Grading of hypertensive retinopathy

Keith and Wegner (1939) have classified hypertensive retinopathy changes into following four
grades:
Patients were grouped according to their ophthalmoscopic findings. As such, this was the first system
to correlate retinal findings with the hypertensive disease state.
Grade I: It consists of mild generalized arteriolar attenuation, particularly of small branches, with
broadening of the arteriolar light reflex and vein concealment.
Grade II: It comprises marked generalized narrowing and focal attenuation of arterioles associated
with deflection of veins at arteriovenous crossings (Salus sign).
Grade III: This consists of Grade II changes plus copper-wiring of arterioles, banking of veins distal to
arteriovenous crossings (Bonnet sign), tapering of veins on either side of the crossings (Gunn sign)
and right-angle deflection of veins (Salus sign). Flame-shaped haemorrhages, cotton-wool spots and
hard exudates are also present.
Grade IV: This consists of all changes of Grade III plus silver-wiring of arterioles and papilloedema.
(copper is cheaper than silver.. So copper comes first)
One of the major limitations of this classification system is the difficulty in distinguishing early
hypertensive retinopathy grades (e.g., grade 1 from grade 2); thus, a modified classification has been
recently proposed.
Scheie classification (1953)
Staging under this system is as follows:

Stage 0 - Diagnosis of hypertension but no visible retinal abnormalities

Stage 1 - Diffuse arteriolar narrowing; no focal constriction

Stage 2 - More pronounced arteriolar narrowing with focal constriction

Stage 3 - Focal and diffuse narrowing, with retinal hemorrhage

Stage 4 - Retinal edema, hard exudates, optic disc edema

The Scheie classification also grades the light reflex changes from arteriolosclerotic changes, as follows:

Grade 0 - Normal

Grade 1 - Broadening of light reflex with minimal arteriolovenous compression

Grade 2 - Light reflex changes and crossing changes more prominent

Grade 3 - Copper-wire appearance; more prominent arteriolovenous compression

Grade 4 - Silver-wire appearance; severe arteriolovenous crossing changes

Scheie Classification

Group Hypertension

Arteriolar sclerosis

No changes

Normal

Barely detectable arteriolar narrowing

Barely detectable light reflex

changes

Obvious arteriolar narrowing with focal

irregularities

Obvious increased light reflex

changes

Grade 2 plus retinal hemorrhages or exudates Copper wire arterioles

Grade 3 plus papilledema

Silver wire arterioles

Modified Scheie classification

Staging is as follows:

Grade 0 - No changes

Grade 1 - Barely detectable arterial narrowing

Grade 2 - Obvious arterial narrowing with focal irregularities

Grade 3 - Grade 2 plus retinal hemorrhages and/or exudates

Grade 4 - Grade 3 plus disc swelling

Classification of hypertensive retinopathy by Wong and Mitchell

Grades

Description

Systemic associations

No retinopathy No detectable retinal signs

None

Mild retinopathy
(retinal
arteriolar signs
only)

One or more of the following arteriolar

signs: Generalised arteriolar
narrowing Focal arteriolar narrowing
Arteriovenous nicking Arteriolar
wall opacity (silver wiring)

Modest* association with risk

of clinical stroke, subclinical
stroke, coronary heart
disease, and mortality.

Moderate
retinopathy

One or more of the following retinal

signs: Haemorrhage (blot, dot, or
flame shaped) Microaneurysm
Cottonwool spot Hard exudates

Strong association with risk

of clinical stroke, subclinical
stroke, cognitive decline,
and cardiovascular mortality

Malignant
retinopathy

Moderate retinopathy plus optic disc

swelling

Strong association with

mortality

Grading of DR:
1. Mild NPDR: At least one microaneurysm or intraretinal hemorrhage.
Hard/soft exudates may or may not be present.
2. Moderate NPDR: Moderate microaneurysms/intraretinal hemorrhage.
Early mild IRMA.
Hard/soft exudates may or may not present.
3. Severe NPDR. Any one of the following (4-2-1 Rule):
Four quadrants of severe microaneurysms/ intraretinal hemorrhages.
Two quadrants of venous beading.
One quadrant of IRMA changes.
4. Very severe NPDR. Any two of the following (4-2-1 Rule):
Four quadrants of severe microaneurysms/ intraretinal hemorrhages.
Two quadrants of venous beading.
One quadrant of IRMA changes.
Proliferative diabetic retinopathy (PDR)
1.
PDR without HRCs (Early PDR) and
2.
PDR with HRCs (Advanced PDR). High risk characteristics (HRC) of PDR are as
follows (Fig. 11.14F):
1.

NVD 1/4 to 1/3 of disc area with or without vitreous haemorrhage (VH) or pre-retinal haemorrhage
(PRH)
2. NVD < 1/4 disc area with VH or PRH
3. NVE > 1/2 disc area with VH or PRH

clinically significant macular edema (CSME) if one of the following three criteria are present on slitlamp examination with 90D lens:
1.
Thickening of the retina at or within 500 micron of the centre of the fovea.
2.
Hard exudate at or within 500 micron of the centre of fovea associated with adjacent
retinal thickening and not residual hard exudates remaining after the disappearance of
retinal thickening
3.
Development of a zone of retinal thickening one disc diameter or larger in size, at
least a part of which is within one disc diameter of the foveal centre.

DME
1.
2.
3.
4.
5.
6.

Based on OCT DME can be classified into different pattern such as

cystoid macular edema,
spongy swelling of the retina,
hard exudates,
serous detachment,
macular traction,
taut posterior hyaloid membrane.

Grading of trachoma
McCallan's classification
McCallan in 1908, divided the clinical course of the trachoma into following four stages:

Stage I (Incipient trachoma or stage of infiltration). It is characterized by hyperaemia of

palpebral conjunctiva and immature follicles.

Stage II (Established trachoma or stage of florid infiltration). It is characterized by appearance

of mature follicles, papillae and progressive corneal pannus.

Stage III (Cicatrising trachoma or stage of scarring). It includes obvious scarring of palpebral
conjunctiva.

Stage IV (Healed trachoma or stage of sequelae). The disease is quite and cured but
sequelae due to cicatrisation give rise to symptoms.
WHO
TF = trachomatous inflammation (follicular): five or more follicles (>0.5 mm) on the superior tarsus
TI = trachomatous inflammation (intense):diffuse involvement of the tarsal conjunctiva, obscuring 50%
or more of the normal deep tarsal vessels; papillae are present
TS = trachomatous conjunctival scarring: easily visible fibrous white tarsal bands
TT = trachomatous trichiasis: at least one lash touching the globe
CO = corneal opacity sufficient to blur details of at least part of the pupillary margin

WHO grading of Xerophthalmia

XN = night blindness
X1 = conjunctival xerosis (X1A) with Bitot spot (X1B)
X2 = corneal xerosis
X3 = corneal ulceration, less than one-third (X3A); more than one-third (X3B)
XS = corneal scar
XF = xerophthalmic fundus

Grading of nucleus hardness on slit-lamp biomicroscopy

Grade I: Soft, White or greenish yellow
Grade II: Soft-medium, Yellowish
Grade III: Medium-hard, Amber
Grade IV: Hard, Brownish
Grade V: Ultrahard, Blackish (rock-hard)

Grading of severity of Chemical Injury

Grading is performed on the basis of corneal clarity and severity of limbal ischaemia (Roper-Hall
system); the latter is assessed by observing the patency of the deep and superficial vessels at the
limbus (Fig. 21.29A).
Grade 1 is characterized by clear cornea (epithelial damage only) and no limbal ischaemia
(excellent prognosis).

Grade 2 shows hazy cornea but with visible iris details (Fig. 21.29B) and less
than one-third of the limbus being ischaemic (good prognosis).
Grade 3 manifests total loss of corneal epithelium, stromal haze obscuring iris details (Fig.
21.29C) and between one-third and half limbal ischaemia (guarded prognosis).
Grade 4 shows opaque cornea (Fig. 21.29D) and more than half limbal ischaemia (very poor
prognosis).

PVR Gradings: (Retina Society Terminology Committee, 1983)

Grade A: vitreous changes (RPE clumps, protein flare)

Grade B: surface wrinkling, rolled edge of tears, vascular tortuosity
Grade C: full thickness retinal folds
Ryan:
C1,C2,C3: 1,2,3 quadrent respectively
Jakobiec:
C1: Posterior star fold
C2: Posterior confluent irregular folds
C3: Posterior subretinal napkin irregular elevation of retina
C4: Anterior irregular folds
C5: Anterior smooth circumferential retinal fold in coronal plane
C6: Anterior circumferential fold of retina at insertion of posterior hyaloid
Grade D: Fixed Retinal Fold in four quadrents
D1: Wide Funnel Shape
D2: Narrow Funnel Shape
D3: Closed Funnel Shape
This classification system has following disadvantages:
There was no clinical correlation between the most severe form (grade D) and visual prognosis.
There was limited quantification of extent of disease.
This system did not include PVR anterior to the equator.

The new classification system consists of the following modified PVR grades:
A Pigment clumps in the vitreous cavity, vitreous haze
B Retinal wrinkling breaks with rolled edges, retinal rigidity, vascular tortuousity, and decreased
vitreous mobility
C Full thickness fixed folds (subdivided into anterior and posterior forms)
Extent of involvement expressed in clock hours (subdivided into contraction types):
CP1-12
CA1-12

1. Focal posterior single or multiple isolated folds posterior to vitreous base.

2. Diffuse posterior confluence of focal epicenters posterior to vitreous base.
3. Subretinal proliferations bands of moth eaten sheets; extent quantified if retina is elevated.
4. Circumferential traction along the posterior edge of vitreous base with central displacement of
retina and radial folds posteriorly.
5. Anterior traction vitreous base displaced to pars plicata, iris or pupillary margin.
Shortcomings of these classifications are that they do not take into account important features
that influence the prognosis.
1. Number, location and size of retinal breaks
2. Number and type of previous operation
3. Time course and biological activity of the proliferative process.

Stages of development of PVR (CPEC)

1.

Cellular activation

2.

Proliferation

3.

Extracellular matrix elaboration and remodeling

4.

Contraction

Eales Disease (PINK)

Charmis Classification:
1.
Stage of Active Phlebitis
2.

The Stage of Persistent Ischaemia

3.

The Stage of Vascular Proliferation

4.

The Stage of Complications

Eales disease staging system (Saxena S)

This classification system is based on both fundoscopic and fluorescein angiographic variables that
have been shown to be prognostic of visual outcome.
A. Eales disease
Stage 1a Periphlebitis of small caliber vessels with superficial retinal hemorrhages
Stage 1b Periphlebitis of large caliber vessels with superficial retinal hemorrhages
Stage 2a Peripheral capillary nonperfusion
Stage 2b Neovascularization elsewhere /Neovascularisation of the disc
Stage 3a Fibrovascular proliferation
Stage 3b Vitreous hemorrhage
Stage 4a Traction / combined rhegmatogenous detachment
Stage 4b Rubeosis iridis, neovascular glaucoma, complicated cataract, and optic atrophy
B. Central Eales disease

Macular Hole
0: premacular hole
1: impending macular holes
small yellow spot (stage lA) or yellow ring (stage IB) in the center of the fovea.
2: A stage 2 macular hole represents the progression of a foveal pseudocyst to a full thickness
dehiscence, as a tractional break develops in the roof (inner layer) of the pseudocyst (<400um)
3: A stage 3 macular hole is a fully developed hole (>400 um diameter),
4: A stage 4 macular hole is a fully developed hole with a complete posterior vitreous detachment
signified by a Weiss ring

Gass classification of ERM

Grade 0 cellophane maculopathy
So called due to cellophane-like sheen seen on ophthalmoscopic examination
No associated visual distortion
Grade 1 crinkled cellophane maculopathy
Membrane causes an irregular wrinkling of inner retinal surface (Figure 5)
Contraction of the membrane causes formation of retinal folds
Fine superficial folds extend out from the margins of the membrane
If wrinkling is severe enough, paramacular vessels may be pulled towards the fovea in a corkscrew
formation. This is seen well on FFA
Normally cystoid macular oedema, retinal haemorrhage, exudates and retinal pigment epithelial
disturbances are absent
Patient will report visual disturbance and VAs of 6/12 or worse are common
Grade 2 macular pucker
Membrane will be thick and opaque, especially for those membranes which develop following
retinal detachment surgery
Full thickness puckering of the macula may be present along with oedema, small hemorrhages,
cotton-wool spots and sometimes localised retinal detachment
Vision will be severely debilitated with VAs often worse than 6/60

Classication of the posterior vitreoretinal interface

0: No PVD
1: Incomplete perifoveal PVD in up to 3 quadrants
2: Incomplete perifoveal PVD in all 4 quadrants with residual attachment to the fovea and optic disc
3: Incomplete PVD over the posterior pole with residual attachment to the optic disc
4: Complete PVD identied biomicroscopically, but posterior hyaloid face not visible on OCT imaging

Stages of Age-Related Posterior Vitreous Detachment

Stage 1: Perifoveal separation with vitreofoveal adhesion.
Stage 2: Complete vitreomacular separation.
Stage 3: Widespread vitreous separation except at the optic disk margin.
Stage 4: Complete, clinically recognizable PVD.

Grading of angle width

Shaffer system
The Shaffer system records the angle in degrees between two imaginary lines tangential to the inner
surface of the trabeculum and the anterior surface of the iris about one-third of the distance from its
periphery. In practice, the angle is graded by many according to the visibility of various structures.
The system assigns a numerical grade to each quadrant of the angle as below (Fig. 10.17); it should
be borne in mind that most angles are narrowest superiorly.
Grade 4 (3545) is the widest angle, characteristic of myopia and aphakia, in which the ciliary body
can be visualized with ease.
Grade 3 (2535) is an open angle in which at least the scleral spur can be identified.
Grade 2 (20) is a moderately narrow angle in which only the trabeculum can be identified.
Grade 1 (10) is a very narrow angle in which only Schwalbe line, and perhaps also the top of the
trabeculum, can be identified.
Slit angle is one in which there is no obvious iridocorneal contact but no angle structures can be
identified.
Grade 0 (0) is a closed angle due to iridocorneal contact and is recognized by the inability to identify
the apex of the corneal wedge. Indentation gonioscopy will distinguish appositional from synechial
angle closure (see Fig. 10.20).
R P C classification
Grade 0
Grade 1
Grade 2
Grade 3
Grade 4
Grade 5
Grade 6

Closed
dipping of light
Schwalbes line visible
anterior trabecular meshwork
posterior T M scleral spur
ciliary body band visible
root of iris visible

Grade the amount of TM pigment :

Scheie suggested a system of grading
0 none, +1 trace, +2 mild, +3 moderate, +4 severe
(+3 corresponds to iris pigmentation)

Grading anterior chamber cells (SUN-Standardization of uveitis

nomenclature)
Other grading systems are Schlaegels & Hogans.
<1
-0
15 -
615 -+1
1625 -+2
2650 -+3
>50 -+4

Grading of aqueous flare (SUN Working Group Grading Scheme)

Nil
-0
Just detectable
-+1
Moderate (iris and lens details clear)
Marked (iris and lens details hazy)
Intense (fibrinous exudate)

+2
+3
+4

Grading of vitreous haze

According to EVS:

Good view of nerve fibre layer (NFL)

Clear disc and vessels but hazy NFL
Disc and vessels hazy
Only disc visible
Disc not visible

0
+1
+2
+3
+4

The grading of arteriolosclerosis:

Grade 1: subtle broadening of the arteriolar light reflex, mild generalized arteriolar attenuation,
particularly of small branches, and vein concealment.
Grade 2: obvious broadening of the arteriolar light reflex and deflection of veins at arteriovenous
crossings (Salus sign).
Grade 3:
Copper-wiring of arterioles (Fig. 13.51C).
Banking of veins distal to arteriovenous crossings (Bonnet sign).
Tapering of veins on both sides of the crossings (Gunn sign) and right-angled deflection of veins.
Grade 4: Silver-wiring of arterioles associated with grade 3 changes.

Staging of ROP

The following five stages are used to describe the abnormal vascular response at the junction of
immature avascular peripheral retina and vascularized posterior retina. Because more than one ROP
stage may be present in the same eye, staging for the eye as a whole is determined by the most
severe manifestation.
Stage 1 (demarcation line) is a thin, flat, tortuous, grey-white line running roughly parallel with the ora
serrata. It is more prominent in the temporal periphery. There is abnormal branching or arcading of
vessels leading up to the line (Fig. 13.60A).
Stage 2 (ridge) arises in the region of the demarcation line, has height and width, and extends above
the plane of the retina. Blood vessels enter the ridge and small isolated neovascular tufts (popcorn)
may be seen posterior to it (Fig. 13.60B).
Stage 3 (extraretinal fibrovascular proliferation) extends from the ridge into the vitreous (Fig. 13.60C).
It is continuous with the posterior aspect of the ridge, causing a ragged appearance as the
proliferation becomes more extensive. The severity of stage 3 can be subdivided into mild, moderate
and severe depending on the extent of extraretinal fibrous tissue infiltrating the vitreous. The highest
incidence of this stage is around the post-conceptual age of 35 weeks.
Stage 4 (partial retinal detachment) is divided into extrafoveal (stage 4A Fig. 13.60D) and foveal
(Stage 4B). The detachment is generally concave and circumferentially orientated. In progressive
cases the fibrous tissue continues to contract and the detachment increases in height and extends
anteriorly and posteriorly.
Stage 5 is a total retinal detachment.

1.

Grading of North Carolina macular dystrophy

Grade 1 is characterized by yellow-white, drusen-like peripheral (Fig. 15.33A) and macular deposits
which develop during the 1st decade and may remain asymptomatic throughout life.
2. Grade 2 is characterized by deep, confluent macular deposits (Fig. 15.33B). The long-term visual
prognosis is guarded because some patients develop neovascular maculopathy (Fig. 15.33C) and
subretinal scarring.
3. Grade 3 is characterized by coloboma-like atrophic macular lesions (Fig. 15.33D) associated with
variable impairment of visual acuity.


1.
2.
3.

Grading of binocular vision

simultaneous perception, SP
fusion
stereopsis

NVG

(a) rubeosis iridis, (b) secondary open-angle glaucoma and (c) secondary synechial angle-closure
glaucoma.

Stages of Proliferative retinopathy

Stage 1 shows peripheral arteriolar occlusion and ischaemia.

Stage 2 is characterized by peripheral arteriovenous anastomoses of dilated pre-existing capillary
channels (Fig. 13.55A).
Stage 3
Sprouting of new vessels from the anastomoses; these have a sea-fan configuration and are usually
fed by a single arteriole and drained by a single vein (Fig. 13.55B and see Fig. 13.56A).
About 3040% of sea-fans involute spontaneously as a result of auto-infarction and appear as greyish
fibrovascular lesions (Fig. 13.55C). Involution most frequently occurs about 2 years after the
development of retinopathy.
Stage 4. The neovascular tufts may continue to proliferate and bleed into the vitreous (Fig. 13.55D).
Stage 5 is characterized by extensive fibrovascular proliferation (Fig. 13.55E) and retinal detachment

ocular GVHD

Jab et al. described four stages of ocular GVHD:

Stage I hyperemia; Stage II hyperemia with serosanguinous chemosis; Stage III
pseudomembranous conjunctivitis; and Stage IV pseudomembranous conjunctivitis with corneal
epithelial sloughing.

OCP

The disease progression of OCP has classically been documented into one of four stages.[7] Stage I
denotes chronic conjunctivitis with subepithelial fibrosis. Stage II refers to inferior fornix
foreshortening. Stage III describes symblepharon formation typically involving the inferior fornix.
Finally, stage IV is the end-stage characterized by ankyloblepharon formation and corneal scarring

neurotrophic keratitis

Mackie[45] characterized three stages of neurotrophic keratitis. Stage one includes an often subtle
irregular corneal surface, which later develops into an easily recognized punctate keratitis. Stage two
is characterized by a frank epithelial defect, which typically is associated with mild anterior stromal
inflammation ( Fig. 4-17-9 ). Folds in Descemets membrane often develop. The epithelium at the
edges of the defect tends to be characteristically heaped up with grayish, swollen epithelium. The
ulcer typically found in the lower, exposed, paracentral cornea and is generally oval in shape ( Fig. 417-10 ). Stage three involves stromal melting and occasionally perforation. Other characteristic
symptoms include red eye, mild foreign body sensation, blurred vision, and lid edema. The severity of
the anesthesia generally corresponds to the severity of the keratitis.

spheroidal degeneration

Three stages of the primary form have been described:

Grade I fine shiny droplets are present only peripherally without symptoms.
Grade II the central cornea is involved and vision may be as low as 20/100 (6/30).
Grade III there are large corneal nodules and vision is no better than 20/200 (6/60).

PSR

Because PSR can lead to severe vision loss, it was classified into five stages by Goldberg. [2] [12]
[15] This progression of retinopathy typically occurs in the third or fourth decade of life but has been
noted as early as the second decade. The five stages are as follows:
1. Peripheral arteriolar occlusions.
2. Arteriolar-venular anastomoses.
3. Neovascular proliferation.
4. Vitreous hemorrhage.
5. Retinal detachment.

Lyme disease

is characterized by three main stages:

Primary, or initial, phase with rash noted at the site of the inoculum (erythema chronicum migrans).
Associated flu-like symptoms can be noted.
Secondary or dissemination phase with systemic signs and symptoms including dermatologic,
neurologic, and cardiac manifestations.
Tertiary or late phase with associated arthritis, meningoencephalitis, polyneuropathies involving both
cranial and peripheral nerves, and carditis.

Sarcoidosis

Stage I consists of bilateral hilar adenopathy alone.

Stage II adds parenchymal involvement.
In stage III, parenchymal disease predominates without prominent hilar involvement.
Stage IV is advanced disease characterized by pulmonary fibrosis.

RHABDOMYOSARCOMA

There are four stages:

I. Localized tumor, completely resected
II. Regional spread, positive nodes, grossly resected
III. Gross residual tumor remaining after incomplete resection
IV. Distant metastases

OSD

Van Bijsterveld created a grading scale for rose bengal dye that divides the ocular surface into three
zones: nasal bulbar conjunctiva, cornea, and temporal bulbar conjunctiva, each graded 03 (0, none;
3, confluent staining).[36] Lemp and the National Eye Institute/Industry Workshop group[15] suggest
that the conjunctiva be divided into six areas and graded in a similar manner ( Fig. 4-23-4 ).
Alternatively, lissamine green stains for cell death or degeneration, as well as cell-to-cell junction
disruption, but does not irritate the eye.

RAPD

Grade I: weak initial constriction followed by greater redilation;

Grade II: a slight stall in movement, followed by a definite dilation;
Grade III: immediate pupillary dilation [i.e., pupillary escape];
Grade IV: pupillary dilation during prolonged illumination of the contralateral eye for 6 seconds,
followed by constriction;
Grade V: immediate pupillary dilation and no signs of constriction), these systems are subject to interobserver errors and are affected by pupillary size; e.g., the small pupil may not show a detectable
initial constriction.
The amount of pupillomotor input asymmetry (the RAPD) may be estimated roughly using the
alternating light test (without any neutral density filters) and the subjective grades +1, +2, +3, or +4 for
asymmetry of pupillary response.
This subjective grading also may be categorized according to the amount of pupil escape, or
dilatation of the pupils, as the light is alternated between the eyes.[13] However, most subjective
grading of RAPDs has serious limitations, such as some large-scale errors that arise from age
variations in pupil size and pupil mobility. For example, a patient who has small pupils and small
pupillary contractions to light may have a large RAPD, but this may appear deceptively small on the
basis of small differences in pupil excursion observed as the light is alternated between the two eyes.
However, the amount of neutral density filter needed to dim the better eye until the small contractions
are equal represents substantial input damage. To estimate the size of RAPDs without using filters is
very much like the estimation of an ocular deviation by Hirschberg without a prism cover test. More
accurate quantification of RAPDs is accomplished by determination of the log unit difference needed
to balance the pupil reaction between the two eyes. [4] [5] Photographic neutral density filters
(49mm, screw mount, 0.3 log, 0.6 log, and 0.9 log) often are available through local photography
stores.

VAN HERRICK GRADING OF THE PERIPHERAL ANTERIOR

CHAMBER DEPTH
4: > 1 PCT
3: to PCT
2: PCT
1: < PCT
Slit: Dangerously narrow

limbal chamber depth method

The limbal chamber depth method of grading the peripheral anterior chamber is a recent modification
of the van Herick test.[37] Instead of the four grades used in the van Herick method, it has seven
grades that are expressed as a percentage fraction of the thickness of the adjacent cornea: 0%, 5%,
15%, 25%, 40%, 75%, and 100%. The limbal chamber depth method has been demonstrated to
perform better in the detection of established PACG and is now widely used in epidemiologic
research.

GRADING OF HYPERDEVIATION

Trace: 5
1+: 10
2+: 20
3+: 30

4+: 45

BESTs Disease
Best's disease has been described as going through four phases based on fundus examination.
1.
The first, the previtelliform stage, is characterized by a normal fundus appearance.
2.
The second stage, the vitelliform stage, usually occurs in early childhood and is
characterized by a well-circumscribed 0.5-2-disk-diameter yellow lesion that looks like the
yolk of an egg and appears to be located under the pigment epithelium. This is usually 0.5-2
optic disk diameters in size. Acuity is usually normal or slightly reduced. The lesion may be
unilateral, and a yellowish change may be noted in the RPE throughout the fundus.
3.
During the teenage years, or thereafter, the yellow lesion can break through the RPE
into the subretinal space, and the yellow material can accumulate inferiorly in the macula in
the subretinal space to form pseudohypopyon (the third stage).
4.
A scrambled-egg appearance to the fundus then follows, with yellow deposits
scatteredthroughout the posterior pole (the fourth stage).

Lasers
Lasers are divided into four classes based on their strength of output.
Class 1 lasers, with a maximum output that is <0.4 mW, are considered the safest lasers and are
believed incapable of causing damage even if viewed for long periods of time.
Class 2 lasers have a maximum output <1 mW. These are also felt to be extremely unlikely to result
in ocular injury because of protective mechanisms conferred by the bodys natural blink response and
aversion reflexes.
Class 3A lasers have a maximum output between 1 mW and 5 mW, and although they cannot cause
immediate eye injury, they can induce damage if stared directly at for sustained periods of time.
Most laser pointers that are available in the United States are class 2 or class 3A lasers.
Class 3B lasers are much more powerful, with a maximum output between 5 mW and 500 mW.
These are believed to be capable of producing ocular damage immediately upon viewing. Although
these lasers are illegal in some countries, they can be obtained quite easily via the Internet.
Class 4 lasers are the most powerful lasers, boasting a maximal output >500 mW. These are typically
used in military and occupational settings, such as laser shows. They are capable of producing
extensive ocular damage. Given the brevity of our patients exposure that still resulted in retinal injury,
the laser involved was most likely a class 3B laser.

VKH
1.
Prodromal phase lasting a few days is characterized by neurological and auditory
manifestations.
Meningitis causing headache and neck stiffness.
Encephalopathy is less frequent and may manifest with convulsions, paresis and cranial nerve
palsies.
Auditory features include tinnitus, vertigo and deafness.
2.
Acute uveitic phase follows soon thereafter and is characterized by bilateral
granulomatous anterior or multifocal posterior uveitis and exudative retinal detachments.
3.

Convalescent phase follows several weeks later and is characterized by:

Localized alopecia, poliosis and vitiligo (Fig. 11.69).

Focal depigmented fundus lesions (sunset glow fundus) and depigmented limbal lesions (Sugiura
sign).
4.
Chronic-recurrent phase is characterized by smouldering anterior uveitis with
exacerbations.

Coats Disease:
stage 1, telangiectasia only;
stage 2, telangiectasia and exudation (2A, extrafoveal; 2B foveal);
stage 3, exudative retinal detachment (3A, subtotal; 3B total);
stage 4, total detachment with secondary glaucoma; and
stage 5, advanced end-stage disease.

House-Brackmann Facial Nerve Grading System

Grade Description Characteristics
I Normal Normal facial function
II Mild dysfunction Very slight weakness found on close inspection; good forehead
function; complete and quick eyelid closure
III Moderate dysfunction Obvious but not disfiguring asymmetry; mild synkinesis; slight
forehead movement; complete eyelid closure with effort
IV Moderately severe dysfunction
Disfiguring asymmetry; no forehead movement; incomplete
eyelid closure
V Severe dysfunction Barely perceptible facial movement; incomplete eyelid closure
VI Total paralysis No movement

FUCHS DYSTROPHY
The first stage is asymptomatic, but guttae can be seen centrally on the posterior
aspect of a thickened Descemet membrane. In the second stage, the patient may
experience increased glare and a painless decrease in vision due to corneal edema.
The cornea may begin to decompensate. In the third stage, vision deteriorates
further owing to advanced corneal edema, and the patient may experience pain from
the formation of epithelial and subepithelial bullae. The fourth stage is characterized

by profound vision loss due to subepithelial scarring, which histologically appears as

diffuse avascular subepithelial connective tissue.

Corneal Ulcer
Stage 0: Stage of Infiltrate
Stage 1: Progressive Stage
Stage 2: Regressive Stage
Stage 3: Healing Stage
CHARACTERISTIC

SIZE
DEPTH
INFILTRATE
SCLERA

MILD

<2mm
<20%
SUPERFICIAL
NOT
INVOLVED

MODERATE

SEVERE

2-5 mm
20 50 %
MID
STROMAL
NOT INVOLVED

>5mm
>50 %
DEEPER
MAY BE
INVOLVED

PAPILLOEDEMA
1
2
3
4

Early
Established
Chronic
Atrophic

Stages of Filtering Bleb Infections

Stage 1:

Purulent bleb

+/- AC reaction
Stage 2:

Purulent bleb

Moderate AC inflammation
Stage 3:

Endophthalmitis with marked AC reaction, vitritis

Grading system of atrophia and phthisis bulbi

I Atrophy bulbi without shrinkage
II Atrophia bulbi with shrinkage
III Atrophia bulbi with shrinkage and disorganization (phthisis bulbi)
IV Phthisis bulbi with intraocular ossification
V Phthisis bulbi with intraocular calcium deposition

posterior staphyloma
A posterior staphyloma is a backward ectasia of the fundus, the hallmark being tessellation and pallor of the area
involved (Figure3). Posterior staphyloma can be of five types[7]:Type 1- The area of tessellation and pallor includes the region of the optic disc and macula. It is the most
common type
Type 2- includes the region of the macula
Type 3- involves the peri-papillary region
Type 4- extends nasally from the disc
Type 5- most rare and involves the fundus inferior to the optic disc

Chorioretinal Laser coagulation Grades

Grade 1/Light: Barely visible blanching of retinal pigment epithelium (RPE)
Grade 2/Mild: Hazy, faint white retinal coagulation
Grade 3/Moderate: Opaque, dirty white retinal coagulation
Grade 4/Heavy: Dense white, chalky retinal coagulation

Ectropion Grading (Rubin et al)

grade 1 the lower punctum just pointing upwards away from globe (punctal ectropion)
grade 2 partial everted lower lid and visible scleral show
grade 3 the presence of conjunctival hyperemia and gross mucosal thickening and
grade 4 as for grade 3 with additional exposure keratitis
Depending upon the degree of outrolling, ectropion can be divided into three grades.
In grade I ectropion only punctum is everted.
In grade II lid margin is everted and palpebral conjunctiva is visible,
In grade III the fornix is also visible.

Cortical Visual Impairment

Roman-Lantzy phases
Phase is a period in the resolution of CVI that indicates degree or severity of CVI.
Phase 1: building visual behavior
Phase 2: integrating vision with function
Phase 3: resolution of remaining CVI characteristics

Classifications in Ophthalmology

CLASSIFICATION OF KERATOREFRACTIVE SURGICAL

PROCEDURES
Optical
Zone
Superficial

Addition

Subtraction
PRK, LASEK, EpiLASIK

Relaxation

CoagulationCompression
Corneal molding

Optical
Zone

Addition

Subtraction

Relaxation

CoagulationCompression

Epikeratophakia
Synthetic
epikeratophakia
Intrastromal
Keratophakia
Intracorneal
lenses

LASIK,
IntraLASIK

Lamellar
keratotomy

Keratomileusisin
situ
Keratomileusis

Peripheral
cornea

Intracorneal ring
segments

Wedge resection
Radial
keratotomy
Hexagonal
keratotomy

Thermokeratoplasty
Compression
sutures

Arcuate
keratotomy

Red-green color vision deficiency:

Red-Green color vision defects fall into two categories depending on which cone class does not
contribute to color vision. The noncontributing cone class is indicated by the prefixes:
Protan-for absence of L cone contribution to vision.
Deutan-for absence of M cone contribution to vision.
Further categorization of color vision defects depends on whether the remaining color vision is based
on two (dichromacy) versus three (anomalous trichromacy) spectrally distinct types of cones. The
suffix -opia denotes dichromacy. The suffix -anomaly denotes anomalous trichromacy in which two of
the cone classes are more similar in spectral sensitivity than the corresponding normal cones:
Deuteranopia. color vision mediated by L and S cones.
Protanopia. color vision mediated by M and S cones.
Protanomaly. color vision mediated by S and two spectrally distinct classes of M cone.
Deuteranomaly. color vision mediated by S and two spectrally distinct classes of L cones

International Clinical DR Scale

International Classification
Level of DR

ETDRS Level of DR

No apparent retinopathy

Level 10: DR absent

International Classification
Level of DR

ETDRS Level of DR

Mild NPDR

Level 20; very mild NPDR

Moderate NPDR

Levels 35, 43, 47; moderate NPDR

Severe NPDR

Levels 53A-E; severe to very severe NPDR

PDR

Levels 61,65,71,75,81,85; PDR, high-risk PDR, very

severe or advanced PDR

International Clinical DME Scale

Disease
Severity
Level

Findings

DME vs. ETDRS scale

DME
apparently
absent

No apparent retinal
No DME
thickening or hard
exudates (HE) in posterior
pole

DME
apparently
present

Some apparent retinal

thickening or HE in
posterior pole

Mild DME: some retinal thickening or HE in

posterior pole but distant from center of the
macula(ETDRS: DME but not CSME)
Moderate DME: retinal thickening or HE
approaching the center but not involving the
center(ETDRS: CSME)
Severe DME: retinal thickening or HE involving
the center of the macula (ETDRS: CSME,
center involved)

Coats' Disease
type I included cases of abnormal exudation without apparent vascular changes;
type II included both exudation and abnormal vessels; and
type III exhibited exudation surrounding a large retinal angioma.

Drusen
Small drusen have been defined in most studies as having a greatest linear dimension of less than 50
m or less than 63 m in diameter.
Large:
64 to >125 m (medium),
125 to <250 m (large), and
250 m (very large).

AMD

AREDS has provided the following clinical classification which can be used to describe adults at risk
for AMD or vision loss from AMD:
No AMD. Absence of any drusen or presence of a few small drusen (>63 m diameter drusen
occupying >125 m diameter circle [equivalent to 5-15 small drusen]) in the absence of any RPE
abnormalities or any later stages of AMD.
Early AMD. Extensive small drusen (occupies at least 125 m diameter circle), or nonextensive
medium size drusen (63 to >125 m diameter drusen) with or without pigment abnormalities
(increased pigment or depigmentation) and no other later stages of AMD.
Intermediate AMD. Extensive medium drusen (occupying an area of at least 360 m diameter
circle, which is equivalent to 20 drusen) if the boundaries are indistinct or occupying an area of 656
m diameter circle (equivalent to 65 drusen) if the boundaries are distinct or at least one large druse
(125 m, approximately the width of a retinal vein as it crosses the optic nerve) or the presence of
GA that spares the foveal center (nonfoveal GA).
Advanced AMD. Geographic atrophy involving the center of the fovea or CNV or disciform scar.

Finger Classification of Radiation Retinopathy

Stage 1 (Findings Are Limited to Outside the Macula)
Cotton wool spots
Retinal hemorrhages
Retinal microaneursyms
Ghost vessels
Exudate
Uveal effusion
Choroidal atrophy
Choroidopathy
Retinal ischemia <5 DA
Stage 2 (Findings from Stage 1 but Found Within the Macula)
Stage 3 (Any Stage 12 in Addition to the Following)
Retinal vascularization
Macular edema
Stage 4 (Any Stage 13 in Addition to the Following)
Vitreous hemorrhage
Retinal ischemia >5 DA

Classification of Giant Retinal Breaks

1.

Giant retinal tear (90 or more)

Extent in degrees (90360) or clock hours (312)
Location (superior, temporal, nasal, inferior)
Configuration
Giant tear without detachment
Giant tear with detachment with
Flat or undisplaced posterior flap
Rolled posterior flap
Inverted posterior flap
Associated with posterior extensions (radial rips) at or within the tear margins
Associated proliferative vitreoretinopathy (absent to severe)
Cause (e.g., spontaneous, trauma, postoperative, systemic syndrome)

2.
3.

Giant dialysis
Giant retinotomy

Stickler's syndrome
Type 1 Stickler's syndrome is characterized by a membranous vitreous appearance and has been
associated with mutations in the COL2A1 gene;
type 2 Stickler's syndrome manifests a different beaded vitreous phenotype and is caused by
COL11A1 mutations.
In addition, one other group of Stickler's syndrome has only systemic abnormalities. This non-ocular
type 3 Stickler's syndrome, with a phenotype displaying characteristic systemic abnormalities such as
facial abnormalities, cleft palate, hearing loss, and arthropathies, but without high myopia, vitreoretinal
degeneration, or retinal detachments, is caused by mutations in COL11A2,[2628] a gene which is
not expressed in ocular tissue.

Spheroid degeneration
Spheroid degeneration has been classified into three basic types.
Type 1 occurs bilaterally in the cornea without evidence of other ocular pathology.
Type 2, or secondary, spheroid degeneration occurs in the cornea in association with other ocular
pathology.
Type 3 is the conjunctival form of the degeneration and may occur concurrently with types 1 and 2.

BRVO
according to site of blockage,
(A) Major at the disc;
(B) major away from the disc;
(C) minor macular;
(DF) peripheral not involving the macula

The Werner Classification of Eye Findings in Graves Disease

NO SPECS
No signs or symptoms
Only signs
Soft tissue involvement (signs and symptoms)
Proptosis
Extraocular muscle involvement
Corneal involvement
Sight loss (optic nerve compression)

Hughes Classification for chemical injuries

Mild :- Good prognosis
Erosion of corneal epithelium, faint haziness of cornea
No ischemic necrosis of conjunctiva or sclera
Moderately severe :- Guarded prognosis
Corneal opacity blurs iris details
Minimal ischemic necrosis of conjunctiva and sclera

Very severe : Poor prognosis

Blurred pupillary outline
Blanching of conjunctiva and sclera

Roper hall (ballen) classification

Grade I : Excellent prognosis
Corneal epithelial damage
No ischemia
Grade II : Good prognosis
Cornea hazy but iris details visible
Ischemia affects <1/3 of limbus
Grade III : Guarded prognosis
Ischemia affects 1/3-1/2 of limbus, stromal haze
Grade IV : Poor prognosis
Ischemia affects > of limbus, cornea opaque

COLOBOMA
Ida Manns classification(1937)
1-above the optic disc
2-superior border of optic disc
3-seperated from the optic disc by normal narrow area of retina
4-inferior crescent below the disc
5- isolated gap in the line of fissure
6-area of pigmentary disturbance
7-extreme peripheral coloboma
Lingam Gopals Optic Disc in Fundal Coloboma:
Six types of disc involvement were identified:
(1) normal disc outside fundus coloboma (27.8%);
(2) disc outside the fundus coloboma and abnormal (10.4%);
(3) disc outside the fundus coloboma and independently colobomatous (8.9%);
(4) disc within the fundus coloboma and normal (5.0%);
(5) disc within the fundus coloboma and colobomatous (44.3%); and
(6) disc shape not identified but blood vessels seen emanating from the superior border of the large
fundus coloboma (2.9%).
Visual acuity was better in types I, II, and III compared with IV, V, and VI. Microphthalmos was more
common with the more severe anomalies. High myopia was more common in the less severe
anomalies.

Accommodative Esotropia
Von Noorden classified Accommodative Esotropia on the basis of underlying etiology as
1. Refractive Accommodative Esotropia
2. Non-refractive Accommodative Esotropia
3. Hypo Accommodative Esotropia
4. Partially Accommodative Esotropia

The Classification of Eye Movement Abnormalities and Strabismus[2] (CEMAS) group classified and
defined this entity asAccommodative Esotropia

Pure Refractive: esotropia eliminated by hyperopic spectacles

Non-Refractive: esotropia at near only and eliminated with plus lenses at near, e.g. bifocal
Mixed: esotropia at distance and greater at near associated with hyperopia and responds to
hyperopic correction at distance with bifocal for near

Mixed (Partially Accommodative) Esotropia

Hyperopia with incomplete response to spectacles and bifocals.

Sturge Weber Syndrome

The Roach Scale is used for classification, as follows:

Type I - Both facial and leptomeningeal angiomas; may have glaucoma

Type II - Facial angioma alone (no CNS involvement); may have glaucoma

Type III - Isolated LA; usually no glaucoma

Normal posterior vitreous detachment:

_ Stage 0: No PVD (seen in 29% of subjects)
_ Stage 1: Incomplete perifoveal PVD in up to 3 quadrants (seen in 47.8%)
_ Stage 2: Incomplete perifoveal PVD in all quadrants with residual attachment to the fovea, optic
nerve, and mid-peripheral retina
_ Stage 3: Incomplete PVD over the posterior pole with residual attachment to the optic nerve and
mid-peripheral retina (1.9%)
_ Stage 4: Complete PVD identified biomicroscopically but not with OCT due to instrument limitation
(8.6%)