also found in many strong household cleaners. In research and industrial applications, sodium and potassium hydroxide are used to control the pH of various products.

Ocular side effects

Direct ocular exposure

Certain

1.Ocular irritation a. Eye pain

2. Lacrimation

3. Non-specific blepharospasm

4. Conjunctiva

a.Hyperemia

b.Edema

c.Blanching of vascular bed

d.Symblepharon

5. Cornea

a.Edema

b.Scarring

c.Ulceration

d.Vascularization

e.Perforation

f.Fibrovascular pannus

6. Cataracts

7. Increased or decreased intraocular pressure

a.Glaucoma

b.Hypotony

c.Phthisis bulbi 8. Entropion

9. Iritis

Clinical significance

Many severe ocular injuries occur every year from exposure to alkalis. A data pull covering the years 2002–2005 from the American Association of Poison Control Centers Toxic Exposure Surveillance System database revealed 34 ocular injuries from alkalis that were rated as ‘major’ (indicating some type of significant residual disability). This number did not include injuries due to ammonia, detergents or other products with an alkaline pH. The total number of emergency visits for ocular exposure to alkalis was greater than 3000, a number rivaled only by gasoline and bleach exposures. Some automobile airbags release minor amounts of sodium hydroxide, which may complicate ocular injuries received via direct trauma during motor vehicle accidents.

Alkalis owe their toxicity to their ability to penetrate the eye surface more readily than other chemicals, including acids. The corneal epithelium and its mucoid coating are effective barriers to many substances, but they are quickly distorted in the presence of strong alkalis. The concentration of hydroxyl ion and the nature of its associated cation play a role in the ocular injury pattern caused by the different alkalis, but the pH of the substance seems to correlate most closely to the extent of the damage. As the pH of a substance rises above 11, there is a large increase in its potential for ocular damage. Of the three most common alkalis, ammonium hydroxide (see section on ammonia) penetrates the eye most rapidly, followed by sodium hydroxide and then calcium hydroxide (see section on lime). Magnesium hydroxide is another alkali known to cause ocular injury, and is a common ingredient in fireworks so chemical injury with this compound is often accompanied by thermal injury.

If the eye is exposed to concentrated lye, the initial response is one of pain, lacrimation and blepharospasm. The latter makes

immediate irrigation of the eye more difficult. Conjunctival injuries may include ischemic necrosis of the limbal tissue and loss of the vascular bed. Later, severe dry eye may ensue along with the development of symblepharon and entropion. Severe ocular burns from alkalis can injure sensory nerves and lead to ocular anesthesia, a bad prognostic sign. As the lye causes corneal epithelial necrosis and disruption of the surface barriers, it immediately begins to penetrate to the deeper layers of the cornea, potentially arriving in the anterior chamber within a minute. The presence of lye in the stroma may lead to permanent corneal opacification, corneal vascularization, stromal thinning, and perforation. Lye in the anterior chamber raises the pH, causing damage to the trabecular meshwork and elevated intraocular pressure. Although some patients eventually develop chronic intraocular pressure elevation, damage to the ciliary body may occur, leading to hypotony and phthisis bulbi. The lens may be permanently injured by the elevated intraocular pH, leading to cataract. There are also case reports of retinal toxicity from alkali injury.

The true severity of an ocular injury from lye may not be known for a few days. Healing may be retarded by chronic inflammation, an imbalance in collagen synthesis/degradation and death of limbal stem cells. Sterile ulcers may form and eventually a fibrovascular pannus may cover the cornea.

Recommendations

The most important intervention in ocular exposure to lye or other alkalis is immediate irrigation. Many studies have been done to identify the optimal irrigating solution for various types of chemical exposure, but the subtle advantages of one solution over another are far less important than the rapidity of applying irrigation. In an industrial setting, eyewash stations are often prevalent. If an ocular exposure to a strong alkali occurs away from such resources, rescuers should immediately apply whatever non-toxic aqueous solution is at hand.

Once a victim is in a medical care center, extensive irrigation must be started immediately using normal saline or sterile­ water. This is aided by the use of topical anesthetic and a lid speculum. One liter of fluid should be used to flush the eye surface over a period of 10 minutes. A few minutes should be allowed to pass following this first liter for accurate testing of the pH of the conjunctival cul-de-sac using litmus paper accurate in the neutral range. If the pH does not drop below 8, one should continue cycles of irrigation for 15 minutes followed by a check of the pH. Some experts advocate irrigation for at least 2 hours to help neutralize the anterior chamber pH while others have advocated anterior chamber paracentesis and washout. After the initial round of irrigation, a brief ocular exam should take place, checking vision and intraocular pressure and examining the conjunctival fornices for foreign bodies, which may be acting as a reservoir for the alkali. At this point, the necrotic corneal epithelium should be removed.

Following irrigation and neutrality of pH, medical therapy should ensue. Topical cycloplegic eye drops, antibiotic ointment and corticosteroid eye drops should be instituted for the first week. After this time, corticosteroids may inhibit wound healing. Antiglaucoma therapy should be started if necessary. High dose oral ascorbate is possibly helpful and of low toxicity. Many other substances have been advocated via both oral and topical routes to aid in healing from these injuries, but none have become the standard of care. The surgical care of the late sequelae of severe ocular burns from alkalis is a complicated subject and beyond the scope of this text.

Class: lkaliA