Professional Documents
Culture Documents
Gradings in Ophthalmology
Gradings in Ophthalmology
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:
Grade 0 - Normal
Scheie Classification
Group Hypertension
Arteriolar sclerosis
No changes
Normal
Grade 0 - No changes
Description
Systemic associations
None
Mild retinopathy
(retinal
arteriolar signs
only)
Moderate
retinopathy
Malignant
retinopathy
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.
Grading of trachoma
McCallan's classification
McCallan in 1908, divided the clinical course of the trachoma into following four stages:
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
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).
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
Cellular activation
2.
Proliferation
3.
4.
Contraction
3.
4.
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
Closed
dipping of light
Schwalbes line visible
anterior trabecular meshwork
posterior T M scleral spur
ciliary body band visible
root of iris visible
+2
+3
+4
0
+1
+2
+3
+4
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.
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.
simultaneous perception, SP
fusion
stereopsis
NVG
(a) rubeosis iridis, (b) secondary open-angle glaucoma and (c) secondary synechial angle-closure
glaucoma.
ocular GVHD
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
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
Sarcoidosis
RHABDOMYOSARCOMA
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
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.
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.
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
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
Purulent bleb
+/- AC reaction
Stage 2:
Purulent bleb
Moderate AC inflammation
Stage 3:
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
Classifications in Ophthalmology
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
ETDRS Level of DR
No apparent retinopathy
International Classification
Level of DR
ETDRS Level of DR
Mild NPDR
Moderate NPDR
Severe NPDR
PDR
Findings
DME
apparently
absent
No apparent retinal
No DME
thickening or hard
exudates (HE) in posterior
pole
DME
apparently
present
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.
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
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
Type II - Facial angioma alone (no CNS involvement); may have glaucoma