Corneal edema causes

Levenson JE. Corneal edema cause and treatment. Surv Ophthalmol 1975 20 190-204. 

Causes severe eye irritation that can progress to severe corneal edema. Temporary blindness has been reported. Causes skin irritation, nausea, headache, and vomiting. Inhalation is irritating to the mucous membrane and upper respiratory tract. May cause sensitization by skin contact. 

Causes irritation to skin, eyes, and respiratory system, CNS stimulation, skin irritation, sensitization. Causes severe eye and skin burns. May cause severe tearing, conjunctivitis, and corneal edema. Inhalation may cause difficulties ranging from coughing and nausea to accumulation of fluid in the lungs (pulmonary edema). 

Toxicology. AT-ethylmorpholine is an irritant of the eyes and mucous membranes prolonged exposure to low concentrations causes corneal edema. 

In an experimental study, humans exposed to 100ppm for 2.5 minutes experienced irritation of eyes, nose, and throat, whereas 50 ppm produced lesser irritation. Distortion of vision can occur at levels much lower than those that cause irritation. Workers exposed to low vapor concentrations (3-11 ppm) for several hours reported temporary fogged vision with rings around lights. Corneal edema has been observed in workers when air concentrations of substituted morpholines exceed 40 ppm. The symptoms usually appear at the end of the workday and clear within 3-4 hours after cessation of exposure. ... 

Human subjects experienced irritation of the nose and throat after brief exposure to 10-20ppm. Workers complained of transient visual disturbances (haloes around lights) after exposure to the vapor for 8 hours, probably due to mild corneal edema, which usually cleared within 3 hours. The liquid is also capable of causing severe eye burns that may cause permanent visual impairment. Isopropylamine in both liquid and vapor forms is irritating to the skin and may cause skin burns repeated lesser exposures may result in dermatitis. ... 

In industrial use, some instances of skin and respiratory tract irritation have been observed but no chronic effects have been reported. A human exposure to 12,000 ppm for 1.5 minutes in a laboratory produced nose irritation and cough mouth pipetting of the liquid caused a severe sore throat and reddened mucous membranes. Workers exposed for several hours to low vapor concentrations complained of foggy vision with rings around lights, the results of corneal edema, which cleared within 3-4 hours after cessation of exposure. ... 

Tests of single drops of aqueous solutions applied to the eyes of animals have shown that 1% solution causes severe irritation, 5% causes hemorrhagic conjunctivitis, and 16% causes severe reaction with conjunctival hemorrhages, corneal edema, and opacities, followed by some clearing but much vascularization. ... 

In a second experiment, Ayers and Stahl studied the effects of discharging a CS pen-gun cartridge into a rabbit eye at a distance of 20 cm. At that distance, the wad caused less damage than the blast and the particles of CS. Only three of 10 animals suffered severe eye lesions, which appeared to combine mechanical damage (lacerations) from the wad and conjunctivitis, intraocular hemorrhage, keratitis, and corneal edema probably from the blast and CS particles driven into the eye. The other animals showed only mild conjunctivitis, which cleared after 3 d. 

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. 

Topically applied anesthetics may cause corneal endothelial toxicity when used after perforating ocular trauma or when used topically for cataract extraction. When injected inttacametally, benzalkonium chloride, the primary preservative used in topical ocular anesthetics, can cause irreversible corneal edema in rabbits. 

Osmotherapy was introduced to ocular therapeutics in 1904 with the use of oral hypertonic saline to reduce elevated intraocular pressure.Topical ocular use of hyperosmotic agents has been proven clinically useful in the treatment of corneal edema, particularly when the cause is endothelial dysfunction. 

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. 

Adapted from Boruchoff SA. Clinical causes of corneal edema. Int Ophthalmol Clin 1968 8 581 -600. 

If there is a treatable cause, its management is necessary for resolution of the edema. If, however, the corneal edema appears to be due to changes in endothelial function, hyperosmotic therapy with 5% sodium chloride solution four to eight times a day and 5% sodium chloride ointment in the conjunctival sac at bedtime is the most appropriate treatment.Treatment with hypertonic agents... 

Patients with bullous keratopathy should have their lOP measured (even though corneal edema results in underestimated lOP) because angle-closure glaucoma can cause similar corneal edema. In addition, patients with Fuchs dystrophy have an increased risk of developing open-angle glaucoma in addition to the bullous keratopathy. Topical carbonic anhydrase inhibitors should be avoided in these patients because of the potential of worsening the corneal decompensation. 

Slit-lamp examination typically reveals moderate to severe edema and inflammation of the lid and conjunctiva, a purulent discharge, and ulceration of the corneal epithelium (Figure 26-43). As previously described, these ulcerations can take on many appearances, usually accompanied by surrounding corneal edema and stromal infiltration beneath the ulcer. A mild to severe anterior chamber reaction, which can cause hypopyon, cataracts. 

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... 

Dorzolamide eye-drops can cause irreversible corneal edema in glaucoma patients with endothelial compromise (25). 

The eye is the most sensitive tissue to sulfur mustard effects. Sulfur mustard vapor or liquid may cause intense conjunctival and scleral pain, swelling, lacrimation, blepharospasm, and photophobia however, these effects do not appear for an hour or more. Miosis due to cholinergic effects may occur. High concentrations of vapor or liquid can cause corneal edema, perforation, blindness, and later scarring. 

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. 

CN is a potent irritant and is more likely to cause serious eye effects than CS. The ocular irritation caused by CN signals avoidance and the intense lacrimation and blepharospasm initiates a defense mechanism. High concentrations of CN may result in chemical injury to the eye with corneal and conjunctival edema, corneal edema, erosion or ulceration, chemosis, and focal hemorrhages. CN-induced ocular effects on the rabbit eye following treatment with various CN formulations has been investigated by Ballantyne et al. and Gaskins et al." Ocular effects included lacrimation, chemosis, iritis, blepharitis, and keratitis severity was dependent on the formulation. 

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

ACUTE HEALTH RISKS irritation to eyes, nose, and throat olfactory fatigue corneal edema distortion of vision blue-gray vision optical halos drowsiness cough labored breathing shortness of breath abdominal pain vomiting diarrhea may cause severe sore throat and redness of mucous membranes exposure to high concentration may result in death. 

Morpholine (lelrahydro-I.A-oxazine [CAS 110-91-8)) Corrosive extremely Irritating upon direct contact severe burns may result. Well absorbed dermally. Vapors irritating to eyes and respiratory tract. Exposure to vapors has caused transient corneal edema. May cause severe liver and kidney Injury. 

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