Ординатура / Офтальмология / Учебные материалы / Ocular Traumatology Springer

–Lesions elsewhere in the retina cause a scotoma only, unless blood vessels are also disrupted and intraocular bleeding occurs [1].

•Presence or absence of defenses, such as refractive error (i.e., ametropia), blink, and aversion reflexes to bright light.

3.2.3.2Solar Retinopathy

Whether self-inflicted [6], caused by ignorance (not wearing suitable eye protection during a solar eclipse [21]), or being influenced by religious rituals [5] or hallucinogenic drugs [22], gazing at the sun can quickly lead to photochemical damage to the photoreceptors and RPE.

3.2.3.2.1 Clinical Features

The clinical features are as follows:

•Most patients present within a few days postinjury, although some people delay their visit to the ophthalmologist for months or even years.

•The most common initial symptoms are decreased visual acuity , central scotoma , and a negative afterimage of the sun, which may last several hours. The damage may be bilateral or unilateral (usually in the dominant eye).

•The typical ophthalmoscopic lesion is a small, yellow-grayish spot in or near the fovea, surrounded by macular edema. The edema resolves in days or weeks, after which the macula may look normal or show minor pigmentary disturbance. Foveolar depression or pseudohole may be observed, but a true macular hole is rare [9].

•The FLAG is usually normal, although a macular window defect is occasionally observed.

It can be much larger if focal damage to the nerve fiber layer has also occurred.

Retinal damage has been reported following direct observation of the sun through sunglasses, smoked glass, or exposed film, and even after exposures lasting only a few seconds.

Visual acuity worse than 20/80 is exceptional.

Can be identified even in the presence of 20/20 acuity.

•Ophthalmoscopically, the typical finding is a perifoveal, round to oval area of RPE change.11 The shape of the lesion corresponds to the shape of the illuminating source.12 The lesion is usually inferior to the fovea and outside the foveal avascular zone. Progressive pigmentation of the lesion may be observed over the next several months, distinguishing the acute maculopathy from an old scar.

•The FLAG shows a sharply demarcated, mottled hyperfluorescent lesion.

Table 3.2.1 provides a summary of recommendations to prevent iatrogenic photic retinal trauma from ophthalmic light sources.

3.2.3.4Welding Arc-related Retinopathy

In marked contrast to the commonly encountered photokeratitis, injury to the retina from radiation emitted by welding arcs is rare [18]. The clinical features are very similar to those described above in acute solar retino­ pathy.

3.2.3.5Laser-induced Eye Injuries

The laser’s light beam is coherent, monochromatic, monodirectional, and minimally divergent. Accidental injuries threaten (Fig. 3.2.1) if proper safety precautions are not implemented. The injury occurs directly (the victim looking at the laser source) or indirectly (reflection from a mirror or another nearby object13). Unexpected discharge of the laser device has also been reported [7].

11The early and therefore rarely observed sign is a grayish lesion at the level of the RPE.

12e.g., a horizontally oval lesion if the microscope illuminator has horizontally oriented filaments

13e.g., photographic paper or a plastic membrane.

Minimize the length of surgery

Use as low a light intensity1 as possible

Use noncoaxial microscope light when possible. Oblique illumination will place the intense image of the illuminating beam at the retinal periphery rather than in the foveal area

Use selective filters to eliminate UV and IR wavelengths2

Use corneal shields against retinal exposure whenever possible

If using an endoilluminator during vitrectomy, minimize direct exposure to the fovea by:

–Reducing the power (using too much power is especially tempting in the “Photon3 era” and with small-gauge surgery)

–Increasing the distance between the probe and the retina

–Intermittently illuminating the fovea and parafoveal areas, instead of keeping the

–light over the same site for extended periods of time

–Directing the light away from the fovea whenever possible

1 Whether it is the indirect ophthalmoscope, operating microscope, or the endoilluminator during vitrectomy

2  Filters are commonly used but their benefit has not adequately been tested

3  i.e., the endoilluminator for vitreous surgery (Synergetics, East Windsor Hill, Conn.)

ZPearl

Individuals at high risk of laser exposure should undergo ophthalmoscopic screening prior to employment as well as after its termination, mainly for legal reasons. Lacking effective treatment, periodic eye examinations are not indicated.

3.2.3.5.1 Clinical Features

The clinical features are as follows:

Fig. 3.2.1  Macular injury caused by laser. Note the spread of the lesion from less than 0.1 mm (original beam diameter) to over 1.5 mm. The spread explains why the vision eventually deteriorates in eyes with a parafoveal laser-induced retinal injury

•Almost all of the reported injuries were caused by short-pulse lasers,14 explaining why the clinical courses are so similar.

•The victim experiences a sudden and severe, monocular visual disturbance, often preceded by a visible flash of bright-colored light. An audible “pop” is common but pain is unusual [3].

•The visual acuity is markedly decreased15 and a visual field defect is present. The anterior segment is typically unaffected and the IOP is normal. On ophthalmoscopy, one or more localized areas of retinal edema, burns, or holes are seen, typically in or near the macula, with or without accompanying subretinal, subhyaloid, or vitreous hemorrhage.

•Over the next few days to weeks there is marked improvement, mainly due to clearing of the hemorrhage accompanied by waning of the inflammation.

14Mostly YAG, operating in the visible and near-IR spectrum, and emitting a few tens of millijoules per pulse of duration in the nanosecond range.

15Commonly to 20/200 or worse.

508 Yaniv Barkana, Michael Belkin, Ferenc Kuhn

•Long-term the visual acuity remains stable, although it may also worsen due to late complications such as chorioretinal scarring, or the development of a macular hole or EMP.

•While there is no treatment of the laser-induced trauma itself,16 certain complications (e.g., EMP) may improve with proper treatment.

:Controversial

It remains to be determined whether early intervention (see Chap. 2.9) or just observation should be recommended for a laser-induced macular hole [19].

3.2.3.5.2 Laser Pointers

Laser pointers emit a continuous, narrow beam of usually red light of up to 5 mW of power. If shone directly into an immobile eye for at least 10−20 s, retinal injury occurs since the retinal irradiance is similar to that caused by sun gazing [16]. Under normal circumstances, however, long exposure and thus retinal damage are unlikely17. While the risk of eye injury from these inexpensive and widely available devices is negligible, their use for flash blinding may lead to accidents.18

Since visible radiation is not absorbed by tissues at the front of the eye, pain or irritation should not be blamed on laser pointers.19

16Corticosteroids and “neuroprotective” compounds have been attempted, but their benefit has never been proven.

17Due to the blink reflex and aversion response.

18Convictions in criminal court have followed the directing of laser pointers into airplane cockpits.

19If these occur, they are most likely due to eye rubbing.

3.2.3.5.3 Military Lasers

Representing an increasingly important hazard, lasers can be employed as adjuncts to weapons20 or as weapons21. Certain military-type lasers are available even over the Internet, and may become a serious medical/societal problem in the future.

3.2.3.5.4 Prevention

Prophylaxis against laser-induced retinal trauma is relatively simple in the civilian environment by wearing proper protective goggle. There is no effective defense against military lasers unless the wavelength of the weapon the enemy uses is known22.

3.2.3.6Heat-induced Damage

In experimental models damage to the blood-retina barrier and the photoreceptors by electromagnetic radiation has been reported [10, 13].

3.2.3.7Lightning-induced Trauma

A whole array of symptoms and pathologies can be caused by a lightning strike, including temporary blindness, keratitis, uveitis, cataract, macular edema and hole, RPE and photoreceptor damage, and optic neuropathy [12, 20]. The treatment depends on the type of damage; the prognosis after cataract extraction is generally good.

20e.g., for range finding and target identification.

21e.g., jamming of enemy equipment, damaging sensors, blinding combatants, physically destroying targets.

22The emitted beam can be made to reach a circle of a few meters at a distance of a few kilometers from the source.

DO:

•explain to the public how observation of a solar eclipse should and should not be observed

•prevent iatrogenic photic damage to the retina from ophthalmic illumination sources

DON’T:

•try to predict the visual outcome after a laser-induced macular injury since the vision can both improve or worsen

Summary

Electromagnetic waves can cause a variety of ocular consequences; some of these are very painful but insignificant (e.g., welder’s keratopathy),

others can cause permanent blindness. The ophthalmologist’s inter­ vention options are unfortunately very limited.

References

[1]Blankenstein M, Zuchlich J, Allen R, Davis H, Thomas S, Harrison R (1986) Retinal hemorrhage thresholds for Q-switched neodymium-YAG laser exposures. Invest Ophthalmol Vis Sci 27: 1176−1179

[2]Boettner E, Wolter J (1962) Transmission of the ocular media. Invest Ophthalmol Vis Sci 1: 776−783

[3]Boldrey E, Little H, Flocks M, Vassiliadis A (1981) Retinal injury due to industrial laser burns. Ophthalmology 88: 101−107

[4]Buettner K, Rose H (1953) Eye hazards from atomic bomb light. Sight Sav Rev 23: 1

[5]Cangelosi G, Newsome D (1988) Solar retinopathy in persons on religious pilgrimage. Am J Ophthalmol 105: 95−97

[6]Ewald R, Ritchey C (1970) Sun gazing as the cause of foveomacular retinitis. Am J Ophthalmol 70: 491−497

[7]Foroozan R, Buono LM, Savino PJ (2003) Traumatic cataract after inadvertent laser discharge. Arch Ophthalmol 121: 286−287

[8]Ham WT Jr, Ruffolo JJ Jr, Mueller HA, Guerry D III (1980) The nature of retinal radiation damage: dependence on wavelength, power level and exposure time. Vision Res 20: 1105−1111

[9]Jacobs NA, Headon M, Rosen ES (1985) Solar retinopathy in the Manchester area. Trans Ophthalmol Soc UK 104 (Pt 6): 625−628

[10]Kiryu J, Ogura Y, Moritera T, Yoshimura N, Honda Y (1993) Breakdown of the blood-retinal barrier after radiofrequency-induced ocular hyperthermia. Ophthalmologica 206: 107−110

[11]Kuhn F, Morris R, Massey M (1991) Photic retinal injury from endoillumination during vitrectomy. Am J Ophthalmol 111: 42−46

[12]Lagreze W, Bomer T, Aiello L (1995) Lightning-induced ocular injury. Arch Ophthalmol 113: 1076−1077

[13]Liggett PE, Pince KJ, Astrahan M, Rao N, Petrovich Z (1990) Localized current field hyperthermia: effect on normal ocular tissue. Int J Hyperthermia 6: 517−527

[14]Lindquist T, Grutzmacher R, Gofman J (1986) Light-induced maculopathy: potential for recovery. Arch Ophthalmol 104: 1641−1647

[15]Marshall J (1970) Thermal and mechanical mechanisms in laser damage to the retina. Invest Ophthalmol Vis Sci 9: 97−115

[16]Marshall J (1998) The safety of laser pointers: myths and realities. Br J Ophthalmol 82: 1335−1338

[17]McDonald H, Irvine A (1983) Light-induced maculopathy from the operating microscope in extracapsular cataract extraction and intraocular lens implantation. Ophthalmology 90: 945−951

[18]Naidoff M, Sliney D (1974) Retinal injury from a welding arc. Am J Ophthalmol 77: 663−668

[19]Newman DK, Flanagan DW (2000) Spontaneous closure of a macular hole secondary to an accidental laser injury. Br J Ophthalmol 84: 1075

[20]Norman ME, Albertson D, Younge BR (2001) Ophthalmic manifestations of lightning strike. Surv Ophthalmol 46: 19−24

[21]Ridgway A (1967) Solar retinopathy. Br Med J 3: 212−214

[22]Schatz H, Mendelblatt F (1973) Solar retinopathy from sun-gazing under the influence of LSD. Br J Ophthalmol 57: 270−273

  3.3  The Effects of Systemic Trauma

on the Eye

Wolfgang Schrader and Ferenc Kuhn

3.3.1Introduction

Certain systemic injuries, even if the eye is not directly involved, may indirectly cause ocular pathologies, usually by one of the following mechanisms:

•Changes in rheologic conditions

•Hypoxia

•A sudden increase of the intravascular pressure.

Because of a great variety of retinal findings and a still somewhat vaguely understood retinal response, the pathomechanisms are not completely understood. The retinal findings may be caused by:

•Embolic damage (e.g., air, blood products, fat)

•Increased intraluminal pressure with endothelial vascular damage

•Mechanical forces acting at the vitreoretinal interface

ZPearl

All physicians, and especially those working in the ER, should know that bodily trauma can cause sight-threatening ocular complications even in the absence of direct eye involvement.

Patient complaints about visual loss whether voiced hours or months after the trauma, should result in an instant referral to an ophthalmologist. If the patient is unconscious or mentally incompetent, ophthalmological examination should be initiated to rule out a direct or indirect traumatic retinopathy. The findings should be meticulously documented for medical and legal purposes (see Chap. 1.8).