Introduction One of the true ophthalmic emergencies. Serious damage results from either strongly basic (alkaline) compounds or acidic compounds. Alkali injuries -more common,more deleterious. Immediate, prolonged irrigation, followed by aggressive early management and close long-term monitoring to promote ocular surface healing and to provide best opportunity for visual rehabilitation.
Pathophysiology Severity : type, volume, concentration, duration of exposure, and degree of penetration of the chemical. Acid Injury Acids dissociate into hydrogen ions and anions in the cornea. The hydrogen molecule damages the ocular surface by altering the pH, while the anion causes protein denaturation, precipitation, and coagulation. Protein coagulation generally prevents deeper penetration of acids and is responsible for the ground glass appearance of the corneal stroma following acid injury. Hydrofluoric acid is an exception; it behaves like an alkaline substance because the fluoride ion has better penetrance through the stroma than most acids, leading to more extensive anterior segment disruption.
Pathophysiology Alkali Injury Alkaline substances dissociate into a hydroxyl ion and a cation in the ocular surface. The hydroxyl ion saponifies cell membrane fatty acids, while the cation interacts with stromal collagen and glycosaminoglycans. This interaction facilitates deeper penetration into and through the cornea and into the anterior segment. Subsequent hydration of glycosaminoglycans results in stromal haze. Collagen hydration causes fibril distortion and shortening, leading to trabecular meshwork alterations that can result in increased intraocular pressure (IOP). Additionally, the inflammatory mediators released during this process stimulate the release of prostaglandins, which can further increase IOP. Presentation History History of a liquid or a gas being splashed or sprayed into the eyes or of particles falling into the eyes. Specific nature of the chemical and the mechanism of injury (eg, simple splash vs high-velocity blast) Common complaints Pain (often extreme) Foreign body sensation Blurred vision Excessive tearing Photophobia Red eyes
Presentation A thorough physical examination should be deferred until the affected eye is irrigated copiously, and the pH of the ocular surface is neutralized. Physical Decreased visual acuity Increased IOP Conjunctival inflammation Particles in the conjunctival fornices Perilimbal ischemia Corneal epithelial defect Stromal haze Corneal perforation Anterior chamber inflammatory reaction Adnexal damage/scarring
Common sources of alkali Common sources of acids Cleaning products (eg, ammonia) Fertilizers (eg, ammonia) Drain cleaners (eg, lye) Cement, plaster, mortar (eg, lime) Airbag rupture (eg, sodium hydroxide) Fireworks (eg, magnesium hydroxide) Potash (eg, potassium hydroxide)
Classication of severity of ocular surface burns by Roper-Hall
Grade Corneal appearance Limbal Ischemia Prognosis Grade I Clear cornea:Corneal epithelial damage None Good Grade II Corneal haze : Iris details visible <1/3 Good Grade III Total epithelial loss: Stromal haze:Iris details obscaured 1/3-1/2 Guarded Grave IV Opaque cornea: Iris details obscured >1/2 Poor
Severe Ocular Burns Harold Merle,1 Max Gerard2 and Norbert Schrage3 European Ophthalmic Review, 2011;5(2):1303
The worst ocular lesions are chemical burns caused by strong bases and acids. Associated with the destruction of limbal stem cells (LSCs). There are repeated epithelial ulcerations, chronic stromal ulcers, deep stromal neovascularisation, conjunctival invasion and even corneal perforations. The initial clinical examination is difficult because the symptomatology is severe, but nevertheless it helps to classify the lesions, to establish a prognosis and to guide the therapeutic care. The classification system used most is that implemented by Hughes and modified by Roper-Hall. It is now completed neatly by those proposed by Dua and Wagoner, which are based on the importance of the deficit of LSCs. Management of ocular surface chemical burns Jean-Jacques Gicquel Br J Ophthalmo Feb 2011 Vol 95 No 2 Joseph et al noticed that the clinical outcome of patients with a Grade IV of Roper-Hall who had received similar treatments was highly variable Dua et al drew the conclusion that Roper-Hall lacked precision and proposed a new classification on an analogue scale expressed as the number of clock hours of limbal involvement and percentage of conjunctival involvement, which could be broken down into six grades Conjunctival involvement is of major importance. Even if the limbus is entirely destroyed, if a sufficient amount of conjunctiva remains, it will still be able to re-epithelialise the corneal surface, prevent stromal perforation and secure the ocular surface for possible secondary LSCT at a later date. Grade Prognosis Clinical Findings Conjunctival involvements Analogue scale I Very good 0 clock hours of limbal involvement 0% 0/0% II Good 3 clock hours of limbal involvement 30% 0.1-3/1-29.9% III Good >3-6 clock hours of limbal involvement >30%-50%
3.1-6/31-50% IV Good to guarded >6-9 clock hours of limbal involvement >50%-75%
6.1-9/51-75% V Guarded to poor >9-<12 clock hours of limbal involvement >75%-<100%
9.1-11.9/75.1- 99.9% VI Very poor Total limbus involvement ( 12 clock hours) Total conjunctival involvement ( 100%)
12/100% Classification of Dua Grade 1 ocular surface burn. Large corneal burn following accidental exposure to ammonia. There is no limbal or conjunctival involvement.
(A) Grade 3 (4.5/30%) ocular surface burn. (B) and (C) the surviving limbal epithelium demonstrates circumferential migration of tongue-shaped projections approaching limbal epithelial cover to denuded limbus. (D) The entire limbus has healed with limbal epithelium and the corneal surface too is almost completely healed with corneal (limbal derived) epithelium. The conjunctival defect is closing with conjunctival epithelium. Fluorescein stained diffuse view of the cornea. Grade 3 (5/35%) ocular surface burn following an accident involving an industrial alkaline chemical. Five clock hours of the limbus and 35% of the conjunctiva were involved. (A) Diffuse view with patient looking straight illustrating the extent of limbal involvement. (B) Diffuse view with patient looking up and out and (C) looking up and in to show the extent of conjunctival involvement. Treatment Medical Care Common goals of management include the following: Removing the offending agent - Ideally, the irrigation solution should be balanced salt solution or Ringers lactate solution. In alkali burns, some authors recommend the useof an amphoteric solution such as diphoterine. Promoting ocular surface healing - non-preserved tear substitutes (promoting the re- epithelialisation in a context in which the tear film is abnormal due to the destruction of goblet cells) Topical mucomimetic agents such as sodium hyaluronate should be used in order to increase the wetability of the surface and the tear-film stability. This also reduces conjunctival fibrosis.
Controlling inflammation - Topical steroids instilled on an hourly basis in order to prevent a secondary destruction of the surrounding tissues. - They will limit the inflammatory processes by diminishing chemotaxis of inflammatory cells and by stabilising cellular and lysosomal membranes of polymorphonuclear leucocytes. - For a long time, steroids were considered to be a contraindication for fear of provoking corneal perforations by countering the action of tissue inhibitors of metalloproteases. - Recent studies have contradicted this dogma. - After the acute phase, teroids may slow down the re-epithelialisation process as well as healing of the collagen matrix. - They should be stopped after 7-10 days but can be reintroduced 6 weeks after the burn, in order to reduce chronic ocular surface inflammation.
Preventing infection Controlling IOP Control pain - paracetamol, Soft CL bandage, AMT
*The amniotic membrane (AM) is avascular and acellular. It will facilitate epithelial healing acting as a basement membrane (it sharescommons collagen isoforms with theconjunctival basement membrane)
Medical Care Ascorbate Critical cofactor necessary for collagen fibril synthesis. The antioxidant properties of vitamin C eye-drops limit the effects of free radicals released after an ocular surface chemical burn. Endogenous vitamin C being secreted physiologically in the aqueous humour by the ciliary body and quickly depleted after a severe chemical burn). Its use is recommended for the treatment of Grade II burns and over. Systemic vitamin C does not have a proven efficacy.
*The combined effect of citrate/ascorbate treatment in alkali-injured rabbit eyes. Pubmed. Cornea.1991 Mar;10(2):100-4. Pfister RR, Haddox JL, Yuille-Barr D. Source:Eye Research Laboratories, AMI/Brookwood Medical Center, Birmingham, AL 35209. The average depth of ulceration was significantly less for the citrate/ascorbate group
Treatment Surgical care Remove inciting chemical Promote ocular surface healing Debride necrotic conjunctival/corneal tissue Temporary amniotic membrane patching Limbal stem cell transplant Cultivated corneal epithelial stem cell sheet transplantation Lysis of conjunctival symblepharon. Prevent infection: Cyanoacrylate tissue adhesive may be applied for the treatment of small corneal perforations. Visual rehabilitation Penetrating keratoplasty with or without cataract extraction Keratoprosthesis Control IOP: Glaucoma filtering surgery or aqueous tube shunt placement may be used for cases of increased IOP refractory to medical management.