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

Phthisis Bulbi

A blind, scarred eye that is shrunken and hypotonic is termed phthisis bulbi. This end stage eye is often painful. A blind, painful eye usually is treated with enucleation.

Non perforating Anterior Segment Trauma

Corneal Abrasion

A corneal abrasion occurs when the corneal epithelium is removed. This creates severe pain, tearing, and photophobia. Patients usually feel there is something in the affected eye, even in the absence of a foreign body. Cor neal abrasions heal by the sliding of existing epithelium to fill in the areas of abraded epithelium. After careful examination to rule out corneal foreign body or infiltrate, antibiotic ointment and a pressure patch are placed on the eye. Place the tape obliquely in parallel strips from the forehead to the cheek. In most cases, a corneal abrasion will heal after 24 to 48 hours of being patched. Antibiotic ointment is typically used for 2 to 3 days after the patch is removed and then discontinued.

If the abrasion is associated with contact lens use, an ophthalmology consultation is indicated to rule out a bacterial corneal infection. The dif ferential diagnosis of a corneal abrasion includes herpes keratitis, bacterial ulcer, or retained corneal foreign body.

Conjunctival and Corneal Foreign Body

Common conjunctival and corneal foreign bodies include dust, dirt, or metallic slivers. Metallic foreign bodies usually are the result of a hammer or a hand tool made of forged steel striking something hard, like a rock. Metal from forged steel is under stress and when it cracks, a metal sliver explodes off at high speed. Retained metallic foreign bodies will cause a rust ring in the cornea. To remove a foreign body, first anesthetize the eye with topical drops (eg, tetracaine). If the foreign body is visualized, remove it with a ster ile cotton tipped applicator. Even superficial corneal foreign bodies can be removed in this manner. Deep corneal foreign bodies or foreign bodies that cannot be removed easily should be removed by an ophthalmologist. Once

Figure 23 5.

A, Photograph of a small hyphema that is layered inferiorly, plus some diffuse blood. A small hyphema is a hyphema that occupies less than or equal to one third of the anterior chamber. B, Total hyphema secondary to blunt trauma. The anterior chamber is full of clot and takes on a black or 8-ball appearance. This patient required surgical evacuation of the clot.

with diabetes, intraocular tumors, or retinal vascular occlusive disease) or iris tumors such as juvenile xanthogranuloma. The skin lesions are much more obvious than the iris lesions (Figure 23 6). The mechanism of bleed ing associated with blunt trauma is thought to be external compression and secondary expansion of the angle with tearing of the iris root. This results

Figure 23 6.

Juvenile xanthogranuloma of scalp: multiple raised, orange nodules that later regressed.

in rupture of the vascular arcade of the iris. Because a hyphema indicates severe ocular trauma and concurrent injuries to the retina or other ocular tissues can occur, an ophthalmology consultation is required.

The most important complications of a hyphema include late re bleeds into the anterior chamber, increased intraocular pressure, and corneal blood staining. Increased intraocular pressure can occur from red blood cells, red blood cell remnants (ghost cells) or sickled erythrocytes in patients with sickle cell anemia that block the trabecular meshwork outflow, or pupillary block glaucoma secondary to a large central blood clot that occludes the

pupil. Damage to the trabecular meshwork associated with angle recession can cause glaucoma that presents acutely or late (ie, months or even years after the trauma).

Corneal Blood Staining

Corneal blood staining may occur in association with large hyphemas that occupy the entire anterior chamber. Hemoglobin and hemosiderin from the hyphema infiltrate through the endothelial cells into the posterior aspect of the corneal stroma and produce an amber opacity (Figure 23 7). In children, it is important to avoid the complication of corneal blood

staining because this can produce a severely blurred retinal image, resulting in amblyopia.

Another important complication of hyphema is optic neuropathy associ ated with sickle cell hemoglobinopathies. Even slightly elevated intraocular pressures (>25 mm Hg) will cause optic neuropathy in patients with SC, SS, or S Thal disease. A sickle cell prep or hemoglobin electrophoresis should be part of the workup of patients with hyphemas who are at risk for hav ing a sickle cell hemoglobinopathy. The ischemic optic neuropathy can be avoided if the intraocular pressure is kept under 25 mm Hg. If the hyphema is causing increased intraocular pressure, the pressure may be lowered with topical or oral glaucoma medications. Oral methazolamide is preferred over acetazolamide for patients with sickle cell disease because methazolamide slightly raises the pH within the eye, while acetazolamide lowers the pH, thus predisposing it to sickling.

Medical Management of Traumatic Hyphemas

Controversy persists as to the medical management of traumatic hyphe mas. The classic treatment is hospitalization with bed rest for at least 5 days. Hyphemas resolve as blood is absorbed via the iris and trabecular mesh work. Since hyphema clots contract approximately 3 to 5 days post trauma, the greatest incidence of re bleeds occur at this time. An alternative to hos pitalization is treatment with bed rest at home. This outpatient treatment has been shown to be safe; however, it should be only used for patients who are reliable and can return to the office for daily checkups. In general, patients with small hyphemas (hyphemas less than one third of the anterior cham ber) have a good prognosis, with re bleed rates of 7% to 14%. These cases are

Figure 23 7.

Photograph of corneal blood staining several weeks after removal of an 8-ball hyphema. Note the yellowish-amber appearance of the cornea that represents iron deposition in the posterior corneal stroma.

often followed as outpatients. Hyphemas larger than one third of the anterior chamber, however, have an increased risk of developing re bleeds. Patients with large hyphemas may benefit from hospitalization and bed rest. Some authorities advocate no medical treatment, not even topical drops, while others suggest long acting cycloplegic agents to minimize ciliary spasm and prescribe topical corticosteroids to reduce inflammation.

The use of systemic antifibrinolytic agents such as aminocaproic acid may decrease the incidence of re bleeding; however, this is controversial because adverse effects such as nausea, emesis, hypotension, and prolonged absorption of the clot can occur. Those who advocate the use of antifibrino lytic agents restrict their use to small hyphemas less than one third of the anterior chamber in size. These agents are contraindicated in patients who are pregnant or have renal failure, blood dyscrasias, coagulopathies, and thrombotic disease. Previous reports have stated that antifibrinolytic agents reduce the re bleed rate in patients with small hyphemas. Others, however, have shown that the re bleed rate of small hyphemas is similar without anti fibrinolytic agents. An important disadvantage of aminocaproic acid is that it retards absorption of the clot and the clots take longer to dissolve. Still, in

appearance. The head trauma is usually quite severe, associated with loss of consciousness or amnesia. Most authorities recommend a short course of high dose corticosteroids. If this treatment plan does not improve vision, optic nerve decompression may be considered in selective cases. Patients who have no light perception have a poor prognosis for visual recovery regardless of treatment. Frontal head trauma can also cause injury to the chiasm, resulting in a bitemporal visual field defect. This is an unusual com plication of severe closed head trauma and often is associated with diabetes insipidus or a skull fracture.

Optic Nerve Avulsion

Optic nerve avulsion is caused by severe blunt anterior trauma to the eye that produces a pressure wave, pushing the optic disc posteriorly behind the lamina cribrosa. Visual acuity is usually NLP. On fundus examination, the optic disc may be recessed or absent.

Chemical Burns

Acid or alkaline solutions that come into direct contact with the surface of the eye can cause severe damage. A chemical burn is a true ophthalmic emergency and deserves immediate irrigation and lavage in the field prior

to the patient arriving at the emergency department. Once in the emergency department, lavage should be continued using at least 3 L of normal saline.

Litmus paper can be used to check the pH of the conjunctival fornix.

Alkaline Burns

Alkaline burns are especially damaging because the base will denature proteins and lyse cell membranes. This enhances the alkaline penetration into the eye and increases the damage. Surface damage includes removal of the corneal epithelium and obliteration of conjunctival blood vessels. The prognosis is proportional to the clock hours of avascular conjunctiva and sclera whitening. If more than 50% of the limbus is blanched, the prog nosis is very poor. After the acute burn, damage and corneal breakdown continue. Collagenase is released from regenerating tissue, producing even more destruction. Over time, symblepharon and cicatricial entropion may occur. In severe cases, the cornea undergoes progressive degeneration and

melt, leading to eventual perforation. The treatment for late alkaline burns includes anti collagenases such as acetylcysteine, artificial tears for dry eye, and topical antibiotics to prevent infection. In addition, a conformer (a plas tic shield placed directly on the cornea under the eyelids) is used to prevent symblepharon and preserve the conjunctival fornix.

Acid Burns

Acid burns can cause severe damage; however, because the acid tends to pre cipitate proteins, the area and depth of necrosis are more limited than with alkaline burns. The treatment is generally the same as for alkaline burns.

Radiation Injury

Radiation therapy of ocular tumors (eg, retinoblastoma and choroidal mela noma) and orbital tumors (eg, rhabdomyosarcoma and lymphoma) can cause ocular injury. Radiation cataracts can form with a single fraction dose as low as 200 rad, but they are usually not progressive and are not visually significant. Doses greater than 800 rad, however, can cause a progressive cataract that develops over 2 to 3 years. Doses above 5,000 rad can cause injury to the lacrimal gland, resulting in a dry eye syndrome that occurs within 3 months to a year after radiation therapy. Radiation keratopathy and conjunctivitis can occur as a consequence of dry eye syndrome and also from direct epithelial damage. This keratopathy is characterized by superfi cial punctate epithelial erosions that may become confluent and form a large epithelial defect. The use of artificial tears is critical for successful treatment of the keratitis.

Radiation retinopathy is caused by retinal vascular ischemia initiated by damage to retinal capillary endothelial cells. Radiation retinopathy devel ops 2 to 3 years after high dose radiation therapy (usually >5,000 rad). The majority of patients receiving more than 8,000 rad develop retinopathy. The retinopathy begins with areas of cotton wool spots, the first sign of radia tion retinopathy, representing early retinal ischemia. As the retinal ischemia progresses, large areas of capillary non perfusion develop. Next, microan eurysms and telangiectatic neovascularization occur. Late changes include iris rubeosis, glaucoma, hyphema, and vitreous hemorrhage. The retinal