Cornea Corneal edema

Acute angle closure and difficulty with accommodation can occur from the anticholinergic effects of antipsychotic agents. In addition, pigment deposits may develop in the cornea and lens. Pigmentary retinopathy has been reported with thioridazine. Keratopathy and corneal edema may occur occasionally during pharmacotherapy with chlorpromazine and fluphenazine... 

Acute injuries of the eyes, primarily from effects of blast and missiles, may occur from tear-gas weapons, such as pen guns. The lnmeulate effects of these Injuries include swelling and edema of the lids, with penetration of skin, conjunctiva, cornea, sclera, or globe by gunpowder and CN conjunctival ischemia and chemosls corneal edema, erosion, Inflammation, or ulceration and focal hemorrhage. 13,20... 

There is a parallel to draw between the Thill and assistant study and the study by Kubota and Fagerlhom [15] who have demonstrated that the importance of the initial corneal edema, resulting from a bum, is correlated to the importance of the sequelar cicatricial leukoma that causes the drop of vision. The stromal lacunae, fonned by the edema, will be colonized by the keratocytes. After the resorption of the edema and at the level of these lacunae, the keratocytes form a zone of cicatricial tissue, which is the origin of the leukoma. These keratocytes also produce an unorganized network of collagen fibrillae, thus causing the drop of transparency of the cornea. 

A variety of clinical situations can give rise to corneal edema (Box 15-1). Because the endothelium is the main structure involved in maintaining normal corneal deturges-cence, it plays a role in stromal hydration and compensates for the driving force of intraocular pressure. Also, the active transport system involved in the movement of water and electrolytes from the cornea to the aqueous humor must be maintained to prevent fluid retention. Endothelial feilure, a frequent cause of corneal edema, can occur due to defects in the transport system or stromal compression resulting from elevation of intraocular pressure, which can induce water movement toward the epithelium. 

Despite their apparent efficacy, the usefulness of sodium chloride solutions in the treatment of edematous corneas with a traumatized epithelium appears to be limited. The intact corneal epithelium exhibits limited permeability to inorganic ions. In the absence of an intact epithelium the cornea imbibes salt solutions, which reduces the osmotic effect. In the management of corneal edema associated with traumatized epithelium, hypertonic saline solutions may be of limited value due to their increased ability to penetrate the epithelial barrier. 

External examination reveals erythema and swelling of the affected skin areas. Slit-lamp examination reveals diffuse conjunctival injection and pimctate epithelial erosions of the cornea with corresponding NaFl staining. If the epithelial lesions are extensive and if lacrimation is profuse, corneal edema also may be noted. 

Deep corneal edema with folds in Descemet s membrane, in the presence of an intact epithelium, can develop from 3 to 4 months after acute HZO. This disciform keratitis may involve the full thickness of the cornea and may be surrounded by a ring-like cellular infiltrate called a Wessley ring. It is considered to be an immune response to viral antigens and responds quickly to topical steroids, especially when initiated early. Unfortunately, it is common to have recurrences when steroids are tapered or discontinued and can lead to corneal scarring or, more seriously, corneal melt.There is often an associated anterior uveitis with keratic precipitates as well as diffuse corneal edema, endothelial cell loss, and increased lOP secondary to trabeculitis. 

Contact lenses can produce changes in corneal shape and/or corneal thickness substantive enough to cause lOP measurement error. This may be particularly true of patients who are prescribed orthokeratology for the management of refractive error. In addition, there is evidence that many soft lens wearers may develop corneal edema during the day. Low levels of contact lens-related edema (<5%) may produce a stiffening of the corneal tissue with a corresponding measured increase in lOP When edema levels increase beyond 6% to 10% (which is less common in contact lens wear), the cornea becomes substantially softer with subsequent lower measured lOP... 

The cornea is the clear, external layer of the eye over the visual axis. The most common toxicologic disorder of the cornea results from irritant or caustic injury and results in edema (swelling) or erosion of the surface cells (abrasion). Patients with only mild corneal edema or erosion may experience halos around bright objects and pain. This typically heals rapidly... 

In the conjunctiva and cornea, sulfur mustard exposure causes loosening of epithelial cells accompanied by corneal edema and opacification (Warthin Weller, 1919). Even low-dose exposure of sulfur mustard to the eyes can be incapacitating (ocular ICt5o = 50 to 100 mg-min/m3). Only limited studies of sulfur mustard-induced eye injuries in animals are available (Kadar et al., 1996 Maumenee Scholz, 1948 Warthin Weller, 1919). These suggest that the microscopic pathology is similar to most chemical injuries with the exception of acid and alkali bums. 

The biocompatibility of poly(CPP), poly(TA), and copolymers of CPP SA and CPP TA implanted in the corneas of rabbits was studied. Six weeks after implantation, the cornea remained clear and showed no evidence of corneal edema or neovascularization, indicating biocompatibility of the polymer matrix implant. 

Corneal edema is a clinical sign of corneal endothelial dysfunction, and topical osmotic agents may effectively dehydrate the cornea. Identifying the cause of corneal... 

French DD, Margo CE. Postmarketing surveillance of corneal edema, Fuchs dystrophy, and amantadine use in the Veterans Health Administration. Cornea 2007 26 1087-9. 

Case reports Three patients who took amantadine developed diffuse corneal edema [272 ]. In two cases the symptoms started within a few weeks and in the third case after 6 years. In the first two cases withdrawal of amantadine resulted in resolution of the corneal edema. However, the other patient received a full-thickness corneal transplant while still taking amantadine, and edema developed in the grafted cornea withdrawal of amantadine then resulted in resolution of the comeal edema in both eyes, but the ungrafted comeal eventually also became edematous, requiring transplantation. Histopathology showed significant loss of endothelial cells. As in the last of these cases, another report documented comeal edema in a corneal transplant until amantadine withdrawn [273" ]. 

Blanchard DL. Amantadine caused corneal edema. Cornea 1990 9(2) 181. 

Hughes B, Feiz V, Flynn SB, Brodsky MC. Reversible amantadine-induced corneal edema in an adolescent. Cornea 2004 23 (8) 823-4. 

At such a step and every 48 h, there must be a thorough clinical examination of the corneal edema, because it is certainly a cause of the noncicatrization of the cornea. A good illustration of this phenomenon is the image of a roof collapsing because it is supported by a too weak structure. The epithelial... 

Administered to mice, 49,000 ppm for 51 minutes resulted in narcosis, muscular hypotonia, disappearance of corneal reflexes, then coma followed by death. The LC50 was estimated to be 21,000 ppm in rats exposed for 3 hours. Repeated exposure of rats to concentrations ranging from 100 to 5000 ppm for 12 weeks caused a dose-related increase in irritation of the mucous membranes. At the 5000 ppm level there was marked edema or opacity of the cornea, salivation, and discharge or bleeding in the nasal mucosa. 

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