Ординатура / Офтальмология / Английские материалы / Primary Care Ophthalmology_Palay, Krachmer_2005
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180CHAPTER 10 • Retina
•The risk of contralateral eye involvement with active CMV retinitis is approximately 20%.
•Primary care physicians should keep in mind that all antiviral therapies are virostatic. Should the patient discontinue systemic treatment, CMV retinitis probably will recur.
Toxoplasmosis
Toxoplasma gondii is an obligate intracellular parasite common among humans and animals (e.g., cats). Ocular toxoplasmosis is a potentially blinding, necrotizing retinitis that may recur.
Symptoms
•Vision is blurred or decreased.
•Wavy or distorted vision (metamorphopsia) may occur.
•Floaters may be seen.
•Pain is variable.
Signs
•Vitreous debris is seen.
•Iritis or cells are present in the anterior chamber.
•Yellow-white areas of retinitis are observed.
•The optic nerve is yellow-white and swollen (Fig.10–28).
•Retinal vascular infiltrates (due to periarteritis) may be observed.
•Old chorioretinal scars are found in the affected or fellow eye.
•Macular edema can occur.
FIGURE 10–28 Left eye of a young man with elevated toxoplasmosis titers. Note the old, healed toxoplasmosis lesion (black) nasal to the optic nerve. The optic nerve has an area of active inflammation and reactivation of infection, with overlying vitreous involvement that obscures the disc margin.
Postsurgical Endophthalmitis |
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Differential Diagnosis
Considerations in the differential diagnosis include the following:
•Uveitis
•Sarcoidosis
•Acute retinal necrosis, with herpes zoster infection the presumed etiologic process
•Toxocara canis infection, syphilis, and HIV infection
Treatment
Treatment of sight-threatening lesions—that is, those involving the macula and optic nerve or those with significant intraocular inflammation—is as follows:
•“Triple therapy” for 4 to 6 weeks:
Pyramethamine and folate
Sulfadiazine, sulfisoxazole, or Triple Sulfa
Clindamycin
•Alternatively, trimethoprim and sulfamethoxazole (Bactrim DS)
•Oral prednisone: 40 to 60 mg every day for 3 to 4 weeks, then tapering; used to limit the inflammation-mediated retinal destruction
•Oral atoquavone: 750 mg four times daily; has been suggested to kill the encysted form of toxoplasmosis
Postsurgical Endophthalmitis
Any invasive ophthalmologic procedure may result in endophthalmitis. This condition should be considered in the etiology of significant postoperative pain or inflammation.
Symptoms
•Pain is not always present.
•Reddening of the eye is apparent.
•Vision is decreased.
•Floaters are seen.
Signs
•Hypopyon, or layering cells in the anterior chamber, is observed (Fig. 10–29).
•Conjunctival injection is present.
•Hazy vitreous or obscuration of the posterior pole (vitritis) may be noted.
Treatment
•Either a vitreous culture with intraocular injection of antibiotics or, in more severe cases, vitrectomy surgery with intravitreal antibiotics is necessary.
•Immediate ophthalmologic referral is essential when endophthalmitis is suspected.
182 CHAPTER 10 • Retina
FIGURE 10–29 Endophthalmitis. Acute postoperative hypopyon in the inferior portion of the anterior chamber (1). Note the conjunctival injection in this painful, infected eye.
1
FIGURE 10–30 Intraocular metallic foreign body in a young man who was pounding a metal hammer on a metal post when he felt a sudden sharp pain in the eye. The small metal fragment may be difficult to see through an undilated pupil and is shown here surrounded with a small amount of vitreous hemorrhage. This fragment could be readily detected with a plain skull film or a computed tomography scan.
Trauma-Associated Endophthalmitis
Failure of the emergency department physician or primary care provider to diagnosis or detect a retained intraocular foreign body may have significant medical-legal implications. Unfortunately, missed diagnosis in such cases can occur. These cases are considered ophthalmologic emergencies and should be referred immediately to an ophthalmologist. Similarly, any full-thickness, perforating, or penetrating wound to the eye (by definition, an open globe injury) necessitates urgent ophthalmologic referral.
Post-traumatic endophthalmitis should be suspected in all cases, particularly with trauma involving an intraocular foreign body, a dirty wound, or a history such as pounding metal on metal (Fig. 10–30). Any patient history suggestive of an intraocular foreign body necessitates radiologic imaging (usually with a skull film or computed tomography [CT] scan) to rule out the presence of foreign material in the eye. Many open globe injuries are treated with intravitreal and/or systemic intravenous antibiotics. Other accompanying injuries should be suspected in the setting of ocular trauma, such as neck, sinus, or central nervous system injuries.
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Endogenous Endophthalmitis
Endogenous endophthalmitis results from septic emboli to the retinal or choroidal circulation. Patients usually are sick from the underlying sepsis and present with vitritis, focal areas of retinitis, and anterior chamber reaction. In the anterior chamber, a few cells to a layering of cells (hypopyon) may be present. Intravenous drug abusers, immunocompromised patients, and hospitalized patients with chronic indwelling catheters or central lines are at risk for endogenous endophthalmitis. Endophthalmitis due to Candida or other fungi usually appears as a small area of focal choroiditis or chorioretinitis that expands into fluffy white opacities that may extend into the vitreous. Infection may progress to complete opacification of the vitreous.
Intravitreal amphotericin and treatment of the systemic infection are indicated. Vitreous surgery may be required in severe cases. Vitreous cultures are helpful and may reveal the causative organism.
Posterior Vitreous Detachment
Posterior vitreous detachment occurs in most persons with time. The detachment usually occurs in the fifth to seventh decades of life. In highly myopic (very nearsighted) persons, development of a posterior vitreous detachment at an early age is likely because of the larger size of the eye. The vitreous is firmly adherent in the peripheral retina, less firmly adherent at the optic nerve and along the major retinal vessels, and weakly adherent along the surface of the retina. When the vitreous separates from the posterior retina, traction is transferred to the peripheral retina, where tears or breaks may occur.
Symptoms
•Patients report flashing lights.
•New floaters are commonly seen, sometimes stringy or circular.
Treatment
•Because the symptoms of a posterior vitreous detachment may herald a retinal detachment, indirect ophthalmoscopy by an ophthalmologist is required and should be performed within 24 hours of diagnosis.
•No treatment is indicated.
•Laser photocoagulation or cryotherapy may be used for any new retinal tears associated with symptoms.
Retinal Detachment
A retinal detachment occurs when fluid separates the neurosensory retina from the underlying RPE. A rhegmatogenous (from the Greek rhegma, meaning “breakage”) retinal detachment typically occurs when the vitreous separates from the retina (posterior vitreous detachment), causing a tear or break (Fig. 10–31). Liquefied vitreous fluid then dissects the neurosensory retina from the underlying RPE, resulting in a
184 CHAPTER 10 • Retina
FIGURE 10–31 Horseshoe-shaped retinal tear that occurred after a posterior vitreous detachment and led to a retinal detachment.
detached retina. Serous or exudative retinal detachments occur following the leakage of fluid caused by a process occurring under the retina without a tear or break in the retina. The fluid leakage may be due to abnormal neovascularization, incompetence of the RPE barrier to fluid, tumors, or inflammation. A tractional retinal detachment results from scar tissue formation on the surface of the retina, leading to contraction with subsequent retinal distortion, elevation, and swelling. Tractional retinal detachments commonly occur with proliferative diabetic retinopathy as the result of repeated vitreous hemorrhage.
Symptoms
•Flashes are noted.
•Floaters are seen.
•A visual field loss occurs, which patients often describe as a curtain, shadow, or bubble of fluid.
•Vision is wavy or distorted (metamorphopsia).
•Vision is decreased.
Signs
•A relative afferent pupillary defect may be observed.
•The visual field loss is unilateral and may be sectoral, quadrantic, hemifield, or total.
•Retinal hydration lines, or rugae, have an appearance similar to that of ripples on a pond.
Workup
•Retinal detachments are difficult to diagnose with a direct ophthalmoscope. A simple technique using a direct ophthalmoscope allows the clinician to compare the
Epiretinal Membrane |
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red reflexes of the two eyes from a distance of several feet. Any differences in the quality of the reflex dictate further evaluation. An eye with a retinal detachment may have a lighter-colored reflex (yellow or orange) than in the fellow eye.
Treatment
•Patients should be referred for immediate ophthalmologic evaluation.
•Surgical intervention is necessary because untreated retinal detachments may lead to blindness in the affected eye.
•The cause of a serous retinal detachment should be determined, especially to rule out the presence of a tumor.
Epiretinal Membrane
A thin sheet of fibroglial tissue, or an epiretinal membrane, may form on the surface of the retina, often after a posterior vitreous retinal detachment. Contraction of the membrane wrinkles and distorts the retina (Fig. 10–32).
Symptoms
•Vision is decreased.
•Vision is wavy or distorted (metamorphopsia).
•Patients report difficulty reading with the affected eye.
Signs
•Amsler grid distortion is found on testing.
•A whitish, folded membrane is evident on the retinal surface (Fig. 10–32).
•The retinal vasculature is distorted.
•Macular edema may be present.
FIGURE 10–32 With contraction of the epiretinal membrane (1), the retinal elements are pulled centrally, with formation of accompanying wrinkles, folds, and vascular distortions.
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186 CHAPTER 10 • Retina
Treatment
•Ophthalmologic referral is indicated.
•Occasionally an epiretinal membrane breaks free from the retina and vision spontaneously improves, but this is rare. If the patient’s vision is minimally affected, no treatment is required.
•If vision is significantly affected, surgical removal of the membrane is necessary to improve the vision and distortion.
Follow-up
• The overall visual prognosis is good.
Vitreous Hemorrhage
Vitreous hemorrhage is the result of an underlying vascular process and occurs in many disorders. Because visualization of the retina may be impossible, ophthalmic ultrasonography may be necessary to determine the presence of an accompanying retinal detachment. Treatment is directed at management of the underlying etiologic process.
Differential Diagnosis
Considerations in the differential diagnosis include the following:
•Proliferative diabetic retinopathy
•Posterior vitreous detachment with an avulsed retinal vessel
•Retinal tear through a vessel (with or without a retinal detachment)
•Macroaneurysm
•Trauma
•Subarachnoid or subdural hematoma (Terson syndrome)
•Any retinal vascular lesion
Retinal Surgery
Advances in retinal surgery over the last 20 to 30 years have been dramatic because of the development of microsurgical techniques, wide-field viewing, and a better understanding of complex biologic processes. Many formerly blinding conditions, such as diabetic retinopathy, recurrent retinal detachments, and retinopathy of prematurity, are now managed more effectively. The two primary forms of retinal surgery are scleral buckling and vitrectomy surgery. The primary indication for surgery is a retinal detachment.
Standard scleral buckling surgery usually involves the placement of a solid silicone band around the equator of the eye to relieve the circumferential traction and support the retina in the region of the retinal tear (Fig. 10–33). The scleral buckle alters the internal fluid dynamics and decreases the rate of subretinal fluid accumulation. Either laser treatment or cryotherapy is used to form an adhesion (retinopexy) of the retina to the underlying choroid in the area of the tear. The combination of a buckle and
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FIGURE 10–33 The external placement of a silicone scleral buckle. The element is sewn to the scleral surface. Note that black silk sutures are supporting the rectus muscles. The white infusion tubing and gold plug represent sclerotomy entry sites into the eye for vitreous dissection instrumentation.
the chorioretinal adhesion serves to repair most rhegmatogenous retinal detachments (80%). In certain situations, an intraocular gas bubble along with retinopexy may be used to reattach the retina. This technique is referred to as pneumatic retinopexy.
During vitrectomy surgery, the surgeon begins by making three small incisions in the sclera. One sclerotomy accommodates an infusion line; the other two are used to place instrumentation into the posterior segment of the eye. The surgeon views the inside of the eye through a surgical microscope that contains various lenses to help visualize the abnormal anatomy. Various instruments such as illuminated picks, scissors, endolaser probes, and forceps are used to perform delicate manipulation of the retina. Heavy liquids, air, gas, or silicone oil may be used to reattach the retina. Laser photocoagulation seals the retinal tear and may be used to treat ischemic retina (panretinal photocoagulation).
CHAPTER 11
Glaucoma
ALLEN D. BECK
Related Anatomy
Aqueous humor is produced by the epithelium of the ciliary body (Fig. 11–1). The aqueous flows past the lens, around the iris, into Schlemm’s canal by way of the trabecular meshwork, and then into aqueous and episcleral veins. The trabecular meshwork is the site of the greatest resistance to aqueous outflow and is located at the junction between the cornea and the iris. This region of the eye is referred to as the anterior chamber angle.
Turnover of the entire volume of aqueous occurs approximately every 100 minutes. Intraocular pressure (IOP) is determined by the balance between production and outflow of aqueous humor. The range of normal IOP measurements is 10 to 21 mm Hg. An IOP measurement of 22 mm Hg or greater is considered abnormal. Diurnal variations in IOP are well documented for both normal and glaucomatous eyes. These pressure swings mean that the IOP may be in the normal range at certain times of the day in patients with glaucoma.
Damage from glaucoma is manifested by optic nerve cupping (Fig. 11–2). Loss of neurons and glial tissue causes glaucomatous cupping secondary to mechanical and ischemic mechanisms.
The damage to the optic nerve results in characteristic patterns of visual field loss (Fig. 11–3). Visual field loss in glaucoma classically respects the horizontal meridian. Visual acuity and the central visual field usually remain normal until late in the disease process.
Definitions and Epidemiology
The term glaucoma refers to a group of diseases with progressive optic nerve damage and visual field loss. In most cases of glaucoma the IOP is consistently above the normal range, although in some cases the IOP may always be within the normal range.
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190 CHAPTER 11 • Glaucoma
FIGURE 11–1 Anatomy of the anterior portion of the eye, demonstrating the flow of aqueous humor from the ciliary body to the trabecular meshwork.
The prevalence of glaucoma is approximately 0.5% of the total population. Elevated IOP without signs of optic nerve or visual field damage (ocular hypertension) occurs in approximately 1.5% of the total population. Glaucoma can be broadly categorized into open-angle glaucoma and angle-closure glaucoma. Most cases of glaucoma are of the open-angle type, in which the eye has a structurally normal outflow pathway (see Fig. 11–1). In angle-closure glaucoma, blockage of aqueous flow between the lens and iris causes a forward shifting of the iris and closure of the anterior chamber angle (Fig. 11–4). Patients with angle-closure glaucoma may experience acute symptoms of severe pain and blurred vision, whereas those with a chronic form of angle-closure glaucoma have slow elevation of IOP with no symptoms.
Open-Angle Glaucoma
Symptoms
•Patients usually have no symptoms, although decreased vision may be noted late in the disease course.
Signs
•IOP is elevated.
•Optic nerve cupping occurs (see Fig. 11–2).
Associated Factors and Diseases
•Increasing patient age is associated with a progressive increase in the prevalence of glaucoma.