Lecture 4: Toddler and Elementary PDF

Lecture 4 – Toddler and Elementary Tinea Capitis and Tinea Corporis Tinea corporis (ringworm of the body) is extremely common. It is seen in children of all races. Tinea capitis (ringworm of the scalp) is relatively common. It is more common in African- American and Hispanic children. It is much...

Lecture 4 – Toddler and Elementary Tinea Capitis and Tinea Corporis Tinea corporis (ringworm of the body) is extremely common. It is seen in children of all races. Tinea capitis (ringworm of the scalp) is relatively common. It is more common in African- American and Hispanic children. It is much more common in children than in adults. Tinea corporis or ringworm of the body is an appropriate name, as tinea corporis typically presents as a red, scaly ring with central clearing (Figure 4.1) (Figure 4.2) (Figure 4.3). In darkly pigmented children there may be hyper- or hypopigmentation. There may be mild pruritus. Tinea corporis may involve the trunk, arms, legs, or face; not the palms, soles, or groin area. The most common causative organisms of tinea corporis are Trichophyton rubrum, Microsporum canis, and Trichophyton mentagrophytes. Tinea capitis typically presents as areas of hair loss with some scaling on the scalp (Figure 4.4) (Figure 4.5). There is often some erythema, and in some cases, there are also pustules. It typically is not particularly itchy or painful, but cases with inflammation may be itchy or painful. The most common causative organism of tinea capitis is Trichophyton tonsurans. Both tinea capitis and tinea corporis are caused by fungi that survive by digesting keratin. This type of fungi is called dermatophytes, and infections are limited to keratinous structures (stratum corneum, hair, nails). These organisms’ natural reservoirs are humans (anthropophilic), animals (zoophilic), or soil (geophilic). Anthropophilic strains typically cause non-inflammatory infections, while zoophilic and geophilic organisms cause inflammatory infections. The scaling associated with these infections is one of the defenses against them. Since the infection is limited to the stratum corneum, if the stratum corneum can be shed faster than the organism can proliferate, the organism will be removed from the skin. This phenomenon accounts for the ring shape of tinea corporis. In the clear, central area the stratum corneum was shed and the organism was cleared. At the scaling border, the fungus is still proliferating. Tinea corporis and tinea capitis can both be diagnosed with potassium hydroxide (KOH) preparations or by fungal culture. For KOH preps, some of the scale are collected on a glass slide and 10% KOH is added to dissolve keratin, but not fungi, which have cell walls made of chitin. The preparation is examined microscopically, and since the keratin has been dissolved, the fungi are readily visible. Tinea corporis is treated with topical agents. The azole group of anti-fungals (ketoconazole, miconazole, econazole, clotrimazole) work by inhibiting 14-lanosterol demethylase, an enzyme involved in lipid synthesis for fungal cell membranes. These agents prevent fungal proliferation but do not kill fungi, so an intact immune system or continued scaling is necessary to clear the fungus. The allylamine group of anti-fungals (terbinafine, butenafine) work by inhibiting squalene epoxidase, another enzyme involved in lipid synthesis for fungal cell membranes. In addition to inhibiting synthesis, the enzyme substrate, which is toxic, accumulates in the fungus, killing the organism. Thus, an intact immune system or continued scaling is not necessary to clear the fungus. Both types of agents are effective in the vast majority of patients. The allylamine group is more effective in recalcitrant cases. Tinea capitis must be treated with oral agents, because the organism is present deep in the hair follicle and is also present inside the hair shafts. The first line agent is griseofulvin, which disrupts microtubule formation. Typical treatment is for 6-8 weeks. In addition to oral therapy, an anti-fungal shampoo, such as ketoconazole, should also be used. The shampoo decreases the transmissibility of the infection immediately. It is important to examine all family members, as tinea capitis can be spread by fomites, such as hair brushes. Molluscum Molluscum contagiosum is extremely common in children. It is more common in children with atopic dermatitis. Molluscum presents with small (1-3 mm), shiny, skin colored papules with a central dimple (Figure 4.6) (Figure 4.7). Lesions can be present anywhere on the body. Molluscum can occasionally present in an adult who did not have molluscum as a child. In addition, individuals with severely impaired immune function, as in advanced HIV, may exhibit extremely large molluscum lesions (>1 cm) (Figure 4.8). Molluscum contagiosum virus is a DNA virus classified as poxvirus. It replicates in the cytoplasm of keratinocytes. Virus is released from the central dimple of lesions, and can cause the spread of lesions to other skin sites or to other individuals. Individuals with atopic dermatitis, or any form of dermatitis, are more susceptible to molluscum because their stratum corneum provides a less effective barrier against the virus. Molluscum lesions will resolve spontaneously once the virus is recognized by the immune system, so treatment is not always necessary. However, they may be present for several years prior to spontaneous resolution, so treatment is often desired. Lesions can be treated by gently scraping them off with a curette or a scalpel blade, applying salicylic acid, liquid nitrogen, or imiquimod (Aldara, an immune stimulator). Periungual Warts Warts are extremely common and can present anywhere on the body. Common locations vary by age group. In children, warts near the fingernails and on the hands are most common. Warts are generally not difficult to recognize. The hallmark is the rough, “verrucous”, surface and the presence of brown or black dots under the surface (Figure 4.9). These black dots represent thrombosed capillaries deep in the wart. Warts are caused by human papillomaviruses (HPVs). Well over 70 different HPVs have been described. HPVs are double-stranded DNA viruses that can infect epithelial keratinocytes (cutaneous, genital, or oral epithelia). Specific HPV types more efficiently infect specific areas. HPV 1 tends to cause plantar warts; HPV 2 causes periungual warts, HPV 3 causes “flat-warts” on the face or legs. HPV 6 and 11 cause benign genital warts. HPV 16, 18, 31, and 33 cause genital warts that have the potential to turn into squamous cell cancer. There are several important HPV proteins. L1 and L2 (Late 1 and 2) are the proteins that form that viral capsid, which protects the viral DNA and is thought to be important in binding to cellular membranes. Other important genes are E5, E6, and E7 (Early 5, 6, and 7). These genes encode viral proteins that play a role in “hijacking” cellular proliferation. Specifically, E6 causes degradation of p53, and E7 interferes with retinoblastoma function. By inactivating these two brakes on cellular proliferation, E6 and E7 promote excessive proliferation of keratinocytes, which is important because the HPV depends completely on cellular proteins to replicate the viral genome, and this can only occur when the cell is proliferating. Periungual warts are difficult to treat. Care should be taken avoid unnecessary trauma or damage to the fingernail. Useful treatments include salicylic acid (Compound W) and liquid nitrogen. Duct tape can be wrapped around the finger/wart, left in place, and changed once a week. Laser therapy is useful and should be kept in mind for recalcitrant cases. Pyogenic Granuloma (PG) PGs occur in children and adults, but are most common in children. PGs are red nodules that are often moist (Figure 4.10) (Figure 4.11) (Figure 4.12), and typically occur following minor trauma. They grow quickly, then stabilize in size. They may be painful, but are typically asymptomatic. If traumatized, they typically bleed briskly. PGs represent an excessive wound healing response. The tissue produced is relatively normal granulation tissue, but for some reason, the proliferative phase of wound healing proceeds beyond the point at which it typically stops, leading to the raised, vascular nodule. PGs are usually treated by surgical removal followed by cauterization of the base of the lesion. It is not rare for PGs to recur after removal, in which case a second procedure is performed in which a larger amount of tissue is removed. Hand-Foot-Mouth (HFM) Disease and Herpangina HFM and herpangina are both fairly common in children, and more common in children with significant exposure to other children. HFM typically presents with vesicles or pustules on the hands and feet that are usually palmoplantar (Figure 4.13) (Figure 4.14) in conjunction with small, well defined erosions in the mouth. The oral erosions are usually on the tongue, inner cheeks, and posterior oropharynx. Herpangina typically presents with isolated oral erosions. The erosions look similar to the erosions in HFM, but they are typically distributed more posteriorly than the lesions in HFM. Also, there are no extra-oral lesions in herpangina. HFM and herpangina are both caused by pircornaviruses, a subgroup of enteroviruses. These are single-stranded RNA viruses. Coxsackievirus A16 is the most common cause of HFM, while herpangina is caused by several strains of Coxsackieviruses A and B, as well as echoviruses. These diseases are self-limiting and resolve spontaneously. Reassurance is typically sufficient. Viral Exanthems Viral exanthems are extremely common. Viral exanthems are relatively non-specific eruptions, typically consisting of widespread erythematous papules, occasionally with small vesicles or urticarial lesions also present (Figure 4.15). The child will often have a concurrent low-grade fever and may feel ill overall. Enteroviruses are the most common cause of non-specific viral exanthems in children. There will often be community-wide “epidemics” as a given virus is passed among susceptible children. Adults are typically spared, as they are likely to already have acquired immunity. In general, there is no available diagnostic test, and this is a clinical diagnosis. The exanthems are self-limited and resolve spontaneously. Reassurance is typically sufficient. Papular Acrodermatitis of Childhood (a.k.a. Gianotti-Crosti) The mean age of presentation is 2 years, and most cases present in the spring and early summer. Papular acrodermatitis presents as symmetric, monomorphic, pink, sharply circumscribed papules (Figure 4.16). The face, buttocks, and extensor surfaces of the limbs are involved, while the trunk is largely spared. There may be a mild fever and diffuse lymphadenopathy. Papular acrodermatitis can be thought of as a specific type of viral exanthem. It mainly differs from the typical viral exanthem by the distribution (sparing of the trunk) and the sharp borders of the papules, and the duration of the rash, with papular acrodermatitis lasting 1-2 months while the typical viral exanthem lasts 1-2 weeks. Papular acrodermatitis occurs secondary to viral infections. In Europe, hepatitis B is the most commonly associated viral disease. In the US, Epstein-Barr virus is most commonly associated, but many different viruses have been associated. The disease is self-limited and will resolve spontaneously. If there is pruritus, a low strength topical steroid can be prescribed for symptomatic relief. If there is reason to suspect possible hepatitis infection (maternal infection, history of blood transfusion, etc.), then bloodwork should be sent to evaluate for hepatitis B and C. Unilateral Thoracic Exanthem (UTE) UTE is fairly common in toddler aged children. UTE usually presents as a non-specific eruption localized to one axilla or flank (Figure 4.17). It then spreads to involve the chest, back, and arm. It will frequently eventually spread to the contralateral side of the body, but remains much more prominent on one side of the body. A viral etiology is strongly suspected, but no specific virus has been isolated. UTE will resolve spontaneously in 1-2 months. Reassurance is all the treatment necessary. Roseola Infantum Roseola is extremely common. Most children are affected before the age of 3. Children initially have a high fever (up to 105 F), which lasts for 3-5 days. A reproducible feature is that children feel well, and do not act sick, despite the high fever. When the fever resolves, the child breaks out in a non-specific, widespread eruption of pink macules and papules. The rash resolves spontaneously over several days. The main diagnostic features are that the child feels well during the fever and the rash begins as the fever resolves. Roseola is caused by human herpesvirus 6 (HHV6) and HHV7. These viruses are lymphotrophic. After the acute infection, the viruses remain latent in the body and may reactivate if the patient becomes immunosuppressed. Typically no treatment is necessary, other than acetaminophen to lower the high fevers. Erythema Infectiosum/Fifth Disease Fifth disease spreads via respiratory secretions and is most common in winter and early spring. School aged children are the most affected age group. Can also be spread by blood products or vertically from mother to fetus. The eruption begins with bright red, macular erythema on the cheeks (Figure 4.18). The nose and perioral areas are spared. This “slapped cheek” appearance persists for up to one week, then a more diffuse eruption occurs, which has a “lacy” appearance and is predominant on the extremities. The more generalized rash lasts for 1-4 weeks, then fades. Warm conditions or physical exertion may make the eruption become much more pronounced. Some patients have mild prodromal symptoms, and some will have mild arthritis or fatigue associated with the rash. Fifth disease is caused by parvovirus B19, a single stranded DNA virus. The virus has a strong tropism for erythroid progenitor cells. The rash typically coincides with the appearance of IgG directed against the virus, indicating that the rash is a manifestation of the immune response against the virus. Due to the erythroid progenitor trophism, individuals with compromised hematopoietic function may experience significant anemia as a result of infection. This is especially true for individuals with sickle cell disease. Treatment is often not necessary for patients with only a rash. If there is significant anemia, red cell transfusion should be considered. Of importance, the disease can be mimic lupus (facial rash, arthritis, anemia), but bloodwork (negative ANA) and course of the disease should differentiate the two. Varicella Varicella has become relatively uncommon, as most children receive the varicella vaccine. Varicella typically begins with a prodrome consisting of a low grade fever and general malaise. The eruption consists of small vesicles on erythematous bases (dewdrops on a rose petal) (Figure 4.19). The eruption is most prominent on the face and trunk, with the extremities significantly less involved (Figure 4.20). The individual vesicles rupture, scab over, and heal. The key clinical finding is that after the initial couple of days, there will be lesions in different stages (i.e., some vesicles, some ruptured vesicles, and some scabs) because new lesions continue to develop. This is opposed to smallpox, in which all lesions will be in the same stage of development. Varicella is caused by the varicella zoster virus (VZV), and is typically spread by respiratory droplets. Blister fluid is also infectious. The incubation period between exposure and onset of prodromal symptoms is typically 10-21 days. After the virus infects respiratory epithelial cells, it replicates in the regional lymph nodes, leading to a primary viremia. Once in the blood, the virus seeds the liver and spleen, and more replication occurs there. Then there is a secondary viremia, and the virus reaches the skin by invading cutaneous capillary endothelial cells during this viremia. A live, attenuated vaccine prevents disease completely in about 75% of immunized persons, and typically causes a milder disease in patients who still get varicella after the vaccine compared to un-immunized individuals. Varicella immune-globulin is available for immunocompromised individuals who are exposed to the virus, but it must be administered within 96 hours of exposure (before the primary viremia occurs). For patients with varicella, the duration and severity of disease can be significantly lessened by early treatment with antiviral medications, such as acyclovir, valacyclovir, and famciclovir. Pediculosis Capitis (Lice) Lice are most common in children from preschool age through elementary school. The presenting feature is typically intense scalp pruritus, due to hypersensitivity to lice saliva or stool. Hypersensitivity (and therefore itch) may take as long as six weeks to develop after the infection starts. On examination, excoriations may be noted. Adult insects are occasionally seen, and when identified, they will be mobile. More commonly, eggs, called nits, are seen. Nits are firmly attached to hairshafts, and look like small white to gray grains of sand. Female lice live for about 1 month, and each female louse lays 5-10 nits per day. Lice mainly spread by head-to-head contact. Spread can also occur via fomites such as combs, brushes, and hats. Each louse needs to have a blood meal every 4-6 hours. Classically, treatment consisted of topical permethrin (either synthetic or natural). However, significant resistance has developed, so other treatments such as topical Malathion and oral ivermectin are becoming more commonly used. Most treatments do not kill all nits, so re- treatment one week after the first treatment is recommended. The shells of nits remain attached to the hairshaft even when there are no viable organisms, presenting a practical problem, as it is difficult to tell if any viable nits remain after treatment, or if all the remaining nits are non-viable. Removal of nits can be accomplished with either special combs or enzymatic shampoos which degrade the attachment, or by shaving the head. The practical problem of nits is most significant in school aged children, since many schools have “no nit” policies, which prohibit children with any visible nits from returning to school. It is important to remember that nits are almost always non-viable following effective treatment. Atopic Dermatitis Atopic dermatitis was previously discussed in infants. As children age, the appearance and distribution of lesions tend to change. The distribution in older children favors the antecubital and popliteal fossae (Figure 4.21). The sides of the neck are also commonly involved (Figure 4.22). Any area of the body may be affected, but the above are by far the most consistently involved. The appearance also changes somewhat as children age. The rash is not as brightly red and is much less “weepy”. There tends to be more scaling, skin thickening, and hyperpigmentation, especially in the fossae and neck folds. Other areas may show a more dry (xerotic) appearance. Periocular involvement can lead to chronic rubbing, causing periocular hyperpigmentation and accentuated infraocular lines (Morgan-Dennie Lines) (Figure 4.23). Small hyperkeratotic papules at hair-follicle orifices are common. These are called keratosis pilaris, and are most common on the outer, upper, arms. Palmar hyperlinearity is also a common finding. Finally, areas of slight hypopigmentation may develop on the cheeks, called pityriasis alba (Figure 4.24). In general, atopic dermatitis is treated similarly in infants and in slightly older children. There is no effective treatment for palmar hyperlinearity, and fortunately, patients seldom seek treatment for this specific finding. Topical steroids are often avoided when treating periocular disease due to side effect concerns. Topical tacrolimus is often used instead. Keratosis pilaris often responds well to mild topical acids, such as lactic acid/ammonium lactate (Am-Lactin). Pityriasis alba is usually treated with moisturization and a mild topical steroid, like hydrocortisone 1%. It takes several months of treatment before the hypopigmentation improves. Henoch-Schonlein Purpura (HSP) HSP is an uncommon disease, affecting approximately 1 in 10000 children each year. It occurs in children and adults, but is more common in children. HSP presents most commonly with purpuric papules (“palpable purpura”) on the legs and buttocks (Figure 4.25) (Figure 4.26) (Figure 4.27). It may affect anywhere on the body, but these are the most common areas. Associated findings include general malaise, abdominal pain, bloody stools, joint pain, and dark colored urine. Most cases will not manifest all these findings, but the rash is probably the most consistent finding across cases. The syndrome typically lasts 1-6 months, but rare patients will have chronic, protracted disease. Most patients will not experience any long term sequelae, but occasional patients develop chronic renal failure, sometimes months or years after the disease has gone into remission. HSP is a vasculitis in which IgA is deposited in the walls of vessels and capillaries, inciting an inflammatory reaction. The manifestations of the disease represent vasculitis affecting different organs. Bloody stools and abdominal pain are manifestations of vasculitis of the GI tract; blood in the urine, a vasculitis of the kidneys; the rash, a vasculitis of the skin. Many cases of HSP are associated with preceding upper respiratory tract infections or with medication intake. Other cases have no identifiable triggering factor. Treatment for HSP is not always necessary. In cases without renal or significant GI symptoms, supportive care with non-steroidal anti-inflammatories may be sufficient for symptomatic relief while waiting for the syndrome to resolve. In cases with significant GI or renal involvement, oral steroids are frequently useful. During the acute phase, patients with GI pain or bloody stools should be monitored carefully for signs of an acute abdomen, because if GI vasculitis is severe, intestinal perforation is possible. Following resolution of the acute syndrome, in rare cases, there can be slow deterioration of renal function. As such, renal function should be monitored long term, approximately once every six months for at least 5 years.