Allan J. Flach, PharmD, MD
The personal tragedy and economic loss associated with impaired vision or even blindness as a result of occupational eye injuries can be prevented by identifying workers at risk and instituting appropriate safety programs. Proper maintenance of tools and equipment by the employer and effective use of protective devices, such as safety glasses or face shields, by the employee will reduce the number of injuries, such as ocular contusions, trauma as a consequence of penetrating and nonpenetrating foreign bodies, conjunctival and corneal abrasions, lid lacerations, and optic nerve damage.
Recognition of the toxic effects of chemical agents and protection from those that may be splashed into the eyes are vital for prevention of visual damage. The ready availability of facilities for cleansing and irrigation of the face and eyes in the workplace is of the utmost importance because initial steps for treatment of chemical burns—especially those caused by strong alkalis and acids—must be carried out immediately by the employee, fellow workers, or anyone else near at hand. There is no time to wait for specialized medical care, so employee education programs for emergency care of chemical burns are essential.
The risks of ocular damage for x-ray technicians, glassblowers, welders, and other workers exposed to ionizing, infrared, and ultraviolet radiation have long been known, but damage caused by exposure to excessive amounts of visible light has been recognized only recently. Wearing protective lenses that filter the most offending wavelengths of visible light may become commonplace in the future.
ANATOMY & PHYSIOLOGY
A brief review of ocular anatomy and function will help in understanding the mechanisms of several kinds of eye injuries and how they affect the visual system (Figure 12–1). The orbit, eyelid, and conjunctiva are protective mechanisms for the eye. The orbit and its bony rim offer excellent mechanical protection from injuries, with the exception of those coming from the direct anterior or temporal directions. The eyelid and conjunctiva are essential for normal maintenance of the smooth, moist, clear anterior surface of the cornea, which, in turn, is essential for clear vision. The normal blinking mechanism depends on the third cranial nerve to open the lids and the seventh cranial nerve to close them. Moistening of the conjunctiva by lacrimal fluid depends in part on activation of the reflex arc between the sensory fifth innervation of the anterior eye and the parasympathetic secretomotor fibers that accompany the seventh cranial nerve along the petrous temporal bone into the middle fossa and then through the orbit to the lacrimal gland. Moistening of the corneal epithelium is aided by mucus from the goblet cells of the conjunctiva, particularly those on the tarsus of the upper lid. Reflex tear production by the lacrimal gland helps to dilute and wash away irritating substances that find their way into the conjunctival sac. The rich blood supply of the conjunctiva and lid also helps in resisting and limiting infections of the anterior eye.
Figure 12–1. View of the inferior half of the right eye.
Internal structures of the eye can be conveniently divided into anterior and posterior segments. The anterior segment includes the cornea, anterior chamber, iris, lens, and ciliary body. These structures comprise the essential optical elements of the eye. The regular pattern of the collagen fibers and posterior endothelial layer of the cornea maintain its optical clarity. Because the cornea and lens are avascular, they require a specialized source of nutrition, which is provided by aqueous humor. The ciliary body produces aqueous humor at a nearly constant rate, bathing the lens and posterior surface of the cornea and then draining near the base of the cornea through the structures associated with the Schlemm canal. A normal rate of production and drainage of aqueous humor maintains the intraocular pressure at between 10 and 21 mm Hg. Injuries causing sustained elevation of pressure can lead to significant glaucomatous visual field loss. The iris and its pupil adjust the amount of light entering the eye. Contraction of the ciliary muscle changes the shape of the lens, thereby allowing for accommodation (adjustment of focusing for seeing at different distances).
The posterior segment of the eye is the light-sensing portion of the visual system and contains the retina and its supporting vascular layer, the choroid. The retina has more than 1 million nerve fibers that arise from the ganglion cells and collect in the optic disc to form the optic nerve, which transmits visual information to the posterior visual system. These nerve fibers are second-order neurons similar to the myelinated sensory tracts of the spinal cord and are not capable of healing with restoration of visual function following injuries such as penetrating wounds of the orbit or posterior orbital fractures involving the optic canal. Depending on the severity of the injury, the fibers may disappear partially or completely, resulting in either partial or complete atrophy of the optic disc (optic nerve). The optic chiasm, optic tracts, and visual radiations to the cortex usually are not involved directly in eye injuries except those involving the bones of the head and the intracranial structures.
Visual acuity depends on the optical clarity of the cornea, lens, and vitreous and proper functioning of the fovea, which is the avascular center of the retinal macula and is composed entirely of specialized cones that are color-sensitive and capable of resolving the finest images. If this small area (<0.5 mm in diameter) is damaged, no adjacent portion of the retina is capable of assuming the fine function that provides maximum visual acuity.
Eye injuries causing retinal detachment or vitreous hemorrhage can lead to loss of peripheral vision, and injuries of the extraocular muscles or their nerves can produce diplopia (double vision).
HISTORY & EYE EXAMINATION
Caution: For chemical burns (see the section “Chemical Burns of the Eye”), emergency treatment should be started immediately, and the history and examination of the patient can proceed in due course. In cases of suspected ruptured or lacerated globe (see below), care must be taken to prevent further damage to the eye during transport to the hospital and initial evaluation.
History
The occupational medical history should include a variety of questions not always considered pertinent to general histories. In addition, the worker should be asked about vision before and after the injury and whether any visual loss was sudden or gradual. Sudden loss of vision without obvious injury may be caused by central retinal artery occlusion or ischemic damage to the optic nerve, occasionally caused by giant cell arteritis. These problems require emergency treatment. Progressive loss of vision following facial bone fractures or head injuries is sometimes a result of optic nerve damage, which may respond to surgery if recognized in time.
In cases of mechanical injury, the worker should be asked about previous tetanus inoculations and about the nature of the forces involved during the injury. Was the eye struck with a small, rapidly moving object that may have penetrated the globe, as sometimes occurs when a steel hammer strikes a steel tool? Or was the eye hit by a large, slowly moving object that may have caused a contusion injury or rupture of the globe? If the presence of a foreign body is suspected, the worker should be asked about the type of material that might be involved (a magnetic metal such as iron or steel, a nonmagnetic metal such as aluminum or copper, or an organic material such as wood) because this information is helpful for determining the method of treatment and for prognosis. Soluble metallic salts from iron-or copper-containing foreign bodies can cause irreversible toxic damage to the retina, best prevented by their prompt removal. Less-soluble materials, such as aluminum, plastic, or glass, are associated with a better prognosis. Organic foreign bodies, such as pieces of wood or splinters of plant material, may introduce an intraocular infection that frequently is difficult to treat and has a very poor prognosis.
If a chemical burn is present or suspected, the type of chemical (alkali or acid) will influence how quickly and deeply it penetrates the eye. If eye injuries are thought to be caused by long-term exposure to chemicals, the various substances to which the worker is exposed should be identified and a material safety data sheet (MSDS) obtained for each. The worker also should be asked about exposure to aerosols, surfactants, detergents, dust, and smoke, all of which can damage the corneal epithelium.
Examination
Even if an injury is thought to have affected only one eye, both eyes should be examined carefully. If swelling prevents easy opening of the eyes for inspection, a sterile topical anesthetic can be instilled through nearly closed eyelids by applying the drops along the lid fissure. After a few minutes, smooth sterile retractors may be used carefully to lift the lids for eye examination.
A. External Eye Examination
1. Eyelids—Note symmetry of the lids of both eyes. Look for lacerations that cross the lid margins and for perforating wounds through the skin of the lid above or below the lid margin. Except in the case of a suspected ruptured or lacerated globe, the lid can be everted to search for foreign bodies on the upper tarsus. To evert the lid, the patient is asked to look down while the physician pulls gently on the lashes and applies mild pressure on the upper surface of the lid.
2. Orbits—Palpate the orbital rims, and note discontinuities and crepitus caused by subcutaneous air from fractures of the paranasal sinuses. In orbital fractures, injury to the inferior or superior orbital nerves as they pass through the floor or roof of the orbit can cause decreased sensibility of the lids and face.
3. Conjunctiva—To examine the conjunctiva, evert the lids by applying gentle pressure over the superior orbital rim of the upper lid or over the malar eminence of the lower lid, thereby avoiding direct pressure on the globe. Look for foreign bodies, hemorrhage, laceration, and inflammation.
Inflammation caused by trauma usually produces a watery discharge (tears), in contrast to the purulent mucoid discharge of bacterial conjunctivitis. Viral or chlamydial conjunctivitis is characterized by lymph follicles in the inferior fornix of the conjunctival sac along with a watery discharge. Preauricular lymph nodes are also frequently present.
4. Corneas—With a bright light, look at the light reflection on the normally smooth corneal surface. Irregularities indicate disruptions of the corneal epithelium. Because the cornea is normally clear and lustrous, the surface texture of the iris is seen easily and clearly. A corneal wound with incarceration of the iris also may be indicated by asymmetry of the pupil. A fluorescein paper strip moistened with sterile saline or a topical anesthetic can be used to stain the tears on the surface of the cornea. The stain diffuses into any area of disrupted epithelium and stains it bright green. The color is enhanced with a blue light. Details of the cornea and the anterior eye are much more easily examined with magnification such as a 2× to 4× loupe or (and preferably) with a slit lamp and microscope, if one is available.
5. Anterior chambers—The anterior chambers should appear deep and clear. Hyphema (hemorrhage into the anterior chamber) is almost always a sign of significant injury. Hypopyon (purulent material in the anterior chamber) is characterized by a white or gray layer of inflammatory cells at the chamber bottom. Hypopyon usually is caused by an infection following a penetrating injury or a bacterial or fungal corneal ulcer.
6. Pupils—The pupils should appear round, black, and equal in size. Pupillary reactions to light should be noted carefully. Normally, both pupils constrict and dilate equally and simultaneously when one pupil is stimulated by light. While the illuminated pupil is demonstrating the direct-light response, the unilluminated pupil is showing the consensual-light response. The direct-light responses of the two eyes can be compared by moving a flashlight back and forth between the eyes and pausing a few seconds at each eye to observe the pupil. Normally, each pupil constricts when illuminated; failure of one pupil to constrict but to dilate instead indicates the presence of an afferent pupillary defect (Marcus Gunn pupil), which may be the result of an optic nerve injury or extensive retinal damage on that side.
B. Test of Ocular Motility
If there are no severe eye injuries, the ocular movements may be tested safely by comparing the excursions in all directions to make sure that they are the same in both eyes. Limitation of upward or downward gaze occurs frequently in orbital floor fractures and may be the result of accompanying edema or mechanical restriction of the ocular muscles. It also can result from direct trauma to a muscle when a penetrating injury of the orbit occurs.
C. Ophthalmoscopic Examination
1. Red reflex—The presence of a good bright-red reflex demonstrates normal optical clarity of the eye. A direct ophthalmoscope with a good bright light is used to observe the red reflex (the red glow reflected from the fundus). Examination should take place in a darkened room with the instrument set at 0 or +1, and the eyes should be observed at arm’s length, approximately 60 cm (2 ft), so that the reflex in both of them can be seen at the same time and compared. An opacity in the cornea, anterior chamber, lens, or vitreous or a gross change in the color of the retina will appear as a dark form against a red background or as a dull or absent red reflex.
2. Optic discs—The examiner should be as close to the patient as possible to maximize the relative size of the pupil. The optic discs should be examined for the presence of papilledema. Optic discs usually are well vascularized and have a good pink color. When nerve fibers in the optic nerve die as the result of various injuries, the blood supply to the disc decreases in proportion to the loss of fibers. The disc will show a faint pallor if only a few fibers are missing, or it may appear completely white as a result of optic atrophy following total destruction of the nerve.
3. Optic cups—The width of each optic cup is usually one-third or less the diameter of the whole optic disc. If it is as large as half the diameter, or if the optic cups are not similar in both eyes, there is an increased risk for glaucoma. Therefore, estimating the cup size is useful for screening patients for glaucoma.
4. Retinal vessels—The vessels should be examined along the upper and lower arcades proceeding from the optic disc, and the presence of hemorrhages, exudates, and other alterations in the appearance of the retina should be noted.
5. Maculae and foveae—Each macula should be checked for alterations in its usual relatively featureless appearance. Its center, the fovea, always can be located 2.5 disc diameters temporal to the optic disc. Its concave center usually shows a small, bright foveal light reflex.
D. Measurement of Intraocular Pressure
If a lacerated or ruptured globe is suspected, intraocular pressure should not be measured. In other injuries, pressure can be measured with a Schiotz tonometer or with an applanation tonometer, if one is available on a slit lamp. If a tonometer is not available, a general impression of extremely high or low intraocular pressure can be obtained by gently palpating each globe in turn with one finger of each hand through the closed upper eyelid. Comparison of the firmness of the two eyes is occasionally useful when the intraocular pressure is extremely high, as in angle-closure glaucoma.
Angle-closure glaucoma accounts for only approximately 5% of all glaucoma; it usually presents with acute aching pain in the involved eye with moderate redness of the globe and blurred vision, sometimes described as colored halos around bright lights. It occurs when the iris root touches the back of the cornea, blocking aqueous out-flow and causing intraocular pressure to rise very rapidly, thus leading to the symptoms. Angle-closure glaucoma can occur only in eyes with anatomically shallow anterior chambers and narrow chamber angles. An attack of angle-closure glaucoma requires prompt treatment. The first approach is to lower the pressure medically with topical miotics such as pilocarpine 1–4% every 15 minutes for 1–2 hours. The production of aqueous humor is reduced with a topical ophthalmic β-adrenergic blocker and a carbonic anhydrase inhibitor. Intraocular pressure can be lowered quickly by increasing the osmolarity of the blood that moves water out of the vitreous humor, thus reducing the ocular volume and the intraocular pressure. Intravenous urea or mannitol infusions are effective, but oral ingestion of glycerin is as effective, safer, and more easily available. Subsequent attacks are prevented by making an opening in the peripheral iris (iridectomy), which passes aqueous humor directly from the posterior chamber to the anterior chamber, keeping the filtration angle open. The iridectomy usually is made with a laser.
Open-angle glaucoma accounts for most cases of glaucomatous visual loss (90%). Its onset is insidious, there is no pain, and visual symptoms are noticed only after severe irreversible loss of visual field has occurred. Therefore, it becomes the physician’s responsibility to see changes in the optic cup. Asymmetric cups or cups as large as one-half the disc diameter are suspicious. Such changes are an indication to request visual fields. Early lowering of intraocular pressure is the only way to prevent loss of visual field. All adults should be encouraged to have their intraocular pressures measured every 1 or 2 years.
The remaining 5% of cases of glaucoma have a variety of causes. Contusion injuries to the eye can tear the iris root and the ciliary body’s attachment to the sclera, damaging the filtration angle, reducing aqueous outflow, and raising pressure. This is called angle-recession glaucoma. Blood in the anterior chamber (hyphema) and inflammatory cells in cases of chronic inflammation, such as uveitis, can block aqueous outflow channels, causing secondary glaucoma.
Although many investigators discuss enhancing blood flow and neuroprotection as potential therapies, the only treatment of open-angle and secondary glaucoma proven effective is lowering of the intraocular pressure. This can be done by medically reducing the production of aqueous humor with a topical β-adrenergic blocker, a systemic carbonic anhydrase inhibitor, or a sympathomimetic drug. Parasympathomimetics, sympathomimetics, and prostaglandin analogues increase the outflow of aqueous humor. If these measures fail to lower the pressure adequately, a surgical procedure can be used to increase the drainage of aqueous humor into the subconjunctival space.
E. Test of Visual Acuity
Visual acuity always should be tested and the results recorded before treatment is instituted. This is important both from the point of view of good care and for medicolegal reasons because patients do not always remember the amount of visual loss that occurred at the time of a severe injury. Visual acuity should be measured with a Snellen chart, if possible, or with a near-acuity card and recorded appropriately. Each eye should be tested separately, first without correction (glasses or contact lenses) and then with correction; each acuity measurement should be recorded for the right eye followed by the left. If a near-acuity card is used, it is important to record the distance at which the measurements were made and whether they were made with or without the patient’s glasses. If visual acuity is poor and a refractive error is suspected, the chart or card can be read through a pinhole as a substitute for corrective lenses; an improvement in acuity will confirm the presence of a refractive error. If acuity is less than 20/200, the greatest distance at which fingers can be counted should be noted for each eye. If the patient cannot see the fingers well enough to count them, the greatest distance at which hand movements can be seen should be recorded. If vision is poorer than this, light perception can be tested with a bright flashlight held as close to the eye as possible, and the ability to perceive light in each of the four quadrants is recorded. If there is no light perception, it should be recorded as such. Visual acuity measured with a Snellen chart is based on a visual angle of 1 minute of arc; this is considered the best resolving power of the eye and is the standard used to design all types of test charts. The 20/20 letters are formed of black lines separated by white spaces, each 1 minute of arc wide; the whole letter is 5 minutes of arc high, measuring 8.7 mm (Figure 12–2). When letters of this size are read accurately at a distance of 20 ft (6 m), 20/20 vision is determined. Other letters on a chart increase in multiples of this standard dimension. The 20/200 letter is 10 times larger or 87 mm high and would appear the same size as a 20/20 letter when seen at a distance of 200 ft. Metric visual acuity charts use 6 m as the standard test distance; therefore, 6/6 = 20/20. The peak of the light-sensitivity curve of the eye is at a wavelength of about 555 nm. This means that our best vision is in yellow-green light.
Figure 12–2. Measurement of visual acuity. Visual acuity measurements are based on a visual angle of 1 minute of arc subtending each part of a test letter. Each letter is made up of five equally sized black or white parts; therefore, the whole letter subtends a visual angle of 5 minutes of arc. The 20/20 letters are 8.7 mm high; the 20/40 letters are twice as large, or 17.4 mm high. This drawing is not to scale.
There are two techniques for objectively estimating visual acuity—optokinetic nystagmus and visual evoked response—that may be useful in certain situations, particularly when the patient is unable or unwilling to respond to the usual subjective measures of visual acuity. Optokinetic nystagmus is a visually stimulated response to relatively large targets. These eye movements are observed in the intact visual system by passing an alternating series of dark and light stripes of equal width before the patient’s eyes. Involuntary nystagmus is produced—slow following movement in the direction of movement of the stripes alternating with a quick recovery movement. The stimulus is usually presented as a series of vertical stripes 1–2 cm in width on a handheld drum 10–15 cm in diameter. The drum is held 20–30 cm from the patient and turned slowly while observing the patient’s eyes to see the induced nystagmus. The stripes also can be presented on a 50-cm-long cloth strip with the stripes running across the 10–12-cm width. Normally, the nystagmus can be induced in any direction, and its rate will vary with the speed of the stimulus.
The visually evoked response is an electroencephalographic recording over the visual cortex (occipital lobe) in response to visual stimuli. The stimulus can be a simple light flash giving an on-off response, or an estimate of visual acuity can be made by presenting an alternating pattern of dark and light squares in a checkerboard pattern on a television screen. The squares can be made progressively smaller until the response is no longer recorded, and the size of the smallest squares eliciting a cortical recording can be related to standard visual acuity measurements. The responses are involuntary and cannot be controlled by the subject; acuity measurements in the range of 20/400 to 20/20 have been recorded even in infants younger than 1 year of age. This technique usually is available through neuro-ophthalmologic or neurologic consultation. It can be particularly valuable when evaluating patients with compensation or forensic problems.
F. Test of Visual Fields
Visual fields should be tested, especially in patients with suspected head injury or a significant decrease in visual acuity. Each eye is tested separately by confrontation. The patient is asked to look at the examiner’s eye while the examiner’s hand moves toward the center of the visual field. The point at which the patient can accurately count fingers in each of the four quadrants is determined, and the results in the two eyes are compared carefully.
CHEMICAL BURNS OF THE EYE
Etiology & Pathogenesis
Strong alkalis and acids can cause the most severe and damaging chemical injuries to the eye and eyelids. Alkali burns are commonly caused by sodium and potassium hydroxide used as cleaning agents, by calcium hydroxide used in mason’s mortar and plaster, and by anhydrous ammonia used in fertilizer. Battery acids and the strong acids used to clean metal in the electroplating industry are also common causes of severe eye injury.
Alkalis affect the lipid in cell membranes and thereby reduce the normal barriers to diffusion. This allows the chemical to penetrate rapidly the interior of the eye. Because alkalis are not neutralized quickly by tissue, their destructive action can continue for hours if they are not diluted and removed immediately by irrigation of the eye. In contrast, acids tend to be fixed by protein in tissues, and this neutralizes them in a relatively shorter period and keeps them from penetrating as deeply.
The corneal endothelium, which is essential for corneal clarity and good vision, is particularly vulnerable to chemical insult. There is often severe damage within the anterior chamber, including the aqueous outflow pathways, leading to glaucoma. Obliteration of the blood vessels of the conjunctiva and sclera can cause severe ischemia of the anterior eye, including the periphery of the cornea and the underlying ciliary body and iris. Ischemia, as well as the associated reduction in blood supply, is one of the major causes of the poor prognosis in patients with severe chemical burns.
Clinical Findings
The skin on the face and eyelids shows edema and erythema, sometimes associated with sloughing of the surface. Eye examination may require use of a topical anesthetic unless nerve damage is severe enough to cause anesthesia. The conjunctiva may be mildly hyperemic, show small hemorrhages, or be blanched and have the appearance of white marble. Testing the pH of the conjunctival surface with indicator paper will help to confirm the presence of acid (low pH) or alkali (high pH) injuries. The severity of injury (Table 12–1) usually is judged by the degree of corneal opacity using the normal clarity of the pupil as a guide. The cornea may appear gray or cloudy because of epithelial and stromal edema. If the cornea is not cloudy, the anterior chamber can be seen clearly. In some cases, the iris and pupil appear hazy and indistinct. Visual acuity is decreased in proportion to the severity of corneal damage. Injuries of the nasopharynx and upper respiratory passages frequently are found in association with aspiration of the chemical irritant.
Table 12–1. Classifications of chemical burns of the eye.
Prevention
Chemical burns can be prevented by safety measures such as keeping chemicals in unbreakable containers and providing splash-protection shields and eyeglasses to employees who must handle chemicals. Workers at risk should be taught emergency treatment measures for themselves and their fellow workers.
Treatment
Emergency treatment (Table 12–2) should be started in the workplace by the patient or anyone immediately available. Any source of water (drinking fountain, hose, etc) is adequate and should be used immediately to wash the eyes with copious amounts of water until the patient can be taken to an emergency facility. At least 1 L of saline or other isotonic solution then should be used to irrigate each eye carefully, with the lids held open to thoroughly cleanse the conjunctival sac. Use of a sterile topical anesthetic may be necessary.
Table 12–2. Emergency treatment of chemical burns of the eye.
(1) In the workplace: Wash the eyes with copious amounts of water until the patient can be taken to an emergency facility.
(2) In the emergency facility:
(a) Irrigate each eye with at least 1 L of saline or other isotonic solution, with the lids open to flush the conjunctival sac.
(b) Use sterile topical anesthetic as necessary.
(c) Remove particulate matter with cotton-tipped applicators.
(d) Test the pH of the conjunctival surface, and continue irrigation until the pH approaches neutral.
(e) Remove loose or damaged epithelium from the cornea and conjunctiva.
(f) Dilate the pupil with cyclopentolate or scopolamine.
(g) Give topical antibiotic drops, patch the eyes, and refer the patient to an ophthalmologist.
Moist cotton-tipped applicators should be used to sweep the conjunctival surface free of particulate matter, such as the granules found in drainpipe cleaners and plaster. The pH of the conjunctival surface should be tested with pH test paper strips or urine pH test strips and irrigation repeated until the pH approaches the normal level of 7. As a general rule, there is no practical limit to the amount of irrigation that may be helpful. If there is any doubt about its efficacy, irrigation may be repeated for several hours while waiting for ophthalmologic consultation.
During irrigation, the gray color or cloudiness of the cornea may appear to clear, giving a false impression of improved clinical status. The change is usually a result of sloughing of the damaged corneal epithelium, which reveals the clearer corneal stroma underneath.
After irrigation is completed, cycloplegic drops (eg, cyclopentolate or scopolamine) may be instilled to dilate the pupil and thus prevent posterior synechiae (adhesions between iris and lens). Antibiotic drops should be instilled before the eye is patched. The patch prevents blinking and should provide some comfort. The patient should be referred to an ophthalmologist.
Specific ophthalmologic treatment may include the use of topical corticosteroids and antibiotics to reduce the severe inflammatory response that occurs shortly after injury. These medications—particularly the corticosteroids—must be used with caution because they enhance the possibility of secondary infection and discourage the formation of new vessels in ischemic areas. Irrigation of the anterior chamber with saline solution may help to restore the pH to more normal levels. After the initial reaction subsides and the conjunctiva and cornea have epithelialized, the severity of the injury can be judged. A scarred cornea can be replaced by a corneal transplant, and a damaged lens (cataract) can be removed surgically and replaced with a clear synthetic lens. Glaucoma as a consequence of scarring of aqueous outflow pathways may be controlled medically—and if not, a surgical fistulization procedure may be done.
Prognosis
Emergency treatment of chemical burns usually is followed by a period of weeks or months of effort to rehabilitate the damaged ocular tissues. The degree of blanching or ischemia of the conjunctiva is an important factor influencing the final outcome. Ischemic damage, even in the presence of apparent healing, makes ultimate restoration of vision difficult. The survival of a corneal transplant depends on normal function of structures in the anterior eye. The survival of the cornea and the anterior segment of the eye are directly related to the degree of damage to the corneal endothelium, aqueous drainage pathways, and ciliary body. If the ciliary body fails to produce enough aqueous humor, the entire eye becomes soft and ultimately atrophies. In patients with severe burns, deep penetration and extensive destruction of ocular tissues can lead to perforation of the globe, infection, and loss of the eye. Milder burns in which chemical penetration is shallower may heal with little scarring.
THERMAL BURNS OF THE EYE & EYELID
Thermal burns of the eyelids and upper face may involve the eyes. However, in cases of flash burn caused by a sudden gas explosion, most individuals forcibly close their eyes, and this reflex lid closure usually protects the ocular surface. Direct contact with molten metal or glass can cause severe injury to the lids and even to the open eye. Thermal injury occurs rapidly at the time of contact. Tissue destruction is not progressive, as is the case with some chemical burns.
Eye examination may require topical anesthesia and careful use of lid retractors. Irrigation may be necessary to remove particulate matter, especially in injuries caused by explosions.
Depending on their severity, thermal burns of the eye structures are treated in the same manner as burns occurring elsewhere on the body. Extensive loss of lid skin can lead to exposure and drying of the cornea. This can be prevented by covering the eye with a transparent plastic sheet and sealing it to the surrounding skin with a sterile antibiotic ointment, thus producing a humidity chamber over the eye. Healing of lid skin frequently is followed by scarring, contraction, and distortion of the lids, which result in some degree of exposure of the globe. Plastic surgery with skin grafting may be necessary to restore lid function.
MECHANICAL INJURIES OF THE EYE & EYELID
Mechanical injuries range from superficial abrasions to complete disruption of the globe depending on the nature of the force striking the eye. Small, sharp, fast-moving objects can penetrate or lacerate the globe, whereas larger objects may exert enough compressive force to cause contusion injury or to rupture the eyeball.
Laceration of the Eyelid
Lid lacerations result from two common mechanisms: (1) contact with sharp, fast-moving objects such as glass or metal parts that cut the skin and subcutaneous tissues (partial-thickness lacerations) or involve the posterior layers, the tarsus, and the conjunctiva (full-thickness lacerations) and (2) avulsion injuries that are caused by blunt trauma (eg, a blow to the malar eminence) and cause abrupt traction of the lid and tear it from its attachment to the medial canthal ligament. The type and extent of injury determine the method of treatment.
Partial-thickness lacerations can be closed by direct suturing with generally good results. Full-thickness lacerations require meticulous repair in two layers by an ophthalmic or oculofacial plastic surgeon to accurately restore the continuity of the lid margin. If notching of the margin occurs with healing, the cornea may not be moistened adequately by tears and protected from abrasions and other trauma. Deep stab wounds above the upper lid may sever the levator muscle of the lid. The cut end of the levator is easier to retrieve and repair if surgery is performed immediately after injury. Inadequate repair can result in chronic ptosis. Severe damage to the upper lid and blinking mechanism also can place the patient at risk for superficial corneal injuries.
In avulsion injuries, lid structures that have pulled away from the globe should be examined carefully and placed as close to their anatomic positions as possible to protect the eye while the patient is awaiting treatment by an ophthalmic surgeon. Retention of avulsed lid structures is important. They frequently can be repaired and usually heal well because of their rich blood supply. It is difficult to substitute skin grafts or skin flaps for the normal lid structures, particularly the tarsal and conjunctival structures that are essential for normal functioning of the lid. Avulsion of the medial canthal ligament sometimes disrupts the lacrimal drainage system, and failure to repair it will result in epiphora (the overflow of tears).
Injuries to the Iris
Injuries to the iris can be caused indirectly by contusion and directly by perforating or penetrating injuries of the eye.
Contusion of the globe transmits force to the iris by the rapid displacement of aqueous humor. Because water is incompressible and the eye is essentially inelastic, these forces can be very large and destructive.
Iridoplegia is caused by damage to the pupillary sphincter. The pupil may react to light either directly or consensually and only slightly or not at all. The iris root, where it attaches to the ciliary body, may be torn, producing an iridodialysis. Sometimes the ciliary body with the iris root intact is torn away from its scleral attachment, producing an angle recession that can damage the aqueous outflow, causing a form of glaucoma.
Penetrating injuries, foreign bodies, stab wounds, corneal lacerations, and ruptured globes all may perforate, tear, or disrupt the iris. Iris tissue frequently herniates through corneal or scleral wounds.
Iris injuries usually do not require treatment other than incidental repair of the associated major injuries. Except for an increase in the amount of light entering an eye, it may have quite useful vision without an iris or with an iris with multiple holes. An eye with more than one pupil still sees only one image.
Injuries of the Retina
Retinal injuries are caused by both blunt trauma (contusion) and penetrating wounds. When the eye is struck in a contusion injury, the force is transmitted by the fluid contents throughout the interior of the globe. Posteriorly, the retina may become edematous in a discrete area, frequently including the macula—a condition called commotio retinae or Berlin edema. Vision is reduced but may improve to nearly normal when the edema clears. This process may require several weeks to a month to complete. Contusion injuries also cause forceful displacement of the vitreous, resulting in traction at its anterior attachment on the surface of the retina at the posterior edge of the ciliary body. This may disinsert the retina from the ciliary body or tear a hole in the peripheral retina. Hemorrhage may result, clouding the vitreous for a time.
Retinal tears or holes frequently cause retinal detachments, which require prompt surgical repair. Visual prognosis depends on macular involvement. If the macula is intact, vision is usually good; if the macula is detached for even a few days, the prognosis is apt to be poor. Penetrating injuries cause direct perforations and tears in the retina, causing hemorrhage and detachments. Treatment of retinal detachments requires localization and closure of the tears or holes. This is done by creating an adhesion and scar between the retina and the choroid surrounding the hole. A freezing probe placed on the scleral surface over the hole will cause an inflammatory reaction in the choroid that will adhere to the retina. Sometimes it is necessary to bring the scleral, choroidal, and retinal surfaces together. Usually this is done by placing an encircling band of silicone rubber around the entire globe; it also may be done by pushing them together from the inside by injecting a gas bubble into the vitreous space.
Ruptured or Lacerated Globe
If a ruptured or lacerated globe is present or suspected, placing a metal shield or other protective covering (eg, the bottom half of a paper cup) over the injured eye will prevent external pressure from causing further damage during transport to the hospital. Patching the other eye will reduce ocular movements and thus help to prevent further trauma to the injured eye.
Visual acuity should be measured and recorded. Severe injuries almost always are associated with some degree of visual loss, lid swelling, orbital swelling, exophthalmos, and hemorrhage. If lid swelling is extreme, it may be necessary to use a sterile topical anesthetic and lid retractors to lift the lids away from the globe during initial examination.
If the cornea is clear and the pupil is round and reacts to light, the globe probably is intact. Global rupture usually is characterized by the presence of brownish or grayish tissue beneath the conjunctiva (subconjunctival hemorrhage), which is caused by exposure or herniation of uveal tissue, an irregular or disrupted corneal surface, or the presence of blood or gross alteration in the appearance of the iris and pupil. Pupillary light reflexes may be abnormal. The pupil pulled or peaked toward one side of the cornea usually indicates that the iris has herniated through a laceration in that direction.
Ophthalmoscopic examination may be difficult because of corneal irregularities and hemorrhage in the anterior chamber and vitreous. If the fundus can be examined and the disc and vessels appear relatively normal, gross disruption of the globe is unlikely. A bright red reflex usually indicates that the interior of the globe is intact. Intraocular pressure should not be measured if a ruptured or lacerated globe is suspected. A radiograph for detection of any radiopaque material in the region of the globe is an essential part of the initial examination.
Definitive examination and treatment should be performed by an ophthalmic surgeon. Until a surgeon is available, both eyes should be covered again, with a sterile eye pad used on the injured eye to minimize contamination. The patient should be supported with parenteral fluids and be considered a candidate for general anesthesia. The repair of a ruptured globe or corneal laceration usually is done under general anesthesia. A local anesthetic is not considered safe because the distortion from its injection might cause additional damage.
The eye is examined safely under anesthesia, usually with an operating microscope, and the repair is carried out by suturing the torn sclera or lacerated cornea. Exposed intraocular structures such as the iris or ciliary body may be replaced in the eye or excised depending on their condition. When the repair is complete, the eye is filled with saline or an electrolyte solution that simulates aqueous humor. Antibiotics are injected subconjunctivally after the globe is closed and are continued intravenously for 4–5 days to prevent infection that may have been introduced by the injury.
A ruptured globe has a grave prognosis for restoration of vision. Corneal lacerations have a better prognosis because their surgical repair usually is accomplished easily. If scarring occurs, corneal transplant can be performed.
Contusion Injuries
Blunt trauma to the eye causes various contusion injuries ranging in severity from ecchymosis of the eyelids (black eye) to major intraocular damage. Compression injuries of the anterior eye are characterized by corneal edema, anterior chamber hemorrhage, and increased intraocular pressure. These symptoms usually resolve without treatment. In some cases, however, return of normal intraocular pressure is followed several weeks or months later by another increase, which indicates the presence of angle-recession glaucoma. This is caused by a tear in the attachment of the iris and ciliary body from the internal surface of the sclera at the anterior chamber angle, damaging the aqueous outflow pathway. Patients with compression injuries always should receive follow-up care at the hands of an ophthalmologist so that angle-recession glaucoma can be detected and treated to prevent progressive damage to the optic nerve. Treatment usually begins with twice-daily drops of an ophthalmic β-blocker.
Hyphema (hemorrhage into the anterior chamber) frequently clears spontaneously, but secondary hemorrhage occurs after several hours or days in up to one-third of patients as a result of lysis of the thrombus in the injured vessels of the iris or ciliary body. Secondary hemorrhage frequently continues until the anterior chamber is completely filled with blood, during which time the intraocular pressure may rise to 50–60 mm Hg (normal 12–20 mm Hg). Lysis and reabsorption of this blood clot may take many days and cause damage to the aqueous filtration pathways and subsequent glaucoma. Breakdown products of blood also can diffuse into the cornea, stain it, and cause long-term reduction of vision. If reabsorption of the blood clot is prolonged, it sometimes can be aspirated successfully. If not, the anterior chamber is opened, and the clot is removed directly. Secondary hemorrhages may require surgical treatment. The prognosis for good vision in patients with secondary hemorrhage is poor.
The prevention of secondary hemorrhages is difficult. Bed rest with binocular patching has been a standard treatment for many years. More recent experience comparing patients treated with bed rest and others allowed normal activity showed no significant difference in the incidence of secondary hemorrhages.
Aminocaproic acid has been used to retard fibrinolysis in the injured vessels to prevent secondary hemorrhages to the benefit of many patients. This treatment slows the lysis of the primary hyphema but, when given for 5–7 days, does reduce the occurrence of secondary hemorrhages. There are significant side effects, so use of aminocaproic acid must be considered carefully and monitored.
Retinal edema, particularly in the macula, causes acute reduction of vision. Vision usually improves with clearance of edema in a few days to several weeks. Clearance is not always complete, and there may be permanent damage to the macula. In ruptures of the choroid, blood spreads beneath the retina at the time of injury, and reabsorption of blood will reveal a crescent-shaped scar concentric with the optic disk. There is no treatment. Other contusion injuries include dislocation of the lens (partial or complete), traumatic cataracts, and tears in the region of the anterior attachment of the retina to the ciliary body, which lead to vitreous hemorrhages and detachment of the retina.
A damaged lens—either dislocated or cataractous—may reduce vision or may be displaced anteriorly, causing increased intraocular pressure by closing the aqueous filtration angle. In either case, the lens is removed by using one of the cataract surgery techniques. Vitreous hemorrhages are removed with a suction-cutting vitrectomy instrument. Following this procedure, the retinal detachment is repaired by creating an adhesive scar between the choroid and retina, usually by freezing through the scleral surface (cryotherapy) over the area of the retinal tear or hole. The sclera then may be buckled inward to push the adhesion against the retina. This is usually done by compressing the globe with an encircling band of silicone rubber. Sometimes, an intraocular gas bubble is used to push the retina, choroid, and sclera into contact.
Intraocular Foreign Bodies
An intraocular foreign body should be suspected on the basis of the occupational history, particularly if the worker complains of an irritating sensation in the eye and no superficial foreign body is found. For example, when steel tools are used to hammer other steel objects, the hammered steelwork hardens to a glassy surface from which small, sharp chips can fly and penetrate the globe with a minimum of discomfort at the moment of impact. Vision may be nearly normal if the entry wound is small. In cases such as this, in which a radiopaque foreign body is suspected, a radiograph should be taken. Ultrasonography usually will demonstrate nonradiopaque objects (eg, glass and plastic). If a foreign body is found, referral to an ophthalmologist for further evaluation and early treatment is essential.
Failure to remove iron or copper foreign bodies can cause severe impairment or loss of vision owing to their toxic effects on ocular tissue. A retained iron or copper foreign body may dissolve away in several months to a year, but the damage done to the retina by the soluble metallic salts is irreversible, and marked visual loss—even blindness—results. The prognosis for these foreign bodies is good if they are removed before they have time to dissolve. Inert materials such as glass or plastic may cause mechanical damage to the eye, but in the absence of a local toxic reaction, the long-term prognosis is better. It is not necessary to remove every foreign body made of inert material; some of them may be left in place depending on their position in the globe and their effect on visual function. Iron-containing magnetic foreign bodies usually are removed with an ophthalmic magnet—sometimes through the entry wound or through a surgical incision made as close as possible to the foreign body. Nonmagnetic foreign bodies are removed with grasping instruments specially designed for ophthalmic microsurgery. Penetrating wounds caused by potentially contaminated objects such as agricultural implements or by wood fragments thrown from woodworking machinery can introduce severe intraocular infections that lead to complete disruption and loss of the globe; therefore, microbiologic studies and treatment with appropriate systemic and local antibiotics are required.
Injuries to the Orbit & Optic Nerve
Orbital floor (“blowout”) fractures frequently are associated with herniation of intraorbital contents into the fracture line. Usually there is severe edema within the orbit that restricts eye movements for 7–10 days. If restriction continues, surgical repair of the fracture may be indicated to free the entrapped extraocular muscles.
Facial bone and orbital fractures that extend to the posterior orbit may involve the optic canal, with damage to the optic nerve indicated by the presence of an afferent pupillary defect. Initial and later evaluations of the patient should include documentation of visual acuity. If there is progressive loss of vision, surgical decompression of the optic nerve in the canal may preserve or, occasionally, even improve the remaining vision.
Orbital injuries may cause severe hemorrhage, marked exophthalmos of the globe, and a dramatic and abrupt increase in intraocular pressure owing to compression. Although this increased pressure usually is relieved by the normal dissipation of interstitial fluid in a short period of time, it occasionally results in occlusion of the central retinal artery or vein. Pressure sometimes can be reduced by the application of gentle external massage to the globe through the closed lids. Surgical lysis of the lateral canthus of the lids may be required.
Penetrating wounds can damage the optic nerve directly by advancing through the funnel-shaped orbit to reach its apex, where the nerve and its blood supply are trapped by the optic canal. Contusion of the nerve causes severe visual impairment and sometimes is treated with large doses of systemic corticosteroids in a manner similar to treatment of spinal cord injuries.
Injuries of the Corneal Epithelium (Abrasions & Superficial Foreign Bodies)
Abrasions of the corneal epithelium can be caused by superficial mechanical trauma (eg, prolonged wearing of contact lenses); by the presence of a foreign body; or by exposure to ultraviolet radiation, chemicals, aerosols, dust, smoke, and other irritants. The occupational medical history should be taken, as described in Chapter 2.
Photokeratoconjunctivitis (welder’s flash) is a specific ocular injury caused by unprotected exposure to ultraviolet radiation with wavelengths shorter than 300 nm (actinic rays). This radiation is generated by the welder’s arc and damages the exposed corneal and conjunctival epithelium. Injuries are caused both by direct observation of the arc and in persons nearby who often are not wearing protective filters.
In the first few hours after exposure, there may be only mild discomfort and slight conjunctival redness. After a latent period of several hours—even as long as 6–8 hours—the injured epithelial cells slough, causing an acute onset of severe pain sometimes said to be “as though someone had thrown hot sand in my eyes.” Marked tearing, photophobia, and blepharospasm (tightly closed lids) are usual.
Examination requires a sterile topical anesthetic, which may be introduced through nearly closed eyelids by placing several drops along the lid margins. When the eyes open, more anesthetic may be instilled, along with fluorescein from a sterile paper strip. The fluorescein will diffuse over the cornea where the epithelium has sloughed, staining it bright green—best observed with a blue light. Epithelial loss is confined to the area exposed in the lid opening.
Treatment consists of instillation of an antibiotic ointment and patching the eye or eyes to prevent lid movement or blinking. The epithelium will not heal rapidly and in some cases not at all if it is frequently wiped and disturbed by blinking. It will require 12–24 hours for healing to occur; in some cases, several days may be necessary. The eyes should be examined daily. Anesthetic drops and fluorescein help in following the progress of reepithelialization. Continue to patch with antibiotic ointment until healing has occurred. Corneal epithelium heals without scarring. Antibiotic solutions or ointments containing corticosteroids sometimes are recommended for the treatment of welder’s flash burns. The steroids may speed clearing of the associated hyperemia and edema, but they increase the incidence of secondary bacterial, viral, and fungal infections. If steroids are used, frequent examination (every 12–24 hours) is essential to detect early signs of infection until healing occurs. In addition, prolonged use of topical steroids (10–14 days or more), even in low doses, can raise intraocular pressure and, in time, can cause significant glaucomatous field loss. This unpredictable response occurs in approximately 10% of the population. It is therefore probably best to avoid the routine or frequent use of topical corticosteroids in the treatment of corneal and conjunctival injuries and infections.
The patient should not be given anesthetic drops or ointment to use at home. Anesthetics slow and may even prevent epithelial healing, and when used in these circumstances, they have led to severe scarring of the cornea and even the loss of an eye.
These injuries are easily prevented by wearing adequate protective filters in the face masks for the welder and goggles or ultraviolet filter glasses by visitors and workers in nearby areas where the welding flash can be seen.
Symptoms and signs of corneal abrasions include severe ocular pain, tearing, and blurring of vision. Inspection of the anterior eye with a flashlight usually shows irregular light reflections on the corneal surface in the area of the abraded epithelium. Use of sterile topical anesthetic and fluorescein paper strips is helpful for further examination. The fluorescein dye diffuses into the area of disrupted epithelium, stains it bright green, and can be observed easily with a blue light. If further evaluation reveals normal pupillary reactions, a bright red reflex, and no disruption of the anterior segment, the injury usually is confined to the anterior external layer of the cornea.
Small foreign bodies on the surface of the cornea or conjunctiva may be seen directly or detected by evidence of damaged epithelium from the fluorescein stain. Foreign bodies usually can be removed with a cotton-tipped applicator, but a sharp instrument is helpful occasionally. The side bevel of a disposable hypodermic needle can be used to gently detach foreign bodies that are firmly attached to the corneal surface. Rust deposited in the anterior layers of the cornea frequently can be removed by the same gentle scraping maneuver. If all the foreign body or rust is not removed easily, it usually can be left to slough or absorb by itself without causing damage. After foreign bodies are removed, treatment is the same as for abrasions.
Abrasions are treated by applying a sterile ophthalmic antibiotic ointment effective against both gram-positive and gram-negative organisms (eg, gentamicin, tobramycin, or a mixture containing bacitracin, polymyxin, and neomycin) and covering the affected eye with a patch dressing to keep the lids closed. Corneal epithelium usually heals promptly if the surface of the cornea is allowed to rest without blinking the lid. The initial process of healing is one in which the normal epithelial cells slide from the edge of the wound over the smooth surface of the cornea to fill the gap. The eyes should be inspected in 12–24 hours to determine if healing has occurred and to rule out corneal infection, which appears as a white or gray haze in the area of the wound. If the abrasion is not healed completely, a second application of the ointment and patch dressing for an additional 12–24 hours may be required. This process should be continued until the epithelial defect is healed. Scarring usually does not occur, and vision is restored to normal.
Caution: After the initial examination with topical anesthetic, sharp pain may return until the epithelium begins to heal. Under no circumstances should the patient be supplied with anesthetic drops or ointment to use during the healing process because topical anesthetics will delay healing and place the patient at risk for severe corneal infection and scarring. Antibiotic mixtures containing corticosteroids should not be used for treatment because they provide inadequate protection against bacterial infection and enhance the growth of viral and fungal pathogens.
Abrasions caused by fat-soluble petroleum products splashed into the eyes are treated initially by copious irrigation with water or saline solution to remove any remaining material. Staining with fluorescein will demonstrate the amount of epithelial loss, which may vary from a few punctate areas to complete denudation of the cornea. In either case, treatment is the same as outlined above. If the abraded area is large, the corneal stroma may appear slightly gray owing to some degree of edema. This clears rapidly with healing of the epithelium.
Exposure to aerosols (eg, paint sprays), detergents, surfactants, dust, smoke, and vapors can produce both acute and chronic symptoms of abrasion. Acute symptoms almost invariably include marked tearing and blepharospasm, which act to protect the eyes and wash away the offending material. Treatment for acute symptoms is as for other abrasions (see above). Chronic exposure to low-level irritants causes fatigue of the lacrimal reflex and subsequent sensations of dryness and burning of the eyes. Some degree of redness is common. Irrigation with saline solution prevents most of these chronic symptoms. Adequate ventilation and avoidance of irritants in the workplace are obviously the best preventive measures.
Exposure to some chemical substances causes a delayed loss of corneal epithelium. For example, formaldehyde fumes cause diffuse damage to epithelial cells, leading to their accelerated sloughing with normal blinking. Fortunately, the abrasion will heal without scarring when the fumes are avoided subsequently. The long list of other substances that produce this effect includes butylamine, diethylamine, hydrogen sulfide, methyl silicate, mustard gas, osmium tetroxide, podophyllum resin, and sulfur.
INDIRECT INJURIES TO THE EYE
In massive crush injuries, compression of the abdominal and chest vessels can cause sudden vascular engorgement of the retina. This leads to marked edema and diffuse hemorrhages in the fundus and can result in permanent ocular damage. Purtscher retinopathy is one form of this condition. There is no treatment. The prognosis for vision depends on the amount of damage done to the macula or optic nerve. Slow improvement in vision occurs as hemorrhages absorb for periods of up to several months.
In fractures of the long bones, fat emboli can migrate to the retina and produce small embolic changes that have the appearance of cotton-wool spots and sometimes are associated with flame-shaped hemorrhages in the fundus. Fat emboli, thrombi from heart valve disease and endocarditis, and emboli from a variety of sources occasionally obstruct branches of the retinal artery and cause infarction of a segment of the retina. Cholesterol crystals shed from atheromatous plaques in the carotid arteries also may migrate to the retina and appear as glistening intra-arterial bodies. In intravenous drug abuse, the injected drugs frequently contain inert substances such as talc, which may be seen in the retina as small white deposits. The prognosis for each of these conditions depends entirely on their location and whether or not the macula is involved. There is no ocular treatment. Clearing of the effects of these emboli—hemorrhages and edema—requires several weeks to a month. Cholesterol crystal emboli are an indication to investigate the patency of the carotid arteries.
Rarely, a septic embolus from a distant systemic infection causes endophthalmitis. Endophthalmitis generally has a poor prognosis. Specific diagnosis requires aspiration of vitreous fluid and sometimes aqueous humor for the isolation of organisms. Periocular injection of antibiotics adjacent to the scleral surface, occasionally intravitreal injection of appropriate doses of antibiotics, and intravenous antibiotics are the usual methods of treatment. The poor prognosis is a result of delay in diagnosis while the infection advances and of the unpredictable and sometimes poor ocular penetration of antibiotics.
SYMPATHETIC OPHTHALMIA
If the uveal tract (ie, the iris, ciliary body, or choroid) of one eye is injured, the uninjured (sympathizing) eye may show inflammation. This rare disorder is thought to be an autoimmune inflammatory response and can be prevented by prompt, adequate treatment of the initial injury to minimize continuing trauma to the damaged uveal tissue. Sympathetic ophthalmia can cause complete loss of vision in both eyes if unrecognized and untreated early in its course. As soon as inflammation is seen in the sympathizing eye, treatment of both eyes with local corticosteroids (topical and periocular injections) and mydriatics should be started. Large doses of systemic corticosteroids are also used frequently.
OCCLUSION OF THE CENTRAL RETINAL ARTERY
Occlusion of the central retinal artery is characterized by sudden painless loss of vision and is considered an ocular emergency. Permanent loss of vision will result if the retina is deprived of blood for 30–60 minutes; consequently, arterial circulation must be restored as soon as possible.
Diagnosis is based on the history and eye examination. Occlusion usually is seen in older patients with arteriosclerosis or following embolism from the great vessels. It also can be caused by pressure from an unusually tight dressing over the eye, particularly when there is orbital edema or hemorrhage. If the visual loss is incomplete, the patient may be able to detect some light. Ophthalmic examination reveals a bloodless retina with thin and thready arteries. Early findings include a faint retinal edema that appears as a grayish or white discoloration and is particularly noticeable around the macula, allowing the normal red color of the choroid in the fovea to show through as a cherry-red spot. Later, red cells in the blood column of the arteries may separate into segments and appear as “boxcars.” The veins also appear thinner than normal. The optic disc retains its normal pink color for several weeks, but the retinal edema becomes more apparent.
Although central retinal artery occlusions usually are not associated with increased intraocular pressures, the most effective treatment is immediate reduction of the normal intraocular pressure in an attempt to dislodge the embolus or thrombus thought to be obstructing the artery at a restricted area of the vessel as it passes through the scleral shell just posterior to the optic disc. The pressure can be reduced by using two fingers to alternately massage and press the globe through the closed lids. This maneuver should be repeated four or five times over 10–15 minutes to accelerate the expression of aqueous humor and applies intermittent pressure on the artery. The patient’s use of a rebreathing bag will increase the amount of carbon dioxide in the cerebral and ocular blood vessels, sometimes effecting vascular dilation.
If these maneuvers fail, paracentesis of the anterior chamber may be indicated. After a topical anesthetic is given, the conjunctiva is grasped with fine-tooth forceps. An incision is made through the clear cornea at the periphery of the anterior chamber, with the sharp scalpel blade held in the plane of the iris so as not to touch either the iris or the lens. The blade then is turned slightly to allow some of the aqueous humor to escape abruptly. This lowers the intraocular pressure and sometimes restores circulation to the retina.
Anterior Ischemic Optic Neuropathy
This condition is characterized by an acute, painless loss of vision in individuals 50–70 years of age. The ischemia of the optic nerve is in or just behind the disc. The disc appears swollen or edematous at first, clearing with time and leaving various amounts of optic atrophy and usually a severe loss of vision. The same process in the 70- to 80-year-old age group may be a result of giant cell arteritis, frequently associated with temporal arteritis. Systemic steroids sometimes are helpful in the latter group to prevent involvement of the second eye.
OCCLUSION OF THE CENTRAL RETINAL VEIN
Occlusion of the central retinal vein produces painless visual loss and is seen most commonly in older patients with diabetes, hypertension, or other vascular occlusive diseases. Findings include a swollen optic disc, distended and tortuous retinal veins, and an edematous retina with flame-shaped hemorrhages.
There is no effective emergency treatment, although anticoagulants have been tried occasionally. An ophthalmologist should follow these patients. The prognosis for improvement of vision is slightly better for patients with an occluded retinal vein than it is for those patients with an occluded retinal artery.
EYE INJURIES CAUSED BY RADIATION EXPOSURE
See Chapter 12 for a description of the electromagnetic spectrum and a discussion of methods to prevent occupational exposure to radiation.
Injuries Caused by Ionizing Radiation
X-rays, beta rays, and other radiation sources in adequate doses can cause ocular injury. The eyelid is particularly vulnerable to x-ray damage because of the thinness of its skin. Loss of lashes and scarring can lead to inversion or eversion (entropion or ectropion) of the lid margins and prevent adequate lid closure. Scarring of the conjunctiva can impair the production of mucus and the function of the lacrimal gland ducts, thereby causing dryness of the eyes. X-ray radiation in a dose of 500–800 R directed toward the lens surface can cause cataracts, sometimes with a delay of several months to a year before the opacities appear. Treatment for these injuries is the appropriate oculoplastic repair of lid deformities and scarring. Deficiencies of tears and mucus can be improved by the topical use of artificial tears and protection from evaporation by wearing protective glasses with side shields that seal to the face. Radiation cataracts can be removed surgically by the appropriate standard technique.
Injuries Caused by Ultraviolet Radiation
Ultraviolet radiation of wavelengths shorter than 300 nm (actinic rays) can damage the corneal epithelium. This is most commonly the result of exposure to the sun at high altitudes and in areas where shorter wavelengths are readily reflected from bright surfaces such as snow, water, and sand. Exposure to radiation generated by a welding arc can cause welder’s flash burn, a form of keratitis. After a latent period of several hours, the injured epithelial cells soften and slough, causing sudden onset of pain. Treatment of these injuries consists of applying antibiotic ointment and patches until the epithelial cells have had an opportunity to heal (see the section “Injuries of the Corneal Epithelium (Abrasions & Superficial Foreign Bodies)”).
Wavelengths of 300–400 nm are transmitted through the cornea, and approximately 80% are absorbed by the lens, where they may cause cataractous changes. Accidental exposure to an inadequately shielded dental instrument used to accelerate the hardening of plastic fillings has caused significant lens opacities in dental personnel. Epidemiologic studies suggest that exposure to solar radiation in these wavelengths near the equator is correlated with an increased incidence of cataracts. They also indicate that workers exposed to bright sunlight in occupations such as farming, truck driving, and construction works appear to have a higher incidence of cataracts than do those who work primarily indoors. Experimental studies show that these wavelengths cause changes in the lens protein that lead to cataract formation in animals.
Cataract
Any opacity in the lens is called a cataract. Some degree of opacity is present in almost all lenses, and the significance of the changes depends solely on their effect on vision. Peripheral opacities, for example, that do not interfere with vision are of no clinical significance.
The lens is composed of lens protein arranged in an ordered pattern of cytoplasmic fibers produced by the lens epithelium. These cells continue to produce new fibers at a slow rate throughout life. The lens thus slowly increases in volume—mainly in thickness—pushing the iris forward.
Changes in the chemistry and hydration of the lens protein create various types of cataracts. These changes may be induced by a variety of agents, including near-ultraviolet radiation of 300–400 nm. These wavelengths are absorbed by the central lens fibers, causing the brownish discoloration of lenticular nuclear sclerosis. Ocular inflammation and corticosteroids, both topical and systemic, produce typical posterior subcapsular cataracts.
Types of Cataracts
A. Age-Related Cataracts
Age-related (senile) cataract is the most common type seen. Some degree of opacity is almost universal. The progress of change and the related reduction in vision is usually quite slow. Nuclear sclerosis—an increasing density in the central mass of protein—causes a myopic change that can be corrected by changing glasses for some years—in many instances restoring vision to near normal.
B. Congenital Cataracts
These can be unilateral or bilateral, and many are thought to be of genetic origin. Some are a result of maternal rubella during the first trimester of pregnancy. If the opacity prevents a clear view of the ocular fundus, surgical removal at an early age—even 2 months—is indicated to aid in the development of useful vision.
C. Traumatic Cataracts
Contusion injuries can cause opacities that may appear right away or may develop slowly over weeks or even months. Penetrating wounds can tear the lens capsule, allowing aqueous humor to soften lens protein, usually creating major opacities. These cataracts almost always need to be removed acutely—in many cases at the time of wound repair.
D. Secondary Cataracts
These changes result from inflammatory processes in the eye (uveitis) and usually begin by producing opacities just inside the posterior lens capsule. Similar changes occur in association with retinitis pigmentosa, glaucoma, and rarely, retinal detachments.
E. Cataracts Associated With Systemic Diseases
These are usually bilateral and may appear in patients with myotonia dystrophica, hypoparathyroidism, diabetes mellitus, and Down syndrome, as well as in many other less common conditions.
F. Toxic Cataracts
Lens opacities are reported following exposure to or ingestion of numerous chemicals. They are described at some length in Grant’s Toxicology of the Eye. The most common cause at present is the use of corticosteroids, either topical or systemic.
Treatment
There is no effective medical treatment for cataract. Surgical removal usually results in significant improvement of vision in approximately 90% of patients. The results depend on whether other ocular changes are present, such as macular scars or optic nerve changes. Indications for surgery depend almost entirely on the needs of the individual patient to improve vision. Minimally invasive, small incision phacoemulsification with quick post-op recovery has become the standard of care in cataract surgery all over the world.
Prognosis
The results of cataract surgery generally are excellent. Significant visual improvement is reported in nearly 90% of patients following extraction of age-related cataracts. The reduced expectations in eyes with injuries are a result of unpredictable intraocular complications such as retinal scarring and macular damage.
Injuries Caused by Visible Radiation (Light)
Visible light has a spectrum of 400–750 nm. If the wavelengths of this spectrum penetrate fully to the retina, they can cause thermal, mechanical, or photic injuries. Thermal injuries are produced by light intense enough to increase the temperature in the retina by 10–20°C (18–36°F). Lasers used in therapy can cause this type of injury. The light is absorbed by the retinal pigment epithelium, where its energy is converted to heat, and the heat causes photocoagulation of retinal tissue. Mechanical injuries can be produced by exposure to laser energy from a Q-switched or mode-locked laser, which produces sonic shock waves that disrupt retinal tissue.
Photic injuries are caused by prolonged exposure to intense light, which produces varying degrees of cellular damage in the retinal macula without a significant increase in the temperature of the tissue (usually no more than 1–2°C [1.8–3.6°F]). Recent studies show that photic injuries are not burns in the literal sense but are damage from the light itself. Sun gazing is the most common cause of this type of injury, but prolonged unprotected exposure to a welding arc also can damage the retinal macula. When the initial retinal edema clears, there is usually some scarring that leads to a permanent decrease in visual acuity. The intensity of light, length of exposure, and age of the exposed individual are all important factors. The older the individual, the more sensitive the retina appears to be to photic injuries. Anyone who has had cataract surgery is much more vulnerable because filtration of light by the lens is impaired. In photic injuries caused by exposure to welding sources or other excessively bright light, treatment with systemic corticosteroids may be tried. A large initial dose of prednisone (60–100 mg) is tapered rapidly over a period of 10–14 days. This may reduce the acute edema or inflammatory response, but it is not always effective.
Wavelengths of 500–750 nm are most useful for vision and appear not to cause photic damage to the retina at exposures most commonly encountered. However, repeated exposure to bright sunlight by working outdoors for 3–4 hours each day can cause prolongation of the dark adaptation response, thereby reducing night vision.
Injuries Caused by Infrared Radiation
Wavelengths greater than 750 nm in the infrared spectrum can produce lens changes. Glassblower cataract is an example of a heat injury that damages the anterior lens capsule. Denser cataractous changes can occur in unprotected workers who observe glowing masses of glass or iron for many hours a day.
EFFECTS OF VIDEO-DISPLAY TERMINAL USE
In recent years, employees who spend 6–8 hours a day looking at video-display terminals have complained of eyestrain, headache, and general fatigue. The brightness of the light from such terminals is not great enough to produce any ocular injury. Posture, accommodative fatigue, and the early changes of presbyopia may contribute to feelings of eyestrain and physical stress. Measures to alleviate these problems associated with video-display terminal use are discussed in Chapter 15.
REFERENCES
Blackburn J: A case-crossover study of risk factors for occupational eye injuries. J Occup Environ Med 2012;54:42 [PMID: 22227872].
Constantinou M: Corneal metallic foreign body injuries due to suboptimal ocular protection. Arch Environ Occup Health 2012;67:48 [PMID: 22315936].
Luo H: Socioeconomic status and lifetime risk for workplace eye injury reported by a US population aged 50 years and over. Ophthalmic Epidemiol 2012;19:103 [PMID: 22364578].
Nuzzi R: Ophthalmic evaluation and management of traumatic accidents associated with retinal breaks and detachment: a retrospective study. Eur J Ophthalmol 2012;22:641 [PMID: 22180153].
Pierce JS: An assessment of the occupational hazards related to medical lasers. J Occup Environ Med 2011;53:1302 Review [PMID: 22027542].
Ramakrishnan T: On-the-job ocular injuries. Insight 2012;37:25 [PMID: 22439359].
SELF-ASSESSMENT QUESTIONS
Select the one correct answer to each question.
Question 1: Open-angle glaucoma
a. accounts for most cases of glaucomatous visual loss (90%)
b. is painful at onset
c. distorts vision in its early stages
d. results in smaller optic cups
Question 2: Visual fields should be tested
a. by licensed ophthalmic technicians
b. primarily in a hospital setting
c. in patients with suspected head injury
d. to confirm the diagnosis of macular degeneration
Question 3: Strong alkalis and acids
a. are neutralized in the eye before they cause injury
b. can cause the most severe and damaging chemical injuries to the eye and eyelids
c. are exposure hazards in only a few industrial settings
d. will not cause injuries away from work
Question 4: Iridoplegia
a. is caused by damage to the pupillary sphincter
b. predictably affects how the pupil reacts to light
c. is not associated with injury to the iris root
d. is unrelated to any form of glaucoma
Question 5: Hyphema with secondary hemorrhage
a. clears spontaneously
b. may cause an increase in intraocular pressure
c. requires opening of the anterior chamber
d. has a uniformly good prognosis
Question 6: Photokeratoconjunctivitis (welder’s flash)
a. is caused by unprotected exposure to ultraviolet radiation with wavelengths longer than 300 nm
b. may be caused by the actinic rays of sunlight
c. damages the exposed corneal and conjunctival epithelium
d. does not affect persons passing nearby
Question 7: Sympathetic ophthalmia
a. is a common disorder associated with injury to one eye
b. is not likely to be an autoimmune inflammatory response
c. cannot be prevented by prompt treatment
d. can cause complete loss of vision in both eyes if unrecognized and untreated early in its course