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When capillary occlusion sites dilate, venous beading, margin of the inner nuclear layer, the external margin of the gan venous tortuosity, flame-shaped hemorrhages (surface hemor glion cell layer, the inner margin of the inner nuclear layer, and rhages), and dot and blot hemorrhages (deep hemorrhages) in the ganglion cell layer to the retinal nerve fiber layer (listed from crease. The perifoveal capillary bed only exists as one Described in detail in the next page. There are no retinal blood vessels in the central part of the fovea, Soft exudate (cotton-wool spots) 0. Highly reflectivity remains due to tion and loss of endothelial cells, inversely endothelial cell gliosis after the disappearance of the soft exudates(8). Classification of retinal edema Macular edema patterns and retinal thickness Retinal edema is divided into macular edema and retinal nerve Otani et al. The latter is thickening due to an increase in intracellular stated that visual acuity was most correlated with macular retinal volume caused by a shortage in arterial blood supply, which typ thickness regardless of the type of pattern(9). Lipid accumulation mainly occurs that destroys the foveal photoreceptors leading to permanent vi from the outer plexiform layer to subretinal space, and leads sual impairment. It is further divided into both focal edema and to formation of intraretinal and subretinal hard exudates(12). Serum lipid levels are a risk factor in hard exudate forma Focal edema occurs as a result of leakage from accumulated tion. Diabetic macu sity of cystoid spaces varies from weakly reflective to moderately lar edema are sometimes accompanied by foveal detachment reflective (. Among cystoid spaces, cystoid spaces in the outer properties of accumulating exudates in the cystoid spaces. Some plexiform layer, the fovea and parafovea, and foveal detachment times hemorrhages accumulate in the cystoid spaces, which then are most influential in macular thickening. They are smaller than the hard exudates adherens between Muller cells and photoreceptors at the base of that can be seen in fundus photography. There are distinguishing the outer segments, and thus had very narrow gaps, which limit characteristics in the favorite accumulation locations and distri particularly the movement of large molecules. Optical coherence tomographic characteristics of microaneurysms in diabetic retinopathy. Permanent visual impairment as a result of macular edema is caused by the destruction of the foveal photoreceptor layer. How Ischemic maculopathy ever, edema does not directly cause photoreceptor layer damage. Capillary nonperfusion in diabetic retinopathy typically occurs the mechanism for photoreceptor cell destruction is complex. The capillary nonperfusion involving the spaces into subretinal space, and this phenomenon appears to be macular, particularly the fovea, causes severe visual acuity loss. This leakage repeats its of the capillary bed on the temporal macula extends to the fovea stop-and-resume cycle. These disease conditions are to the mechanical obstruction by the leakage and due to the ac termed ischemic maculopathy. This is an to account for this association is that when macular thickness important factor that impedes visual improvement even after become greater cystoid spaces increase in size and internal pres diabetic macular edema is resolved after treatment(33). Relation between superficial capillaries and foveal neurysms in the human diabetic retina. Optical coherence tomographic screening, and relationships to the neuronal layers. Histology and fluorescein angiography of micro 28) Otani T, Yamaguchi Y, Kishi S. Hyperreflective sign in resolved cotton tion and visual acuity in diabetic macular edema. Characterization of macular edema ischemic diabetic maculopathy: correlation of optical coherence tomo from various etiologies by optical coherence tomography. Optical coherence tomography fea after intravitreal triamcinolone treatment for diabetic macular edema. Association of elevated serum lipid levels with retinal hard exudate in diabetic retinopathy. A prospective study of serum lipids and risk of diabetic macular edema in type 1 diabetes.

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Because gonococcal conjunctivitis can rapidly cause blindness, the cause of all cases of ophthalmia neonatorum should be verified by examination of smears of exudate, epithelial scrapings, cultures, and rapid tests for gonococci. Gonococcal neonatal conjunctivitis causes corneal ulceration and blindness if not treated immediately. Chlamydial neonatal conjunctivitis (inclusion blennorrhea) is less destructive but can last months if untreated and may be followed by pneumonia. Treatment for neonatal gonococcal conjunctivitis is with ceftriaxone, 125 mg as a single intramuscular dose; a second choice is kanamycin, 75 mg intramuscularly. To treat chlamydial conjunctivitis in newborns, erythromycin oral suspension is effective at a dosage of 50 mg/kg/d in four divided doses for 2 weeks. Herpes simplex keratoconjunctivitis is treated with acyclovir, 30 mg/kg/d in three divided doses for 14 days. Other types of neonatal conjunctivitis are treated with erythromycin, gentamicin, or tobramycin ophthalmic ointment four times daily. Crede 1% silver nitrate prophylaxis is effective for the prevention of gonorrheal ophthalmia but not inclusion blennorrhea or herpetic infection. The slight chemical conjunctivitis induced by silver nitrate is minor and of short duration. Accidents with concentrated solutions can be avoided by using wax ampules specially prepared for Crede prophylaxis. The most common cause is cat-scratch disease, but there are many other causes, including Mycobacterium tuberculosis, Treponema pallidum, Francisella tularensis, Pasteurella (Yersinia) pseudo-tuberculosis, C trachomatis serovars L1, L2, and L3, and C immitis. Conjunctival Cat-Scratch Disease this protracted but benign granulomatous conjunctivitis is found most commonly in children who have been in intimate contact with cats. The child often runs a low-grade fever and develops a reasonably enlarged preauricular node and one or more conjunctival granulomas. The disease appears to be caused by a slender pleomorphic gram-negative bacillus (Bartonella [formerly Rochalimaea] henselae), which grows in the walls of blood vessels. With special stains, this organism can be seen in biopsies of conjunctival tissue. The organism closely resembles Leptotrichia buccalis, and the disease was previously known as leptotrichosis conjunctivae (Parinaud conjunctivitis). The organism is commonly found in the mouth in humans and always in the mouth in cats. The conjunctival nodule can be excised; in the case of a solitary granuloma, this may be curative. Systemic tetracyclines may shorten the course but should not be given to children under 7 years of age. Conjunctivitis Secondary to Neoplasms (Masquerade Syndrome) When examined superficially, a neoplasm of the conjunctiva or lid margin is often misdiagnosed as a chronic infectious conjunctivitis or keratoconjunctivitis. Since the underlying lesion is often not recognized, the condition has been referred to as masquerade syndrome. The masquerading neoplasms on record are conjunctival capillary carcinoma, conjunctival carcinoma in situ, infectious papilloma of the conjunctiva, sebaceous gland carcinoma, and verrucae. Verrucae and molluscum tumors of the lid margin may desquamate toxic tumor material that produces a chronic conjunctivitis, keratoconjunctivitis, or (rarely) keratitis alone. Readers are referred to other sections of this chapter for information about inflammatory and 254 degenerative lesions of the conjunctiva (eg, pingueculum and pterygium) that can simulate conjunctival neoplasms.

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The peripheral chorioretinal changes of pathologic myopia include paving stone, pigmentary, and lattice degeneration that may lead to retinal breaks and 444 retinal detachment. There may be reasonably good vision, but untreated, there tends to be slow progression to macular hole and/or retinal detachment. Chronic hyperglycemia, systemic hypertension, hypercholesterolemia, and smoking are risk factors for development and progression of retinopathy. Visual impairment is caused by macular edema or the complications of proliferative diabetic retinopathy comprising vitreous hemorrhage, tractional retinal detachment, and neovascular glaucoma. Retinopathy is rare in type 1diabetics prior to puberty, whereas one third of type 2 diabetics have retinopathy at initial diagnosis. The relative risk for developing diabetic retinopathy is higher in type 1 compared to type 2. Screening Early detection and timely treatment of diabetic retinopathy are essential for prevention of permanent visual loss. Screening should be performed within 3 years from diagnosis in type 1 diabetes, at diagnosis in type 2 diabetes, and annually thereafter in both types. Diabetic retinopathy may progress rapidly 445 during pregnancy, and screening should take place in the first trimester and then at least every 3 months until delivery. Recent advances in imaging particularly wide field fundus photography have improved detection of central and peripheral retinopathy. Chronic hyperglycemia leads to a metabolic response that is mediated by increased glycation end products, polyols, reactive oxygen species, eicosanoids, nitric oxides, and intercellular adhesion molecules, and activation of the protein kinase C pathway, leading to microvascular endothelial damage, retinal capillary leukostasis, and capillary closure. The earliest histopathologic changes are thickening of the capillary endothelial basement membrane and loss of pericytes, leading to outpouchings that form microaneurysms. Superficial flame-shaped hemorrhages in the nerve fiber layer arise from precapillary arterioles, and deep dot and blot hemorrhages arise from the venous end of the capillaries. Cotton-wool spots are evidence of axoplasmic stasis usually due to infarcts of the nerve fiber layer from occlusion of precapillary arterioles. Classification Diabetic retinopathy can be broadly classified into nonproliferative retinopathy, maculopathy, and proliferative retinopathy, of which the latter two may coexist. Moderate nonproliferative diabetic retinopathy showing microaneurysms, deep hemorrhages, flame-shaped hemorrhage, exudates, and cotton-wool spots. Maculopathy can also be due to ischemia, which is characterized by edema, deep hemorrhages, and little exudation. Diabetic ischemic maculopathy with deep retinal hemorrhages, little exudation, and in the right eye, early optic disk neovascularization. Fundus fluorescein angiogram shows capillary nonperfusion (arrows), macular edema, and dye leakage from the optic disk new vessels in the right eye. Fluorescein angiogram of proliferative diabetic retinopathy shows leakage from the neovascular tissue. The fragile new vessels proliferate onto the posterior face of the vitreous and 450 become elevated once the vitreous starts to contract away from the retina. There is very little risk of developing neovascularization and vitreous hemorrhage once a complete posterior vitreous detachment has developed. In eyes with proliferative diabetic retinopathy and persistent vitreoretinal adhesions, elevated neovascular fronds may undergo fibrous change and form tight fibrovascular bands, leading to vitreoretinal traction. This can lead to progressive traction retinal detachment or, if a retinal tear occurs, rhegmatogenous retinal detachment. Advanced diabetic eye disease may also be complicated by iris neovascularization (rubeosis iridis) and neovascular glaucoma.

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To support this discussion, selected rooms are detailed in the form of Design Plates. Each Design Plate includes an axonometric view, foor plan, refected ceiling plan, elevations, room data sheet, and an equipment list. The equipment list provides a comprehensive overview of space planning and utility requirements and locations for the key rooms in this service. Design guide has one plate that represents both Ophthalmology and Optometry on the same plan. For each design plate there are two room content lists; one for Ophthalmology and one for Optometry. Small, hand-held equipment items are not included on the Design Plates, but are indicated in the Room Content Lists. M5027 Table, Multiple Instrument, Ophthalmic 1 V V A multiple instrument ophthalmic table. M5562 Tester, Visual Acuity, Video/Microproces 1 V V Visual acuity tester using video (television sor Based monitor) and microprocessor technology. Wall bracing is required for mounting the unit directly to the wall without support from below. The unit requires an electrical outlet on the far end wall of the examination lane. M6045 Corneal Topography Unit 1 V V Computerized corneal mapping system for pre and post surgical diagnosis of astigmatism, refractive error, irregularly shaped corneas and other eye conditions. M5562 Tester, Visual Acuity, Video/ 1 V V Visual acuity tester using video (television Microprocessor Based monitor) and microprocessor technology. E0204 Worksurface, w/Overhd Cab & Drwrs, 1 V V Typically includes: Wall Mtd, 24" W 2 Vertical Hanging Strips 1 Lockable Flipper Unit 1 Shelf, Storage/Display 1 Light 1 Cantilevered Work Surface 2 Storage Frames 2 Drawers, 3"H 3 Drawers, 6"H E0224 Worksurface, Computer, O/H Cab, Wall 1 V V Typically includes: Mtd, 60" W 3 Vertical Hanging Strips 2 Lockable Flipper Units 2 Shelves, Storage/Display 2 Lights 1 Tack board 2 Tool Rails 2 Paper Trays 1 Diagonal Tray 1 Cantilevered Work Surface 1 Adjustable Keyboard Tray 1 Stationary Pedestal, Box/Box/File F0205 Chair, Side With Arms 1 V V Upholstered side chair, 32" high X 21" wide X 23" deep with arms, padded seats and padded backs. The computer is used throughout the facility to input, manipulate and retrieve information. This table is designed to hold up to three ophthalmologic instruments allowing the patient to turn only slightly between them for testing. The table top is adjustable from approximately 26" to 38" and facilitates complete wheelchair accessibility to all instruments. Unit includes lamps, prism measuring lens marking device, cylinder axis wheel calibrated in two 180 degree segments and a green flter for tinted glass. They provide typical confgurations and general technical guidance, and are not intended to be project specifc. The Monitor unit shall consist of a central processing mini tower, fat panel monitor, keyboard, mouse and speakers. Unit is electrically powered for precise positioning and has an adjustable headrest and armrest. This unit has a plastic laminated fnish, one trail drawer with full suspension, and three storage electrical drawers with single door. Unit consists of a base mounted ophthalmological slit lamp with head and chin rest and manual height and focusing adjustments. The instrument features a microscope head with parallel optics that will accept an applanation tonometer. Unit consists of headband and crown, halogen quartz lamp, multi-coated aspherical lenses, scleral depressor and mirror. Unit features a focusing system, engraved focusing scale, positive fxation for rapid measurements, center and peripheral corneal measurements scale with a range from 30D to 60D. This differs from standard eye examination room confgurations which normally do not have electrical outlets in that wall. Lightweight instrument with interchangeable heads, rechargeable battery handle, mirror, forehead rest and one halogen lamp.