Ординатура / Офтальмология / Английские материалы / Pediatric Ophthalmology for Primary Care 3rd edition_Wright, Farzavandi_2008

Table 15-3. Causes of Neurotrophic Ulcer

Congenital Onset

1.Congenital trigeminal anesthesia

2.Familial dysautonomia

Acquired Onset

1.Fifth trigeminal nerve damage

2.Closed head trauma

3.Intracranial tumors

4.Intracranial aneurysm

5.Neurosurgery

Corneal Disease

1.Herpes simplex keratitis

2.Herpes zoster keratitis

3.Chronic contact lens wear

Chronic Topical Medication Abuse

1.Timolol (topical glaucoma medication)

2.Chronic topical anesthetic

Chemical Burns

Treatment of neurotrophic ulcers includes the use of artificial tears and topical lubricants. Patients should be warned not to use topical anesthetic drops because this is an important cause of a neurotrophic ulcer. In severe cases of neurotrophic ulcer, a conjunctival graft is placed over the cornea, even though it blocks vision. A tarsorrhaphy, a procedure in which the eye lids are sutured together, can be used to protect the cornea and preserve the globe. Unfortunately, in severe cases where the damage to the sensory nerve is permanent, the neurotrophic ulcer can progress to ulceration and perfora tion, with loss of the globe.

Keratoconus

Keratoconus is a noninflammatory, self limiting ectasia of the central por tion of the cornea. It is characterized by progressive thinning and steepen ing of the central cornea. Keratoconus occurs in about 0.15% to 0.6% of the general population; however, data on prevalence of keratoconus vary greatly. Onset of keratoconus occurs during the teenage years—mean age of onset is 16 years, but onset has been reported to occur at ages as young as 6 years. Keratoconus shows no gender predilection and is bilateral in more than 90% of cases. Often, patients with keratoconus have had several spectacle

prescriptions in a short period of time and none has provided satisfactory vision correction. Refractions are often variable and inconsistent. Patients with keratoconus often report monocular diplopia or polyopia and complain of distortion rather than blur at both distance and near vision. Some report halos around lights and photophobia. During the active stage, change may be rapid; although unusual, contact lenses may have to be refit as often as every 3 to 4 months. In general, the disease develops asymmetrically.

Atopic disease (eg, hay fever, atopic dermatitis, asthma) has been sug gested as an etiologic component of keratoconus. Patients with keratoconus are chronic eye rubbers; it is theorized that rubbing indents the cornea and may make the cornea yield at its weakest point, the center. Hormonal influ ence has been addressed as a possible cause, a supposition supported by the initial onset around puberty and tendency to progress during pregnancy or to exacerbate during menopause. Systemic conditions linked to keratoconus include Down syndrome, Ehlers Danlos syndrome, Crouzon syndrome (craniofacial dysostosis), and Marfan syndrome. To date, no single, clear cut cause of keratoconus has been found.

Treatment consists of providing a hard contact lens to establish a smooth surface to the cornea. If the contact lens fails and the cornea becomes thin and distorted causing decreased visual acuity, a corneal transplant may be necessary. It is rare that a child would have severe keratoconus that would require a corneal transplant.

Chapter 16

Eyelid and

Orbital Masses

A mass, or tumor, behind the eye will push the eye forward causing prop tosis (exophthalmos), an important sign that an orbital mass is present. Proptosis often presents with one eye appearing larger than the other eye, as the proptotic eye pushes the eyelids apart, causing a wider lid fissure (Figure 16 1). Anterior orbital masses and eyelid masses cause narrowing of the lid fissure (Figure 16 2). An acquired lid or orbital mass requires

A

B

Figure 16 1.

A, Four-year-old boy with Hand-Schüller-Christian disease and proptosis of the right eye caused by a posterior orbital mass. Note that the lid fissure is wider on the right. B, Axial computed tomography scan of the same patient, demonstrating right lateral orbital lesion with destruction of the lateral orbital wall. Note that the right eye is proptotic and forward as compared with the left eye. From Johnson T, et al. Clinicopathological correlation. Saudi Bul Ophthalmol. 1988;3:31.

immediate evaluation, with orbital imaging to rule out severe orbital disease such as rhabdomyosarcoma. Table 16 1 presents the differential diagnosis of pediatric proptosis.

Capillary Hemangioma

The most common vascular ocular tumor seen in children is the capillary hemangioma. This is a hamartoma, as it is made up of tissue normally found in the eyelid. During the first few weeks of life, the lesion will be small. Over the next few months, it progressively increases in size. The tumor generally shows spontaneous regression by 4 to 7 years of age. If the tumor is super ficial, it has a red or strawberry appearance (Figure 16 2A—nose and right

A

B

Figure 16 2.

A, Infant with large hemangioma involving the left upper lid and orbit, tip of the nose, and superior aspect of right eyebrow. Note that the mass is causing severe ptosis and obstructing the visual axis. B, Contrast-enhanced computed tomography scan of the same child, showing large anterior orbital mass involving the left upper lid and medial orbit.

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