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Sequelae of Radiation Therapy to the region
of the eye
Skin and Adnexa
Skin changes resulting from radiation
therapy may include erythema, hyperpigmentation,
depigmentation, atrophy, telangiectasia, and ectropion or
entropion of the eyelid. Although conjunctival changes are
usually insignificant, a corneal abrasion may result from
the formation of a keratotic plaque in a radiation-injured
conjunctiva. Loss of the cilia from the scalp, eyebrow, or
eyelid may occur after radiation therapy to the ocular area.
Hair loss from the scalp may occur at an exit area of an
external beam portal. Eyebrow loss occasionally occurs when
a 60Co plaque has been used anteriorly and
superiorly to treat choroidal malignant melanoma. The loss
of eyelashes that may accompany the use of x-ray therapy in
the treatment of basal cell carcinoma is usually permanent.
Similar lash loss may follow radioactive plaque therapy of
ciliochoroidal melanomas.
Cornea
Direct corneal injury may result from
irradiation of ocular and adjacent structures. Blodi
classified this damage as purely epithelial with a good
prognosis for recovery or stromal with a poor prognosis.
Experiments indicate that 72 Gy fractionated over 8 days
leads to corneal perforation, but 48 Gy fractionated over
the same time produces mostly reversible epithelial changes
with minimal stromal damage.
Lens
A great concern in the treatment of
ocular disease is the risk of radiation-induced cataract.
Merriam and Focht have shown that as little as 2 Gy in
a single fraction or 8 Gy fractionated delivered at the
level of the lens can significantly elevate the incidence of
cataract development. At higher doses, the percentage of
lenses that develop cataracts increases to 100%. With the
use of improved shielding, beam-control techniques, and more
inherently sharp beams, an 80% reduction in the incidence of
radiation-induced cataracts is expected.
Retina and Choroid
Changes in the retina and choroid are
observed after doses
of 45 to 60 Gy. Vascular damage leads to infarction
of tissue with the formation of exudates and hemorrhages.
Decreased visual acuity may result from damage to the
retinal tissue or from atrophy of the optic nerve. Because
of the extreme radioresistance of the sclera, which may
tolerate doses to 750 Gy or more, only a few cases of
scleral necrosis have been reported
Lacrimal Gland and Bony Orbit
Radiation damage to the lacrimal gland
may decrease tear production and produce irreversible
corneal changes. A particularly distinctive and disfiguring
orbital change that sometimes occurs in children irradiated
for ocular or orbital tumors is the arrested development of
the lateral orbital wall growth center, leading to
subsequent temporal osteomalacia.
Optic Nerve
Parsons described retrobulbar optic
neuropathy in 12 nerves in 131 patients at mean and median
times of 47 and 28 months, respectively. No injuries were
observed in 106 optic nerves that received a total dose of
<59 Gy. Among
nerves that received doses of 60 Gy or higher, the 15-year
actuarial risk of optic neuropathy was 11% when treatment
was administered in fraction sizes <1.9 Gy compared with 47%
when given in larger fractions.
Hypothalamus and Pituitary Dysfunction
Hypothalamus or pituitary function in
children with optic glioma may be impaired by the tumor
itself and by the high cranial irradiation doses used in
treatment. Brauner et al. evaluated the effect of optic
glioma and its treatment on patient growth and pubertal
development in 21 patients (13 boys and 8 girls) treated
with irradiation (45 to 55 Gy). Growth hormone deficiency
was present in only one patient tested before irradiation
and in all patients after irradiation. Precocious puberty
occurred in seven patients—before radiation therapy in five
patients and after irradiation in two. The cumulative height
loss during the 2 years after irradiation was 0.2 ± 0.2
standard deviation (mean ± standard error of the mean) in
seven patients with precocious puberty and 1.1 ± 0.2
standard deviation in 14 prepubertal patients (p
<.01).
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