Ocular hazard from picosecond pulses of Nd: YAG laser radiation.

Seven rhesus monkeys (14 eyes) were exposed to 1064-nanometer radiation in single pulses of 25 to 35 picoseconds fromn a mode-locked Nd: YA G laser. Threshold injury resulted from single pulses with a mnean energy of 13 +/- 3 mnicrojoules. Electron microscopy of the retina revealed that damnage was highly localized in the photoreceptor and pigmented epithelial cells at the oluter retina. Membrane disruption, distorted outer segmtzents, and abnormnal melanin granules resembling fetal premelanosomnies were observed.

Histologic analysis of photochemical lesions produced in rhesus retina by short-wave-length light.

The photopathology of retinal lesions produced by extended exposure (1000 sec) to low corneal power levels (62 microW) of blue light (441 nm) was investigated by light microscopy in 20 rhesus eyes over an interval ranging from 1 hr to 90 days after exposure. Results indicate a nonthermal type of photochemical lesion originating in the retinal pigment epithelium and leading to a histological response with hypopigmentation which requires 48 hr to appear. This type of lesion helps to explain solar retinitis and eclipse blindness and has significance for aging and degenerative changes in the retina.

Photochemical lesions in the primate retina under conditions of elevated blood oxygen.

Under conditions of nonthermal radiant exposure to blue light (440 nm) the primate retina can suffer photic injury by a mechanism that must be photochemical in nature. We have examined the effects of elevated blood oxygen (pO2 of 270 mmHg) on the retinal photosensitivity to blue light in two macaque monkeys by histologic analysis of 12 lesions at 1 to 57 days after irradiation. The retinal image diameter from a xenon arc lamp source was 1 mm, the duration of exposure was 100 sec, and the radiant exposures ranged from 11 to 36 J/cm2. When blood oxygenation is not elevated experimentally, the threshold radiant exposure for a blue light lesion to be visible funduscopically at 2 days postexposure is about 30 J/cm2. At a high blood pO2 level, a radiant exposure of only 11 J/cm2 gave a funduscopically visible lesion at 1-day postexposure. This large increase in retinal sensitivity to blue light damage appears to be due to photodynamic action. The only direct effect of elevated blood pO2 on the retina observed histologically was the presence of numerous granules in the cells of the retinal pigment epithelium (RPE). However, there was no apparent histopathology associated with the elevation of blood pO2 alone. Analysis of the various photic lesions showed only moderate damage to the neural retina, but a strong response was seen in the RPE. This is the histopathologic pattern of a typical blue light lesion shown in previous studies but more severe. So the effect of elevated blood O2 is to increase retinal sensitivity to photic damage, to lower the damage threshold, and to increase the severity of damage at a given radiant exposure. The status of lesions at 23 and 57 days postexposure suggests that such injuries are repairable.

Action spectrum for retinal injury from near-ultraviolet radiation in the aphakic monkey.

We found that the action spectrum for retinal damage (determined by the fundus photographic appearance of a minimal lesion immediately after exposure) extends into the near-ultraviolet by exposing three aphakic eyes from rhesus monkeys to 405-, 380-, 350-, and 320-nm wavelengths produced by a 2,500-W xenon lamp equipped with quartz optics and 10-nm interference filters. Exposure times were 100 and 1,000 seconds and the spot diameter on the retina was 500 micrometers. The retina was six times more sensitive to 350- and 325-nm wavelengths than to blue light (441 nm). Both ophthalmoscopic and histologic data showed that near-ultraviolet lesions differed in important respects from blue-light lesions. Near-ultraviolet produced irreparable damage to rod and cone photoreceptors.

Basic mechanisms underlying the production of photochemical lesions in the mammalian retina.

Extended exposure (100s) of the macaque retina to blue light (400-500nm) produces a photochemical type or types of lesion. The basic mechanisms responsible for such photic damage are unknown but the toxic combination of light and oxygen leading to the free radicals O-.2, H2O2, OH., and O2(1 delta) have been suggested as a possible source of the phototoxicity. To test this hypothesis, the radiant exposure (J. cm-2) to short wavelength light (435-445nm) required for minimal damage in the macaque retina is under investigation as a function of oxygenation and after administration of substances known to either inhibit/scavenge radicals or act as anti-inflammatory/anti-oxidant agents. Substances under study include beta-carotene, steroids, catalase and SOD. Here we report radiant exposure in J.cm-2 needed to produce a minimal lesion vs oxygenation as measured by partial pressure of O2 in arterial blood (Po2). There is a sharp drop in the radiant exposure threshold with increase in the partial pressure of O2 in arterial blood, e.g. 30 J.cm-2 at 75 torr to 10 J.cm-2 at 271 torr, a factor of 3. Methylprednisolone injected intravenously one hour before exposure (125 mg) has been shown to raise the threshold for retinal damage in two macaques by a factor of approximately 2. Another animal fed beta-carotene (7.5 mg daily) over a period of 3 months has been exposed to blue light at several levels of oxygenation. The results suggest a protective effect.

The use of the laser in neurological surgery.

Lasers generate unidirectional beams of monochromatic, and temporally and spatially coherent electromagnetic radiation that are capable of vaporizing and coagulating biological tissue. Specific physical characteristics of laser energies of different wavelengths impart to each form of surgical laser specific potentials for clinical use in neurological surgery. The major advantages of surgical lasers appear to be improved precision, reduction of surgically related mechanical trauma, reduction of blood loss, and decreased operative time. Improvement of operative mortality and morbidity and increased longevity that might result from its use would make the laser cost effective.

Evaluation of retinal exposures from repetitively pulsed and scanning lasers.

Threshold damage in the macaque retina is shown to be equivalent for the argon-krypton (Ar-Kr) 647 nm and the helium-neon (He-Ne) 632.8-nm lines for exposures to continuous wave (CW) radiation from 1 to 1,000 s. This equivalence allows interpolation from experiments with 647-nm, exposures at power levels that are unavailable with the He-Ne laser. To simulate He-Ne laser scanner exposures, 40-microseconds pulses of 647-nm light transmitted through a revolving disk with holes in the periphery were used to expose the retinas of monkeys under deep anesthesia at pulse repetition frequencies (PRFs) of 100, 200, 400, and 1,600 Hz for exposure durations of 1, 10, 100, and 1,000 s. The thresholds between laser exposure at 488 nm (Ar-Kr) and between laser exposure at 647 nm (Kr) are compared to assess thermal versus photochemical effects on the retina. The threshold for 488-nm pulses was consistently lower than that for 647-nm pulses at all PRFs and exposure times. The difference in thresholds increased with exposure time and PRF. The sharp decreases in 488-nm thresholds at 100-s exposure times for each PRF can be interpreted as a basically photochemical effect. The radiant exposure required for damage at 647 nm was several orders of magnitude above the radiant exposure from typical He-Ne scanner applications. From the similarity of the macaque retina to the human retina, it is concluded that no realistic ocular hazard exists from exposure to scanning laser systems of 1 mW or less, operating at higher than 100 Hz.

Ocular hazards of light sources: review of current knowledge.

Retinal damage is the most important hazard from light. There are three types of retinal damage classified as structural, thermal and photochemical; damage type depends on wavelength, power level and exposure time. Photochemical damage from blue light produces solar retinitis and is postulated to accelerate aging which leads to senile macular degeneration. The lens protects the retina from blue light and near ultraviolet (UV) but at the expense of cataractogenesis. Lens removal exposes retina to near UV that is six times more dangerous than blue light. Filters are recommended to protect lens and retina from blue light and near UV.

Potential ocular hazards from xenon flashlamps.

High radiance optical sources used in fast photocopiers represent a potential hazard to the human retina. Primates (macaque monkeys) were exposed to a prototype flashtube assembly similar to that used in fast photocopiers. One animal trained in a restraint chair to perform a visual task for a major portion of his food was exposed to multiple pulses (1000 pulses daily) from two xenon flashtubes placed 22 cm from the eyes. After sixty daily exposures over a period of three months with pupils dilated to 8 mm or greater, no anomalies were detectable in the retina. Examination for defects with the fundus camera was negative even a year after the exposures. Four additional monkeys (eight eyes) were exposed under anesthesia to insure that repetitive exposures on the retina were coincident. Exposure to two xenon flashtubes, each with 160-J input, did not produce a retinal lesion after 4200 flashes spaced 1.7 s apart. Exposure to a single flashtube with 540-J input produced negative results even after fifty flashes focused on the same retinal site. It was concluded that neither of these optical sources was capable of producing a thermal lesion in the monkey retina. Calculations predict that a photochemical-type retinal lesion is possible but only in extraordinary conditions of exposure which would be extremely unlikely, if not impossible, while viewing a photocopier.