Causes More than 25, chemical products with the potential to cause chemical eye injuries have been identified, many of which may be classified as acids or bases, oxidising or reducing agents, or corrosives. Acids and bases are the most frequently implicated chemical agents. The severity of the injury is related to the nature, concentration, quantity and pH of the chemical involved. It also depends upon the duration of contact and surface area of exposure.
History of high-velocity explosive chemical injury should always raise suspicion of an associated intraocular foreign body. Most severe injuries are typically caused by ammonia and lye which are both capable of rapid penetration into the eye. The severity of the injury is dependent on the anion concentration, the dissociation of the alkali, and the quantity of fluid. A wave of hydroxyl ions rapidly advances through ocular tissues, causing massive cell death by saponification of cellular membranes and extensive hydrolysis of glycosa-aminoglycans and collagen within the corneal matrix.
Damage caused by lime injuries is reduced by the precipitation of calcium soaps that hinders further penetration. Presence of magnesium hydroxide in fireworks results in a combined chemical and thermal injury.
The most important agents causing alkali injuries to the eye are:. Weak acidic compounds precipitate proteins within the corneal and conjunctival epithelium, thus acting as a partial barrier to further penetration of the chemical. It leaves a greyish white epithelium, which often obscures all tissue underneath it. Stripping off this opacified epithelium often reveals a relatively clear underlying corneal stroma.
As long as the corneal stem cells near the limbus are not damaged, epithelial recovery is likely, with little or no stromal cloudiness.
Hydrofluoric, sulphuric, sulphurous, chromic, and hydrochloric acids are the most common causes of acid burns. Strong acids ionise completely in an aqueous solution. The strength of an acid depends on its ability to dissociate and lose a proton. The primary mechanism of damage by acids is due to the action of dissociated proton.
Hydrofluoric acid causes most severe acid injury due to its unique properties. Hydrofluoric acid has a unique dissolving action which allows it to quickly penetrate into deeper tissues. Moreover, hydrofluoric acid chelates all calcium and magnesium from cells, thereby halting cellular biochemical activity. Although alkalis typically cause the most serious chemical injuries, the presence of an acid injury does not preclude an equally severe ocular injury. Very strong acids, however, overcome this precipitated obstacle and progress through tissue, much as alkalis.
Indeed, there is no clinically significant difference in course of injury and prognosis between severe acid and alkali burns. The end result of a very severe acid injury is often indistinguishable from that of an alkali injury. The most important agents causing acid injuries to the eye are:.
HF produces severe ocular injury because of its high degree of activity in dissolving cellular membranes. It is highly toxic so that as little as 7 ml of HF, or 2. It is found either in pure form or mixed with agents like nitric acid, ammonium difluoride, and acetic acid. Injury with sulphuric acid may be compounded by thermal burns from heat generated by the reaction of acid with water on the corneal tear film.
Dissolution of concentrated sulphuric acid in water results in release of heat, which causes tissues charring. At first, visual acuity is not severely affected after exposure to sulphurous acid, but it worsens greatly over hours to days as the ocular condition deteriorates.
Other types of ocular chemical injuries are usually less severe than alkali and acid injuries. Lacrimatory agents: Lacrimatory agents are aerosol dispersed chemicals which produce ocular irritation. Chemical Mace nonlethal spray containing purified tear gas and chemical solvent : Chemical Mace and similar compounds can cause minor to severe ocular injury, depending on a number of factors. The ocular injury associated with the original Chemical Mace is caused by the lacrimator chloroacetophenone.
Degree of severity depends upon proximity of spray can to the eye, quantity of chemical entering the eye, duration of exposure, state of normal reflex mechanisms, and the mechanism of propelling the chemical. Extensive exposure leads to damage including loss of ocular surface epithelium, severe persistent stromal oedema, presumably secondary to endothelial damage, stromal clouding, and corneal neovascularisation. Pepper spray Oleoresin capsicum : Pepper spray Oleoresin capsicum is used for riot control or self defence.
Exposure to these chemicals causes ocular stinging, pain, excessive watering and inability to open eyes. Mustard gas Dichlorodiethyl sulphide : Mustard gas Dichlorodiethyl sulphide is a poisonous agent used as a chemical warfare agent. It causes irritation of conjunctiva and sore sticky eyes on exposure or a chronic and delayed mustard gas keratitis manifesting as recurrent corneal erosions. Diagnosis The severity of eye injury depends upon:.
Prior to clinical eye examination, pH of both the eyes should be checked. Eye must be irrigated to bring the pH to a safer range between 7 and 7. Palpebral fissures should be examined and fornices should be swept to remove a retained particulate matter, which can cause persistent damage. Eye should be examined under fluorescein dye. Intraocular pressure should be documented as well to exclude any rise. Emergency treatment of the chemically injured eye must precede any attempt at classification.
Once the condition has been stabilised, determine the anticipated course of the chemical injury by examining the critical features. Understanding and documenting the salient features of an alkali injury of the eye permits proper classification so that appropriate treatment can be initiated and accurate prognosis deduced. Photographic documentation may be obtained, if possible. Include any conjunctival epithelial defects as well, particularly concerning the palisades of Vogt limbal stem cells.
Document all epithelial defects, including those extending into the fornices of the eye. Corneal stromal opacity: Grade corneal stromal opacity on the basis of penlight examination:. Perilimbal ischaemia: To document perilimbal ischaemia, note the clock hours where the conjunctiva is whitened.
The conjunctiva and episclera are devoid of blood vessels in these areas. This whitening should not be confused with less severe injury, where there is chemosis and thrombosed blood vessels, but some of the conjunctiva is still viable. Perilimbal whitening is a useful parameter by which the extent of corneal stem cell damage, and indirectly, injury of the underlying ciliary body and trabecular meshwork, may be judged.
Documentation of these findings allows for more accurate determination of the necessity for corneal stem cell transplantation. These measurements and findings can be applied to the classification of alkali injuries as described by Hughes , and later modified by Ballen , Roper- Hall and Pfister et al This classification, with accompanying drawings and photographs, represents the span of damage encountered after alkali injury. The accuracy of early assessment becomes important in prognostication and treatment plans.
The conjunctival involvement should be calculated only for the bulbar conjunctiva, up to and including the conjunctival fornices. McCulley has divided the clinical course of chemical injury in four distinct phases:.
The clinical findings immediately following chemical exposure may be used to assess the severity and prognosis of the injury. Hughes classification modified by Ballen in , Roper- Hall in and Pfister et al in provides a prognostic guideline based on corneal appearance and extent of limbal ischaemia. The Roper-hall classification system was introduced in the mids and is the most established and commonly applied system. In the acute phase during first week , Grade I injuries heal while Grade II injuries slowly recover with corneal clarity.
Intraocular pressure may be elevated due to inflammation or decreased due to damage to ciliary body. During early reparative phase 7- 21 days , in Grade II injuries, re- epithelialisation is completed with clearing of opacification.
In more severe cases, there may not be a change in clinical appearance and there may be delayed or arrested re- epithelialisation. Keratocyte proliferation occurs with production of collagen and collagenase, resulting in progressive thinning with potential of perforation.
In late reparative phase, re- epithelialisation patterns divide injured eyes into two groups:. Preparation for vision restoration: Preparation for vision restoration must begin immediately after the injury. Deliberate and timely treatment determines successful outcomes in the rehabilitative process. The patients were followed up for 1 year, and parameters including best-corrected visual acuity, epithelial defect area, conjunctival and limbal involvement, and injury-related complications were evaluated.
Median best-corrected visual acuity at presentation was 1. The median initial epithelial defect was mm 2 range, 18 to mm 2 , which healed in all eyes by 3. Initial median limbal involvement was 12 clock hours range, 3 to 12 clock hours , resulting in a residual limbal stem cell deficiency of 6 clock hours range, 0 to 12 clock hours at 1 year.
It can react violently with strong acids and with water. Sodium hydroxide is corrosive. NaOH can react with moisture from the air and may generate heat as it dissolves. This heat can be enough to cause a fire if it is near flammable materials. Sodium hydroxide is useful for its ability to alter fats. It is used to make soap and as a main ingredient in household products such as liquid drain cleaners. Sodium hydroxide is usually sold in pure form as white pellets or as a solution in water.
Sodium hydroxide is used in bar soaps and detergents. Sodium Hydroxide is also used as a drain cleaner to unclog pipes. Some other uses include fuel cell production, to cure food, to remove skin from vegetables for canning, bleach, drain cleaner, oven cleaner, soaps, detergent, paper making, paper recycling, aluminum ore processing, oxide coating, processing cotton fabric, pickling, pain relievers, anticoagulants to prevent blood clots, cholesterol reducing medications, and water treatment.
In the home, some household items like soaps or cleaners contain sodium hydroxide. Accidental ingestion or skin contact with these cleaners could cause harmful exposure. Some industrial workplaces use sodium hydroxide. Here are some workplace exposure limits to NaOH in the air. Remove clothes carefully if they get wet to avoid spreading the sodium hydroxide on your skin. Sodium hydroxide is a potentially dangerous substance. It can hurt you if it touches your skin, if you drink it or if you breathe it.
Eating or drinking sodium hydroxide can cause severe burns and immediate vomiting, nausea, diarrhea or chest and stomach pain, as well as swallowing difficulties.
Damage to the mouth, throat and stomach is immediate. Breathing it can cause severe irritation of the upper respiratory tract with coughing, burns and difficulty breathing. The harmful effects of sodium hydroxide depend on several factors including the concentration of sodium hydroxide, length of time exposed, and whether you touched it, drank it or inhaled it.
Contact with very high concentrations of sodium hydroxide can cause severe burns to the eyes, skin, digestive system or lungs, resulting in permanent damage or death. Prolonged or repeated skin contact may cause dermatitis.
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