Program Director, University of Alaska at Fairbanks
Wessely rings may persist for some time in corneas traumatized by a foreign body medications known to cause weight gain order online avodart, even after the foreign body is removed medications that interact with grapefruit order genuine avodart online. Sclera Nearly 50% of patients with necrotizing scleritis have an associated systemic immunologic or connective tissue disease symptoms 6dp5dt buy avodart 0.5mg cheap. Immune-complex deposition medicine man aurora buy avodart 0.5 mg without a prescription, granulomatous inflammation, and occlusive vasculitis have been implicated in the pathogenesis of scleral inflammation. Diagnostic Approach to Immune-Mediated Ocular Disorders Many, but not all, immune-mediated ocular disorders are secondary to a systemic disease. As with most medical problems, diagnostic investigations need to begin with a complete history, including a review of systems, and a general physical examination, as indicated. Some of the more common laboratory diagnostic tests that are selected to further narrow the differential diagnosis are listed in Table 6-2. In general, except in the case of rheumatoid arthritis, which has a strong predilection for scleral and corneal involvement, the workup for patients with immune-mediated corneal disease in whom an underlying disease is suspected is quite similar to that for the uveitis patient. In a patient presenting with ocular inflammation, diagnosing systemic vasculitis with tests, including antineutrophil cytoplasmic autoantibody tests (see Table 6-2), may be instrumental in instituting early life-saving therapy. Table 6-2 See BCSC Section 9, Intraocular Inflammation and Uveitis, for more information on the diagnostic workup of patients with uveitis. Table 6-3 provides the clinical interpretation of ocular surface cytology for immune-mediated keratoconjunctivitis. Finally, it should be noted that corneal and ocular surface morbidities may result from underlying autoimmune disease. Generally, when a systemic disease is suspected, it is advisable to coordinate care with an internist or rheumatologist, especially if systemic immune suppression is being considered. Immune-Mediated Diseases of the Eyelid Contact Dermatoblepharitis Topical ophthalmic medications, cosmetics, and environmental substances can occasionally trigger a local allergic reaction. These reactions are associated with itching, eyelid erythema and swelling, and conjunctival hyperemia and chemosis (Fig 7-1). Ocular anaphylactic reactions can follow instillation of topical anesthetics and antibiotics such as bacitracin, cephalosporins, and sulfacetamide but often resolve spontaneously. Patients are often sensitized by previous exposure to the offending drug or preservative. An acute eczematous reaction develops with erythema, leathery thickening, and scaling of the eyelid (Fig 7-2). Sequelae of chronic contact blepharoconjunctivitis include hyperpigmentation, dermal scarring, and lower-eyelid ectropion. Medications that are Figure 7-1 Acute anaphylactic reaction to commonly associated with contact topical ophthalmic medication with conjunctival blepharoconjunctivitis include hyperemia and chemosis. Usually, the history provides the necessary clues, but sometimes a "rechallenge" is necessary to confirm a suspicion. Rechallenges should never be done in patients with a known systemic allergy to a drug. Initial management of type I hypersensitivity reactions includes allergen avoidance or discontinuation. Adjunctive therapy may involve the use of cold compresses, artificial lubricants, topical antihistamines, Figure 7-2 Delayed allergic contact dermatitis ma s t - c e l l stabilizers, and/or nonsteroidal antisecondary to topical ophthalmic medication. Topical vasoconstrictors, either alone or in combination with antihistamines, may provide acute symptomatic relief but should not be used long term. In severe cases, a brief (several-day) course of mild topical corticosteroids or tacrolimus (Protopic) ointment 0. The pathogenesis of atopic dermatitis involves a type IV hypersensitivity reaction, increased IgE hypersensitivity, increased histamine released from mast cells and basophils, and impaired cell-mediated immunity. Other ocular findings include periorbital darkening, exaggerated eyelid folds, meibomianitis, ectropion, and chronic papillary conjunctivitis. Infants typically have an erythematous rash, children tend to have eczematous dermatitis with secondary lichenification from scratching, and adults have scaly patches with thickened and wrinkled dry skin. Oral antipruritic agents such as antihistamines and mast-cell stabilizers can alleviate itching but may exacerbate dry eye with their anticholinergic activity. Efficacy and tolerability of topical pimecrolimus and tacrolimus in the treatment of atopic dermatitis: meta-analysis of randomised controlled trials. Immune-Mediated Disorders of the Conjunctiva Hay Fever Conjunctivitis and Perennial Allergic Conjunctivitis Hay fever (seasonal) conjunctivitis and perennial allergic conjunctivitis are largely IgEmediated immediate hypersensitivity reactions. It enters the tear film and comes into contact with conjunctival mast cells that bear allergen-specific IgE antibodies. Degranulation of mast cells releases histamine and a variety of other inflammatory mediators that promote vasodilation, edema, and recruitment of other inflammatory cells, such as eosinophils. In a presensitized individual, the activation and degranulation of mast cells can be triggered within minutes of allergen exposure. Symptoms develop rapidly after exposure to the allergen and consist of itching, eyelid swelling, conjunctival hyperemia, chemosis, and mucoid discharge. Contributing factors, including contact lenses and dry eye, should be identified, as these can play an important role in facilitating allergen contact with the ocular surface. Conjunctival scrapings reveal the characteristic eosinophils, which are not normally present on the ocular surface (see Chapter 6).
Even in the normal eye shakira medicine purchase avodart once a day, laminar trabeculations or pores may be seen as grayish dots in the base of the physiologic cup medications mobic purchase avodart with a mastercard. With glaucomatous optic neuropathy treatment dvt purchase avodart 0.5mg otc, neural atrophy results in more extensive exposure of the underlying lamina cribrosa and may reveal more laminar pores or striations in the optic nerve cup medicine 911 generic avodart 0.5 mg. Nasalization of the central retinal artery and central retinal vein is often seen as the cup enlarges. Although nerve fiber layer hemorrhages usually appear as a linear red streak on or near the disc surface (Fig 3-16), their appearance is highly variable. One-third of glaucoma patients at some time during the course of their disease may develop hemorrhages, which typically clear over several weeks to months. Some glaucoma patients have repeated episodes of optic disc hemorrhage; others have none. Optic nerve head hemorrhage is an important prognostic sign for the development or progression of visual field loss, and any patient with a disc hemorrhage requires detailed evaluation and follow-up. Disc hemorrhages may also be caused by posterior vitreous detachments, diabetes mellitus, branch retinal vein occlusions, and anticoagulation therapy. Axons in the nerve fiber layer of the normal eye may best be visualized with red-free illumination. As the nerve fibers extend from the peripheral retina to converge at the optic nerve head, they appear as fine striations created by the bundles of axons. In the healthy eye, the brightness and striations of the nerve fiber layer are more easily visible superiorly and inferiorly. With progressive glaucomatous optic neuropathy, the nerve fiber layer thins and becomes less visible. Early wedge-shaped defects are sometimes visible only at a distance from the optic disc margin. Diffuse nerve fiber loss is more common in glaucoma than is focal loss but also more difficult to observe. The nerve fiber layer can be visualized clearly i n high-contrast black-and-white photographs, and experienced observers can recognize even early disease if good-quality photographs are available. The combination of red-free filter, wide slit beam, and posterior pole lens at the slit lamp affords the best view. Alpha zone is present in most normal eyes as well as in eyes with glaucoma Figure 3-15 Optic nerve head photograph showing vertical elongation of the cup with localized thinning of the inferior and superior neuroretinal rim in the left eye of a patient with moderately advanced glaucoma. Beta zone is more common and extensive in eyes with glaucoma than in healthy eyes. Other, less specific, signs of glaucomatous damage include nasal displacement of the vessels, narrowing of Figure 3-17 Nerve fiber layer photograph shows a nerve fiber bundle defect peripapillary retinal vessels, and baring of the (arrowheads). It is important to recognize that glaucomatous optic nerve damage is only one type of pathologic change of the optic nerve; other etiologies of optic nerve changes should be considered in the differential diagnosis. Certain conditions may cause apparent cupping of the optic nerve that can be confounded with glaucoma, such as congenital pits of the optic nerve head, coloboma, morning glory syndrome, arteritic ischemic neuropathy or compressive optic neuropathies. With rare exceptions, glaucoma results in increased cupping and pallor within the cup, but not pallor of the remaining rim tissue. The ophthalmologist must also consider drusen or coloboma as possible causes of optic nerve change and visual field loss. Finally, the myopic optic disc represents a challenge when the ophthalmologist is attempting to assess possible glaucomatous damage. The size, tilting, and associated structural changes often preclude the ability to definitively determine the presence of glaucomatous damage. Recording of optic nerve findings Due to the large variability in the appearance of the optic nerve head in healthy subjects, it is frequently not possible to confirm the presence of glaucomatous damage based on a single crosssectional observation. Therefore, glaucoma diagnosis frequently requires longitudinal monitoring and detection of progressive damage over time. Careful documentation is essential in order to allow adequate comparison of the optic nerve head appearance over time, both for diagnosis of the disease in individuals suspected of having glaucoma, and for detection of progression in those with established disease. It is common practice to grade an optic nerve head by comparing the diameter of the cup with the diameter of the disc. The diagram must be of adequate size to allow depiction of important topographic landmarks and morphologic features. However, even very well-detailed descriptions or drawings of the optic nerve head are generally insufficient to detect the subtle changes that may occur as the result of glaucomatous progression over time. Therefore, objective documentation of the appearance of the optic nerve head by photographs or imaging should be obtained whenever possible. Photography, particularly simultaneous stereophotography, is an excellent method for recording the appearance of the optic nerve for detailed examination and sequential follow-up. This record allows the examiner to compare the present status of the patient with the baseline status without resorting to memory or grading systems. If stereoscopic photographs are not available, even simple monoscopic photographs are preferable to drawings in documenting the appearance of the optic nerve head. However, evaluation of optic nerve head photographs is subjective and does not provide direct quantitative information about the degree of neural loss or rates of disease progression. Imaging of the optic nerve head and retinal nerve fiber layer Since the 1850s, the appearance of the optic nerve head has been recognized as critical in assessing the disease status of glaucoma. However, assessment of the optic nerve head at the slit-lamp or through photographs is subjective and shows relatively large interobserver and intraobserver variation. Imaging devices provide an objective means to obtain reproducible and highresolution images of ocular structures relevant to glaucoma. In addition, imaging devices contain normative databases that allow one to determine the probability that observed measurements are within the normal range, assisting in the differentiation of optic nerve damage from normal variation.
Intralesional corticosteroid injection in patients with dark skin may lead to depigmentation of the overlying eyelid skin and thus should be used with caution symptoms lupus buy 0.5 mg avodart amex. Internal chalazia require vertical incisions through the tarsal conjunctiva along the meibomian gland to facilitate drainage and avoid horizontal scarring of the tarsal plates symptoms after embryo transfer avodart 0.5mg without prescription. See also BCSC Section 7 medicine rocks state park avodart 0.5mg on line, Orbit medications with weight loss side effect buy 0.5mg avodart free shipping, Eyelids, and Lacrimal System, for further discussion of chalazion. Structural and Exogenous Disorders Associated With Ocular Surface Disorders Exposure Keratopathy Exposure keratopathy can result from any disease process that limits eyelid closure. Exposure keratopathy is characterized by a punctate epithelial keratopathy that usually involves the inferior one-third of the cornea; however, the entire corneal surface can be involved in severe cases. Large, coalescent epithelial defects may result, which may lead to ulceration, melting, and perforation. Symptoms are similar to those associated with dry eye, including foreign-body sensation, photophobia, and tearing, unless an associated neurotrophic component results in corneal anesthesia. In the earliest stages, nonpreserved artificial tears during the day and ointment at bedtime may suffice. Taping the eyelid shut at bedtime can help if the problem is primarily one of nocturnal exposure. The use of bandage contact lenses can be hazardous in patients with exposure keratopathy because of a high incidence of desiccation and infection. For cases in which the problem is likely to be temporary or self-limited, temporary tarsorrhaphy using tissue adhesive or sutures should be performed. However, if the problem is likely to be long-standing, definitive surgical therapy to correct the eyelid position is mandatory. Correction of any associated eyelid abnormalities, such as ectropion and/or trichiasis, is also indicated. Most commonly, surgical management consists of permanent lateral and/or medial tarsorrhaphy. Insertion of gold or platinum weights into the upper eyelid is also an effective, more cosmetic approach to promote eyelid closure. Reported complications of gold weight implants include infection, shifting, extrusion, induced astigmatism, unacceptable ptosis, and noninfectious inflammatory response to the gold. In cases of paralytic ectropion of the lower eyelid, a horizontal tightening procedure may also be beneficial in correcting the flaccid lower eyelid. See BCSC Section 7, Orbit, Eyelids, and Lacrimal System, for further discussion of thyroid eye disease, lagophthalmos, and proptosis. Patients have a flimsy, lax upper tarsus that everts with minimal upward force applied to the upper eyelid. Clinical findings include small to large papillae on the upper palpebral conjunctiva, mucus discharge, and corneal involvement ranging from mild punctate epitheliopathy to superficial vascularization (Fig 3-21). The problem may result from spontaneous eversion of the upper eyelid when it comes into contact with the pillow or other bed linens during sleep. Direct contact of the upper eyelid with bed linens may traumatize the upper tarsal conjunctiva, inducing inflammation and chronic irritation. The condition may be unilateral if the patient always sleeps in the same position. Treatment consists of covering the affected eyes with a metal shield, taping the eyelids closed at night, or performing surgical eyelid-tightening procedures. Differential diagnosis includes vernal conjunctivitis, giant papillary conjunctivitis, atopic keratoconjunctivitis, bacterial conjunctivitis, and toxic keratopathy. Superior Limbic Keratoconjunctivitis the pathogenesis of superior limbic keratoconjunctivitis (SLK) has not been established, but it is thought to result from mechanical trauma transmitted from the upper eyelid to the superior bulbar and tarsal conjunctiva. It is often bilateral; however, 1 eye may be more severely affected than the other. Patients with SLK should undergo thyroid function tests, including tests for free thyroxine (T4), thyroid-stimulating hormone (TSH), and thyroid antibody levels. Treatments include topical anti-inflammatory agents, large-diameter bandage contact lenses, superior punctal occlusion, thermocauterization of the superior bulbar conjunctiva, resection of the bulbar conjunctiva superior to the limbus, topical cyclosporine, autologous serum eyedrops, amniotic membrane transplant, and conjunctival fixation sutures. Topical cyclosporine A in the treatment of superior limbic keratoconjunctivitis: a long-term followup. Treatment of superior limbic keratoconjunctivitis by thermocauterization of the superior bulbar conjunctiva. Conjunctival fixation sutures for refractory superior limbic keratoconjunctivitis. Recurrent Corneal Erosion Recurrent erosions typically occur either in eyes that have suffered a sudden, sharp, abrading injury (eg, fingernail, paper cut, tree branch) or in patients with preexisting epithelial basement membrane dystrophy. The superficial injury produces an epithelial abrasion that heals rapidly, frequently leaving no clinical evidence of damage. After an interval ranging from days to years, symptoms suddenly recur without any obvious precipitating event. In contrast to shearing injuries, small, superficial lacerating injuries involving the cornea rarely result in recurrent erosions. Poor adhesion of the epithelium is thought to be caused by underlying abnormalities in the epithelial basement membrane and its associated filament network. Gelatinase activity (MMP-2 and MMP-9) is upregulated in the epithelium of patients with recurrent corneal erosions. Chronic activation of MMPs may either result from or cause poor epithelial adherence, which leads to the symptoms of recurrent corneal erosion. Some patients with recurrent corneal erosions have been noted to have MGD, and increased levels of MMPs have been observed in the tear film of patients with MGD.
Electron microscopy reveals that the deposits are composed of randomly oriented Figure 13-4 Verruca vulgaris medicine 2000 buy avodart us. A treatment 2 lung cancer buy avodart 0.5mg cheap, Verruca vulgaris is a form of infection of the eyelid with human papillomavirus (HPV) medications such as seasonale are designed to buy generic avodart 0.5mg online. B medicine 7253 avodart 0.5mg, Occasional koilocytes with nuclear contraction and cytoplasmic clearing are present (arrow). Amyloid deposits within the skin of the eyelid are highly indicative of a systemic disease process, either primary or secondary, whereas deposits elsewhere in the ocular adnexa are more likely to represent a localized disease process. Cysts Epidermoid Cysts Epidermoid cysts, also known as epidermal inclusion cysts, are common in the eyelids. They may arise spontaneously or as a result of the entrapment of epidermis beneath the skin surface following surgery or trauma. Epidermoid cysts are lined with keratinized stratified squamous epithelium and contain keratin (Fig 13-10). Ductal Cysts the eyelid contains the ducts of numerous structures, including the lacrimal gland and the apocrine and eccrine sweat glands. Ducts are typically lined with a double layer of cuboidal epithelium, as are ductal cysts. Cysts arising from sweat ducts are referred to as either apocrine or eccrine hidrocystomas (Fig 13-11). B, In the more central cells, the nuclei are displaced peripherally by large eosinophilic viral inclusions known as molluscum bodies (arrows). The molluscum bodies become more basophilic near the surface of the epithelium (arrowheads). Clinically, it is a well-circumscribed, oval, dome-shaped to verrucoid "stuck-on" papule, varying from pink to dark brown in color. Histologically, although several architectural patterns are possible, all of them demonstrate hyperkeratosis, acanthosis, and some degree of papillomatosis. The acanthosis is a result of the proliferation of either polygonal or basaloid squamous cells without dysplasia. Pseudohorn cysts, which are concentrically laminated collections of surface keratin within the acanthotic epithelium, are a characteristic finding in most types of seborrheic keratosis (Fig 13-12). Irritated seborrheic keratosis, also termed inverted follicular keratosis, shows nonkeratinized squamous epithelial whorling, or squamous "eddies," instead of pseudohorn cysts (Fig 13-13). Granulomatous inflammation consisting of epithelioid histiocytes and multinucleated giant cells (arrows) surrounds clear spaces (lipogranuloma). Because the lipid is dissolved by solvents during routine tissue processing, optically clear ("lipid dropout") spaces remain. Strong evidence supports the idea that keratoacanthomas are a variant of a well-differentiated squamous cell carcinoma. These dome-shaped nodules, which have keratin-filled central craters, may attain a considerable size, up to 2. The natural history is typically spontaneous involution over several months, resulting in a slightly depressed scar. Histologically, keratoacanthomas show a cup-shaped Figure 13-9 Cutaneous amyloid in a patient with multiple myeloma. At the deep aspect of the proliferating nodules, mitotic activity and nuclear atypia may occur, making it difficult to differentiate between keratoacanthoma and squamous cell carcinoma. Many dermatopathologists and ophthalmic pathologists prefer to call this lesion well-differentiated squamous cell carcinoma because of the possibility of perineural invasion and metastasis. Actinic keratosis Actinic keratoses are precancerous squamous lesions that appear, clinically in middle age, as erythematous, scaly macules or papules on sun-exposed skin, particularly on the face and the dorsal surfaces of the hands. Hyperkeratotic types of these lesions may form a cutaneous horn, and hyperpigmented types may clinically simulate lentigo maligna. However, when squamous cell carcinoma arises in actinic keratosis, the risk of subsequent metastatic dissemination is very low (0. All types demonstrate changes in the epidermis with hyperkeratosis and parakeratosis. Cellular atypia (nuclear hyperchromasia and pleomorphism and an increased nuclear-tocytoplasmic ratio) is present and ranges from mild (involving only the basal epithelial layers) to frank carcinoma in situ (full-thickness involvement of the epidermis). Dyskeratosis (premature individual cell keratinization) and mitotic figures above the basal epithelial layer are often found (Fig 13-15). The underlying dermis shows solar elastosis (elastotic degeneration of collagen) (Fig 13-16), which manifests as fragmentation, clumping, and loss of eosinophilia of dermal collagen. A chronic inflammatory cell infiltrate Figure 13-10 Epidermal inclusion cyst in the dermis. Histologic examination of the base of the lesion is necessary to determine whether stromal invasion indicative of squamous cell carcinoma is present. Carcinoma Basal cell carcinoma Basal cell carcinoma (BCC), the most common malignant neoplasm of the eyelids, accounts for more than 90% of all malignant eyelid tumors. Although exposure to sunlight is the main risk factor, genetic factors can play a role in familial syndromes. The lower eyelid is more commonly involved than the upper eyelid, with the medial canthus being the second most common site of involvement.
Pingueculae represent an elastotic degeneration (the material stains for elastin but is not broken down by elastase) of subepithelial collagen with hyalinized connective tissue medicine over the counter purchase discount avodart line. Excision is indicated only when pingueculae are cosmetically unacceptable or when they become chronically inflamed or interfere with successful contact lens wear symptoms 6 days post embryo transfer buy 0.5 mg avodart free shipping. Judicious use of topical corticosteroids may be considered in patients with inflammation symptoms of colon cancer purchase generic avodart line, but their use as a long-term therapy for pingueculae is strongly discouraged due to their adverse effects treatment 12mm kidney stone avodart 0.5 mg amex. Pterygium A pterygium is a wing-shaped growth of conjunctiva and fibrovascular tissue on the superficial cornea (Fig 12-2). As with a pinguecula, the pathogenesis of a pterygium is strongly correlated with UV-light exposure, although environmental traumas such as exposure to dust, wind, or other irritants that cause chronic inflammation may also be factors. The predominance of pterygia on the nasal side in the interpalpebral zone is theorized to result from light passing medially through the cornea, focusing on the nasal limbus area, while the shadow of the nose reduces Figure 12-1 A pinguecula, seen, as is typical, the intensity of light transmitted to the temporal limbus. The histopathology of pterygia is similar to that of pingueculae, only it involves subepithelial fibrovascular tissue. Further discussion of the histopathology of both pingueculae and pterygia can be found in BCSC Section 4, Ophthalmic Pathology and Intraocular Tumors. Pterygia are nearly always preceded by pingueculae, although why some patients develop pterygia whereas others have only pingueculae is not known. Regular and irregular astigmatism, as well as corneal scarring, occurs in proportion to pterygium size. A pigmented iron line (called a Stocker line) may be seen at the central anterior edge of the pterygium on the cornea. A pterygium must be differentiated from a pseudopterygium, which may occur after trauma or secondary to inflammatory corneal disease. Treatment with artificial tears can alleviate associated irritation, but as with pingueculae, long-term use of topical corticosteroids is contraindicated. Excision is indicated Figure 12-2 A pterygium: a wing-shaped if the pterygium approaches the visual axis, exhibits growth of conjunctiva and fibrovascular tissue on the superficial cornea. Conjunctival Concretions Concretions are small, yellow-white dots found in the palpebral conjunctiva of older patients or patients who have had chronic conjunctivitis. Concretions appear to be epithelial inclusion cysts filled with epithelial and keratin debris, as well as mucopolysaccharide and mucin. Concretions are almost always asymptomatic but may erode the overlying epithelium, causing foreign-body sensation. Conjunctival Inclusion Cysts Inclusion cysts of the conjunctival epithelium are typically asymptomatic and are often an incidental finding during routine ophthalmic examination. Most acquired cysts are derived from an inclusion of conjunctival epithelium into the substantia propria. The implanted cells proliferate to form a central fluid-filled cavity that is lined by nonkeratinized conjunctival epithelium. Conjunctival cysts may also form from ductal epithelium of the accessory lacrimal glands; these cysts are lined by a double layer of epithelium. Conjunctival inclusion cysts typically appear clear and can occur in either the bulbar conjunctiva or the conjunctival fornix (Fig 12-3). A corneal epithelial inclusion cyst is rare, but it can occur if trauma, surgery, or chronic inflammation results in conjunctival overgrowth onto the surface of the cornea. Epithelial inclusion cysts are most commonly asymptomatic and therefore may be simply observed. Cysts usually re-form after simple drainage because the inner epithelial cell wall remains. Conjunctivochalasis Conjunctivochalasis is poor adherence of the bulbar conjunctiva. It occurs commonly with chronic inflammation or aging and is often overlooked and asymptomatic. Occasionally, the redundant conjunctiva Figure 12-3 Large conjunctival epithelial overhangs the lower eyelid margin to such an extent that inclusion cyst. These range from the aggravation of dry eye in the mild stages (from exposure of the redundant conjunctiva due to uneven wetting), to secondary tearing due to occlusion of the lower punctum when the chalasis is prominent medially, to exposure-related pain and irritation in its severe stages. The etiology of conjunctivochalasis remains unknown, but increased tear inflammation seems to accompany loss of conjunctival epithelial cohesiveness and increased collagenolytic activity, which may explain the conjunctival laxity. Histologic studies have also revealed elastosis and chronic nongranulomatous inflammation, in addition to collagenolysis, in conjunctivochalasis. Lubricants, anti-inflammatory agents, antihistamines, and nocturnal patching have been suggested as treatments, although none besides lubrication is a potential long-term solution. If these modalities fail, then surgical excision, conjunctival fixation to the sclera, amniotic membrane grafting, or cauterization of the redundant folds may be required. See Chapter 14 for discussion of surgical procedures used for conjunctivochalasis. Conjunctival Vascular Tortuosity and Hyperemia Conjunctival vascular tortuosity and hyperemia can result from many causes. Age-Related (Involutional) Changes As a result of aging, the cornea gradually becomes flatter in the vertical meridian, thinner, and slightly less transparent. Its refractive index increases, and Descemet membrane becomes thicker, increasing from 3 m at birth to 10 m in adults. Occasional peripheral endothelial guttae, sometimes known as Hassall-Henle bodies, can form with age (see the discussion later in the chapter). The average rate of decrease in endothelial cell density throughout adult life is approximately 0. Epithelial and Subepithelial Degenerations Coats white ring A small (1 mm or less in diameter) circle or oval-shaped area of discrete gray-white dots is sometimes seen in the superficial stroma. Referred to as Coats white ring, it represents iron- containing fibrotic remnants of a metallic foreign body.
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