The eye is protected by the lids and orbital margins from direct injury, but it can be injured by light, chemicals and mechanical trauma. Trauma involves ocular foreign bodies, blunt trauma, and penetrating and perforating injuries.
▃Light Damage to the Eye (OP9.5)
UV spectrum is subdivided into:
•UV-A: 400–320 nm (90% of UV [ultraviolet] radiations from sun).
•UV-B: 320–280 nm.
•UV-C: ≤ 280 nm.
The ozone layer (2–3 mm in thickness) is produced in the stratosphere by a photochemical reaction which filters out most of the destructive UV light. The depletion of ozone layer leads to an increase in UV-B radiation.
■Biochemical Mechanism of UV Radiation Damage
For photodamage to occur, the tissue must contain a molecule that absorbs light. Tissue photo damage may occur in two ways:
1.Molecular fragmentation: The molecules containing alternate double bonds (proteins, enzymes, and nucleic acid) resonate with radiation of UV wavelength. The increased intensity of UV radiation breaks the molecular bonds and the new molecules may induce inflammation or affect the immune system.
2.Free radical generation: Free radical light damage requires three components: light absorbing molecule, oxygen, and short-wavelength radiation (Flowchart 19.1).
Ocular Light Damage
Fortunately, the body contains protective free radical scavengers which include superoxide dismutase, vitamin C and E, glutathione peroxidase, and carotene. The shortage of free radical scavengers in premature infants, elderly, or nutritionally impaired persons may cause greater vulnerability to light damage. With age, many of the photoprotective mechanisms of the eye degrade. Excessive exposure to UV radiations can lead to cataract development and risk of macular degeneration.
The reduction of environmental exposure and use of absorptive lenses diminish the risk of light damage to the eye. Also, intake of antioxidant as dietary supplements may slow the development of cataracts and macular degeneration.
Acute sunburn reaction occurs in lids, which is essentially an UV-B-induced response. Clouds do not filter out UV radiation and therefore do not prevent sunburn. Malignant skin changes include basal cell carcinoma, squamous cell carcinoma, and malignant melanoma. Other features include epidermal keratoses and sebaceous hyperplasia.
The most effective range of damaging wavelength is 260 to 290 nm, but as a result of absorption by the ozone layer, radiations of these wavelengths rarely penetrate to the Earth’s surface. The cornea absorbs rays of wavelength <320 nm, that is, UV-B and UV-C. Apart from UV radiation, welding flashes, germicidal lamps, and sun lamps cause superficial punctate keratitis (SPK). Chronic exposure to UV radiations results in pterygium and spheroidal degeneration of cornea.
Short-wavelength radiations are cataractogenic (primarily cortical cataract). Infrared (IR) radiation also has an effect on lens. Lower wavelength of IR radiation closely matches the resonant frequency of water molecules. In glass blowers, lens water absorbs radiations from IR source, resulting in aggregation of insoluble lens proteins and glass blower’s cataract.
Prolonged illumination from indirect ophthalmoscope with a focusing lens, operating microscope, or sun cause maculopathy. Oxygen with fluorescent lights in nursery may enhance damaging potential of oxygen (due to damaging free radicals) in premature infants, as immature retina is devoid of protective free radical scavengers. It may result in retinopathy of prematurity.
Eyes can be protected from light damage by taking the following measures:
•During surgery, light can be blocked by occuluder disc placed on cornea or bubble of air in anterior chamber.
•Intraocular lens (IOLs) with UV filters– These IOLs filter out all wavelengths of light <400 nm and prevent decrease in visual function such as color vision and contrast sensitivity.
•Use of photochromatic lenses: When shorter wavelength light (300–400 nm) interacts with glass photochromatic lenses, they darken (Ag+ → elemental Ag).
Chemical injuries may be due to alkalis or acids. It may be accidental or as a result of an assault.
Alkali burns are more common than acid burns since alkalis are more widely used at home and in the industries.
Most commonly involved alkalis are–
•Lime—usually fresh mortar or white wash Ca(OH)2.
•Caustic potash (KOH).
•Caustic soda (NaOH).
•Ammonia (NH4OH)—It is most harmful.
Alkali burns are more severe than acid burns because alkalis penetrate deeper into tissues and may involve various ocular tissues (Table 19.1). Flowchart 19.2 explains the mode of damage of various eye structures by alkalis.
Thus, alkalis cause extraocular as well as intraocular complications. Ammonia (NH4OH) and sodium hydroxide (NaOH) may produce severe damage due to rapid penetration.
Table 19.1 Various ocular injuries incurred by alkalis
Ocular part affected
Conjunctival congestion, edema, and necrosis, with formation of symblepharon.
Corneal epithelial damage, opacification, and vascularization.
Uveitis and ciliary epithelial damage.
Acids coagulate tissue proteins. The coagulated surface proteins act as a protective barrier and prevent deep penetration of acids (except hydrofluoric acid). So, the main damage is restricted to lids, conjunctiva, and cornea. Therefore, acids produce limbal ischemia, symblepharon, corneal necrosis, and sloughing. Common acids involved are:
•Sulphuric acid (H2SO4)– used in industries and batteries in inverters.
•Hydrochloric acid (HCl).
•Nitric acid (HNO3).
•Sulphurous acid (H2SO3)—refrigerant.
•Hydrofluoric acid (HF)—Used in glass etching and cleaning. It also tends to rapidly penetrate the eye.
■Grading and Prognosis of Chemical Injuries
Severity of chemical injuries is graded to plan the appropriate treatment and indicate the ultimate prognosis. Grading is performed on the basis of severity of limbal ischemia and corneal clarity (Table 19.2).
Table 19.2 Grading of chemical injuries
Limbal ischemia and corneal clarity
No limbal ischemia with clear cornea
<120° limbal ischemia and hazy cornea but with visible iris details
120°–180° limbal ischemia and total epithelial loss, with hazy cornea obscuring iris details
IV (very severe)
>180° limbal ischemia with opaque cornea
◊Emergency treatment (immediate).
Immediate treatment of all chemical burns includes the following considerations:
•Copious irrigation with normal saline or balanced salt solution for at least 30 minute or till pH returns to normal. It can be done by IV infusion line for controlled flow of saline onto the ocular surface. If saline is not immediately available, irrigate with water at once. If irrigation is delayed, prognosis becomes worse.
•Removal of retained particulate matter (such as lime or cement) with forceps after instillation of topical anesthetic. Double eversion of upper eyelid should be performed to remove the trapped particles from the upper fornix.
•Debridement of necrotic corneal epithelium for proper reepithelialization.
Treatment is aimed to reduce inflammation, promote corneal reepithelialization, and prevent corneal melting. Treatment includes the following measures:
•Prophylactic antibiotic drops are given for approximately 7 days.
•Topical cycloplegics—Avoid phenylephrine because it is a vasoconstrictor.
•Topical steroids—Corticosteroids reduce inflammation and the development of symblepharon by preventing the formation of excessive granulation tissue. These can be used safely during the first week to combat uveitis without increasing the risk of corneal melting.
During the 2nd and 3rd weeks, fibroblasts migrate into the acellular burned areas, presumably from the surrounding keratocytes; however, steroids cause reduced collagen synthesis and inhibition of fibroblast migration. Thus, steroids impair stromal healing and enhance corneal melting during this period. Therefore, steroids should be avoided after the initial 7 to 10 days and must be replaced by topical nonsteroidal anti-inflammatory drugs (NSAIDs) which do not affect keratocyte function.
After the 3rd week, fibrocytic repopulation of cornea occurs, that is, there is no fibroblast migration, so steroids can once again be used, if required.
•Ascorbic acid: It promotes collagen synthesis by corneal fibroblasts, so wound healing is improved.
◊Topical sodium ascorbate in artificial tears 10% is administered every 2 hours.
◊Oral sodium ascorbate is given 2 g/day.
•Citric acid: Citrate acts by inhibiting neutrophil activity, thereby reducing the intensity of inflammation. It also causes chelation of extracellular calcium ions, inhibiting collagenase, and consequently preventing stromal damage. Topical sodium citrate 10% is given every 2 hours for approximately 10 days.
•Tetracyclines: These are effective collagenase inhibitors, so they reduce collagenolysis and stromal melting.
◊Oral doxycycline 100 mg B.I.D. is given.
•Tear substitutes: Preservative-free lubricants are used every 1 hour.
•Preservation of symblepharon formation: It is done by:
◊Sweeping the glass rod covered with antibiotic ointment in the fornices twice daily.
◊Fitting of contact lens.
•Limbal stem cell transplantation from patient’s other eye (autograft) or from donor (allograft). The aim of transplantation is to restore normal corneal epithelium.
•Amniotic membrane grafting is done:
◊To promote epithelialization.
◊To suppress fibrosis.
◊To prevent symblepharon formation.
•Division of symblepharon: A variety of approaches have been tried for the successful surgical management of chronic symblepharon. Various materials have been evaluated as a mechanical barrier to keep potentially adhesive surfaces apart after excision of the symblepharon. The raw area created after the excision of symblepharon may be covered by conjunctival autograft, mucous membrane graft, and amniotic membrane transplantation.
•Corneal transplantation (keratoplasty) should be delayed for at least 6 months to allow maximum resolution of inflammation.
▃Ocular Foreign Bodies
Foreign body may be extraocular (superficial) or intraocular.
■Extraocular (Superficial) Foreign Bodies (OP3.8, OP4.8)
The usual foreign bodies (FB) are small particles of coal, iron, dust, emery, sand, husk of paddy, stone, glass, and wings of insects. FB may be impacted on conjunctival or corneal surface. On the conjunctival surface, it may be lodged in sulcus subtarsalis, fornices, or bulbar conjunctiva. A conjunctival FB lodged in the upper sulcus subtarsalis abrades the cornea with each blink. FB retained in upper fornix can be seen on double eversion of upper lid. If retained for a long period in the upper fornix, it may be embedded in a mass of granulation tissue, producing a foreign body granuloma. Corneal FB is usually embedded in the epithelium or superficial stroma. A foreign body can be detected on slit-lamp examination.
Symptoms of conjunctival foreign body includes:
•FB localized on conjunctiva or cornea.
Vertically oriented linear corneal abrasions indicate a FB under upper eyelid. Fluorescein staining is done to reveal the presence of corneal abrasion caused by FB. An infected FB can cause conjunctivitis. Retained FB carries a risk of secondary infection and corneal ulceration.
Iron FB often results in rust staining of the bed of corneal abrasion, but fades away with the time, leaving a corneal opacity.
Treatment aims at removal of FB using slit-lamp under topical anesthesia. After removal of FB, antibiotic eye ointment is applied and eye is bandaged for a day. Protective glasses must be used to protect the eyes.
■Intraocular Foreign Body (IOFB)
Penetrating injury may be associated with retention of FB in the eye (intraocular FB). Once the FB enters the eye, it may lodge in any of the structures it encounters (Fig. 19.1).
Types of FBs
IOFBs could be of three types.
•Foreign bodies producing inflammatory reactions:
◊Iron and steel.
•Foreign bodies prone to result in infection:
◊Spicules of wood.
A piece of glass in anterior chamber is exceptionally difficult to observe because its refractive index is very close to that of aqueous.
Modes of Damage to the Eye
An IOFB can cause damage the eye in three ways:
•By mechanical effects.
•By introduction of infection.
•By specific reactions of FB on intraocular tissues.
Mechanical Effects of IOFB in the Eye
A FB may enter the eye through either cornea or sclera. When it pierces the cornea, it may be retained in the anterior chamber or may be lodged in the iris stroma. It may pass into the lens, vitreous, or retina.
FB in the lens may gain access through the iris or pupil. When it passes through the iris, perforation leaves behind a hole in it at the site of impact. A hole in the iris is of great diagnostic significance since it rarely occurs, except due to perforation by a FB. A FB in the lens produces traumatic cataract.
FB in the vitreous: A FB may access the vitreous by various routes as depicted in Fig. 19.2.