Porth's Essentials of Pathophysiology, 4e

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Disorders of Special Sensory Function: Vision, Hearing, and Vestibular Function

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Disorders of Intraocular Pressure The intraocular pressure reflects that of the aqueous humor that fills the anterior and posterior chambers of the eye. The aqueous humor is produced by the ciliary body and passes from the posterior chamber through the pupil into the anterior chamber 6,25,34,35 (Fig. 38-11A). Aqueous humor leaves through the trabecular mesh- work at the iridocorneal angle between the anterior iris and the cornea. It then drains into the canal of Schlemm, a thin-walled vein that extends circumferentially around the iris, for return to the venous circulation. Intraocular pressure results from a balance of several factors, including the rate of aqueous humor production by the ciliary body, the resistance to flow between the iris and ciliary body, and its rate of removal by the drainage system (trabecular meshwork and canal of Schlemm). Normally, the rate of aqueous humor secretion is equal to the rate of outflow, and the intraocular pressure is maintained within a normal range of 10 to 21 mm Hg. 34 Glaucoma is a chronic, pressure-induced degen- erative neuropathy that produces changes in the optic nerve and visual field loss (see Fig. 38-1D). Glaucoma is commonly classified as open-angle or angle-closure glaucoma depending on the appearance of the iridocor- neal angle, and according to whether it is a primary or secondary disorder. 6,25,34,35 Open-Angle Glaucoma Open-angle glaucoma, which is the most common form of glaucoma, results from an abnormality of the trabecular meshwork that controls the flow of aqueous humor into the canal of Schlemm without obstruction at the iridocorneal angle 34–36 (see Fig. 38-11B). Open- angle glaucoma is usually asymptomatic and chronic, causing progressive damage to the optic nerve and vision loss unless it is appropriately treated. Elevated intraocular pressure is a primary factor; however, some eyes tolerate elevated intraocular pressure without developing disk or visual field changes, whereas others develop glaucomatous changes with consistently normal intraocular pressures (normal-tension glaucoma). Clinical Manifestations. Because open-angle glaucoma is usually asymptomatic, it is often suspected when abnormal intraocular pressure measurements or optic disk abnormalities are found during a routine eye examination. The normal optic disk has a central depression called the optic nerve cup (Fig. 38-12). In glaucoma, the neuroretinal rim of the optic nerve becomes progressively thinner, thereby enlarging the optic nerve cup, a phenomenon referred to as optic nerve cupping . Its cause is loss of retinal ganglionic cell axons, along with supporting glia and vasculature. 6 Because changes in the optic cup precede visual field loss, regular ophthalmoscopic examinations are important to detect damage to retinal ganglion axons before visual field loss occurs. Diagnosis and Treatment. Diagnostic methods include applanation tonometry (measurement of intraocular

develop suddenly at any time. Careful monitoring for metamorphopsia, or distorted vision of straight lines, can aid in the early detection of retinal damage. Neovascular Degeneration. The neovascular form of AMD is characterized by the formation of a choroidal neovascular membrane. These new blood vessels have weaker walls than normal and are prone to leakage; thus, this form is commonly referred to as “wet.” The leakage of serous or hemorrhagic fluid into the subreti- nal space causes separation of the pigmented epithelium from the neurosensory retina. Over time, the subretinal hemorrhages organize to form scar tissue, causing death of the underlying retinal tissue and loss of all visual func- tion in the corresponding macular area (see Fig. 38-10B). Although some subretinal neovascular membranes may regress spontaneously, the natural course is toward irre- versible loss of central vision. Diagnosis and Treatment. The early stages of subretinal neovascularization may be difficult to detect with an ophthalmoscope. Therefore, there is a need to be alert for recent or sudden changes in central vision, blurred vision, or scotomata (visual field areas in which vision is depressed or absent). Persons with late-stage disease often find it difficult to see at long distances (e.g., in driving), do close work (e.g., reading), see faces clearly, or distinguish colors. However, they may not be severely incapacitated because the peripheral retinal function usually remains intact. Effective therapies for neovascular macular degen- eration include thermal laser photocoagulation, pho- todynamic therapy, and intravitreal injections of VEGF inhibitors. 23,31–33 Conventional retinal laser photoco- agulation can achieve direct destruction of a choroidal neovascular membrane. Photodynamic laser therapy involves the intravenous injection of a dye that is subse- quently activated by retinal laser irradiation to produce selective vascular damage. Recognition of the key role that VEGF plays in choroidal neovascularization patho- genesis led to development of VEGF inhibitors, a class of drugs that has now become the preferred treatment for neovascular macular degeneration. These drugs are given by intravitreal injection. In addition to currently used and forthcoming treatments, there is interest in the so-called preventative category of treatments. 21,31–33 Tobacco smoking is consistently identified as a preventable age-related macular degeneration risk; thus, its elimination should be one of the first therapeutic recommendations. Preventative recommendations also include dietary supplementation containing high-dose antioxidants and minerals (vitamins E and C, zinc, and β -carotene) for persons at risk for developing macular degeneration and for slowing the progression of age-related macular degeneration in persons with the disease. 30 However, more experimental data and randomized clinical trials are needed to support their therapeutic value, the most effective composition in terms of single- or multiple- supplement combinations, and dosing of the particular supplements.