Burns and Trauma
Deborah Pavan-Langston
Pedram Hamrah
I. Anterior Segment Burns
may be chemical, thermal, radiation, or electrical.
Chemical burns are among the few true emergencies and are usually caused by alkali or acid in the form of liquid, powder, solid, or vapor. The offending agent should be identified, whenever possible, because the severity of ocular injury is pH dependent. Other forms of anterior segment burns that should be managed as chemical burns are those due to tear gas and mace. These are generally thought not to cause permanent ocular damage, although there have been reports of eyes lost after such burns. In addition, ocular injuries from sparklers and flares containing magnesium hydroxide should be managed as chemical rather than as thermal burns.
Pathology of chemical burns. The most serious chemical burns are with alkali such as lye (NaOH); caustic potash (KOH); fresh lime [Ca(OH)2], i.e., plaster, cement, mortar, whitewash; and ammonia (NH4), which is present in household cleaner, fertilizers, magnesium OH (sparklers), and refrigerant.
Alkali burns are more severe than acid burns, because of their rapid penetration-often less than 1 minute—through the cornea and anterior chamber. Alkali raises the tissue pH, causing saponification of fatty acids in cell membranes, thereby resulting in disruption of the cells and stromal mucopolysaccharide with concomitant tissue softening. Further, penetration of alkali into the corneal stroma destroys the collagen fibers and matrix of the stromal matrix. Damage from alkali burns is related more to the degree of alkalinity (pH) than to the actual cation. Permanent injury is determined by the nature and concentration of the chemical, as well as by the time lapsed before irrigation. The extent of limbal epithelial damage and degree of intraocular penetration are associated with visual prognosis. Extensive limbal epithelial damage and limbal ischemia have the most unfavorable prognosis, because the limbus harbors corneal epithelial stem cells that are necessary for reepithelialization of the cornea. The absence of limbal stem cells will lead to neovascularization and conjunctivalization of the cornea. Moreover, alkali burns can cause corneal melting and severe scarring, as well as uveitis and secondary glaucoma.
Acid burns, such as those caused by battery acid, industrial cleaner (H2SO4), laboratory glacial acetic acid or HCl, fruit and vegetable preservatives, bleach, refrigerant (H2SO3), industrial solvents, mineral refining agents, gas alkylation agents, silicone production agents, and glass etching agents (HFl), cause their maximum damage within the first few minutes to hours and are less progressive and less penetrating than alkaline agents. Acids precipitate and denature tissue proteins that rapidly set up barriers against deep penetration by the chemical. Acids do not cause loss of corneal matrix, and damage is, therefore, localized to the area of contact, with the exception of burns from hydrofluoric acid or acids containing heavy metals, both of which tend to penetrate the cornea and anterior chamber, ultimately giving rise to intraocular scarring and membrane formation.
Mace (chloroacetophenone) and other tear gas compounds are variable in their toxic contents and clinical effects. If sprayed as recommended from more than 6 ft away, not directed at the eyes, and at a conscious individual, only minor chemical conjunctivitis occurs. More direct and concentrated spray toward the
eyes in a person whose defensive reflexes are compromised can result in severe injury, clinically similar to an alkali burn. Mace and other lacrimator ocular burns should be managed in the same manner as alkali burns.
Classification and prognosis of the chemically burned eye is most useful for alkali burns, but also extends to acid and toxic chemical injuries of the eye.
The Thoft burn classification includes the following groups. I. Epithelial damage, no ischemia, good prognosis. II. Hazy cornea, iris detail seen, less than one-third limbal ischemia, good prognosis. III. 100% epithelial loss, stromal haze blurring iris details, one-third to one-half limbal ischemia, guarded prognosis. IV. Opaque cornea, greater than one-half limbal ischemia, poor prognosis.
A mild alkali burn with epithelial defects ranging from scattered superficial punctate keratitis (SPK) to focal epithelial loss will exhibit sluggish reepithelialization and mild corneal haze with ultimate minimum visual handicap regardless of treatment. Moderately severe burns with a large area of epithelial defects and limbal ischemia take variable courses, depending on the extent of the injury. Moderate stromal opacification with increased corneal thickness can follow, and heavy proteinaceous aqueous exudation in a markedly hyperemic eye can be observed. Superficial neovascularization of the cornea may follow the advancing edge of regenerating epithelium, and persistent epithelial defects may ultimately lead to stromal thinning and perforation. Scarring and neovascularization of the cornea may result in permanent visual impairment. In the most severe burns, the corneal stromal integrity may be undisturbed for the first 2 weeks, although anterior iritis may be severe and go undetected. As re-epithelization of the cornea begins, ulceration and perforation may ensue secondary to the release of collagenases, elastases, and other enzymes from the epithelium, polymorphonuclear neutrophil (PMN) leukocytes, and keratocytes, and decreased collagen synthesis due to severe ascorbate deficiency in alkali-burned eyes.
Therapy is classified by time post injury.
Immediate treatment for chemical burns is copious irrigation using the most readily available source of water or normal saline solution (shower, faucet, drinking fountain, hose, or bathtub). The greater the time is between injury and decontamination, the worse the prognosis. The victim should not wait for sterile physiologic or chemical neutralizing solutions. The lids should be held apart and water irrigated continuously over the injured globe(s). The initial lavage at the site of the injury should continue for several minutes so both eyes receive copious irrigation. Orbicularis spasm may make this difficult. Use of a cloth material on the lids will help the irrigator to hold otherwise slippery spastic lids. Skin irrigation may be started simultaneously by pouring water over the affected area but is unquestionably secondary to ocular lavage.
After the initial lavage, the patient should be taken immediately to an emergency room where treatment should be started immediately before further testing is done. In the emergency room, topical anesthetic is instilled q20 minutes to relieve some of the considerable pain, and immediate lavage is begun with at least 2,000 mL of normal saline 0.9% or Ringer lactate solution over a minimum period of 30 minutes using handheld intravenous tubing, a Morgan medi-FLOW lens, or an irrigated lid speculum. Lid retractors should be used if necessary. The conjunctival fornices and palpebral conjunctiva should be swept with sterile cotton-tipped applicators to remove any foreign matter that may have been retained at the time of injury. Cotton-tipped applicators moistened with 0.05 mol/L of 10% ethylenediaminetetraacetic acid (EDTA) make sticky CaOH easier to remove. Double eversion of the upper lid should be performed to exclude foreign material in the upper fornix. If eversion of upper or lower lids reveals embedded chemical in the tissue, 0.01 to 0.05 mol EDTA solution should be used as irrigant or the fornices further swept with cotton-tipped applicators soaked in EDTA. Careful examination after lavage for perforating ocular injury should be made. Direct pressure on the globe during lavage should be avoided if ocular global laceration is at all suspected (see Section VI).
Irrigation should be continued until pH paper reveals that the conjunctival readings are close to normal (pH of 7). Once a relatively normal pH is achieved, the patient should be checked again in 5 minutes to ascertain that the pH is not changing again in the direction of acidity or alkalinity, depending on the nature of the burn. If pH paper is not available, it is better to overtreat the patient with prolonged lavage.
Medications. While the pH is being stabilized near normal, the mydriatic-cycloplegics atropine 1% or scopolamine 0.25% should be instilled to dilate the pupil and prevent massive iris adhesions to the lens (posterior synechiae) as well as to reduce the pain secondary to iridociliary spasm. Phenylephrine should be avoided due to its vasoconstrictive effects. After irrigation is complete, broad-spectrum antibiotics such as moxifloxacin, gatifloxacin, ciprofloxacin, ofloxacin, tobramycin, or polymyxin-bacitracin ointment should be started to protect against super-infection. For alkali or more severe acid burns, there is frequently an immediate rapid increase in intraocular pressure (IOP) secondary to shrinkage of the collagen fibers of the sclera. Carbonic anhydrase inhibitors such as acetazolamide 500 mg intravenously (i.v.) or orally (p.o.) stat., should be given. Whenever possible, the retina should be examined for necrotic retinopathy from intraocular penetration of the agent.
For pain, systemic analgesics should be administered. Acetaminophen, Oxycodone, and acetaminophen/codeine (Percocet), one tablet p.o. q3h, or meperidine, 50 mg to 100 mg intramuscularly (i.m.) or p.o. q4h, are effective.
Depending on the extend of injury, a complete emergency physical examination should not only be done by an ophthalmologist, but also by an otolaryngologist and an internist, because many toxic chemicals are aspirated or swallowed at the time of original injury, leading to concomitant chemical burns of the respiratory or upper gastrointestinal tract. During irrigation, the examiner should always be aware of the possibility of an acute airway obstruction secondary to the chemical burn, inducing laryngeal edema.
Once the immediate emergency situation is controlled, the affected eye(s) may be pressure-patched. Patients need to be followed daily until the cornea is reepithelialized. For very severe burns, the patient may be hospitalized for close monitoring. Topical antibiotic ointments and drops should be continued q4h to q6h along with the mydriatic-cycloplegics. Preservative-free artificial tears or gel should be started q1h if the patient’s eye is not patched.
Midterm therapy is used for several days to weeks immediately postburn.
Elevation of IOP may be noted and is probably due to prostaglandin release. Long-term elevation of pressure is secondary to scarring of outflow channels. Carbonic anhydrase inhibitors such as acetazolamide 250 mg p.o. qid, metha-zolamide 50 mg p.o. tid are usually effective in reducing this pressure and should be continued as long as it is elevated more than 22 to 25 mm Hg. A topical beta-blocker, such as timolol 0.5% bid, an alpha-adrenergic agonist such as brimonidine bid, and other IOP-lowering drops (see Chapter 10 and Appendix A) may be added if needed. Glycerol 50%, 40 to 60 mL p.o. q12h may be used as an oral hyperosmotic agent for a few days in patients with severely elevated pressure. Mannitol 20% solution i.v., 2.5 mL per kg, may be given for short-term pressure control in those patients who cannot take oral medication. Cardiac and renal status should be ascertained before use of any hyperosmotic agent, and long-term carbonic anhydrase inhibitors should be avoided in patients with a history of renal stones.
Topical steroids such as dexamethasone 0.1% or 1% prednisolone acetate q4h to q1h should be used to quiet inflammation for the first 2 weeks post injury to control anterior segment inflammation and limit matrix degradation. After this period, if the corneal epithelium is not 100% intact, particularly in alkali burns, steroids should be markedly reduced or withdrawn because of the increased chance of corneal melting and perforation due to collagenolytic enzyme release, as well as due to the increased chance of infection. Systemic steroids such as prednisone 30 mg p.o. bid may be substituted if iridocyclitis is still uncontrolled.
Calcium (Ca2+) chelators ascorbate or citrate are important in grade 3 and 4 alkali-burned eyes. Ten percent citrate and 10% ascorbate in artificial tear solution q2h while the patient is awake for 1 week then qid inhibits neutrophil activity and inflammatory chemotaxis and may slow or prevent melting. These eyes become rapidly scorbutic, thus interfering with collagen synthesis and leading to ulceration. Ascorbate (vitamin C) 2 g p.o. daily is also given until epithelial tissue is healed. Ascorbate is believed to promote collagen synthesis. Ascorbate should be used with caution in nonalkali burn situations, because ciliary body concentration of the drug will enhance rather than inhibit corneal melting. It should also be used with caution in patients with compromised renal function. Oral tetracyclines (e.g., doxycycline 100 mg p.o. bid) also chelate Ca2+, and thus collagenase should also be used for several weeks. Further, 1% medroxyprogesterone is very effective in suppression of collagen breakdown. If melting of the cornea begins to occur, other collagenase inhibitors, e.g. 10% or 20% acetylcysteine, may be used q4h.
Therapeutic soft contact lenses with high water content may be of great benefit in assisting epithelial healing, which in turn will inhibit enzyme release and stromal melting. The lenses may be placed, if epithelial healing is delayed, and are generally left in place for 6 to 8 weeks. However, immediately after injury, these lenses should be used with caution, because they may trap the offending agent, preventing epithelial healing and further increasing the rate of infection. The decision regarding the use of soft contact lenses should be left to a cornea specialist. Alternatively, a temporary tarsorrhaphy or PROKERA amniotic membrane lenses that are commercially available may be used for severe burns. A scleral shell or ring could be used to maintain the fornices if a symblepharon starts to develop.
Topical antibiotics drops should be used several times daily initially and then tapered to qid, and cycloplegia (atropine, scopolamine) should be maintained as long as there are more than mild cells and flare in the anterior chamber.
Dermal injury should be cared for with the guidance of a dermatologist.
Long-term therapy depends on the severity of the burn and may vary from an antibiotic and artificial tears to surgical reconstruction of the eye with conjunctival flaps or transplants, amniotic membrane grafts, autologous conjunctival or limbal stem cell transplants, patch grafts, penetrating keratoplasty, and keratoprosthesis. These procedures may be performed as soon as 2 weeks following the injury.
II. Thermal Injuries
usually involve injury to the lids. Direct injury to the globe is usually limited due to reflex closure of the eyelids and a good Bell’s phenomenon. Treatment is similar to that of thermal injury elsewhere in the body.
A contact burn of the globe may be mild, such as one caused by tobacco ash, or severe, such as one seen with molten metal, which may produce severe permanent burns of the globe itself. Heat can cause severe inflammation, leading to expression of stromal proteases and collagen melt. Superficial thermal burns are often caused by hair-curling irons. Further, burns can be caused by glass and iron, with a melting point of 1,200°F, as well as with lead, tin, and zinc, with a melting point below 1,000°F. After a molten cast of the eye has been removed from under the lids, a permanently opacified globe can often be found underneath. Further, sympathetic uveitis can occasionally develop in a nonburned contra-lateral eye.
Therapy. For partial-thickness lid burn, topical antibiotic ointment with sterile dressings is used, but with minimum burns no dressing is needed. Frequent saline or lubricated dressing, avoidance of early débridement, prophylactic systemic or topical antibiotics qid for prevention of secondary infection, and protection of the globe are critical factors in successful management. Cycloplegic agents can help relieve ciliary spasm with associated discomfort. Topical steroids such as prednisolone 1% qid may be used to decrease scarring between the lids and globe (symblepharon formation) if the corneal epithelium is intact. Increased IOP from steroid use should be ruled out periodically. Systemic steroids may be used to control secondary
iridocyclitis if topical steroids must be limited because of the severity of the corneal burn.
Exposure therapy. In severely burned eyelids with exposure of the globe, topical antibiotic ointment tid should be placed on the lid and globe. In addition, a piece of sterile plastic wrap should be placed over the eye to protect the globe from exposure by forming a moist chamber. This same technique of a plastic-wrapped moist chamber may be used to protect patients with exposure secondary to marked exophthalmos, severe conjunctival hemorrhage or chemosis, or traumatic avulsion of the eyelid. The covering film is cut in 10 cm × 15 cm rectangular pieces and may be gas autoclaved in individual packages. These pieces are large enough to cover the entire orbit from forehead to cheek. In addition, antibiotic ointment is applied to the skin around the orbit, and the sterile film is placed over the area to be protected. The film will adhere to the skin by static charge and adherence to the ointment.
In mild burn cases with minimum exposure and Bell’s phenomenon, only the inferior conjunctiva is exposed, and antibiotic ophthalmic ointments q4h should suffice to protect the globe until surgical repair, if needed, is possible.
III. Radiation Burns: Ultraviolet (UV) and Infrared
UV radiation is the most common cause of light-induced ocular injury. Sources are welding arcs, sun lamps, carbon arcs, and prolonged exposure to sun. Ultraviolet burns may be prevented by use of ordinary crown glass, regular glass lenses, or special UV-blocking plastics, as they absorb the rays.
After exposure there is a delay of 6 to 10 hours before the burn becomes symptomatically manifest, when the injured epithelial cells are shed. Symptoms may range from mild irritation and foreign body sensation to severe photophobia, pain, and spasm of the lid, but are usually self-limited and improve within 24 hours.
Examination will reveal varying lid edema, conjunctival hyperemia, and punctate roughening of the corneal epithelium. This punctate pattern is easily seen with fluorescein staining. Because of high absorption in the cornea, UV light rarely damages the lens and does so only if intensity has been extremely high.
Therapy is with short-acting cycloplegic drops such as cyclopentolate 1% to relieve ciliary spasm and prophylactic topical antibiotic ointment or drops. A semipressure patch with the eyes well closed underneath is left on for 24 hours to decrease discomfort from eyelid movement. The patient with severe pain may, however, need systemic sedatives and analgesics. Patients should be reassured that the damage is transient and that all symptomatology will improve within 24 to 48 hours.
Infrared burns are also usually of little consequence and produce only temporary lid edema and erythema, with little or no damage to the globe. Therapy is antibiotic ointment bid for 4 to 5 days after injury. Chronic exposure to infrared light is seen in glassblowers and metal furnace stokers who are improperly protected by industrial goggles. These workers develop cataracts after many years of exposure, but no other anterior segment changes are found and the posterior segment is not affected. The mechanization of furnaces has made this problem relatively rare.
Ionizing radiation from cyclotron exposure and beta-irradiation from periorbital therapy of malignancy are frequent causes of radiation burns. The cornea, lens, uvea, retina, and optic nerve may suffer from injury, but also may be protected from it by use of lead screens and leaded glass to absorb x, gamma, and neutron radiation.
Signs and symptoms are conjunctival hyperemia, chemosis, circumcorneal injection, and watery or mucopurulent discharge. Necrosis of the conjunctiva and sclera can occur if radioactive material is embedded in the conjunctiva. The earliest sign of corneal damage is hypesthesia. Radiation keratitis ranges from a punctate epithelial staining to sloughing of large areas of epithelium, and stromal edema with interstitial keratitis and aseptic corneal necrosis. The minimum cataractogenic dose from x-ray is approximately 500 to 800 rad. The younger
the lens, the greater the vulnerability to x-ray. A latency period of 6 months to 12 years exists, depending on dosage, but independent of whether gamma rays or neutrons were the source of injury. The uveal tract may undergo vascular dilation with subsequent boggy edema. Intraretinal hemorrhages, papilledema, and central retinal vein thrombosis may rarely be seen after radiation injury. Late complications are related to loss of corneal sensation, lack of tears, poorly healing corneal epithelium, corneal vascularization, and keratitis.
Therapy of radiation injury is symptomatic. Cycloplegics, such as cyclopentolate 1% or scopolamine 0.25% bid, and topical antibiotic ointments or drops should be used to reduce the pain of ciliary spasm, prevent synechia formation, and protect against infection. Topical steroids are rarely indicated and should not be used in the presence of epithelial ulceration. A therapeutic bandage contact lens with antibiotic eye drops (ointments dislodge the lens) may assist healing of an epithelial defect.
Solar viewing. Unprotected viewing of the sun as in a solar eclipse or psychotic state can cause irreversible macular burns via focusing of visible and short infrared rays on this retinal area. Loss of visual acuity may become permanent or may return toward normal. There is no specific treatment, and prophylaxis is the key to prevention.
Laser burns of an accidental nature are being seen with increasing frequency with industrial use of these machines. These burns are almost always macular, with instantaneous and usually permanent loss of central vision. Prophylactic wearing of absorbing goggles will protect against indirect laser beam scatter, but only avoidance of direct viewing of the beam will prevent the tragic irreversible and untreatable macular burns.
IV. Electric Shock Cataract
After electrical injury is sustained, particularly around the head, a periodic check for cataract formation through dilated pupils should be made, starting a few weeks after injury. The appearance of characteristic vacuoles is a key prognostic factor. The latency period for cataract formation ranges from months to years.
V. Corneal Abrasions and Foreign Bodies
Traumatic corneal abrasions result in the partial or complete removal of a focal area of epithelium on the cornea, producing severe pain, photophobia, foreign body sensation, lacrimation, blepharospasm, and decreased vision. Motion of the eyeball and blinking increase the pain and foreign body sensation.
