurs in most adult patients. Surgery works in male genital lichen scle rosus if it relieves susceptible epithelium from chronic occluded exposure to urine. Surgery fails if it does not achieve this goal or if the damage to urethral structural and functional integrity is beyond intervention and if skin rather than mucosal grafts are used (if a graft is needed). Surgery may inadvertently worsen the problem by increasing the overall incontinence of the distal uri nary system. Fundamental to planning of penile surgery for lichen sclerosus is the recognition of the pernicious role in the initiation and progression of male genital lichen sclerosus played by the chronic occluded exposure of genital skin to urine [67]. In the long term, about 40% of patients will respond to medical treatment: the majority of the remainder will be cured by surgery, usually circumcision [1]. Residual burntout disease on the glans may improve with longterm topical retinoid treatment. Subdermal injection of polydeoxyribonucleotide (a mitogen for fibroblasts, endothe lial cells and adipocytes) is an interesting new approach [68]. Squamous carcinoma of the penis is the most serious potential complication of lichen sclerosus [1,9]. Carcinoma in situ and early microinvasive disease can be difficult to diagnose clini cally against a background of lichen sclerosus [1,9,69]. One third to one half of all established penile cancer is associated with lichen sclerosus [76,79,80].

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Since lip lesions are often of the nodular or morphoeic types asthma symptoms jaw cheap albuterol online mastercard, Mohs micrographic surgery [22], utilizing microscopically controlled excision, potentially offers the highest cure rate with the greatest preservation of tissue. Basal cell carcinoma of the lip Actinic radiation is a major aetiological factor in the development of basal cell carcinoma, greater than 85% occurring on the sun exposed areas of the head and neck [1,2]. Fairskinned individuals who burn and those whose occupations require excessive exposure to sunshine are at greatest risk; the tumour is rare in dark skinned persons, and 95% occur after the age of 40 years [3]. Keratoacanthomas are common selflimiting proliferative tumours that arise most frequently in men after the sixth decade of life [1,2]. Although some believe keratoacanthomas represent welldifferentiated squamous cell carcinomas, significant differences between the two entities have been demonstrated [3]. A number of welldocumented variants, many with generally distributed eruptive keratoacanthomas, have been described. The role of actinic damage is strongly supported by the fact that the majority of lesions occur on sunexposed skin (90%), with up to 10% occurring periorally or on the vermilion border of the lips, often on the lower lip. Keratoacanthomas often manifest at the vermilion border, as indurated domeshaped nodules displaying a characteristic central, keratinfilled, crusted and frequently darkened crater. They usually appear as an ulcer with a rolled margin, usually on the anterior or maxillary gingiva, clinically indistinguishable from squamous cell carcinoma. It is unclear whether intraoral keratoacanthomas regress spontaneously, as all have been excised for diagnosis. When lesions develop intraorally or on the lips, they should immediately be subjected to biopsy for confirmation, since squamous cell carcinomas at these sites frequently metastasize. Intralesional therapy with methotrexate or 5fluorouracil can also be employed with excellent results [14,15]. Treatment is by application of petroleum jelly and avoidance of the adverse environmental conditions. Contact cheilitis Contact cheilitis is an inflammatory reaction provoked by the irritant or sensitizing action of chemicals. Most cases are caused by the deliberate application of lipsticks or lipsalves but many substances have been incriminated, sometimes from accidental contact with an offending substance (Box 110. An eosin impurity used to be an important sensitizer [8] but is now rarely if ever used. Other ingredients occasionally incriminated include azo dyes, carmine, oleyl alcohol [9], lanolin, perfumes, azulene, propyl gallate [10], sesame oil [11], stearates [12], shellac and colophony [13,14]. Petrolatum chapsticks may cause an unusual form of acne with a single row of large open comedones along the cutaneous margin of the upper lip [18]. The keratin of the vermilion loses its plasticity, so that the lips become sore, cracked and scaly. The affected person tends to lick the lips, or to pick at the scales, which may aggravate the condition. Lipstick cheilitis is sometimes confined to the vermilion but more often extends beyond. There may be persistent irritation and scaling or a more acute reaction with oedema and vesiculation. If a small sucked object is responsible, the reaction may be confined to one part of the lips. Azo dyes Carmine Colophony Eusolex Oxybenzone ptertiarybutylphenol Propyl gallate Sesame oil Wax Azulene Castor oil Eosin Lanolin Phenyl salicylate Ricinoleic acid Shellac Benzoic acid Cinnamon Ester gum Oleyl alcohol Propolis Salol Vanilla Diagnosis. If acute eczematous changes are obviously present, the diagnosis of contact cheilitis presents no difficulty. If the changes are confined to irritation and scaling, the various forms of exfoliative cheilitis must be excluded. Topical corticosteroids or pimecrolimus will often give symptomatic relief but the offending substance should be identified and avoided. Metal hair clips, metal pencils, the cobalt paint on blue pencils, nail varnish, and the metal, wooden, nickel and reed mouthpieces of musical wind instruments [15] may be implicated. Apple Banana Cherry Kiwi fruit Mango Parsley Pear Artichoke Carrot Fennel Lemon Onion Parsnip Pineapple Asparagus Celery Garlic Lime Orange Peach Plum 110. Aromatic retinoids such as etretinate and isotretinoin cause cheilitis, dryness and cracking of the lips in many patients [1,2]. Eczematous cheilitis the lips are often involved secondarily to atopic eczema (see Chapter 41). In a large Russian series, almost half the cases had associated thyroid disease [1], but this observation has not been confirmed. Most cases occur in girls or young women, and the majority have a personality disorder [9,10]. The process, which often starts in the middle of the lower lip and spreads to involve the whole of the lower or both lips, consists of scaling and crusting, more or less confined to the vermilion border, and persisting in varying severity for months or years. The patient often complains of irritation or burning, and can be observed frequently biting or sucking the lips. In some cases, the condition appears to start with chapping or with atopic eczema, and develops into a habit tic. In such cases, the clinical features are variable and may simulate carcinoma, lichen planus or lupus erythematosus. Reassurance and moisturizing agents and topical corticosteroids [2], or tacrolimus [5,13] may be helpful in some cases as may Calendula [14] but others require psychotherapy, antidepressants or tranquillizers [4,6,11,15]. The diagnosis is now restricted to those few patients whose lesions cannot be attributed to other causes, such as contact sensitization or light (see Actinic cheilitis, p. Origin Natural Material Collagen Fat (free fat transfer, autologous fat transfer/transplantation, liposculpture, lipostructure microlipoinjection) Hyaluronic acid Hydroxyapatite Synthetic Polyacrylamide PolyLlactic acid Polymethylmethacrylate Silicone *Usually nonresorbable. In simple glandular cheilitis, the lower lip is slightly thickened and bears numerous pinheadsized orifices, from which mucous saliva can readily be squeezed. In the more severe suppurative form the lip is considerably and permanently enlarged, and subject to episodes of pain, tenderness and increased enlargement. The surface is covered by crusts and scales, beneath which the salivary duct orifices may be discovered. In the most severe forms there may be deepseated infection with abscess formation and fistulous tracts. This does, of course, support the suggestion that in many cases glandular cheilitis is a consequence of actinic cheilitis [5]. Cheilitis granulomatosa, cheilitis exfoliativa, and selfinduced changes (Munchausen syndrome) should be considered in the differential diagnosis [7]. If the lips are grossly enlarged, excision of an elongated ellipse of tissue may be required; in other cases shave vermilionectomy may be all that is necessary. Complications may include temporary pain, bleeding, bruising, swelling, seromas (fluid collections), infection or allergy. Clinically, patients may present with painless or painful, diffuse lip/facial swellings, usually of a firm elastic consistency. Granulomatous cheilitis Definition and nomenclature this is a chronic swelling of the lip due to granulomatous inflammation of unknown cause. Melkersson in 1928 [1] described labial oedema in association with recurrent facial palsy. Rosenthal in 1930 emphasized the role of genetic factors and added fissured tongue to the syndrome.

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Such infections are still responsible for a high proportion of deaths in the neonatal period in developing countries asthma 3d animation order albuterol 100 mcg on line. Initially, the infant develops what appears to be straightforward cellulitis, usually affecting the abdominal wall. However, the child becomes disproportionately toxic, and the area affected becomes indurated, discoloured and extends progressively [2,6,7,8]. Purpura and, occasionally bullae, may develop in the centre of the indurated area, often followed quite rapidly by frank necrosis. A wide variety of bacteria have been associated with necrotizing fasciitis, most commonly group A streptococci, but also group B streptococci, Staphylococcus aureus and Escherichia coli [6,7,8]. In many cases, a synergistic infection by aerobic and anaerobic organisms appears to be responsible. Antibiotic (and antifungal) therapy appears to be of limited value in this potentially lethal situation. The most important aspect of treatment is early surgical excision of the necrotic tissue [7,8]. Neonatal listeriosis Listeriosis during the neonatal period is uncommon, but dangerous. The responsible organism, Listeria monocytogenes, may be transmitted to humans principally through contaminated foods [1]. In pregnancy, it causes a nonspecific, mild, influenzalike illness in the mother [2,3], but it may lead to transplacental infection of the fetus. Adult listeriosis has increased in a number of European countries during the early 21st century, but mostly in the elderly and not as yet in pregnancyrelated cases [4]. The earlyonset form results from the development of miliary granulomas following bloodborne dissemination of infection. Severely affected babies tend to be born prematurely and there is a high mortality. The back appears to be the site of predilection for such lesions, which are also seen in the mouth and on the conjunctiva. Other cutaneous lesions have been described in such babies, including purpura and morbilliform rashes. The late form of the disease is commoner, taking the form of meningitis, occurring a week or two after birth. Diagnosis is by culturing the organism from a variety of sites, including cerebrospinal fluid, blood, urine and from biopsy Preorbital cellulitis is restricted to the part of the orbit anterior to the orbital septum and is manifest by eyelid swelling. Orbital cellulitis involves the structures deep to the septum and presents with painful proptosis, eyelid oedema and conjunctival erythema [1]. One should always be alert to the possibility of group B Streptococcus as a rare cause of periorbital cellulitis or any form of cellulitis in a neonate, in view of the high risk of septicaemia with this organism [2,3]. Necrotizing fasciitis this name is given to a distinctive form of cellulitis in which infection tracks along the fascial planes, causing thrombosis of the blood vessels running through the fascia with resulting necrosis of the skin, subcutaneous fat and even muscle [1,2] (see also Chapter 26). Ecthyma gangrenosum Pseudomonas aeruginosa is common in the hospital environment and infections are encouraged by the widespread use of broad spectrum antibiotics (see also Chapter 26). Most, but not all, neonates who develop the skin lesions of ecthyma gangrenosum have P. Occasionally, the lesions develop at the site of direct inoculation of the causative organism. Histologically, the presence of vasculitis, due to bacterial infiltration of the vessel walls, is characteristic, together with haemorrhage and necrosis [5]. Clinically, lesions initially take the form of painful macular erythema or purple ecchymosis [1,2,3,6,7,8]. The centre then generally develops either vesicles (or less commonly bullae) or pustules, which rapidly ulcerate. Subsequently one or more ulcers occur, each with a depressed, necrotic, often black, crusted centre and a raised edge. This infection is potentially dangerous when it occurs in the setting of septicaemia. Appropriate parenterally administered combination antibiotic therapy will be required. Congenital syphilis Congenital syphilis is described in detail in Chapter 29, but its cutaneous manifestations in the neonate will be considered here briefly because of their importance in differential diagnosis [1]. About 15% of children born to mothers with untreated syphilis will contract congenital syphilis, but fetal loss/still birth occurs in about 20% of such pregnancies. The skin is clinically affected in about 40% of neonates with congenital syphilis [1,2]. In such cases, the skin is usually of normal appearance at birth, the initial lesions occurring between the second and eighth week, and occasionally later. Small, round, moist, papular lesions, traditionally termed mucous patches, are frequently present in the mouth and on other mucosal surfaces. Condylomata lata may be present in the anogenital flexures or at other flexural sites, for example between the toes or in the angles of the mouth. Apart from the cutaneous features, the most frequent clinical manifestations of congenital syphilis in the newborn are hepatomegaly, splenomegaly, jaundice, pneumonia and rhinitis, often with a bloodstained discharge. The recent resurgence in the incidence of syphilis in many countries may lead to an increase in cases of congenital disease, especially where antenatal care is poor [2,3,4]. A similar condition may be seen in older children and adults in the context of poor nutrition, delayed growth and immunodeficiency [4,5]. Treatment is with parentral antibiotics and often requires plastic surgery later to repair large facial defects. Purpura fulminans Although in the newborn this condition is most often a reflection of genetically transmitted thrombophilic disorder, it may be caused by acute infections, particularly with endotoxinassociated, Gram negative bacteria such as Neisseria meningitidis [1,2]. Congenital tuberculosis Tuberculosis in the newborn due to transmission of infection in utero is relatively rare (see also Chapter 27). The lungs and/or liver tend to be the predominant sites of involvement, and skin manifestations are unusual. Fungal infections Both Candida and Malassezia species can cause neonatal fungal disease. There are two distinct forms of neonatal candidiasis, present at birth or seen in the first weeks of life. Neonatal candidiasis this is a relatively common disorder that occurs in the early weeks after birth, in the form of oral candidiasis with or without candidiasis in the napkin area (see also Chapter 32). The occurrence of localized palmar pustules in an infant with neonatal oral candidiasis was believed to reflect the inoculation of Candida from the mouth into the skin as a result of sucking [2]. Systemic neonatal candidiasis is a particular problem for preterm babies on intensive care units where it can cause septicaemia and death. Verylowbirthweight infants may have a scalded appearance, and are particularly at risk of systemic infection. When infection is confined to the skin, affected infants are generally well, and the rash clears within a week with appropriate topical antifungal therapy, for example with topical ketoconazole. Skin and mucosal involvement may be complicated by systemic candidiasis, particularly in the premature [2,11]. The lungs may be affected [12]; hepatosplenomegaly and abnormal liver function have also been recorded [6]. Systemic antifungal therapy should be considered in atrisk infants [9]; amphotericin B is probably the drug of choice [8,11]. Studies have shown that intravenous fluconazole prophylaxis in verylowbirthweight infants can reduce both invasive candidiasis and mortality rates [14,15,16] but a Cochrane review using oral antifungal prophylaxis in preterm infants has not shown a definitive benefit [17]. This yeast has been a cause of systemic infections in infants receiving intravenous lipids, and it is presumed that the source of organisms in such cases was the skin [3]. This type of rash was reported to have a frequency of 10% in neonates seen as outpatients in a paediatric dermatology department [5], with pustule contents showing M. A good therapeutic response to the topical application of 2% ketoconazole cream for 15 days was seen in almost every case. A frequency of 66% was reported in one study, with 62% being culture positive for Malassezia [6].

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The patient complains of generalized itching often with signs of excoriation and/or lichenification asthma symptoms for months discount 100mcg albuterol. Opioidinduced pruritus is the most frequent and best recognized primary druginduced Differential diagnosis Box 118. Disease course and prognosis Although considered a mild adverse drug reaction, chronic pruri tus can have a significantly negative effect on quality of life. Although antihistamine medications are frequently prescribed for druginduced pruritus, they are rarely helpful. Alternatively introduction of naloxone, naltrexone (receptor antagonists) or nalbuphine (partial receptor agonist, receptor antagonist) may be tried, but all of these approaches are likely to lead to loss of pain control. Interest ingly, receptor antagonists have also been utilized in other forms of pruritus especially where endogenous endorphins are thought to be pathogenic, such as in cholestatic pruritus [20]. For more resistant cases of druginduced pruritus, photo therapy and other therapeutic options may be of value (see Chapter 83). The medications which most commonly cause druginduced eczema are listed in Box 118. Patients with a contact allergy to ethylenediamine may develop generalized or localized eczema following injec tion of aminophylline preparations containing ethylenediamine as a solubilizer for theophylline [24,25]. Patients with contact allergy to parabens may develop systemic eczema on exposure to drugs containing parabens as a preservative [26]. Similarly, sensitized patients may develop eczema following oral inges tion of neomycin or hydroxyquinolines [27]. Sulphonylureas may also induce eczematous eruptions in sulphanilamidesensitive patients as a result of crossreactivity. Phenothiazines can produce allergic contact dermatitis, photoal lergic reactions and eczematous contacttype dermatitis, and may crossreact with certain antihistamines. Tetraethylthiuram disulphide (disulfiram, Antabuse) for the management of alco holism can cause eczematous reactions in patients sensitized to thiurams via rubber gloves. Pathophysiology the eczematous response is mediated by drugspecific Tcell induced inflammation in the skin (see Chapter 12). The eruption tends to be symmetrical, and may involve first, or most severely, the site(s) of the original der matitis, before becoming generalized. Complications and comorbidities Following drug withdrawal, complications and comorbidities are minimal. Reexposure to the cul prit would be expected to reproduce the same clinical picture. Investigations Patch tests are commonly positive and usually vesicular, although histology of the eruption itself may show leukocytoclastic vasculi tis. Oral challenge with the suspected antigen may be required to substantiate the diagnosis. Therapies utilized to treat eczematous dermatoses, such as topical corticos teroids, are usually effective. Pos tulated explanations include a preferential trafficking of activated memory T cells to these sites as a form of recall phenomenon from previous physical/inflammatory insult. Although excretion of drugs or their metabolites in the site has been postulated, there is no syringotropic inflammation which argues against a central role for sweat glands in the pathogenesis [39]. Definition and nomenclature A benign and selflimiting drug eruption characterized by sym metrical involvement of the gluteal and intertriginous areas, occurring in the absence of systemic involvement. Features that have been described include: superficial perivascular lymphocytic Part 11: ExtErnal agEnts Symmetrical drugrelated intertriginous and flexural exanthem 118. Occasionally, the erup tion may consist of small papules, pustules, vesicles and rarely bullae. Chemotherapeutic reactions such as neutrophilic eccrine hidradenitis/eccrine squamous metaplasia may also have a flexural predilection. Disease course and prognosis the reaction improves quickly on withdrawal of the culprit drug. No active therapy is required although topical or systemic glucocorticoids may hasten recovery [38]. Part 11: ExtErnal agEnts Druginduced urticaria, angiooedema and anaphylaxis Definition Urticaria and angiooedema are physical signs which involve circumscribed skin oedema and erythema (described in detail in Chapters 42 and 43). Anaphylaxis is a constellation of clinical find ings which describes respiratory and cardiovascular compromise (bronchoconstriction and hypotension) in a lifethreatening man ner and is described in Chapter 42. Pseudoallergy (nonimmune mediated) describes a presentation which is clinically indistinguishable from true allergy (IgE medi ated). Anaphylaxis during general anaes thesia is an important problem and can be difficult to investigate if intraoperative exposures are not well recorded. Furthermore, dis tinction between true immunemediated and nonimmunemedi ated reactions can be challenging. Common perioperative causes of anaphylaxis or anaphylactoid reactions include: anaesthetic agents (especially thiopental), neuromuscular blocking agents (may also be nonIgE mediated), analgesics (opioids are usually associated with nonIgEmediated reactions), antibiotics, prota mine and blood transfusions (mechanism unclear) [43]. Recently, anaphylaxis caused by drugs bioengineered onto medical equip ment, such as chlorhexidinecoated central venous catheters, has been recognized [44]. Anaphylaxis usually develops on second exposure to a drug as it is thought that prolonged treat ments may induce tolerization rather than allergy (in contrast to Tcellmediated hypersensitivities). Anaphylaxis and anaphylac toid reactions usually develop within minutes to hours (the vast majority within the first hour) of drug administration. Anaphylaxis and anaphylac toid reactions are often associated with skin or mucosal changes: in less severe cases, there may be premonitory dizziness or faint ness, skin tingling and reddening of the bulbar conjunctiva, fol lowed by urticaria, angiooedema, bronchospasm, abdominal pain and vasomotor collapse. Intravenous administration is associated with more severe reactions and rapid progression, over minutes, to cardiac arrest. In cases of insect stingrelated and foodinduced anaphylaxis, the syndrome evolves more slowly [45]. Epidemiology Urticaria is the second most common type of adverse cutaneous drug eruption [46,47]. It has been estimated that 1 in 1500 of the population of Eng land has experienced anaphylaxis at some point in their lives [48]. The incidence of anaphylaxis during general anaesthesia has been estimated to arise in 1: 4000 to 1: 25000 cases [43]. Differential diagnosis Druginduced urticaria needs to be distinguished from other causes of urticaria, especially infection. Druginduced anaphylaxis needs to be distinguished from other causes of anaphylaxis. However, it is critical that causation is addressed and investigated as necessary to prevent accidental recurrence. Pathophysiology the mechanisms underlying druginduced vasodilation, oedema and itch in urticaria are identical to those seen in angiooedema (deeper in skin) and anaphylaxis (systemic circulation). On exposure to the drug, crosslinking of IgE on the surface of mast cells (and possibly basophils) is followed by inflamma tory mediator release (including histamine), which induces vaso dilation, neuronal activation and smooth muscle contraction (see Chapter 8). Cyclooxygenase inhibitors, such as aspirin and indo metacin, may also cause urticaria or angiooedema by pharmaco logical mechanisms. Other drugs, such as radiocontrast media, local anaesthetics and dextrans (in plasma expanders) may release mast cell mediators directly. Deaths from druginduced anaphylaxis are uncommon (<2%); the major predisposing risk factor for poor outcome is coexistent severe asthma [53,54].

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Clinical features the oral mucosa is almost invariably involved in white sponge naevus asthma symptoms jet order albuterol 100 mcg amex. Nonpainful white plaques primarily involve the non cornified buccal mucosae, gingiva and floor of the mouth. Painless, shaggy or folded white lesions typically affect the buccal mucosa bilaterally but may also involve other areas, although rarely the gingival margins [1,2]. Extraoral lesions most often occur in the oesophagus or anogenital area, but almost invariably follow the development of typical oral lesions. Clinical features the lingual fraenum is tight and the tongue cannot be fully protruded. Complications and comorbidities There may be a family history and sometimes deviation of the epiglottis or larynx [4]. Speech is not usually affected in patients with ankyloglossia but the ability to suckle [8] and to cleanse the buccal sulcus with the tongue may be, and there can be effects on jaw development [9]. The family history and clinical examination are usually adequate to differentiate this from other more common causes of white lesions such as cheek biting, burns, lichen planus and candidosis. Reassurance is all that is required, although some have suggested that tetracyclines might clear the lesions [9,10]. Ankyloglossia superior syndrome is a rare distinct malformation that consists of a fibrous or osseous connection between the tip of the tongue and the hard palate, and additional congenital anomalies such as cleft palate, gastrointestinal malformations and deformed limbs [3]. Epidemiology Incidence and prevalence A common condition affecting more than 5% of the population [1]. Syndromic forms are in many cases due to chromosomal aberrations or monogenic diseases. Orofacial clefts result from an embryopathy in which there is failure of the frontonasal process and/or fusion of the palatal shelves. In the submucous cleft palate, the palatal shelves may fail to join, but the overlying mucous membranes are intact and the muscle attachments of the soft palate are abnormal, causing velopharyngeal insufficiency. Associated diseases Geographic tongue is commonly found in people with fissured tongues. There is an occasional association with psoriasis and reports of improvement during infliximab treatment for psoriasis [3]. Geographic tongue has also been recorded in four patients on treatment with bevacizumab [5] but this requires confirmation. Epidemiology Clinical features Fissures of various morphology on the dorsum of the tongue. The total incidence of facial clefting is between two and three per 1000 live births. Cleft palate as an isolated malformation behaves as an entity distinct from cleft lip with or without cleft palate. The risk of recurrence in subsequent children is about 2% if one child has it, 6% if one parent has it, 15% if one parent and one child have it. Sex Oral hair Oral hair is a rare innocuous anomaly [1,2], not to be confused with hairy tongue or the hair on skin flaps used intraorally in reconstructions as, for example, after cancer resections. Cleft palate is more prevalent in females, while cleft lip is more prevalent in males. Ethnicity There are racial differences with a high incidence of cleft palate in SouthEast Asia and a low incidence in AfroCaribbean races. More than 400 syndromes may include a facial cleft as one manifestation and cleft lip/palate may be associated with many congenital syndromes. Not all cases of clefting are inherited; a number of teratogens (environmental agents that can cause birth defects) have been implicated, as well as defects in essential nutrients. Clefts of the lip with or without cleft palate and cleft palate alone result from the failure of the first branchial arches to complete fusion processes and are the most common of all craniofacial anomalies. The male to female ratio of cleft lip/palate is 2: 1; the ratio for cleft palate alone is just the reverse, 1: 2. Predisposing factors Cleft lip/palate is more prevalent in the lower socioeconomic classes. The teratogens incriminated include isotretinoin, which causes birth defects such as brain malformations, learning disability, heart problems, as well as facial abnormalities. Thalidomide given to pregnant mothers was, and anticonvulsants (phenytoin, valproic acid, lamotrigine, carbamazepine) and corticosteroids may be, associated with an increased incidence. Systemic corticosteroids have been reported to increase the risk (this is controversial) and there are also concerns about possible effects from topical steroids used in the first trimester. There has been concern about aspirin and diazepam as possible causes but there is no real evidence. Clinical features Presentation A person may have a cleft lip, cleft palate or both cleft lip and palate. A cleft may involve only the upper lip or may extend to involve the nostril and the hard and soft palates. Lips are more frequently cleft bilaterally (approximately 25%) when combined with cleft palate. Cleft lip and palate comprises about 50% of the cases, with cleft lip and isolated cleft palate each comprising about 25%. About 85% of bilateral cleft lips and 70% of unilateral cleft lips Genetics Clefts can be seen in over 300 different syndromes (Box 110. True median clefts have been described in association with bifid nose and ocular hypertelorism. Pseudocleft of the middle of the upper lip may occur in orofaciodigital syndrome I. Clefts in the lower lip are rare and usually median but may involve the mandible and sometimes the tongue. Cleft palate may be incomplete involving only the uvula and the muscular soft palate (velum). Clefts are often accompanied by impaired facial growth, dental anomalies, speech disorders, poor hearing and psychosocial problems. Clinical variants Submucous cleft palate can be recognized by a notched posterior nasal spine, a translucent zone in the midline of the soft palate and a bifid uvula, but not all these features are necessarily present and a bifid uvula may be seen in isolation. About 1/1200 births are affected and feeding difficulties, speech defects and middle ear infections may develop in 90% of affected children. Adenoidectomy is contraindicated as it may reveal latent velopharyngeal insufficiency. If the palatal defect is too wide, it can be repaired 3 months later to allow for sufficient palatal growth. These children need a hearing assessment, and if it is impaired, ear ventilation tubes (grommets) may be indicated. Speech, if poor despite the best efforts by the child and the speech pathologist, may be corrected with pharyngoplasty. Palatal ulcers seen in neonates with cleft lip and palate appear to result from trauma from the tongue and resolve if a palatal plate is fitted. Dental abnormalities include malocclusion (almost 100%), hypodontia (50%), hypoplasia (30%) and supernumerary teeth (20%). Children may have a higher prevalence of caries in both the primary and permanent dentitions, and significantly more gingivitis, especially in the maxillary anterior region. Adult cleft lip and palate patients may have poorer oral hygiene and more gingivitis.

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However asthmatic bronchitis with acute exacerbation icd 9 discount 100 mcg albuterol, this is a postinflammatory phenomenon, and always recovers within a few weeks, and is not due to the treatments applied. Although dietary manipulation is common and popular with parents, it needs to be undertaken in an informed and evidencebased manner to ensure it is appropriate and that the essential nutrition, growth and development of the infant is maintained. Prolonged contact with urine induces an irritant erythema, which may break down to form erosions if untreated. Transepidermal water loss and pH are higher in infants with napkin dermatitis than those without [2], emphasizing the importance of skin barrier function in the pathogenesis. Treatment is aimed at keeping the skin dry and using barrier creams or emollients to restore normal epidermis. Topical steroids should only be used in the short term, and only if inflammation is severe; secondary infection should be treated appropriately. The management of infantile atopic eczema for the most part is topical and primarily aimed at restoring skin barrier function [13,14], reducing inflammation, treating secondary infection and providing parental education and support. Although exclusive breastfeeding for the first 6 months appears protective [16], prolonged breastfeeding beyond this time does not appear to confer an advantage. However there appears to be no benefit in delaying weaning onto solids beyond 4 months of age [18,19]. They are thought to be due to the irritant effect of urine compounded by secondary infection, and are considered to be part of the spectrum of presentation of napkin dermatitis, along with infantile gluteal granuloma [1]. However, Jacquet dermatitis is rare nowadays due to the technological advances in absorbency of modern nappies. Infantile gluteal granuloma Overuse of potent, especially fluorinated, steroids under occlusion in infants with napkin dermatitis has been thought to lead to the formation of a granulomatous inflammatory reaction, characterized by reddish brown nodules on the buttocks [1]. Treatment is avoidance of further topical steroids and the use of appropriate emollients to restore the epidermal barrier. Although rarely seen now, a similar eruption has been described in the elderly who wear cloth nappies for incontinence [2]. Infantile psoriasis Onethird of individuals with psoriasis develop the disease in childhood (before the age of 15 years), although infantile psoriasis is less common [1] (see also Chapter 35). Although some authors consider infantile psoriasis to be a self limiting disease [5], it may be a prelude to more typical chronic plaque psoriasis in later life [6]. In the majority of infants, mild topical steroids, often in combination with an anticandidal agent, and emollients usually suffice [6]. Parakeratosis pustulosa Parakeratosis pustulosa is a localized inflammatory condition involving the distal phalanx. Combination topical preparations of potent steroids and antibiotics are usually used. There may be a family history of psoriasis, and the condition is thought to predispose to psoriasis in later life [1]. Infantile acropustulosis is a rare disorder characteristically affecting children between the ages of 1 and 2 years [1]. The differential diagnosis is scabies infestation, and sometimes the condition is seen to follow a genuine scabies infection, as a persistent, reactive, post inflammatory phenomenon. Pityriasis alba Transient, hypopigmented areas on the face, associated in some cases with fine scale, are not uncommon in childhood but are usually seen in slightly older children rather than infants. It is most frequent on the lower cheeks, and lesions are ovoid in shape, with indistinct margins. Although entirely asymptomatic, the condition is most noticeable in children with darker skin types [1], and may be a source of great concern to parents. The condition is considered to be part of the atopic spectrum [2,3] (85% have an atopic history [3]), but no specific treatment is required. Urticaria Uricaria in infancy differs from urticaria in adults in that it presents with haemorrhagic lesions in approximately 50% cases, and angiooedema in 60% [1] (see also Chapter 42). Anaphylactic shock is very rare in the first year of life but incidence increases with age, particularly in industrialized societies [2,3]. Approximately half of infants presenting with urticaria have a personal or family history of atopy [1]. Infection, usually viral, with or without drug intake, appears to be the cause of urticaria in the majority of cases [1]. Cholinergic urticaria, precipitated by Infantile acne Infantile acne is rare, but should be easily distinguished from the transient sebaceous gland hyperplasia/milk spots seen in the neonate (see also Chapter 90). No underlying endocrinopathy was found in infants [1,3], in contrast to older children presenting with preadolescent acne in whom more detailed investigation may be merited. Treatment may be topical (benzoyl peroxide, erythromycin or retinoids) in mild cases [1]. In more extensive disease, the majority of children will clear with oral erythromycin, but trimethoprim can also be used if there is erythromycin resistance [1]. In severe disease, oral isotretinoin has been shown to be safe and effective in infants [2]. Scarring is estimated to occur in 17% of infants with acne [1], reflecting the proportion with more severe disease. Urticaria in infancy may be a feature of systemic disease including systemic lupus erythematosus, juvenile rheumatoid arthritis, mastocytosis and Kawasaki disease [7], but is rarely the only presenting feature. Often this is nonspecific and harmless [1], but some viral infections have very characteristic features that allow a diagnosis to be made. A detailed account of viral infections appears in Chapter 25, but the most frequent or important infections seen in children are highlighted here. Viral exanthems account for the most common presentation to a paediatric emergency department [3]. However, differentiation from exanthems due to other causes (drugs, bacterial toxins, autoimmune disease) must be made [1,2]. Overall, petechial changes are much more likely to occur in exanthems associated with infections, particularly of viral origin (although meningococcal septicaemia should always be considered) [2]. A more reticulate rash then appears on the limbs and body, and palmoplantar erythema is common. The eruption fades over 7 days, but recrudescences are not infrequent, particularly if the child gets hot. Older individuals may develop a papulopruritic eruption in a glove and stocking distribution with parvovirus B19 infection [3], but this pattern is rarely seen in infants. Hand, foot and mouth disease this is a common infection in young children, affecting the oral cavity and extremities. A high fever develops that lasts for 3 days and may rarely be associated with febrile convulsions [4]. As the pyrexia subsides a fine, lacy, macular erythema appears, which may be accompanied by occipital lymphadenopathy. It is most commonly associated with Coxsackie A viral infection, most usually A16 [1], but infection with A6 [2], Coxsackie B [1] and enterovirus 71 [1] have also been described. Spread is by droplets or faecal contamination and the incubation period is 7 days. However, virus may be present in the faeces for several weeks after infection, making isolation impractical [1]. Symptomatic treatment only is required, but it is highly contagious and widespread outbreaks are common. At this age, children would not usually have received their initial vaccination in this county, but herd immunity would have conferred protection. Encouragingly, recent public health campaigns and immunization programmes in schools seem to be increasing uptake again [2]. An initial prodrome of fever and coryzal symptoms is followed after 3 days by the development of small, white Koplik spots on the buccal mucosa. On the fourth day of the illness the rash appears, initially on the forehead, spreading caudally down the face onto the trunk and limbs.