2. Light and Laser Injury
Structural damage to the retina
produced by any type of light source.
3. Mechanism of damage
Photochemical &Thermal retinal damage possible
Potential causes
1 solar eclipse
2 welding arc
3 lightning,
4 ophthalmic
instruments,
5 Laser
4. LIGHT INTERACTION WITH
THE RETINA
The eye primarily perceives radiation in
the optical spectrum, comprised of
the visible (400–760 nm)
Ultraviolet (UV; 200–400 nm), and
Infrared (IR; > 760 nm).
Radiation in this region can be
produced by the sun, ophthalmic
instruments, and lasers
5. Associated features
■ Delayed appearance of the lesion after
the injury by hours to days
■ Variable recovery of vision
■ Severity of damage proportional to
increased duration and intensity of
exposure
6. Mechanisms to reduce retinal light
exposure.
The cornea absorbs most UV-B (280–315 nm) and
UV-C (< 280 nm), as well as some IR radiation, and
reflects up to 60%
of incident light that is not perpendicular to its surface.
The lens absorbs most UV-A (315–400 nm) and visible
blue wavelengths.
Retinal xanthophyl absorption of near-UV and blue light
to protect the photoreceptors,
Choroidal circulation control temperature
Intracellular moleculardetoxification of free radicals and
toxic molecules.
Physiologicalprotective mechanisms include the
eyebrow ridge, squint and blink reflexes, the aversion
response, and pupillary miosis.
7. Light damage to the retina
may occur when
Protective mechanisms are impaired
متعمدDeliberate gazing at a light source.
Young patients may be at increased risk due to
efficient light transmission through ocular
media.
8. PHOTIC RETINOPATHY
Damage disorder of RPE and photoreceptor
Temporally Permanent;
Recovery noted in solar retinopathy welding arc
maculopathy , and operating microscope
phototoxicity .
Mild sever
9. Retinal injury and the visual recovery
depend on multiple factors
The location and area exposded , the duration,
intensity, and spectrum of the light source, and host
susceptibility factors, such as age, nutritional status,
ocular pigmentation, core temperature, clarity of
ocular media, and pre-existing retinal disease.
Emmetropes and hyperopes may be at increased risk
caused by effective focusing of light on the retina.
Systemic photosensitizing agents, such as
tetracycline, hematoporphyrins, and psoralen, may
predispose to photochemical damage.
10. Solar (eclipse)Retinopathy
Religious sun gazing, solar eclipse,,sunbathing,
psychiatric disorders,
Solar radiation damages the retina through
photochemical effects,
Symptoms develop 1 to 4 hours by decreased
vision. usually improves within 6 months
A small yellow spot with a gray margin may be
noted in the foveolar or parafoveolar area
FA reveal transmission defects due to RPE
irregularity
OCT, demonstrates disrupted reflectivity in the
outer retina, or fragmentation of the highly
reflective layer corresponding to the junction
between the IS OS
Oral corticosteroids treat acute lesions,
11. Welding Arc Exposureاللحام
keratitis due to cornea UV absorption.
A yellow edematous lesion occurs
acutely in the fovea which is replaced
over time by an RPE irregularity or a
pseudomacular hole.
Vision usually improves with time
12. البرقLightning Retinopathy
Lesions described include macular edema,
macular hole, cyst, or a solar retinopathy-like
picture, cataract, retinal detachment, retinal
artery occlusions
Visual recovery often occurs over time, even
with severe maculopathy.
High-dose intravenous methylprednisolone
treatment may play a role in recovery of
vision
13. Retinal Phototoxicity from
Ophthalmic Instruments
Retinal injury has been described
following exposure to light produced
by the operating microscop
7% of patients having cataract
operations demonstrated
operating microscope phototoxicity
The mechanism of
intraoperative phototoxicity is
photochemical but may be thermally
after 60 minutes of
operating microscope light exposure,
despite the presence of UV and IR
filters,
14. The lesion is yellow round
FA of the acute lesion
reveals fluorescein
leakage at the level of
the RPE which may
simulate the
appearance of choroidal
neovascularization.
Subsequent weeks, the yellow
lesion fades and is replaced
by permanent areas of RPE
clumping and atrophy
FA blocking and transmission
defects, respectively
Long-term squeal
Retinal surface wrinkling. -
Choroidal neovascularization
15. Measures to avoid this complication
1-Minimizing length of surgery
2-Minimizing light output,
3-Using filters,
4-Rotation of the globe by a superior rectus suture,
5-Maximizing light pipe distance from the retina
6-using eccentric and variable endoillumination
techniques
7-Placement of an air bubble corneal cover
9-Retinal examinations be performed with
the minimal illumination required
16. LIGHT EXPOSURE AND AGE-
RELATED
MACULAR DEGENERATION
An association between long-term solar exposure and
AMD was considered
when AMD was found to be less common in patients
who have nuclear cataract
Solar observation acutely damages the RPE and
produces RPE pigmentary irregularities, which are
similar in appearance to those in AMD
The use of hats and sunglasses to filter UV was
inversely associated with the prevalence of soft,
indistinct drusen.
17. LASER INJURY
Laser applications in industrial, military,
and laboratory situations
account for accidental retinal injury.
-Subtle lesion -Macular hole
-Hemorrhage -Foveal cyst –
-Yellow RPE irregularities
-Epiretinal membrane
-Macular hole - Gliosis.
Recovery of vision is variable and is
related to the extent and location of
the initial injury.
Corticosteroids have been used to
treat laser-induced and laser pointer
retinal injuries.
Foveal cyst
18. In the ophthalmology setting
Lasers operators slit lamp or
operating microscope
contain filters to protect the
operator
Decreased color discriminatio
has been noted in
ophthalmologists who used
the argon blue-green.
Persons in the laser area
are at risk from laser light
scatteredfrom optical
interfaces such as
contact lenses and
mirrors
The risk is related to their
distance from the laser,
Protective goggles
should be worn.
19. LASER
POINTERS
Laser pointers are portable low energy devices that
emit a very narrow coherent low-powered laser
beam of visible light.
These devices are used to illuminate an item of interest
with a spot of brightly colored light
Laser used by ophthalmologists for retinal therapy
generate between 5 and 500mW
The FDA specifies that laser pointers between 1–5 mW
20. LASER POINTERSCont.
There is misuse of these handheld lasers.
.The mechanism of injury is thermal chorioretinal damage
There is visual abnormalities and scotom .
FA demonesterat perimacular hyperfluorescence correspond to RPE
window defect
Visual acuity improved to 20/20 and visual field returned to normal within8
weeks, but a subjective decrease in brightness and foveal RPE
These pointers that exceed recommended standards may produce
permanent retinal injury and visual impairment with resultant
photoreceptor damage
21. COMPLICATIONS OF
THERAPEUTIC RETINAL LASER
PHOTOCOGULATION
Inadvertent photocoagulation of the fovea,
cornea, iris, or lens can be minimized
with use of careful technique
and appropriate laser settings
22. Cont. COMPLICATIONS OF
THERAPEUTIC RETINAL LASER
PHOTOCOGULATIONpanretinal photocoagulation
spread over multiple sessions
Decreases in laser intensity and duration, avoid smaller spot sizes (50 μm),
with the use of the krypton red laser