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Diluted
pilocarpine drops (0.1%) can be used to diagnose a
Holmes–Adie pupil. These drops will not constrict a normal pupil, but will constrict a Holmes–Adie pupil due to denervation sensitivity.
·
Holmes–Adie pupil is an
idiopathic condition, typically affecting young women, presenting with an
enlarged pupil that is poorly reactive to light and accommodation. Absent ankle
jerks are a frequent association. A Holmes–Adie pupil causes no harm, except
blurring vision when reading in some patients. Adie’s pupil is due to a postviral degeneration in the ciliary
ganglion. The pupil is initially dilated, with a tonic reaction to light
and sectorial vermiform movements. The pupil is hypersensitive to 0.125% pilocarpine.
The near vision is impaired by accommodative spasm but this recovers in a few
months. The pupil sphincter later becomes fibrosed and the pupil miosed.
Holmes–Adie syndrome is the combination of Adie’s pupil with hyporeflexi.
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Red desaturation – ie when red looks paler to one eye than
the other – is a sensitive sign of optic nerve dysfunction
·
If
the entire anterior chamber is full of blood and no iris can be seen (a 100% hyphaema), the term ‘8-ball hyphaema’
has been used.
·
CHRPE (congenital hypertrophy of the retinal pigment
epithelium) can be ‘typical’ or ‘atypical’. Typical
CHRPE are grey or black, with depigmented lacunas,
and are found in one quadrant of one eye. They do not affect vision. Atypical CHRPE have a white fishtail, and
are bilateral. They do not affect vision, but if there are more than four
atypical CHRPE in each eye then familial adenosis polyposis or Gardner’s syndrome may be suspected as an
association. Colonoscopy and examination of all family members would therefore
be appropriate. Fluorescein angiography will add nothing in terms of a diagnosis.
The
lesion appears as a cluster of gray to black, well-defined RPE lesions that
have been likened to bear tracks on the retina.
Retinitis pigmentosa causes ‘bone spicule’ pigmentation in the retinal mid-periphery,
along with a waxy disc pallor and retinal arteriolar attenuation. Patients with
retinitis pigmentosa often suffer from night
blindness and restricted peripheral vision (‘tunnel
vision’ when the disease is advanced).
Metastases to the choroid can appear as large dark lesions under the retina, often
with overlying exudative
(as opposed to rhegmatogeneous) retinal detachment.
Potential sources of primary lesions include the gastrointestinal tract, breasts,
kidneys, testes and prostate. However, the appearance does not sound typical of
a metastasis to the choroid. Discrete pigmented spots in the retina, often with
pale rims of atrophy, could be due to either previous laser treatment (in a
diabetic patient with signs of retinopathy and a history of new blood vessel
formation, for example) or scars from previous toxoplasmosis infections.
Congenital
or old toxoplasmosis lesions can reactivate
in adulthood, appearing as pigmented retinal lesions with a white fluffy edge,
often obscured on examination by vitreous inflammatory debris (vitritis); hence the descriptive term for the appearance of
active toxoplasmosis, ‘a headlight in the fog’.
Old inactive lesions require no treatment.
·
Giant-cell
arteritis affects the large- and medium-sized arteries. Ocular involvement is due
to inflammation and occlusion of the ophthalmic artery and its branches to the
optic nerve head, the posterior ciliary arteries.
Occlusive vasculitis causes pallor and swelling of
the optic nerve head (nicknamed ‘pale papilloedema’). This condition is known as
‘anterior ischaemic optic neuropathy’ (AION). Central retinal artery occlusion (CRAO)
is very unusual in giant-cell arteritis.
·
The earliest sign of diabetic
retinopathy is the presence of microaneurysms on fluorescein angiography. The ERG and VEP would
be affected very late in the disease as the patient became blind, as would the
response of the pupil. Autonomic neuropathy in patients with diabetes is
another cause of abnormal pupillometry. Ocular
ultrasound will not be abnormal until there is anatomical derangement of the
eye, as would occur in retinitis proliferans with tractional retinal detachment. (Incidentally, this test is
useful when there is also a cataract and the retina cannot be seen.)
·
Optic nerve
sheath meningioma: ‘railroad-track” sign of a central lucent optic nerve
surrounded by tumor.
·
Hypoplasia of the optic nerve: typical double ring sign is seen. The nerve fiber
layer is practically nonexistent.
·
Another optic nerve atrophy distinguishable from LHON (
nasal, 20-30 yrs, Retinal peripapillary telangiectasis, a
typical finding in LHON, is evident.) is dominant optic atrophy. Visual acuity depression is
mild in dominant optic atrophy ( more temporal
pallor, 4-8 yrs of age).
·
Acute, recurrent toxoplasmosis: headlight in fog
·
CMV retinitis: brushfire border
·
Acute retinal necrosis demonstrating the
hallmark finding of grayish-white patches in the retinal periphery.
·
Bird-shot choroiditis.
The classic finding is a creamy yellow, multifocal choroiditis.
The central vision is excellent; the patient's main complaints were floaters
and peripheral spots.
·
Presumed ocular histoplasmosis
syndrome. The classic findings of juxtapapillary chorioretinal scars and macular scarring, with a greenish
yellow area and blood along the edge, fulfill the clinical picture of choroidal neovascularization.
Peripheral scars are often seen.
·
ocular
sarcoidosis: candle-wax drippings
·
The PORN syndrome is associated with acute
peripheral retinal necrosis, indicated here by the whitish areas located
peripherally in the superior retina
·
masquerade syndrome to
describe eyes with uveitis (or simulated uveitis) in which the cause of inflammation is either neoplastic or nonuveitic in
origin.
·
Fluorescein angiogram
demonstrating the “leopard spots”
pattern resulting from patchy subretinal
infiltrates in a patient with reticulum cell sarcoma.
·
Hollenhorst plaque
within a retinal arteriole in the fundus in an eye
without a clinically evident retinal arterial obstruction
·
Acute hypertensive choroidopathy.
Yellow, “Elschnig's spots” can be seen at the level of
the retinal pigment epithelium.
·
Photodynamic
therapy (PDT) is the treatment of choice for subfoveal
and juxtafoveal classic CNVM. In PDT, vertiporfin, a photosensitizer or
light activated dye is injected intravenously. The area of CNVM is then exposed
to light from a diode laser source at a wavelength (689 nm) that corresponds to
absorption peak of the dye. The light-activated dye then causes disruption of cellular
structures and occlusion of CNVM with minimum damage to adjacent RPE,
photoreceptors and capillaries.
·
Endophthalmitis:
Postoperative cases: Staphylococcus epidermidis
Penetrating trauma: Bacillus cereus and Streptococcus species
Patient with a central venous catheter or prolonged antibiotic therapy:
Candida albicans
·
H
·
·
Pigment dispersion syndrome (PDS) is an autosomal dominant disorder characterized by disruption of
the iris pigment epithelium (IPE) and deposition of pigment granules on the
structures of the anterior segment. Pigment granule accumulation in the trabecular meshwork then leads to progressive trabecular dysfunction and ocular hypertension with or
without associated glaucomatous optic neuropathy. Because the age of onset
often is in the third or fourth decade of life, this disorder is an important
and often underdiagnosed glaucoma affecting younger
people
The classic triad of clinical signs
of PDS consists of a Krukenberg spindle, slitlike,
radial, midperipheral iris transillumination
defects, and pigment deposition on the trabecular
meshwork.
·
Best disease, also
termed vitelliform macular dystrophy, is an autosomal dominant disorder involving the long arm of
chromosome 11 (11q12-q13), which classically presents in childhood with the
striking appearance of a yellow or orange yolklike
lesion in the macula.
Lesions in this disease are
restricted to the eye. No systemic associations exist. Abnormalities in the eye
result from a disorder in the retinal pigment epithelium (RPE). Lipofuscin (periodic acid-Schiff [PAS] positive)
accumulates within the RPE cells and in the sub-RPE space, particularly in the foveal area. The RPE appears to have degenerative changes
in some cases, and secondary loss of photoreceptor cells has been noted
1.
Stage 1 (previtelliform)
- Normal macula or subtle RPE pigment changes, EOG abnormal
2.
Stage 2 (vitelliform)
- Well-circumscribed, 0.5-5 mm round, elevated, yellow or orange lesion;
described as an egg-yolk appearance; usually centered on the fovea; can be
multifocal; the rest of the fundus has a normal
appearance.
3.
Stage 3 (pseudohypopyon)
- Yellow material can break through the RPE and accumulate in the subretinal space in a cyst with a fluid level formed. The
yellow material will shift with extended changes in position (60-90 min). This
stage most often is found in the teenage years, but it has been described in
individuals aged 8-38 years.
4.
Stage 4 (vitelliruptive)
- Scrambled egg appearance is due to the breakup of the uniform vitelliform lesion. Pigment clumping and early atrophic
changes may be noted. Visual acuity may deteriorate moderately.
5.
Stage 5 (atrophic) - As the yellow material
disappears over time, an area of RPE atrophy remains. This appearance is
difficult to distinguish from other causes of macular degeneration. Visual
acuity can deteriorate more markedly at this stage.
6.
Stage 6 (choroidal neovascular/cicatricial) -
Following the atrophic stage, choroidal neovascularization can develop, leading to a whitish subretinal fibrous scar
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