Photomechanical mechanisms

Surgical photomechanical effects include photodisruption, photofragmentation, and photovaporization.¹⁶ Photodisruption occurs in Nd:YAG laser capsulotomy and lamellar keratectomy when infrared laser energy ionizes target tissue molecules, producing plasma and a rapidly expanding shock wave that dissects target tissue.¹⁷ Photofragmentation occurs in excimer laser photorefractive keratectomy when ultraviolet laser energy breaks bonds in corneal surface molecules and residual energy volatilizes molecular fragments. Photovaporization occurs in holmium laser sclerostomy and erbium laser phacolysis when rapid water vapor expansion excavates target tissues.

Most accidental photomechanical retinal injuries are caused by very brief laser exposures ranging in duration from a hundred femtoseconds (10⁻¹⁵ sec) to microseconds (10⁻⁶ sec).^18–22 Their very high retinal irradiances (power densities) produce tissue heating and expansion that cause immediate thermomechanical chorioretinal distortion and bleeding. Photovaporization may occur, but retinal irradiances are generally far too low for other photomechanical effects. Most victims experience a brilliant light flash followed by immediate monocular vision loss. An audible sound (pop) and/or momentary pain occur infrequently at the time of the laser accident.

Photomechanical retinal injuries

A small number of photomechanical laser accidents occur each year.^19–22 Most are caused by laboratory research lasers and military rangefinders or target designators.^20–22 Injuries can be prevented by effective laser safety training and proper protective eyewear. Surgical Q-switched and femtosecond laser systems have numerous safeguards that limit high optical irradiances to small, restricted spatial volumes.

Initial vision loss depends on a laser injury’s retinal location and associated chorioretinal disruption and bleeding.²¹ Blood can spread laterally in subhyaloid, subretinal, or sub-RPE (retinal pigment epithelium) spaces. Chorioretinal scars form and evolve. Vision may improve over days to months. Prognosis is excellent for less severe injuries that do not involve the fovea.

Optical coherence tomography (OCT) and fluorescein angiography are valuable for evaluating, managing, and documenting real and alleged injuries. Anti-inflammatory and neuroprotective drugs for reducing laser damage have been studied experimentally,^23,24 but clinical trials of their efficacy are impractical because injuries are uncommon. Accident victims should be followed for macular holes and choroidal neovascularization that can develop in the months following an injury.^25–29 Macular holes may close and choroidal neovascularization (CNV) may resolve spontaneously but conventional macular hole surgery and CNV therapy are potentially useful when needed.^25–29

In real laser accidents,

Most laser injuries and noninjurious laser exposures are painless.³⁰ Eye rubbing after a laser incident can cause painful self-inflicted corneal abrasions, sometimes falsely attributed to the laser exposure.^30–32 Real retinal laser injuries do not cause chronic headache or other somatic complaints, including head, neck or jaw pain.³⁰

The ease of laser injury diagnosis is directly proportional to the severity of the laser injury.³⁰ In ambiguous cases, subtle retinal findings have an excellent visual prognosis. When a retinal laser injury is alleged and objective findings are absent or within normal limits, diagnosis of laser injury should be deferred pending a rigorous review of the patient’s retinal findings, ophthalmic and systemic tests, clinical course, and past medical history. Such an analysis may take weeks or even months to perform if there is a complex past medical history. A guideline has been published for this type of analysis.³⁰

Pressure from patients or attorneys to reach quick conclusions in alleged but inapparent laser injuries should be resisted.^30,33 There are numerous potential psychiatric, financial or other explanations for complaints of nonorganic origin.^30,33 Differentiating between those origins is challenging, but organic retinal laser injuries do not cause chronic pain, and if a significant visual abnormality is present, it should be reproducible and consistent with a significant chorioretinal abnormality.³⁰

Photothermal mechanisms

Photocoagulation occurs when intense light is absorbed mostly by melanin in the RPE and choroid. Light energy is converted into heat, increasing the temperature of directly exposed pigmented tissues.^2,3,34 Heat conduction spreads temperature elevation to adjacent sites. Overlying neural retina damaged by heat conduction loses its transparency and becomes visible as a focal white lesion (“burn”) because it scatters white fundus illumination light back at an observer. Retinal burns increase in size over time due to postexposure scarring and collateral chorioretinal damage that is not apparent immediately after the exposure.²

Standard clinical photocoagulation produces immediately visible burns, with retinal temperature increases exceeding 20 °C.¹ Photomechanical effects occur at roughly three times the laser exposure needed for a visible lesion. Invisible lesions that are apparent only with fluorescein or autofluorescence imaging occur at half to one-quarter of the exposure needed to produce ophthalmoscopically visible lesions. In clinical parlance, “subthreshold” means ophthalmoscopically invisible or “subvisible.”³ Subthreshold photocoagulation can produce beneficial therapeutic effects with low temperature rises that produce minimal or no apparent retinal damage.³⁵

Most accidental photothermal retinal injuries are caused by pulsed laser exposures ranging in duration from a microsecond to a few seconds. Retinal irradiance is high enough for photocoagulation but too low for photomechanical effects. The magnitude and duration of chorioretinal temperature elevation determine the severity of a retinal burn, along with lesion size, fundus pigmentation, and chorioretinal sequelae.^3,21 Photothermal and photomechanical retinal injuries are managed similarly. Injuries should be followed for retinal holes and CNV that can develop within a few months of the injury.^27,36

Photothermal retinal injuries

Industrial and military photothermal laser accidents are less common than photomechanical ones because they require a narrow range of lower retinal irradiances.

Photochemical mechanisms

Accidental photochemical retinal injuries (known as photic retinopathy or retinal phototoxicity) are caused by prolonged intense light exposures that probably would be well tolerated if experienced only momentarily.⁵ They occur at chorioretinal temperature elevations too low for photothermal damage, at illuminances far exceeding normal environmental levels, in exposures lasting from seconds to minutes. Optical radiation produces highly reactive oxygen radicals that can damage retinal cell membranes, proteins, carbohydrates, and nucleic acids. The extent of a photochemical retinal injury depends on individual defense mechanisms, the location and area of exposed retina, and the duration, intensity, and spectrum of the light exposure.^{5,10,12,47–49}

Photic retinopathy does not occur unless acute cellular damage is so excessive that it acutely overwhelms retinal repair mechanisms.^5,37 People safely undergo bright but much lower irradiances in ophthalmic imaging studies and light therapy for seasonal affective disorder.^12,37,50

Action spectra characterize how effectively different wavelengths cause a photochemical effect.⁵¹ Photic retinopathy can be divided into photosensitizer- and photopigment-mediated phototoxicities which have different action spectra.^4,5,52

The hazardousness of photosensitizer-mediated retinal phototoxicity increases rapidly with decreasing wavelength,^5,47 similar to the absorption spectrum of lipofuscin in the RPE which is its primary mediator.^53,54 Thus, UV radiation is much more hazardous than visible light. In an aphakic eye, UV radiation, violet light (400–440 nm) and blue light (440–500 nm) account for 67%, 18%, and 14% of potential retinal phototoxicity, respectively.^55,56 Photosensitizer-mediated phototoxicity is the basis for the international consensus aphakic standard A_λ phototoxicity function used to estimate industrial acute retinal phototoxicity risks.⁵⁷

In an adult phakic eye, the retina has the additional shielding of crystalline lens attenuation of UV radiation and shorter wavelength visible light. That is why the international consensus phakic standard B_λ phototoxicity function peaks at 440 nm in the blue part of the spectrum. The B_λ function is often termed a “blue light hazard” function, even though blue light has far less retinal phototoxicity than violet light or UV radiation.^4,5,57

The hazardousness of photopigment-mediated retinal phototoxicity⁵⁸ peaks around 500 nm (blue-green), similar to the luminous sensitivity of scotopic vision⁵⁹ because the photopigment rhodopsin mediates both processes.⁵ This type of photic retinopathy requires only 1% of the retinal irradiance needed for photosensitizer-mediated phototoxicity,^10,52,60,61 but experimental studies were performed with highly light-sensitive nocturnal rodents whose primary photopigment is rhodopsin.^5,58,61

Clinical findings are similar in solar and welding arc maculopathies, as they are in operating microscope and endoilluminator injuries.^5,37

Photochemical retinal injuries

Solar and welder’s maculopathy

Figure 90.1 shows a typical yellow-white solar maculopathy lesion.^62,63 Lesions fade over several weeks, resolving completely or leaving foveolar distortion, pigment mottling or even a macular hole.⁶² Welding arc injuries produce similar clinical abnormalities.^5,64,65 Welder’s maculopathy is extremely rare but it may be underreported because its transient clinical symptoms may be masked by those of associated photokeratitis.^5,8,66

Fig. 90.1 Acute solar maculopathy typically produces a small yellow-white foveolar lesion, as seen in this 15-year-old girl with 20/200 visual acuity. The lesion faded and visual acuity returned to 20/40 in the 3 months following the injury.

Common visual complaints after acute solar or welding arc injury are blurred vision, central scotoma and erythropsia. Post-injury visual acuity may be normal or decreased to the 20/40 to 20/200 range. Visual acuity usually returns to 20/20 to 20/40 over 6 months.^5,62 Fluorescein angiography may be normal but more severe injuries may cause foveal RPE defects.^62,67 The characteristic OCT finding is a well-defined outer retinal hyporeflective space primarily involving the photoreceptor inner and outer segment layers, as shown in Fig. 90.2 for a welding arc injury.^5,65,68–73 Spectral domain OCT imaging immediately after an injury reveals overlying outer nuclear layer and underlying RPE abnormalities, as shown in Fig. 90.3.

Fig. 90.2 OCT images taken months to years after solar or welding arc injuries usually reveal a well-defined foveolar outer retinal hyporeflective space.^5,65,68–73 This 34-year-old male had been welding since 11 years of age and complained of vision loss for 5 months prior to the OCT study. A horizontal scan through his fovea shows largely normal retinal pigment epithelium (RPE) and external limiting membrane reflective bands but interruption of the Verhoeff’s membrane (RPE tight junctions and/or apical processes) as well as the inner/outer-segment junction hyperreflective bands. These OCT findings are consistent with chronic damage to photoreceptor inner- and outer-segment layers.⁶²

(Courtesy of Suman Pilli, MD, Muralidhar Ogoti, MD, and Vishwanath Kalluri, MD.)

Fig. 90.3 A spectral domain OCT image taken shortly after a solar injury documents the foveolar outer retinal hyporeflective space observed in older lesions and also abnormalities in the overlying outer nuclear layer and underlying retinal pigment epithelium (RPE). These findings are consistent with histopathological evidence of photoreceptor and RPE damage after acute solar maculopathy in human eyes scheduled for enucleation.^74,136

(Courtesy of Giovanni Staurenghi, MD, and Marco Pellegrini, MD.)

The histopathology of solar retinopathy has been studied in volunteers who stared at the sun monocularly for 10–60 minutes before enucleation for choroidal melanoma.^63,74 Photoreceptor damage included vesiculation and fragmentation of photoreceptor outer segment lamellae, mitochondrial swelling, and nuclear pyknosis.^63,74 Cones appeared more damage-resistant than rods, possibly accounting for good visual outcomes after some injuries.⁷⁴ RPE damage was variable.^63,74 Imaging and histopathological data to date do not permit determination of whether solar and welding arc injuries are primarily of RPE and/or photoreceptor origin.

Foveomacular retinitis is a term used to describe foveal abnormalities resembling photic retinopathy. It occurs after blunt ocular trauma and whiplash injury^75–77 and in people with no history of mechanical or photic trauma.^78,79 Outbreaks were reported in military personnel during World War II and again from 1966 to 1973.^80–83 Those incidents were ascribed to solar exposure,^82,84 consistent with reports of solar maculopathy in young people who have been sunbathing but not sungazing.^85,

Buy Membership for Opthalmology Category to continue reading. Learn more here