Chemical damage to the eyes are one of the really urgent ophthalmic situations. At that time, almost any chemical can cause irritation of the eyes, the most severe damage usually occurs by ingestion of strong acids or alkalis. Damage alkalis are more common and can be more dangerous, especially in the bilateral process that often ends in visual impairment and disability.

There are 5 degrees of severity of burns. The severity of damage is caused by chemical type, volume, concentration, duration of exposure, temperature and the degree of penetration of the chemical. They play a role as the age of the victim (much heavier burns can occur in children), previous condition of the eye and started treatment.

The mechanism of damage to acids and alkalis is slightly different.



Burns acids
As is known, acid burns less dangerous as compared with alkali burns Protein clotting (coagulation) normally prevents deeper penetration acids. The exception is when the concentrated sulfuric acid enters the eye (storage solutions, chemical industry) and nitric acid. High capacity for penetration has also hydrofluoric (hydrofluoric acid).

Burns alkalis
Alkalis cause hydrolysis of the protein structure and cell destruction leading to necrosis of the wet tissues, including - at the deeper structures in contact with the intraocular fluid. In particular, the change in the corneal stroma (hydration, followed by turbidity) and the trabecular meshwork may be that an increase in generation of inflammatory factors can lead to an increase in intraocular pressure (IOP).

Common symptoms of chemical eye burns

Reduced visual acuity. The initial decline may be due to epithelial defect, haze, increased lacrimation, or discomfort. At medium and heavy chemical burns vision immediately after the injury can be a good, if small corneal clouding. But eventually burns effects may become more pronounced and lead to a significant loss of vision.

Increased intraocular pressure (IOP). Immediate increase in IOP may occur due to the deformation, shortening of collagen in the anterior chamber and trabecular apparatus. In the future, it may be associated with inflammation in the anterior part of the eye.

Inflammation of the conjunctiva. Varying degrees of redness and swelling of the conjunctiva are possible even with weak damage. Additionally, it may change the color of the conjunctiva: in contact with chromic acid brown color, and in contact with nitric acid - yellowish.

Fragments of debris in the vaults of the conjunctiva. It often occurs in lesions of the eye solid particles such as plaster, etc. If you do not remove the particles, will continue the selection of chemical substances, so - to grow a chemical burn. These particles must be removed to restore the surface could begin. Carbide lime - is especially dangerous. They should be removed before washing, do not tighten the start of care, otherwise the matter will dissolve the liquid part of the tear, causing heavy damage.

Perilimbalnaya ischemia. Perilimbalnoy degree of ischemia (blanching) is an important predictor of recovery of the cornea in the future as limbal germ cells are responsible for the renewal of the corneal epithelium. In general, more severe ischemia means a poor prognosis.

The defect of the corneal epithelium. The degree of damage to the corneal epithelium can vary from mild diffuse epithelial keratitis point to no epithelium. In the case of complete absence of epithelial defect can badly stain fluorescein in contrast to the usual erosion, moreover - this defect can not be seen. If the epithelial defect is suspected but not identified during the initial inspection, the eyes should be examined later after a few minutes or even hours.

Stromal haze. This feature may vary from the "transparent cornea" (0 ​​degree) to full opacity (degree of 5) inability to examination of the anterior chamber.

Perforation of the cornea. Very rare manifestation is more common after a few days / weeks in the case of heavy damage when the ability to heal the cornea reduced.

The inflammatory response of the anterior eye may vary from single cells and flair to marked fibrinoid reaction in the anterior chamber. Usually more pronounced when damaged by alkalis due to the greater ability to penetrate deeper.

Scarring / damage to the surface of the conjunctiva and eyelid skin. Similar to the chemical damage to other parts of the skin. This manifestation can lead to serious problems if scarring prevents proper closure of the optic fissure, thereby exposing further damage to the eye.

Treatment of chemical eye burns.

Treatment of chemical eye injury may include surgery and therapies for rehabilitation in order to maximize the conservation of both in acute and in the long term.

1) removal of the damaging agent
Immediate copious rinsing is the single most important method of removing chemical burns and treatment in the early stages. If available, the eye must be anesthetized before washing. Local anesthetics are used to reduce pain, blepharospasm, and for better patient cooperation.
Ideally, the eye must be flushed with sterile balanced buffer solution such as normal saline or Ringer's solution. However, immediate irrigation plain tap water (or drinking water without gas out of the bottle and so on. P.), Preferred waiting "perfect fluid".

2) inflammation control
Inflammatory mediators are allocated at the time of injury, cause cell death and involve other participants in the ongoing inflammatory process in the tissues of the eye. This powerful inflammatory response not only inhibits the re-epithelialization, but also increases the risk of corneal ulceration and perforation.
Control of inflammation via topical use of steroids can help break this cycle of inflammation.
Extras can be used citrate or ascorbic acid (altering calcium metabolism in the affected zone). Acetylcysteine ​​(10% or 20%) - can inhibit collagenolysis that prevents the formation of corneal ulcers, but the clinical use to date is debatable.

3) acceleration of the surface of the restoration (epithelialization) eyes
Prior to the final disposal of the harmful chemical can not start full epithelialization. Chemical damage to the eye after phase leading reactive increase tear production in a subsequent gradual decrease in tear production, and therefore the wetting agents (artificial tear preparations, etc.) have an important role in healing.
Ascorbic acid plays a fundamental role in restoring the structure of collagen, resulting in improved recovery of the cornea.
Using medical bandage contact lenses before complete epithelialization may be useful in some cases.
Among the surgical care methods are applied as appropriate:- Partial removal of necrotic areas of the surface of the cornea or conjunctiva tissue;- Temporary cover amniotic membrane;- Transplantation of limbal stem cells;- Transplantation of cultured corneal epithelial stem cells;- Elimination of conjunctival simblefarona (seam conjunctiva century with the conjunctiva of the eyeball).
For the purpose of rehabilitation of visual functions can be performed:- Sequentially or partial keratoplasty, cataract extraction with simultaneous when needed or without it;- Keratoprosthetics.

4) infection prevention
 In the absence of the corneal epithelium susceptible to eye infection. From prevention to the initial stages of treatment using the topical application of antibiotics.
Special cyanoacrylate adhesive for ophthalmic use can be used to treat small area of ​​deep tissue damage to the cornea.

5) control of intraocular pressure
With increased intraocular pressure, both at the initial stage of therapy, and during the late recovery period, pathogenetically justified the use of a blocker generation of intraocular fluid to reduce IOP.
Antihypertensive (penetrating antiglaucoma) operations or operations using the bypass / valve devices can be performed when using the appropriate local antihypertensive drugs increased IOP is maintained. The term is defined individually.

6) Control of pain
Serious burns can be long and extremely painful. The spasm of the ciliary muscle is possible to control the use of cycloplegic drugs; nevertheless, at the initial stage may be required, oral analgesics.complications
The primary complications include conjunctivitis, corneal erosion, corneal cloudiness and edema, acute increase of IOP, the corneal melting, and its perforation.
Secondary complications can be:• secondary glaucoma;• secondary cataract;• scarring conjunctival cavity;• thinning of the cornea, perforation;• corneal ulcer (aseptic or infectious nature);• total disruption of surface clouding and vascularization of the cornea;• subatrophy eyeball (phthisis or consumption).

Complications

The primary complications include conjunctivitis, corneal erosion, corneal cloudiness and edema, acute increase of IOP, the corneal melting, and its perforation.

Secondary complications can be:
• secondary glaucoma;
• secondary cataract;
• scarring conjunctival cavity;
• thinning of the cornea, perforation;
• corneal ulcer (aseptic or infectious nature);
• total disruption of surface clouding and vascularization of the cornea;
• subatrophy eyeball (phthisis or consumption).