Corneal blindness

Herpes simplex keratitis (HSK) is caused by HSV type 1 in adults and is one of the most common infectious etiologies of blindness. It is second only to trauma as a cause of corneal blindness in the United States, where an estimated 50,000 new or recurrent cases are seen each year. Recurrent HSK can be reactivated by many factors in addition to those listed above. Reactivation has been reported in patients after penetrating keratoplasty, argon laser trabeculoplasty, Nd YAG laser peripheral iridotomy, or treatment with excimer lasers, including cases in which ocular herpes had not occurred previously. It is important to realize that because most patients have latent HSV it is possible for a reactivation to occur despite a negative history of a primary infection. 

Whitcher JP, Srinivasan M, Upadhyay MP. Corneal blindness a global perspective. Bull World Health Organ 2001 79 214-21. 

In humans, vitamin A deficiency manifests itself in the following ways night blindness, xerophthalmia, Bitot s spots, and corneal involvement and ulceration. Changes in the skin have also been observed. Although vitamin A deficiency is seen in adults, the condition is particularly harmful in the very young. Often, this results from malnutrition (56). 

Another widespread application of cold storage of tissue for transplantation is that of preservation of the cornea. Inj uries leading to corneal scarring, various kinds of diseases, and the production of comeal opacity are leading causes of blindness. Cornea transplantation is a commonly used and highly successful procedure. It... 

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. 

Eyes are especially susceptible to vesicants. In addition to the immediate corrosive effects, the cornea of the eye can become inflamed (keratitis) after a latency of 6-10 years. This condition can progress to blindness. Corneal lesions may reoccur even after receiving a corneal transplantation. 

Urticant vapors are violently irritating to the eyes, nose, and respiratory tract and cause immediate pain. Very low concentrations can cause inflammation, lacrimation, and temporary blindness higher concentrations can cause corneal corrosion and dimming of vision. Inhalation causes runny nose, hoarseness, and sinus pain. 

Eyes Severe damage. Instant pain, conjunctivitis and blepharospasm leading to closure of eyelids, followed by corneal scarring and iritis. Mild exposure produces reversible eye damage if decontaminated instantly. More permanent injury or blindness is possible within one minute of exposure. 

Deficienqr of vitamin A results in night blindness (rod cells are responsible for vision in low light), metaplasia of the corneal epithelium, dry eyes, bronchitis, pneumonia, and follicular hyperkeratosis. 

Other reported effects of exposure to carbon disulfide are ocular changes (blind spot enlargement, contraction of peripheral field, corneal anesthesia, diminished pupillary reflexes, nystagmus, and microscopic... 

Ophthalmologic effects Optic neuropathy or neuritis may occur at any time following initiation of therapy, in some cases, visual impairment has progressed to permanent blindness. Corneal microdeposits appear in virtually all adults treated with amiodarone. They give rise to symptoms such as visual halos or blurred vision in as many as 10% of patients. Corneal microdeposits are reversible upon reduction of dose or drug discontinuation. Asymptomatic microdeposits are not a reason to reduce dose or stop treatment. Some patients develop photophobia and dry eyes. Vision is rarely affected and drug discontinuation is rarely needed. 

Vitamin A deficiency can result from insufficient dietary intake, from malabsorption and it has been recognized that also malfunction of RAR-receptors can lead to symptoms of vitamin A deficiency. These symptoms include skin lesions, night blindness, corneal ulcerations and conjunctivitis and poor bone remodeling. Vitamin A deficiency associated with malnutrition is wide spread in large parts of the world and may be fatal in infants and young children suffering from kwashiorkor or marasmus. 

The duration of treatment for skin diseases is often longer than it is for malaria, and therefore, dose-related toxicities are important. The most serious toxicities are ophthalmological. Reversible alterations include ciliary body dysfunction and corneal changes with edema and deposits. Irreversible retinopathy also occurs however, it is less common with quinacrine than with the other two drugs. Toxicity may be asymptomatic, but the earliest symptoms are night blindness, scotoma, or tunnel vision. 

L B. Supplement with vitamin A. Vitamin A deficiency symptoms include night blindness that can lead to corneal ulceration. This deficiency can occur in patients with impaired liver storage or fat malabsorption. Dairy products, such as milk, are a good source of vitamin A. (3-Carotene, a vitamin A precursor, is found in pigmented vegetables, such as carrots. When a deficiency is diagnosed, it is appropriate to treat the patient with a supplement rather than to rely on increased consumption of vitamin A-rich foods. A patient with pancreatic disease and malabsorption syndrome will need parenteral supplementation. 

Its garlicky odor, faint at first, Is soon imperceptible. Exposure to H does not cause Immediate discomfort rather, the onset of effects Is delayed and insidious. Troops have been known to remain In contaminated areas until their eyes, skin, and respiratory organs were affected. Exposure of skin produces erythema, then blisters that are painful and slow to heal. Such eye Injuries as conjunctivitis, keratitis, and corneal ulcers cause temporary or permanent blindness. The respiratory effects of H Include rhinitis, laryngitis, bronchitis, and, In severe cases, destruction of mucous membranes. The bone marrow and digestive system are affected by systemic administration of H. The multiple effects of this Insidious agent make It among the most potent used on the battlefield. 

The acute pathologic effects of H on the eye include edematous clouding of the cornea and necrosis of corneal stroma. About 5 h later, infiltration by segmented leukocytes is noted at the sclero-comeal junction and in the corneal stroma. Healing usually occurs in several weeks, but the Injury may result in persistent or recurrent corneal ulceration and blindness. 

Of the long-term complications of wartime exposure to mustard gas, perhaps the best documented and one of the most serious is recurring corneal ulcers, with eventual opacification and blindness. No exact figures are available for predicting the eventual development of such long-term corneal lesions, but it has been reported that a Ct of 100 mg min/m will cause acute blindness for 24-48 h.20 Permanent blindness typically occurred about 14 yr... 

Night blindness (inability to see in dim light), conjunctival xerosis (dry and non-wettable conjunctiva), corneal xerosis (dry and non-wettable cornea and become opaque), keratomalacia (cornea becomes soft and burst open and vision is lost), Bitot s spots, growth retardation, dry and rough skin, sterility due to faulty spermatogenesis. 

Inorganic acids have similar acute toxic properties corrosive action on the skin, the respiratory tract, and especially the eyes where corneal damage may occur. Severe exposures may cause blindness, pulmonary edema, and even death. The onset of symptoms may be delayed for several hours after exposure. Prolonged exposures to low concentrations produce chronic effects such as tooth erosion, chronic bronchitis, and photosensitization of the skin (J >2, ). 

While Raman-based corneal hydration measurements on healthy living human eyes are not yet possible due to the excessive laser excitation light levels required by the method, corneal hydration status has been successfully measured in legally blind patients [16]. 

Egger SF, Huber-Spitzy V, Alzner E, Scholda C, and Vecsei VP (1999) Corneal wound healing after superficial foreign body injury vitamin A and dexpanthenol versus a calf blood extract. A randomized double-blind study. Ophthalmologica 213, 246-9. 

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