PREGUNTAS Flashcards
(283 cards)
1
Q
How do anatomists define the macula?
A
That portion of the posterior retina with xanthophyllic pigment and two or more layers of ganglion cells.
2
Q
How large is the macula?
A
5-6 mm (5000-6000 microns)
3
Q
What is the name for the small, slightly concave portion of the posterior retina that is devoid of capillaries and occupied almost exclusively by cones?
A
Foveal avascular zone.
4
Q
How large is the fovea?
A
1.5 mm, 1500 microns, 1 disk diameter (DD), 5 degrees.
5
Q
What area is defined by the lack of a ganglion cell and inner nuclear layer?
A
Foveola: approx. 350 microns, approx. equal to the foveal avascular zone (FAZ).
6
Q
What is the deepest portion of the retina supplied by branches of the central retinal artery
A
The inner portion of the inner nuclear layer.
6
Q
What is the name for the depression in the center of the foveola?
A
Umbo, clivus, light reflex.
7
Q
What is the exception to the role of retinal blood supply of the choriocapillaris?
A
Choriocapillaris normally supplies the outer portions of the retina up to the outer part of
the inner nuclear layer—a cilioretinal artery can sometimes supply an area of inner retina
8
Q
What makes up the outer portion of the blood-retina border?
A
Tight junctions between adjacent RPE cells (zonulae occludentes).
9
Q
What makes up the inner portion of the blood-retina border?
A
Retinal capillary endothelial cells.
10
Q
What is the chromatophore for all four classes of human visual pigments (rhodopsin, red, blue, and green), and how is it oriented to the plane of the lipid bilayer?
A
11-cis-retinaldehyde is oriented parallel to the plane of the lipid bilayer and, therefore, perpendicular to the path of photons.
11
Q
When are old rod disks and cones shed?
A
Rod disks are shed at dawn and cone disks are shed at dusk.
12
Q
Why is the neuroretina usually devoid of water?
A
The RPE has a high capacity for water transport.
13
Q
What syndrome can be associated with congenital hypertrophy of the RPE?
A
Gardner Syndrome (intestinal polyposis).
14
Q
What are the parts of the ciliary body?
A
The ciliary body has two parts, which are pars plicata ciliaris and pars plana ciliaris. The pars plicata is a circumficial zone about two and a half millimeters in the anterior posterior dimension, extending posteriorly from the iris root and contains 70 to 80 ciliary processes. The pars plana ciliaris is about three millimeters wide nasally and four and a half millimeters temporally, and extends from the pars plicata anteriorly to the ora serrata posteriorly. The posterior part of the pars plana is covered with vitreous base.
15
Q
What artery is the origin for both the choroid and the central retinal artery?
A
Ophthalmic artery.
16
Q
How is pars plana vitrectomy performed?
A
There are three incisions made in pars plana, for which one is used for infusion of fluid to maintain intraocular pressure. The second port is used for illumination with fiber optics. The third opening is used to allow a vitrectomy instrument to be used in the vitreous cavity. Other instruments (such as laser probes, intraocular scissors, etc.) are interchangeable through one of these openings.
17
Q
When is open sky vitrectomy performed?
A
Open-sky vitrectomy is an operation used for desperate cases of detached retina. One of the best indications for this procedure is grade V ROP.
18
Q
What is the best predictor of metastatic potential for retinoblastoma histopathologically?
A
Optic nerve invasion.
19
Q
What wavelengths of light pass through the vitreous gel?
A
The vitreous body is a clear gel that allows the transmission of about 90% of light
wavelengths between 300 to 1400 nm.
20
Q
What is the most common cause of cotton wool spots?
A
Diabetic retinopathy.
21
Q
What forms the external limiting membrane of the retina?
A
It is formed by tight junctions between the photoreceptor inner segments and the lateral margins of Müller’s cells.
22
Q
What is a highly characteristic histologic finding in the iris pigment epithelium of diabetics?
A
Lacy vacuolization of the iris pigment epithelium.
23
Q
What organ is the most common site of metastasis for uveal melanomas?
A
Liver.
24
What type of collagen is vitreous composed of?
Type II collagen, which is specific for vitreous.
25
What is the most abundant component of the vitreous body?
Water is the major component of the vitreous body. It comprises 98% of its volume.
26
What is the optical function of the vitreous?
It acts as an ultraviolet filter. There is decreased transmission at 350 to 300 nm wavelength and zero thereafter as well as decreased infrared transmission at 800 nm wavelength and zero after 1600 nm
27
How often do patients with acute posterior vitreous detachment and vitreous hemorrhage have retinal breaks?
70% will have peripheral retinal breaks.
28
How far is the ora serrata from the limbus?
6 mm
29
Where do we make the incision for pars plana vitrectomy?
An incision that is made three to four millimeters posterior to the limbus goes to the anterior part of the pars plana and avoids the vitreous base and the pars plicata. The blood vessels for pars plana are radially oriented and the circumficial incision rarely causes any bleeding into the eye.
30
Is the insertion of the superior rectus muscle anterior or posterior to the ora serrata?
Posterior
31
How far is the equator from the limbus?
16 mm.
32
How often is there no family history of retinitis pigmentosa in a patient with the disease?
40% of patients with retinitis pigmentosa will have no family history of the disease.
33
What is the probability that the next child of a patient with a history of bilateral retinoblastoma will develop the disease?
50%.
34
In what other tumor besides retinoblastoma may Flexner-Wintersteiner and
Homer Wright rosettes be seen?
Medulloepithelioma.
35
What are Elschnig spots?
They are choroidal infarcts seen in severe hypertensive retinopathy.
36
What is Terson’s syndrome?
Retinal and vitreous hemorrhage associated with posttraumatic subarachnoid and subdural hemorrhage.
37
What is the most common cause of spontaneous vitreous hemorrhage in adults?
Diabetic retinopathy.
38
A 60-year-old patient has an acute, spontaneous vitreous hemorrhage that prevents visualization of the fundus. What diagnostic test should next be requested for in this case?
Ultrasonography to rule out the possibility of retinal detachment or a neoplasm.
39
What is Cloquet’s canal?
It is the embryological remnant of the hyaloid vascular system.
40
What can be observed in essentially normal eyes that are remnants of the fetal vasculature?
Mittendorf’s dot, vascular loops, Bergmeister’s papilla.
41
At what time during embryonic development does the primary vitreous first form
During the 3rd through 9th weeks.
42
What is the source of the secondary vitreous?
Vitreous fibrils are formed by the inner retina while the Müller cells produce hyaluronic
acid
43
By which month is Cloquet’s canal formed?
5th month.
44
The tertiary vitreous forms what ocular structures?
Zonular fibers.
45
What is the most common presentation of PHPV?
Leukocoria.
46
What are the most common characteristics of PHPV?
Unilateral in 90% of cases, normal full term infants, microphthalmia, shallow AC, natural course leads to blindness.
47
What are the most common fundus abnormalities that are seen in hereditary vitreoretinopathies?
Equatorial and perivascular (radial) lattice, retinoschisis, chorioretinal atrophy, optic atrophy.
48
What are the 2 hereditary vitreoretinopathies most commonly not associated with systemic abnormalities?
Wagner’s Disease and Jansen’s Disease.
49
What differentiates Wagner’s and Jansen’s Disease?
Jansen’s Disease has a high incidence of retinal detachment. Wagner’s Disease is not
associated with retinal detachment.
50
What disease is associated with heredity vitreoretinopathies and systemic abnormalities?
Stickler’s Syndrome.
51
What systemic abnormalities are generally found in Stickler’s Syndrome?
1. Hyperextensibility and enlargement of joints.
2. Arthritis and spondyloepiphyseal dysplasia.
3. Orofacial findings include mid-facial flattening, cleft palette, and the Pierre-Robin
malformation complex (micrognathia, cleft palette, and glossoptosis).
52
Why is it important to recognize Stickler’s Syndrome?
Because of the high incidence of retinal detachment which are normally very difficult to repair.
53
What is the most common inheritance pattern in Stickler’s Syndrome?
AD
54
What are the findings in ocular ischemic syndrome?
Stenosis of the carotid artery can lead to ocular ischemia, ipsilateral absence of arcus
senilis, iris neovascularization and midperipheral retinal hemorrhages.
55
What composes asteroid hyalosis?
Calcium soaps.
56
What is the ratio of pericytes to retinal vascular endothelial cells in normal retinal blood vessels?
1 to 1 ratio.
57
What type of configuration can choroidal melanomas assume on B-scan ultrasound?
Collar button configuration.
58
What are the criteria for diabetic clinically significant macular edema (CSME)?
Retinal thickening within 500 microns of the center of the fovea.
Hard exudates at or within 500 microns of the center of the fovea if associated with thickening of adjacent retina.
Retinal thickening 1 DD in size or larger if within 1 DD from the center of the fovea.
59
What are the retinal findings of preproliferative diabetic retinopathy?
Cotton wool spots, dark blot hemorrhages, vascular changes (beading, looping, sausage-
like), and intraretinal microvascular anomalies (IRMA).
60
What did the Diabetes Control and Complications Trial demonstrate?
Aggressive efforts to normalize blood sugars with insulin pumps may initially worsen the retinopathy in some patients during the first few months of treatment. Ultimately, strict control of blood sugar with intensive insulin therapy:
Reduced the risk of development of retinopathy in patients without retinopathy by 76%
Reduced by 47% the risk of development of severe nonproliferative and proliferative retinopathy in patients with mild to moderate nonproliferative retinopathy, and slowed the progression of retinopathy in patients with mild to moderate nonproliferative retinopathy by 54%.
61
What group of patients can show a worsening of diabetic retinopathy with intensive control?
Patients with mild or moderate NPDR at the time of change to intensive control.
62
What treatment did the DRS recommend for high-risk PDR?
PRP - 1200 or more 500 micron burns separated by 1/2 burn width.
63
What were the conclusions of the Early Treatment Diabetic Retinopathy Study
(ETDRS)?
Focal laser coagulation should be considered for all eyes with CSME because treatment reduces the risk of visual loss by 50%.
Panretinal photocoagulation (PRP) should be considered in patients who are at high risk of developing proliferative diabetic retinopathy (PDR) while mild to moderate nonproliferative diabetic retinopathy (NPDR) can be observed.
Systemic aspirin (650 mg/day) does not prevent the development of PDR, nor does it increase the risk of visual loss or vitreous hemorrhage.
64
Describe Severe NPDR as defined by the ETDRS.
Severe NPDR was defined by the ETDRS as any one of the following: intraretinal heme and microaneurysms in 4 quadrants; venous beading in 2 quadrants; IRMA in 1 quadrant. Remember the 4:2:1 rule for severe NPDR.
65
How did the ETDRS define very severe NPDR?
2 of 4,2,1
66
What groups of patients are predisposed to poor visual acuity even after photocoagulation?
Those with diffuse macular edema, macular ischemia, hard exudates in the fovea, or marked CME.
67
What is the risk of developing high-risk PDR within one year for patients with very severe NPDR?
Very severe NPDR - 45% risk of developing high-risk PDR within one year.
68
What systemic conditions may lead to a worsening of diabetic retinopathy?
Hypertension, severe carotid vascular disease, and pregnancy.
69
Is photocoagulation recommended if high-risk PDR develops during pregnancy?
YES
70
Which should be treated first, CSME or high-risk PDR?
CSME
71
Describe the technique for focal laser photocoagulation.
Focal - a 50-100 micron spot size, 0.1 second or less duration, attempt to whiten or darken all leaking microaneurysms between 500 and 3000 microns from the center of the macula.
72
Which should be done first - focal laser or cataract extraction?
Focal laser.
73
What type of lasers may be more successful for PRP in patients with vitreous heme?
Krypton red or diode lasers.
74
What are potential adverse effects of panretinal photocoagulation of diabetic retinopathy?
1. Angle closure glaucoma from choroidal effusion.
2. Decreased night vision.
3. Central scotoma from worsening diabetic macular edema.
4. Retinal detachment from regression and contracture of neovascular fronds.
75
What are the different types of central retinal vein occlusions?
Nonischemic CRVO. Ischemic CRVO. Papillophlebitis.
76
What is the probability that the next child of a patient with unilateral retinoblastoma but without a family history of the disease will develop retinoblastoma?
6%
77
What is the most common primary intraocular malignancy?
Uveal malignant melanomas.
78
Where is the most frequent primary site of choroidal metastatic tumors?
Women: breast.
Men: lung.
Other causes include kidney, GI tract, prostate (rarely).
79
What are the layers of Bruch’s membrane?
1. The inner basal lamina of the RPE.
2. The inner collagenous zone.
3. Band of elastic fibers.
4. Outer collagenous zone.
5. Basal lamina of the choriocapillaris.
80
What are Roth spots and what can cause them?
They are white spots in the middle of an intraretinal hemorrhage, which are thought to represent a fibrin thrombus occluding a ruptured blood vessel. They can be caused by:
1. infectious endocarditis
2. leukemia
3. anemia
4. hyperviscosity syndromes, eg. Multiple myeloma, Waldenstrom macroglobulinemia.
81
What are some of the causes of a bull’s eye maculopathy?
1. Drugs (chloroquine, chlorpromazine, thioridazine, tamoxifen).
2. Cone dystrophy.
3. Stargardt’ s disease.
4. Inverse (central) retinitis pigmentosa.
5. Batten’ s disease.
82
What are the risk factors for the development of choroidal neovascularization in DMAE
1. Cigarette smoking.
2. Elevated serum cholesterol.
3. Large, bilateral, soft drusen.
4. Pigment irregularities in the macula.
83
What factors decrease the risk of choroidal neovascularization in age-related macular degeneration?
1. Exogenous estrogen use in postmenopausal women.
2. Increased serum carotenoid levels.
84
How can retinoblastoma present clinically?
Leukocoria
Strabismus.
Secondary glaucoma.
Pseudouveitis (hypopyon, hyphema, red eye, pain) in older children. Proptosis.
Orbital inflammation.
85
What are the most common organs involved with hematogenous spread of retinoblastoma?
Bones, lymph nodes and liver.
86
What is the fundus appearance of retinoblastoma?
Endophytic tumors project into vitreous, while exophytic tumors present as retinal
detachment.
87
What is the treatment for retinoblastoma?
1. Enucleation.
2. Radiotherapy if good vision is present.
3. Photocoagulation for tumors <3mm diameter or <2 mm thickness.
4. Cryotherapy for tumors <3.5 mm or <2 mm thickness.
5. Systemic chemotherapy for orbital recurrences and metastatic disease (skull, orbit,
long bones, viscera, spinal cord, lymph nodes).
Note: photocoagulation and cryotherapy are contraindicated if vitreous seeding is present.
88
What are retinal capillary hemangiomas called?
Von Hippel’s disease.
89
How many patients with Von Hippel’s disease are associated with systemic lesions (Von Hippel-Lindau’s syndrome)?
Twenty five percent have systemic lesions such as:
1. Hemangioblastomas of the cerebellum, brainstem and spinal cord.
2. Cysts of the kidneys, pancreas, lungs, ovaries, and epididymis.
3. Phaeochromocytoma and hypernephroma.
90
How would you workup patients with Von Hippel’s disease and their relatives?
1. Physical examination.
2. Urinalysis.
3. 24-Hour urine collection for levels of vanillylmandelic acid (VMA).
4. Renal ultrasonography.
5. Abdominal CT scan.
6. Brain CT or MRI scan.
91
What is the treatment of Von Hippel Lindau’s disease?
1. Photocoagulation or cryotherapy if it is affecting or threatening vision.
2. Genetic counseling.
3. Refer for medical treatment of the systemic lesions of Von Hippel-Lindau’s
syndrome.
92
What is Wyburn-Mason syndrome?
1. It is a phacomatoses consisting of
2. Large, dilated, tortuous vessels forming AV communications in the retina,
3. Racemose hemangiomas in the midbrain causing seizures and hemiparesis, and
4. Hemangiomas in the ipsilateral pterygoid fossa, mandible and maxilla.
93
What are the causes of peripheral retinal neovascularization?
1. Diabetes mellitus.
2. V ein occlusion.
3. Sickle cell anemia.
4. Retinal vasculitis (sarcoidosis, collagen vascular disease, radiation retinopathy, pars
planitis).
5. Retinopathy of prematurity.
6. Familial exudative vitreoretinopathy.
7. Eales disease.
94
What are the critical signs of sickle cell retinopathy?
Peripheral neovascularization (sea fans), sclerosed peripheral vessels, and a dull gray
peripheral fundus resulting from ischemia.
95
How would you manage sickle cell retinopathy?
1. Photocoagulation to areas of capillary nonperfusion.
2. Pars plana vitrectomy for tractional retinal detachment or vitreous hemorrhage.
96
What is the cause of retinal and optic disc colobomas?
Incomplete closure of the fetal fissure.
97
What other ocular features may be associated with retinal colobomas?
Posterior embryotoxon. Non-rhegmatogenous retinal detachment. Strabismus.
Nystagmus.
Posterior lenticonus.
98
What is the mode of inheritance of choroideremia?
X-linked recessive.
99
What are the ERG findings in choroideremia?
It may be normal in the early stages, but the scotopic ERG will eventually become non-
recordable and the photopic ERG severely diminished by the end of the first decade.
100
What metabolic error is present in gyrate atrophy?
Inborn error of the mitochondrial enzyme ornithine aminotransferase, leading to increased levels of ornithine in CSF, aqueous, serum and urine.
101
How is gyrate atrophy treated?
Pyridoxine and arginine-restricted diet.
102
What is the mode of inheritance of Stargardt’s disease?
AR
103
What systemic diseases may be associated with congenital hypertrophy of the retinal pigment epithelium?
Gardner’s syndrome and familial adenomatous polyposis (FAP). At least 4 lesions in each eye are generally considered necessary to suggest the possibility of either FAP or Gardner’s syndrome.
104
What systemic diseases may be associated with angioid streaks?
1. Paget’ s disease.
2. Pseudoxanthoma elasticum.
3. Ehlers-Danlos syndrome.
4. Hemoglobinopathies (homozygous sickle cell disease, thalassemias).
5. Acromegaly.
6. Calcinosis.
7. Senile elastosis.
105
What posterior segment features may be caused by Ehlers-Danlos syndrome?
High myopia and retinal detachment from giant tears.
106
When does the retina become vascularized in an infant?
The nasal retina is usually vascularized by 36 weeks gestation, while the temporal retina
is usually completely vascularized by term.
107
Which infants are at risk for developing retinopathy of prematurity (ROP)?
Infants born less than 36 weeks of age, weighing less than 2000 g and who have received
supplemental oxygen.
108
When should neonates at risk for ROP be screened?
Initially, they should be screened between postconceptual ages of 32 and 36 weeks after birth then every 2 weeks until 36 weeks if the fundi are normal and weekly if there is evidence of zone 1 or 2 disease present.
109
How often does ROP in infant eyes spontaneous regress?
85%.
110
What is a retinal detachment?
It is a separation of the sensory retina from the RPE by subretinal fluid.
111
What is the significance of pigment cells (tobacco dust) in the retrolental space of a patient complaining of sudden onset of floaters and flashing lights?
It suggests the possibility of a retinal tear. The cells represent macrophages containing RPE cells.
112
What potential complication can occur in areas of “white-without-pressure”?
Giant tears can occur along the posterior border of “white-without-pressure.”
113
Do snail-track degenerations have the same complications as lattice
degeneration?
Yes. Large round holes can form in areas of snail-track degeneration, and there is a high risk of retinal detachment.
114
What is retinoschisis?
It is a splitting of the neurosensory retina into two layers.
115
Where does the splitting occur in degenerative retinoschisis?
Degenerative retinoschisis can either be typical (split at outer plexiform layer) or reticular (split at nerve fiber layer).
116
What group does degenerative retinoschisis occur more frequently in, myopes or hypermetropes?
Hypermetropes (70%).
117
What are the clinical features of juvenile X-linked retinoschisis?
It is a bilateral, vitreoretinal degeneration in children characterized by tiny cystoid spaces in a bicycle wheel pattern in the macula eventually resulting in an atrophic macular scar and associated with retinoschisis in up to 50% of cases. Retinal detachment and vitreous hemorrhage can also occur in up to 40% of cases.
118
What is a characteristic ERG finding found in juvenile X-linked retinoschisis?
The b-wave is disproportionately decreased as compared to the a-wave.
119
What type of visual field defects do retinoschisis and retinal detachments produce?
A retinal detachment produces a relative scotoma while a retinoschisis produces an absolute scotoma.
120
How can retinoschisis produce a retinal detachment?
For a retinoschisis to cause a retinal detachment there should be an outer wall hole present. There are two possible scenarios. In the first case, only outer wall hole(s) of schisis cavity is/are present. This results in the content of the schisis cavity to slowly detach the retina. In the second type of retinal detachment secondary to retinoschisis, there is a hole in both the inner and the outer walls of the cavity.
121
How are retinal detachments classified?
There are three main classes of retinal detachment including rhegmatogenous retinal
detachment, tractional retinal detachment and exudative retinal detachment.
122
What is a tractional retinal detachment?
Tractional retinal detachment is caused by vitreous membranes produced by penetrating injuries or proliferative retinopathy, which can cause traction on neurosensory retina and pull it away from the retina pigment epithelium layer.
123
Describe the appearance of the retina in tractional retinal detachment.
The retina has a smooth surface and is immobilized. The detachment is concave toward
the anterior segment of the eye and rarely extends to the ora serrata.
124
How are tractional retinal detachments repaired?
Treatment may require both vitrectomies to release the traction on the detached retina and
a scleral buckle procedure to seal the break.
125
When does exudative retinal detachment occur?
Exudative retinal detachment is seen when there is damage to the retinal blood vessels or the EPR. This allows the passage of fluid into the subretinal space. The most common causes of this exudative retinal detachment are neoplasia and inflammatory disease. This can present as a “shifting fluid” in appearance, which responds to the force of gravity, detaching the area of the retina in which it accumulates.
126
What are signs of long-standing rhegmatogenous retinal detachments?
Pigment demarkation (high-water marks). Secondary intraretinal cysts.
Retinal thinning.
Subretinal fibrosis.
127
What is the most common cause of rhegmatogenous retinal detachment?
The most common cause of rhegmatogenous retinal detachment is lattice degeneration which is found in 8-10% of the general population, however, only a small number of affected individuals develop retinal detachment. It is estimated that 20-40% of all rhegmatogenous detachments has lattices degeneration as the underlying cause.
128
What is the most common cause of failure to repair a rhegmatogenous retinal detachment?
Proliferative vitreoretinopathy (PVR).
129
How do we classify PVR?
PVR is classified according to its location, type, and extent of retinal contraction. If the PVR is posterior to the equator, it is considered as posterior PVR, and if it is anterior to the equator, it is considered as anterior PVR. Anterior and posterior PVR can be further classified based on the extent of the proliferation or retinal contraction.
130
What is the treatment for a retinal giant tear?
A giant retinal tear is a retinal tear greater than 90 degrees in circumferential extent. Following the vitrectomy the retinal flap can be unfolded with air, silicone oil, or perflurocarbon. After reattachment of the retina, long acting tamponade gas or silicone oil is used to reattach the retina with the extensive laser photocoagulation therapy around the retinal tear to stabilize the retina. Using these recent techniques the patient can be in supine position during the surgery, unlike the earlier techniques which require the prone position to permit the unfolding of the giant tear.
131
What are potential complications of drainage of subretinal fluid?
1. Postoperative endophthalmitis.
2. Retinal incarceration.
3. Vitreous prolapse.
4. Choroidal hemorrhage.
5. Iatrogenic retinal breaks.
6. Fishmouthing of U-tears.
132
What are causes of early failure of retinal detachment surgery?
1. Failure to find all retinal breaks.
2. Buckle failure due to inadequate size, height and positioning.
3. Fishmouthing of the retinal tear.
4. Missed iatrogenic breaks during drainage of subretinal fluid.
133
What are the indications for vitrectomy?
1. Non-resolving vitreous opacities, eg. Bleeding, inflammation, neoplastic.
2. Proliferative retinopathy.
3. Complicated retinal detachments, including giant tears.
4. Macular epiretinal membranes.
5. Dislocated crystalline lens or lens fragments after cataract surgery.
6. Diagnostic vitrectomy for uveitis.
7. Aphakic cystoid macular edema in which vitreous is incarcerated in the wound.
134
What are the intraoperative complications of vitrectomy?
1. Iatrogenic DR or retinal breaks.
2. Severe hemorrhage.
3. Cataract formation.
4. Pressure induced optic nerve damage.
135
What are the POP complications of vitrectomy?
1. Endophthalmitis.
2. Retinal detachment.
3. Recurrent vitreous hemorrhage.
4. Phthisis bulbi.
5. Sympathetic ophthalmia.
6. Glaucoma.
7. Anterior segment neovascularization.
8. Flat anterior chamber.
9. Cataract.
10. Fibrin formation.
11. Inflammation.
12. Recurrent corneal erosions.
136
What did the Diabetic Retinopathy Vitrectomy Study (DRVS) evaluate?
The benefit of early (1-6 months) versus late (at 1 year) vitrectomy for eyes with severe
vitreous heme and visual loss of 5/200 or worse
137
What did the DRVS show concerning vitrectomy in patients with vitreous hemorrhage?
Benefit of early vitrectomy was clearly demonstrated in IDDM patients. No such
advantage was found in NIDDM patients.
138
What can cause a traumatic retinal break?
Retinal breaks can result following perforating eye injuries by direct retinal perforation,
contusion, and vitreous traction, which is produced by fibrocellular proliferation
139
When is pneumatic retinopexy used?
It is used to treat uncomplicated retinal detachments with a small retinal break or a group of breaks over an area of less than two clock hours located in the upper two-thirds of the retina. Air, sulfur hexafluoride (SF6) and perfluoropropane (C3F8) are most commonly used.
140
Which of the gases used in fluid-gas exchange lasts the longest inside the eye?
Perfluoropropane (C3F8) lasts 55-65 days, while sulfur hexafluoride (SF6) and
perfluoroethane (C2F6) last 10-14 days and 30-35 days respectively.
141
What are the indications for treatment of macular holes with vitrectomy and fluid-gas exchange?
Full thickness macular holes less than one-year-old and associated with a visual acuity worse than 20/60.
142
When is an inferior iridectomy performed when using silicone oil as a permanent tamponade?
Inferior iridectomy is placed in an aphakic eye when silicone oil is used to fill the vitreous cavity. This is to minimize the anterior segment complications by preventing the prolapse of silicone oil into the anterior chamber.
143
What are the most common causes of spontaneous vitreous hemorrhage in adults?
1. Diabetic retinopathy (39-54%).
2. Retinal break without detachment (12-17%).
3. Posterior vitreous detachment (7.5-12%).
4. Rhegmatogenous retinal detachment (7-10%).
5. Retinal neovascularization from BRVO and CRVO (3.5-10%).
144
What are the main methods used in intraocular surgery to create a chorioretinal scar?
1. Photocoagulation.
2. Cryotherapy.
3. Diathermy.
145
What is the mechanism of action of photocoagulation?
The light energy is absorbed by an opaque tissue and is converted into heat that produces thermal damage. The chorioretinal adhesion is made during photocoagulation by different wavelengths of light, which produces burns in the retina and pigment epithelium. Photocoagulation should be used in the area that the retina is in contact with the pigment epithelium.
146
What is the mechanism of action of diathermy?
The diathermy probe conducts the radiofrequency energy to the ocular tissue. The energy is then converted to heat as it penetrates the tissue, and produces a burn within the ocular tissue.
147
What is the disadvantage of using diathermy to create a chorioretinal scar?
The main disadvantage of diathermy is that it causes shrinkage and weakening of the
sclera. It also requires scleral dissection for best results.
148
What is cryotherapy?
Cryotherapy is a common method used to create a chorioretinal adhesion during intraocular surgery. Cryotherapy causes dissolution of cellular membrane by freezing. When the temperature is rapidly lowered during cryotherapy, intracellular ice crystal form, which can cause mechanical damage. During the thawing, water and electrolytes separate, which results in a change in the PH with rupture of the cell membrane. The longer the cryoprobe is used on the sclera, the stronger the adhesion is between the retina and the retina pigment epithelium.
149
What are causes of choroidal folds?
1. Hypermetropia.
2. Ocular hypotony.
3. Choroidal tumors.
4. Posterior scleritis.
5. Orbital disease, eg. Thyroid ophthalmopathy.
150
What is retinal telangiectasia?
It is defined by an exudative retinal detachment associated with telangiectatic vascular
anomalies. It is found predominantly in males, usually unilateral and not hereditary.
151
What are the types of retinal telangiectasias?
1. Coat’ s disease (children).
2. Leber’ s miliary aneurysms (adults).
3. Idiopathic juxtafoveolar telangiectasis (adults).
152
What are causes of leukocoria in children?
1. Retinoblastoma.
2. Coat’ s disease.
3. Persistent hyperplastic primary vitreous (PHPV).
4. Cataract.
5. Toxocariasis.
6. Cicatricial ROP .
7. Incontinentia pigmenti (Bloch-Sulzberger syndrome).
8. Retinal dysplasia.
9. Retinal astrocytoma.
10. Inflammatory cyclitic membranes.
153
What is Coat’s disease?
It is a severe form of unilateral retinal telangiectasia mainly occurring in boys and resulting in massive exudative retinal detachment. It typically presents in the first decade of life with visual loss, leukocoria, or strabismus.
154
What are risk factors associated with retinal vein occlusion?
Systemic risk factors: age, systemic hypertension, and diabetes mellitus, blood dyscrasias Ocular risk factors: glaucoma,hypermetropia, periphlebitis, and congenital anomalies of the central retinal vein.
155
At what site in the retina do branch retinal vein occlusions occur in?
At AV crossings.
156
At what site does a central retinal vein occlusion usually occur in?
At the prelaminar layer of the optic nerve head.
157
What percentage of eyes with nonischemic CRVO will convert to ischemic CRVO?
Fifteen percent of cases within 4 months and 34% of cases within 3 years.
158
When does rubeosis iridis develop in eyes with ischemic CRVO?
Rubeosis iridis usually develops within 2-4 months in approximately 50% of eyes.
159
In what percentage of people is a cilioretinal artery present?
It is present in up to 30% of individuals.
160
What is Eales’ disease?
It is an idiopathic vasculitis in young boys or men with associated positive reaction to PPD, epistaxis, constipation and occasionally with potentially fatal cerebral vasculitis.
161
What are lacquer cracks?
Lacquer cracks are large breaks in Bruch’s membrane found in highly myopic eyes.
162
What is a Fuch’s spot?
It is pigmentary proliferation following absorption of macular hemorrhage from choroidal neovascularization in highly myopic eyes.
163
What does visual loss in acute retinal necrosis (ARN) syndrome usually result from?
Visual loss in ARN can result from optic neuritis, which may occur early in the disease, and proliferative vitreoretinopathy and retinal detachment.
164
What viruses have been implicated in ARN syndrome?
Herpes simplex and varicella zoster.
165
What is the appropriate treatment for ARN syndrome?
Intravenous acyclovir for 5 to 10 days, followed by oral acyclovir.
166
What are causes of bull’s eye maculopathy?
1. Chloroquine toxicity.
2. Cone dystrophy.
3. Bardet-Biedl syndrome.
4. Batten’ s disease.
5. Inverse retinitis pigmentosa.
6. Benign concentric annular macular dystrophy.
7. Fenestrated sheen dystrophy.
8. Stargardt’ s disease.
167
What are angioid streaks?
They are cracks in Bruch’s membrane radiating from the optic disc with secondary changes in the choriocapillaris and RPE.
168
What ocular complications can occur from angioid streaks?
Foveal involvement.
Choroidal neovascularization. Choroidal rupture from trauma.
169
What systemic diseases are associated with angioid streaks?
Ehlers-Danlos syndrome. Pseudoxanthoma elasticum.
Paget disease.
Sickle cell diseases and thalassemias.
170
What systemic diseases may be associated with lattice degeneration?
Marfan’ s syndrome.
Stickler’ s syndrome.
Ehlers-Danlos syndrome.
171
What are the main indications for prophylactic treatment of lattice degeneration?
1. Retinal detachment in the opposite eye
2. Highly myopic eye with extensive lattice degeneration
3. Family history of retinal detachment
4. Systemic diseases associated with lattice degeneration
172
What clinical features are suggestive of a malignant change of a choroidal nevus into a melanoma?
1. Evidence of growth.
2. Presence of symptoms.
3. Lipofuscin pigment on the surface.
4. Dilated vessels within the tumor.
5. Posterior margin of the lesion is within 3 mm of the optic disc.
6. Subretinal fluid.
7. Cystoid changes of overlying retina.
173
What is Leber’s congenital amaurosis?
It is an autosomal recessive congenital blindness presenting at birth or within the first few years of life.
174
What are the ERG findings in Leber’s congenital amaurosis?
The ERG is nonrecordable, even if the fundus appears normal.
175
What is the oculodigital syndrome, which commonly occur in children with Leber’s congenital amaurosis?
Constant rubbing of the eyes by the child in an effort to stimulate the retina causes enophthalmos as a result of resorption of orbital fat.
176
What is the volume of the vitreous?
4ML
177
What are causes of selective or predominant decrease in the amplitude of the b- wave?
1. Siderosis.
2. Congenital stationary night blindness.
3. Central renial artery or vein occlusion.
4. Quinine or methanol toxicity.
5. Juvenile X-linked retinoschisis.
178
What is the implicit time?
It is the time between the flash of light and the peak of the b-wave.
179
How can rod responses to the ERG be isolated?
A fully dark adapted eye is stimulated with a flash of very dim light or with blue light.
180
What ERG techniques are used to isolate cone responses?
1. Stimulation of a fully light-adapted eye with a bright flash of light or red light.
2. Flicker light stimulus of 30-40 Mhz to which rods cannot respond.
181
What does the electro-oculogram (EOG) measure?
The EOG measures the standing action potential between the electrically negative cornea and the electrically positive back of the eye. It reflects the activity of the RPE and the photoreceptors.
182
Will a patient with optic atrophy resulting from demyelinating optic neuritis have a recordable EOG?
Yes. Widespread disease of the RPE is needed to affect the EOG response significantly. Eyes with lesions proximal to the photoreceptors will have a normal EOG
183
What is the mode of inheritance of Best’s disease?
AD
184
What electrophysiologic findings are present in Best’s disease?
The EOG is subnormal (decreased light peak:dark trough ratio), while the ERG is normal.
185
What are the stages of Best’s disease?
Previtelliform (normal fundus, abnormal EOG).
Vitelliform (egg-yolk stage).
Pseudohypopyon.
Vitelliruptive (scrambled egg).
Macular scar.
186
Give two complications that may be produced by choroidal nevi.
Malignant transformation and choroidal neovascular membranes.
187
What is the classic triad of clinical findings in retinitis pigmentosa?
Retinal bone-spicule-like pigmentation. Arteriolar attenuation.
Waxy disc pallor.
188
What are the ERG and EOG findings found in retinitis pigmentosa?
The ERG is abnormal with reduced amplitude of photopic and scotopic b-waves and a delayed implicit time. The EOG shows an absence of the light rise.
189
What other ocular findings may be associated with retinitis pigmentosa?
1. Posterior subcapsular cataracts.
2. Myopia.
3. Optic disc drusen.
4. Keratoconus.
5. Open angle glaucoma.
6. Intermediate uveitis.
7. Posterior vitreous detachment.
190
What is the name of the syndrome characterized by retinitis pigmentosa and sensorineural hearing loss?
Usher Syndrome.
191
What is Refsum’s disease?
It is an accumulation of phytanic acid, resulting in pigmentary retinopathy, cataracts, hypertrophic peripheral neuropathy, and cerebellar ataxia, deafness, ichthyosis, arrhythmias and elevated CSF protein.
192
What is Oguchi’s disease?
It is a recessive form of stationary night blindness characterized by a 2-12 hour delay in attaining normal dark-adapted rod thresholds and associated with Mizuo’s phenomenon.
193
What is Mizuo’s phenomenon?
It is a change in fundus color from a golden brown fundus in the light-adapted state to a
normal color in the dark-adapted state. It is found in Oguchi’s disease
194
What are the ERG findings in cone dystrophy?
The photopic response will be subnormal or non-recordable, while the scotopic response
will be normal.
195
What is the mode of inheritance of Stargardt’s macular dystrophy and fundus flavimaculatus?
AR
196
What is Stickler’s syndrome?
It is an autosomal dominant vitreoretinal degeneration characterized by high myopia, an empty vitreous cavity, large areas of lattice degeneration with RPE hyperplasia, retinal detachment in 30% from multiple breaks and gian tears, presenile cataracts in 50% of cases. Ectopia lentis and glaucoma develops in 10% of cases.
197
What is a characteristic retinal lesion found in sphingolipidoses such as Tay- Sachs disease (Gm2 gangliosidosis type 1) and Neiman-Pick disease?
Cherry-red spot in the macula.
198
What drugs can cause crystalline deposits to be deposited in the macula?
Tamoxifen, canthaxanthin, and methoxyflurane.
199
At what CD4 lymphocyte count level does CMV retinitis become more common?
CMV retinitis becomes more common when CD4 lymphocyte countsdrop to 50 cells/mm3 or less.
200
How often does iris neovascularization and neovascular glaucoma occur following a central retinal artery occlusion?
5%
201
What is Wyburn-Mason syndrome?
This is a phacomatoses consisting of AV malformations in the retina and midbrain.
202
How does verteporfin work in photodynamic therapy for CNVin age-related macular degeneration (AMD)?
Verteporfin is a photosensitizing drug that is administered intravenously and selectively accumulates in neovascular tissue of AMD by attaching to low-density lipoproteins. Because cells in CNV are actively dividing and growing, they need higher levels of lipoprotein compared with normal cells. Therefore, high concentrations are absorbed rapidly in these areas. When activated by laser light, free radicals and singlet oxygen is produced, which damages cell components.
203
How is the laser treatment delivered to activate verteporfin after it is administered to the patient?
The laser treatment is administered 15 minutes after verteporfin infusion intravenously at a predetermined spot size through the slit lamp and contact lens at 689 nm targeted by a low intensity helium-neon beam for 83 seconds, with 50 J/cm2 delivered to the lesion.<
204
What precautions should be taken during photodynamic therapy with verteporfin?
Following infusion of verteporfin, care should be taken to avoid exposure of skin and eyes to direct sunlight or bright indoor lights for 5 days with dark sunglasses and long- sleeved shirts and pants. In the event of extravasation during infusion, the area should be thoroughly protected from direct light until the swelling and discoloration have faded to avoid a severe burn.
205
Why should patients receiving photodynamic therapy be encouraged to expose their skin to ambient indoor light rather than stay in the dark?
This helps inactivate the drug through a process called photobleaching.
206
A child is diagnosed with Leber’s congenital amaurosis. What is the chance that succeeding children will also have this condition?
There is a 1 in 4 chance that succeeding children will have Leber’s congenital amaurosis because it is transmitted in an autosomal recessive fashion.
207
What is the most common form of congenital defect in color vision?
Deuteranomalous trichromatopsia, which affects 5 percent of the male population.
208
What is the incidence of lattice degeneration in the general population?
7 to 8 percent.
209
What is the long-term risk of retinal detachment in patients with lattice degeneration?
1%.
210
What is the incidence of progressive retinal detachment from atrophic retinal holes in phakic eyes with lattice degeneration?
2%
211
How much carotid artery stenosis is required to cause ocular ischemic syndrome?
90% or greater ipsilateral obstruction.
212
What is the most accurate way of measuring intraocular pressure for a patient with intravitreal gas bubble?
The most accurate method of measuring intraocular pressure for a patient with intraocular gas bubble is by applanation tonometry. Indentation (Schiötz) tonometry can give a falsely low reading presumably because of the compressibility of the gas.
213
What is the 5 year mortality rate of patients with ocular ischemic syndrome?
40%
214
What is the most common opportunistic ocular infection in acquired immunodeficiency syndrome (AIDS)?
Cytomegalovirus (CMV) retinitis.
215
In a patient with CMV retinitis and rhegmatogenous retinal detachment, where is the most common location for retinal breaks?
The most likely position for retinal breaks is within or adjacent to the area of retinal necrosis.
216
What is the role of vitrectomy in management of proliferative diabetic retinopathy?
There are two main objective of vitrectomy for proliferative diabetic retinopathy. First, it is used to remove media opacities such as vitreous hemorrhage or cataract. The second objective is to relieve vitreous traction causing detachment or distortion of the macula.
217
What was the recommendation of the Diabetic Retinopathy Vitrectomy Study group (DRVS) for type I versus type II diabetes?
The DRVS was designed to evaluate the risks and benefits of performing early pars plana vitrectomy in eyes with advanced proliferative diabetic retinopathy. In patients with Type I diabetes, early vitrectomy (after one month) offered a greater chance of visual recovery, however, in type II and mixed type diabetes no significant difference was noted between the early versus late (after one year) vitrectomy.
218
When is silicone oil used during vitrectomy surgery?
Silicone oil can be used to provide a long-term or permanent internal tamponade in some cases of severe retinal detachment including giant tears and retinal detachment complicated by proliferative vitreoretinopathy.
219
What is the specific gravity of silicone oil?
0.975, which is slightly less than fluid in the vitreous cavity.
220
What are the commercially available silicone oil viscosities?
Silicone oils of 1,000 to 5,000 centistokes are used for vitreous surgery. The viscosity of silicone oil is related to the length of the polymer chains that make the oil. The average molecular weight of the silicone oil molecules of 1,000 centistokes is about 25,000, and the average molecular weight of silicone oil with a viscosity of 5,000 centistokes is about 50,000. In the United States, commercially available silicone oil is 5000 centistokes.
221
What are the most common complications of silicone oil?
Most complications of silicone oil are due to its entering the anterior chamber or causing pupillary block with secondary shallowing of the anterior chamber. These complications include band keratopathy, generalized corneal decompensation, iritis, chronic inflammation glaucoma, hypotony, cataract, and retinal damage.
222
What proportion of patients with an acute symptomatic PVD have a retinal
tear?
10%
223
What is usually present in the history of a majority of patients with superonasal retinal dialyses?
Head or eye trauma.
224
What is the prevalence of lattice degeneration in patients with rhegmatogenous retinal detachment?
25-30%.
225
What are the important histologic features of lattice degeneration?
Discontinuity of the internal limiting membrane.
Pocket of overlying liquified vitreous.
Vitreoretinal condensation and adherence at the margin of the lesion. Sclerotic vessels.
V ariable degrees of retinal atrophy.
226
What color and wavelength of light is absorbed by fluorescein?
Blue – 490 nm.
227
What color and wavelength of light is emitted by stimulated fluorescein?
Yellow-green – 530 nm.
228
What are the five broad categories of hyperfluorescence?
Leakage, staining, pooling, transmission, and autofluorescence.
229
How does one differentiate leakage and pooling?
The borders of leakage become increasingly blurred, while the borders of pooling remain
distinct.
230
Nausea, vomiting, or vaso-vagal reaction occur in what percentage of FA patients?
10%
231
At what wavelength does fluorescence peak for ICG?
835 nm.
232
What is the difference between classic and occult CNV during FA?
Classic hyperfluoresces very early and has distinct boundaries, while occult hyperfluoresces later, may be associated with RPE detachment and may have indistinct borders.
233
How longs does it take the cones and rods to reach their threshold in dark adaptation?
Cones - 5-10 minutes, Rods - 30 minutes.
234
What is the range of human color vision?
Between 400-700 nm.
235
What is protan color deficiency? Deutan? Tritan?
Protan - lack or deficiency of red sensing cones. Deutan - lack or deficiency of green sensing cones. Tritan - lack of blue sensing cones.
236
A Tritan deficiency almost always signifies what type of disease?
Acquired.<
237
In what group of patients is central serous retinopathy (CSR) most common?
Men between 30 and 50.
238
What is most likely defective in patients with CSR?
RPE barrier or pumping functions.
239
Describe the fluorescein pattern in CSR.
A small area of hyperfluorescence that increases in size and intensity - 10% have “smokestack.”
240
What is the purpose behind sending patients home with an Amsler Grid?
Testing for metamorphopsia and scotoma, which may be early symptoms of CNV.
241
What is pathologic myopia?
Changes in the retina associated with very abnormal elongation of the eye, usually with
axial lengths >32.5mm and spherical equivalents >-8.00 diopters.
242
What is the most serious complication of pathologic myopia?
CNV.
243
What are Fuch’s spots?
Area of RPE hyperplasia found in pathologic myopia presumably developing in response
to a small area of CNV that does not progress to disciform scarring.
244
How do epiretinal membranes (ERM) develop?
A dehiscence of the internal limiting membrane allows retinal glial cells (myofibroblasts and fibroblasts) to proliferate along the retinal surface. Contraction of these membranes causes cellophane maculopathy or macular pucker. Detachment of the posterior vitreous is present in almost all eyes.
245
What is an indication for surgery for ERM?
Visual acuity of 20/60 or worse.
246
What can angiography show in VMTS?
Angiography may show leakage from vessels in the macular region and from the optic disc
247
What percent of stage 1 macular holes will undergo spontaneous resolution?
Approximately 50%.
248
What is the incidence of bilaterality of idiopathic macular holes?
Between 25% and 30%.
249
What is considered protection from developing macular holes?
Complete posterior vitreous separation.
250
What can occur in the retina after a sudden rise in intra-abdominal pressure?
Valsalva retinopathy - the rise in intraocular venous pressure may be sufficient to rupture small capillaries in the macula.
251
Where is the hemorrhage located in valsalva retinopathy?
Under the internal limiting membrane.
252
What is the prognosis for valsalva retinopathy?
Excellent - most recover completely in 2-3 months.
253
Where is the pathology usually centered in Purtscher’s retinopathy?
Surrounding the optic disc.
254
What is the pathophysiology of Purtscher’s retinopathy?
Injury activates complement, which causes granulocyte aggregation and leukoembolization. Complement-mediated leukostasis and obstruction may follow local retinal vascular injury.
255
What may cause Purtscher’s-like retinopathy?
Acute pancreatitis, collagen vascular diseases, and childbirth.
256
How are the fundus findings caused by fat embolism different from Purtscher’s?
Heme is found in the paramacular area and cotton wool spots are generally found more peripherally.
257
The syndrome of intraocular hemorrhages associated with abrupt intracranial
hemorrhage is known as what?
Terson Syndrome.
258
What is the suspected cause of Terson Syndrome?
The acute intracranial hemorrhage may cause an abrupt rise in intraocular venous
pressure resulting in a rupture of peripapillary and retinal vessels.
259
What percentage of patients with subarachnoid hemorrhage will have associated intraocular hemorrhage, and what percent will have vitreous hemorrhage?
Approximately 33% will have associated intraocular hemorrhage and 6% will have vitreous hemorrhage.
260
Describe the five stages of hypertensive retinopathy with the Modified Scheie Classification.
Grade 0 - No changes.
Grade 1 - Barely detectable arterial narrowing.
Grade 2 - Obvious art. narrowing with focal irregularities. Grade 3 - Grade 2 + retinal heme and/or exudate.
Grade 4 - Grade 3 + disc swelling.
261
In what type of patient do we normally see hypertensive choroidopathy?
Young patients experiencing acute hypertension, such as in preeclampsia, eclampsia,
pheochromocytoma, or accelerated hypertension.
262
What are Elschnig spots?
Hyperpigmented patches with a surrounding zone of hypopigmentation found over zones
of choroidal nonperfusion.
263
What are Siegrest streaks?
Linear configurations of hyperpigmentation that develop over choroidal arteries in
patients with uncontrolled hypertension.
264
Describe the FA of a patient with hypertensive choroidopathy.
Early choroidal hypoperfusion and late leakage.
265
What syndrome is AR, carried on chromosome 16 and characterized by obesity, polydactyly, hypogonadism, mental retardation and pigmentary retinopathy?
Bardet-Biedl syndrome.
266
What diseases share ichthyosis and pigmentary retinopathy?
Refsum disease and Sjögren-Larsson syndrome.
267
Histologically, what is the difference between oculocutaneous albinism and ocular albinism?
Oculocutaneous albinism is characterized by a reduction in the amount of primary melanin found in each melanosome, while ocular albinism has an absolute decrease in the number of melanosomes.
268
What is the inheritance pattern of oculocutaneous albinism? Ocular albinism?
Oculocutaneous albinism is AR, while ocular albinism is X-linked.
269
What therapy can prevent or treat the retinal degeneration associated with abetalipoproteinemia?
Vitamin A and E.
270
How common is cobblestone degeneration in patients over the age of 20?
Cobblestone degeneration is found in 22% of the population >20yo.
271
What is Shafer’s sign?
Small clumps of pigmented cells, called tobacco dust, seen in the vitreous or AC. This sign can be helpful in diagnosing the type of retinal detachment when no hole can be found.
272
What cells are responsible for PVR?
RPE and glial cells.
273
Why is a macula on detachment a more urgent case than a macula off detachment?
If the macula is spared 87% of eyes will attain 20/50 or better, while only 37% will reach that level of acuity if the macula is detached. A macular detachment should be repaired within the first week because studies have shown a decline in post-op VA in eyes repaired >1 week out.
274
How soon should a patient with an exudative retinal detachment be scheduled for surgery?
They should not be scheduled for surgery because the treatment of exudative detachments is aimed at treating the underlying condition (usually neoplasm or inflammatory disease).
275
What are the most common quadrants for retinal break following trauma?
1. Inferotemporal, which is noted to be the least protected (i.e., less bony structure) area of the globe.
2. Superonasal (due to the coup contrecoup effect).
276
What’s the most common quadrant for a spontaneous (i.e., non-traumatic)
retinal break? How does age affect this risk?
1. Less than 20 years of age: superotemporal quadrant, followed by inferotemporal, followed by superonasal, followed by inferonasal.
2. 20-40 years of age: superotemporal quadrant, followed by inferotemporal and superonasal (equal), followed by inferonasal.
3. Over 40 years of age: superotemporal quadrant, followed by superonasal, followed by inferotemporal, followed by inferonasal.
277
What must you rule out when a patient presents with posterior scleritis?
1. Syphilis.
2. W egener’ s granulomatosis.
3. Inflammatory bowel disease.
4. Rheumatoid arthritis.
5. Relapsing polychondritis.
6. Systemic lupus erythematosus.
7. Sarcoid.
278
Name the four stages of macular hole formation, according to the Gass system.
Stage I is a foveal detachment, with loss of foveal pigment (i.e., yellow spot). Stage II is a full-thickness macular hole, less than 400 microns. Stage III is a full-thickness macular hole, greater than 400 microns. Stage IV is a full-thickness retinal hole greater than 400 microns, with detached vitreous. Typically, Stages II-IV are repaired operatively. Stage I holes are observed. A macular cyst can be a precursor to a macular hole.
279
What is the differential diagnosis of intraretinal crystals?
Crystals can be from Tamoxifen, canthaxanthine, cystinosis, primary hyperoxaluria, Bietti’s crystalline dystrophy, idiopathic juxtafoveal telangiectasia Type II, diabetic macular edema, talc retinopathy and methoxyflurane toxicity.
280
With regard to intraocular foreign bodies, which substances are more reactive, or more significant, than others are are?
Aluminum, zinc, glass, stone and plastic are especially well tolerated. Copper (containing more than 85%) causes chalcosis and iron causes siderosis. Cooper and iron are the main metals that cause extensive damage with ERG changes, initially producing a large A-wave and a normal B-wave. As the siderosis progresses, the B-wave amplitude will diminish and eventually become extinguished. ERG’s are useful for following these patients with intraocular foreign body. Vegetable matter is an organic foreign body that can cause a severe inflammatory response, and an increased risk for endophthalmitis. The copper from chalcosis can produce a KF (Kaiser-Flescher) ring.
281
What were the conclusions of the Age-Related Eye disease Study (AREDS)?
1. People at high risk for developing advanced AMD reduced their risk by 25 percent when treated with antioxidants plus zinc and also reduced the risk of central visual loss by 19 percent.
2. The risk of developing advanced AMD in people at high risk was reduced by 21 percent by zinc alone and reduced the risk of central visual loss by 11 percent.
3. The risk of developing advanced AMD in people at high risk was reduced by 17 percent by antioxidants alone and reduced the risk of central visual loss by 10 percent.
282
What were the specific daily amounts of antioxidants and zinc used in the AREDS study?
500 mg of vitamin C
400 international units of vitamin E 15 mg of beta-carotene
80 mg of zinc as zinc oxide
2 mg of copper as cupric oxide.
