Causes of alkali burns with serious consequences.
Corneal alkali burns are mostly caused by strong alkaline substances (PH >11.5) such as potassium hydroxide, ammonia and lime, etc. When alkaline substances enter the eye, they rapidly produce a necrotic reaction, and more severe reactions can produce irreversible damage within minutes. Because these substances are biphasic soluble (water-soluble and lipid-soluble), they can easily pass through the epithelial barrier. Therefore, corneal damage from alkaline substances is more complex and severe than that from acid burns.
Clinically, according to the degree of ocular tissue damage and the nature of the lesion, it is divided into 3 stages and 4 degrees.
I. Clinical stages.
1, acute stage: within a few seconds to 3 days after the burn, the early manifestation of the conjunctiva and cornea occurrence of progressive necrotic reaction, pain and eye irritation symptoms are obvious.
2, nutritional disorders: 3 days to 3 weeks after the burn, early manifestation of corneal edema degeneration, and gradually develop into non-inflammatory necrotic ulcers. In the later stage, a large number of new blood vessels grow in, some tissues begin to repair, and repeatedly gradually reduce.
3, scarring period: burn 3 weeks corneal white spot formation. Various ocular complications appear one after another, lid adhesions, increased intraocular pressure or ocular atrophy.
Second, clinical grading.
Degree 1: only corneal epithelial damage, good prognosis.
Degree 2: slight clouding of the cornea, but the iris texture can be seen, ischemia at the corneal limbus, good prognosis.
Grade 3: total epithelial damage, corneal clouding, and poorly visible iris texture. Corneal limbal ischemia between 1/3-1/2 weeks. Visual acuity loss, corneal perforation.
Degree 4: Heavy corneal clouding, poor visibility of the iris. Ischemia at the corneal limbus greater than 1/2 week. Poor prognosis.
Emergency treatment and early treatment of alkali burns:
1, first aid at the scene: immediately remove the alkaline material retained in the eye with large amounts of water, this is very critical.
2.Self-blood subconjunctival injection
3.Application of vitamin C corticosteroids and collagenase inhibitors:
5, corneal transplantation: early post-burn corneal ulceration, with the risk of thinning and perforation.
6, late treatment.
(1) Treatment of dry inflammation: Severe alkali burns with extensive conjunctival necrosis destroy the cup cells of the conjunctiva, making it impossible to produce adhesions, and the destruction of the main lacrimal ducts, leading to dry inflammation and lid bulb adhesions. If this state is not improved, any surgery to restore vision will fail.
(2) Lid bulb adhesion separation and formation surgery: This surgery must be done only after the alkali burn reaction has completely subsided (i.e., at least 1 year after the injury); premature surgery will result in increased inflammatory reaction after surgery, recurrence of adhesions, failure of surgery, and increased adhesions and scarring, which is harmful.
(3) Corneal transplantation surgery treatment.