Ординатура / Офтальмология / Английские материалы / Handbook of Pediatric Eye and Systemic Disease_Wright, Spiegel, Thompson_2006
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malformations; this percentage decreases to 52% if the child is infected during weeks 9 to 12 of gestation. If infection occurs during the second trimester, approximately 25% to 30% of children will develop malformations, whereas third-trimester infections rarely manifest abnormalities.94 Congenital rubella can also result in spontaneous abortion or stillbirth, low birth weight, or, in some cases, normal-appearing infants.27
Children with congenital rubella may develop transient thrombocytopenia, purpura, hepatitis, and hemolytic anemia. The most common permanent manifestation of congenital rubella is unilateral or bilateral sensorineural deafness, although mental retardation and cardiac anomalies are relatively common.118 Additionally, children with congenital rubella appear to be at increased risk for progressive endocrine complications, including insulin-dependent diabetes mellitus, hypothyroidism, and hyperthyroidism.75,118
INHERITANCE
Not inherited.
TREATMENT
Treatment of children with rubella is primarily supportive. Cataract surgery can be performed for children with cataracts but may be complicated by a severe inflammatory response. This severe postoperative inflammatory response may be associated with retained rubella virus within the lens. Complete removal of all lens material and aggressive postoperative topical corticosteroids and cycloplegics is essential in these children. Medical therapy is the initial treatment for rubella-associated glaucoma. Surgical therapy may be necessary when the intraocular pressure cannot be controlled by medications.108
PROGNOSIS
The prognosis for children with rubella retinopathy is generally good. Visual loss secondary to choroidal neovascularization is uncommon and typically occurs later in life. Glaucoma associated with rubella is often difficult to control; therefore, the visual prognosis for these children is guarded. In some children with keratitis, glaucoma, and cataract, severe visual loss may occur.
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Varicella-Zoster
Varicella or chickenpox is an extremely contagious disease of childhood characterized by a generalized exanthematous rash. It is a disseminated disease resulting from primary infection with varicella-zoster virus (VZV). The virus eventually spreads from the peripheral lesions to the dorsal root ganglia of the corresponding dermatome, where it becomes latent in virtually all patients. Reactivation of the latent virus results in a focal infection affecting one or two dermatomes, herpes zoster.47,48 Ocular involvement can occur in both varicella and herpes zoster; however, the complications associated with herpes zoster ophthalmicus (HZO) have a greater potential for significant ocular morbidity.
INCIDENCE
Before 1995, approximately 4 million cases of varicella occurred in the United States each year. In 1995, a varicella vaccine was licensed in the United States for routine use in children, and increasing use of this vaccine will reduce the annual incidence of varicella. Current information concerning the incidence of herpes zoster is lacking. However, previous reports indicate an annual incidence of herpes zoster in children of 0.74 per 1000 in children from 0 to 9 years of age and 1.38 per 1000 from ages 10 to 19.56
ETIOLOGY
The virus responsible for varicella and herpes zoster is the vari- cella-zoster virus. This virus is a member of the herpes family of viruses and is spread by airborne droplets and by direct contact with infected lesions.40,66 It is highly contagious to those individuals who are not immune. Varicella is communicable 1 to 2 days before the onset of vesicles and up until all the lesions have crusted over; however, the disease is most communicable during the prodromal phase. Congenital varicella results from transplacental spread of the virus by an infected mother.
Reactivation of latent virus results in herpes zoster with a characteristic unilateral vesicular rash affecting one to two dermatomes. Reactivation of varicella zoster virus latent in the trigeminal ganglion results in HZO. The mechanisms for reactivation of varicella-zoster are unknown but are probably related to both the host and virus. Herpes zoster is very uncommon in healthy children and is usually encountered in children with
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cancer or those who are immunocompromised, as well as children who developed primary varicella during the first year of life.2,47,50,123 Additionally, a recent report suggests that the psychological stress of severe child abuse might result in the development of herpes zoster.48
CLINICAL FEATURES
Ocular complications of varicella are not uncommon. The most common manifestations are papillary conjunctivitis and conjunctival vesicle formation. Other less-frequent manifestations include epithelial keratitis that may be punctate or dendritic, subepithelial infiltrates, stromal keratitis, disciform keratitis, or mild nongranulomatous anterior uveitis.61 The keratitis associated with varicella infection is not recurrent and only rarely leads to permanent scarring. There are isolated reports of neuroophthalmic manifestations of varicella including internuclear ophthalmoplegia and oculomotor palsy.85,111 In children with congenital varicella, chorioretinitis is the major ophthalmic manifestation.
The onset of HZO is heralded by the development of a maculopapular eruption followed by the development of vesicles over the forehead, eyelids, and along the side of the nose. Ocular involvement may occur with the involvement of any branch of the trigeminal nerve but is most likely to occur if the nasociliary branch is involved. Inflammation from herpes zoster has the potential to affect virtually any orbital, adnexal, or ocular tissue. Cranial nerve palsies have been reported during the first week following the onset of the rash. Dermatitis of the eyelids may lead to secondary bacterial infections, as well as lid notching, loss of cilia, entropion, trichiasis, and stenosis of the lacrimal puncta. Follicular conjunctivitis, episcleritis, and scleritis may also occur in children with HZO. Corneal manifestations include superficial or stromal keratitis that can include pseudodendrites, punctate epithelial keratitis, anterior stromal infiltrates, endotheliitis, and neurotrophic keratitis. Corneal hypesthesia often develops in conjunction with HZO-associated keratitis. Iridocyclitis is not uncommon and can be severe in some patients. Elevated intraocular pressure is often present and may lead to glaucoma in some children. Posterior segment manifestations include optic neuritis and the acute retinal necrosis syndrome. Rarely, patients who are severely immunocompromised, such as those with advanced AIDS, may develop the progressive outer retinal necrosis syndrome (PORN).
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CLINICAL ASSESSMENT
Infection with herpes simplex can resemble herpes zoster; therefore, it may be difficult to distinguish between the two. Tissue culture methods can be used to obtain a specific diagnosis of varicella-zoster virus. Fluorescent antibody staining of cells in scrapings from vesicles may also be useful. Serological tests may be useful in some patients, although they are less timely than other methods because acute and convalescent serum is required to establish the diagnosis.
SYSTEMIC ASSOCIATIONS AND NATURAL HISTORY
Varicella is primarily a disease of childhood, although adults are infected uncommonly. In most patients, the first manifestations include a prodrome of fever, malaise, and anorexia. The characteristic cutaneous exanthem appears 1 to 2 days later and lasts for about 10 to 14 days. The exanthem is characterized by maculopapules with vesicles and scabs in various stages of evolution (Fig. 9-5). Following the onset of the rash, patients develop pruritus, malaise, and anorexia.
FIGURE 9-5. Child with varicella and multiple facial lesions in various stages of development. Numerous lesions are present on the eyelids of the left eye.
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FIGURE 9-6. Eight-year-old girl with leukemia and herpes zoster ophthalmicus of the left eye. Crusted vesicles are visible along the nose and upper forehead. Early scarring is also present along the bridge of the nose and above the brow.
Herpes zoster ophthalmicus is characterized by a vesicular rash affecting the ophthalmic division of the trigeminal nerve. Some patients may experience prodromal symptoms for 2 to 3 days before the onset of the rash, including dermatomal pain, headache, fever, malaise, and chills. In children, pain is not typically a part of the disease as compared to adults. These symptoms are followed by the development of erythematous maculopapular lesions within the affected dermatome that quickly evolve into vesicles and bullous lesions. The lesions continue to develop over a 3- to 5-day period and resolve over the ensuing 3 to 4 weeks (Fig. 9-6). As with herpes zoster in general, HZO in children typically follows a more benign course as compared to adults.
INHERITANCE
Not inherited.
TREATMENT
Most of the ocular complications associated with primary varicella infection are self-limited and require no therapy. However,
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anterior uveitis or stromal keratitis with decreased visual acuity may require therapy with topical corticosteroids; this is especially important in children who are susceptible to the development of amblyopia. Systemic acyclovir should be considered in immunocompromised children who develop varicella infection.
The treatment of herpes zoster in children is similar to that in the adult population. The cutaneous lesions can be treated with moist compresses and antibiotic ointments to help loosen lid crusting and to prevent secondary infection. Topical corticosteroids may be necessary to treat associated uveitis, stromal keratitis, or disciform keratitis. Systemic administration of corticosteroids may be indicated for either optic nerve or cranial nerve involvement and have been utilized in the treatment of adult patients with these complications.74 Topical antiviral agents are not effective for any of the ocular manifestations of HZO. Oral acyclovir should be considered for children with involvement of the ophthalmic branch of the trigeminal nerve if treatment can be initiated within 72 h following the onset of the rash. The recommended dosage is 80 mg/kg/day in four or five divided doses to a maximum of 4 g/day for both children and adolescents.101 Intravenous acyclovir is typically not used in healthy children but may be utilized in the treatment of immunosuppressed patients.
PROGNOSIS
The prognosis for children with varicella-associated ocular disease is generally good. Most of the ocular complications are transient or treatable with topical corticosteroids. However, the prognosis is somewhat guarded for children who develop acute retinal necrosis associated with VZV infection. Overall, the visual prognosis is most dependent on the extent of the retinitis and the severity of the intraocular inflammation. Early aggressive systemic therapy is probably the key to a better visual outcome in children with this syndrome.
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