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Clinical Methods of Ophthalmology For Medical StudentsDr - Baburao Dasari - M.S (Oph) ., D.O.

The document outlines the clinical methods of ophthalmology for medical students in India, aligning with the competency-based undergraduate curriculum set by the NMC. It includes detailed chapters on anatomy, clinical examination techniques, and a comprehensive list of clinical skills and cases for assessment. The curriculum emphasizes practical skills, theoretical knowledge, and clinical competencies essential for aspiring ophthalmologists.

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0% found this document useful (0 votes)

102 views380 pages

Clinical Methods of Ophthalmology For Medical StudentsDr - Baburao Dasari - M.S (Oph) ., D.O.

Uploaded by

uday kiran

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CLINICAL METHODS OF OPHTHALMOLOGY FOR MEDICAL STUDENTS AS PER THE

COMPETENCY BASED UNDERGRADUATE CURRICULUM OF NMC , INDIA

Clinical Methods of Ophthalmology for

Medical students
Begin a clinical course of Ophthalmology with
clinical methods
Dr.BabuRao Dasari . M.S (Oph ) ., D.O.
Professor of Ophthalmology

Begin the subject of Ophthalmology with

clinical methods
Clinical methods of ophthalmology for medical students as per the
competency based undergraduate curriculum of NMC , India
CLINICAL METHODS OF OPHTHALMOLOGY FOR MEDICAL STUDENTS
AS PER THE COMPETENCY BASED UNDERGRADUATE CURRICULUM OF

Clinical Methods of Ophthalmology for

Medical students

Dr.BabuRao Dasari . M.S (Oph ) ., D.O.

Professor of Ophthalmology
4.Contents

Chapter 1: Clinical Anatomy and Physiology of the Eye

Chapter 2: Ocular Symptoms

Chapter 3: History taking and plan of case sheet writing

Chapter 4: Visual acuity and other visual functions of the eye

Chapter 5: Practical Refraction

Chapter 6: Clinical Examination of the of the Eyebrow

Chapter 7: Clinical Examination of the Eye Lids

Chapter 8: Clinical Examination of the Lacrimal Apparatus

Chapter 9: Clinical Examination of the Orbit and Periorbita

Chapter 10: Clinical Examination of the Eye Ball

Chapter 11: Clinical Examination of the Conjunctiva

Chapter 12: Clinical Examination of the Cornea

Chapter 13: Clinical Examination of the Sclera

Chapter 14: Clinical Examination of the Anterior Chamber

Chapter 15: Clinical Examination of the Iris

Chapter 16: Clinical Examination of the Pupil

Chapter 17: Clinical Examination of the Crystalline Lens

Chapter 18: Clinical Case Discussion of Cataract

Chapter 19: Salient clinical findings for documentation of cataract for diagnosis

Chapter 20: Diagnosis of Cataract

Chapter 21: Comparative clinical signs of cataract (four pages)

Chapter 212: Treatment of Cataracts

Chapter 23: Examination of the Posterior Segment (fundus oculi)

Chapter 24 Visual pathway and defects

5.List of Clinical Skills: Psychomotor Skills (DOAP, AETCOM)

Clinical skills are derived from competencies. AN 41.1. Integration. OP. Competency: 1,2,3,4,5,6,7,8,9

33. Demonstrate the clinical examination of the patient

Clinical skills: 54 numbers, i.e., OSCE, DOAP, demonstration (by withred eye, i.e., corneal luster, pupil abnormalities
the student): observe, assist, or perform clinical skills in Anterior chamber depth with a torch light
ophthalmology described in competency topics and clinical
sessions (S, SH, DOAP). 34. Demonstrate the clinical examination of aqueous
flare, hypopyon, and hyphemia. Write a brief note to
1. Demonstrate the steps for recording visual acuity for demonstrate and interpret the depth of AC with a slit
distance, near, and pinhole examinations. lamp by Van Herick’s method.
2. Color vision
36. Demonstrate Examination of Iris Shadow 37. Describe
3. Demonstrate eversion of the upper eyelid (Method 1, 2). gonioscopy, and what are the structures of the angle of
4. Demonstrate MRD-1, MRD-2, and MRD-3 in the Ptosis A.C. seen in the gonioscopy?
Exam.
5. Demonstrate Measurement of Excursion of 38. Demonstrate Examination of Direct and Indirect Pupil
Reaction and Swinging Flash Light Test for RAPD and Pupil
Levatorpalpebrae Superioris Muscle
Reaction for TAPD
6. Demonstrate measurement of the interpalpebral
aperture and examination of lagophthalmos. 39. Demonstrate visual field examination by the
7. Demonstrate an Assessment of Entropion confrontation method
8. Demonstrate an Assessment of Ectropion 40. Demonstrate A-Scan Biometry
9. Demonstrate the epilation procedure.
41. Demonstrate examination with a direct
10. Demonstrate the clinical signs of Hordeolum externum,
ophthalmoscope
Hordeolum Internum, Chalazion, and the incision and
curettage procedure. 42. Demonstrate examination with an indirect
11. Demonstrate the Basics of a Slit Lamp ophthalmoscope.
12. Demonstrate Schirmer’s test. 43. Demonstrate techniques of examination of the
13. Demonstrate Tear Film Breakup Time (TBUT) cataractous lens for confirmation.
14. Demonstrate Regurgitation Test
44. Demonstrate ND YAG capsulotomy and iridotomy
15. Demonstrate the Syringing Procedure
with an Abraham lens.
16. Demonstrate Luedde’s Exopthalmometry
17. Demonstrate Hertel’s exopthalmometery. 45. Demonstrate Worth Four-Dot Test
18. Demonstrate Naphzeigers’s sign. 46. Demonstrate the FRIEND Test
19. Demonstrate Hirschberg’s Corneal Light Reflection Test.
20. Demonstrate Cover Test 47. Demonstrate Bagaloni Glasses
21. Demonstrate the correct method of examination of 48. Demonstrate stereo acuity (fly test)
extraocular movements of the eye ball (uniocular or
49. Demonstrate measurement of the angle of squint,
binocular).
i.e., Hirschberg’s corneal reflection and prism bar cover
22. Demonstrate Bell’s Phenomena tests
23. Demonstrate digital bedside tonometry.
24. Demonstrate Schiotz tonometry. 50. Demonstrate lacrimal massage technique in
congenital dacryocystitis.
25. Demonstrate Applanation Tonometry
26. Demonstrate the window reflex test. 51. Demonstrate eye drop instillation in a simulated
27. Demonstrate Placido’s disc examination. environment.
28. Demonstrate examination of corneal sensitivity. 52. Demonstrate the examination of + 78 D + 90 D with a
29. Demonstrate fluorescein staining of Cornea slit lamp.
30. Demonstrate methylene blue staining.
31. Demonstrate Rose Bengal staining 53. Demonstrate the examination of the retinoscopy
procedure.
32. Demonstrate removal of extraocular corneal and
conjunctival F.B. in a simulated environment. 54. Demonstrate the identification of spheres, cylinders,
prisms, and mirrors.

-------------------------------
6. List of diagrams to draw and learn

1. Draw and label a section of the eye, the cavities of the eye ball, and a diagram of the anterior
appearance of the eye.
2. Draw and label a diagram of the clinical anatomy, histological layers, and lymphatic drainage of the
conjunctiva.
3. Draw and label a diagram of clinical anatomy and the layers of the eyelid.
4. Draw and label a diagram of clinical anatomy, the lacrimal apparatus.
5. Draw and label a diagram of clinical anatomy and an optical section of the cornea.
6. Draw and label a diagram of clinical anatomy showing the angle of the anterior chamber of the eye.
7. Draw and label a diagram of the clinical anatomy of the iris.
8. Draw and label a diagram of the optical section of the crystalline lens.
9. Draw and label a diagram of the layers of the retina and the indirect ophthalmoscopy appearance of
the fundus oculi.
10. Draw and label a diagram of the potential spaces of the orbit.
11. Draw and label a diagram of the afferent and efferent pupillary light reflex pathways.

12. Draw and label a diagram of the sympathetic pathway to the eye and discuss the clinical

aspects
13. Draw and label a diagram of the central and peripheral visual fields (VF) and write the
principles of recording of VF. Describe the bedside clinical method, i.e., confrontation.
method of recording of VF.
14. Draw and label a diagram of the visual pathway and discuss the common visual field
defects.and lesions that affect the field defects.
rd
15. Draw and label the diagram of the oculomotor (3 cranial nerve) and its clinical
Importance.
th
16. Draw and label the diagram of the trochlear (4 cranial nerve) and its clinical importance.
17. Draw and label the 6th (abducent nerve) cranial nerve and its clinical importance.
7. List of OSPE (List of Long and short cases for UG clinical examination)

List of Long Cases

 All types of cortical and Nuclear cataract

Immature cataract
Mature cataract
Hyper mature cataract
Nuclear sclerosis cataract
 Corneal ulcer
26. Ciliary staphyloma
List of Short cases
27. Equatorial staphyloma
1. Preseptal cellulitis 28. Intercalary staphyloma
2. Lid edema 29. Buphthalmos
3. Contusion lid 30. Phthisis bulbi
4. Blepharoptosis 31. Atrophic bulbi
5. Hordeolum externum 32. Red eye
6. HordeolumInternum 33. Chemosis of the conjunctiva
7. Chalazion 34. Conjunctival cyst
8. Madarosis 35. Subconjunctival haemorrhage
9. Tylosis 36. Phlycten
10. Ectropion 37. Dry eye spots: Bitot spots and xerosis
11. Entropion 38. Pterygium
12. Lagophthalmos 39. Spring catarrh
13. Blepharitis 40. Symblepharon
14. Trichiasis 41. Corneal ulcer
15. External ocular dermoid 42. Leucoma/macula
16. Limbal dermoid 43. Adherent leucoma cornea
17. Derma lipoma 44. Keratoconus
18. Chronic dacryocystitis 45. Herpes zoster ophthalmicus
19. Mucocele 46. F.B. on the cornea, conjunctiva, and lids
20. Encysted mucocele 47. Hyphema
21. Lacrimal fistula 48. Hypopyon
22. Acute dacryocystitis 49. Keratic precipitates
23. Squint case 50. Mydriatic pupil
24. Proptosis 51. Miosis pupil
25. Anterior Staphyloma 52. Posterior synechiae
Page 8.OSCE
OSCE : Images method of learning -- Students are requested to make a diagnosis basing on the image and write a brief note
of differential diagnosis and treatment
1 2 3 4 5 6 7 8

9 10 11 12 13 14 15 16

17 18 19 20 21 22 23 24

25 26 27 28 29 30 31 32

33 34 35 36 37 38 39 40

41 42 43 44
Page 9. OSCE
45 46 47 48 49 50 51 52

53 54 55 56 57 58 59 60

61 62 63 64 65 66 67

68 69 70 71 72 73 74

75 76 77 78 79 80 81

82 83 84 85 86 87 88

89 90 91 92
Page - 10 OSCE
93 94 95 96 97

98 99 100 101 102 103 104

105 106 107 108 109 110

111 112 113 114 115 116 117

118 119 120 121 122 123

124 125 126 127

Page -11 OSCE
128 129 130 131 132 133

134 135 136 137 138 139

140 141 142 143 144 145 146

147 148 149 150 151 152 153

154 155 156 157 158 159 160

161 162 163 164 165 166 167

168 169 170 171 172

Page 12. OSCE
173 174 175 176 177

178 179 180 181 182

183 184 185 186 187 188 189

190 191 192 193 195 196

194

197 198 199 200 201

202 203 204 205 206

Chapter 1. Competencies in anatomy and physiology
Competency based undergraduate curriculum for the Indian Medical Graduate
Department of Ophthalmology
Column C: K- Knowledge, S – Skill, A - Attitude / professionalism, C- Communication
Column D: K – Knows, KH - Knows How, SH - Shows how, P- performs independently,

Column F:DOAPsession– Demonstrate,Observe,Assess,Perform

Number COMPETENCY Domain LevelK Core( Suggested Suggeste Num Vertical/ G Sig.
The student should be /S/A/C /KH/S Y/N) Teaching d ber Horizonta r Faculty
able to l
H/P Learning Assessm requ Integratio a Date
method ent ired n d
method to e
certi
fy P
AN41.1 Describe ,demonstrate K/S SH Y Practi Written/V Ophthalm
parts and layers of eyeball cal, iva voce ology
Lectur
e,Sma
llgrou
p
discus
sion
AN 30.5 Explain effects of K KH N Lecture Written Ophthalm K KH
pituitary tumors ology
in the visual
pathway
AN 31.3 Describe the K KH N Lecture Written Ophthalm K KH
anatomical basis ology
of Horner’s
syndrome
PY Describe and K KH Y Lecture, Written/vi Ophthalm
10.17 discuss the Small va ology
functional group
anatomy of the discussion
eye ,Physiology
of pupil and light
reflex
PY Demonstrate and discuss K KH Y Lecture, Written/vi
10.18 the physiological basis of Small va
lesions in visual path way group
discussion
PY Demonstrate testing of field S P Y DOAP Skill 1 ENT,
10.20 of vision in session assessme Ophthalm
volunteer/simulated nt /Viva ology
environment
voce
AN 31.5 and PY10.18 , is written in Chapter 25. AN 31.3, PY 10.17 is written in the chapter Pupil . ,Py10.20 is written in
chapters visual acuity chapter.

1
Chapter 1. Clinical anatomy of the eye ball and its Parts
AN41.1 Describe& demonstrate parts and layers of eyeball
Section of the eye ball

Figure 1.1

Figure 1.2 The eye lids and anterior aspect of the eye ball

2
The anatomy of the eye can be described as coats of the eye ball and Tenon’s capsule which covers the eye
ball , contents of the eye ball, Ocular adnexa, Extra ocular muscles , Vascular supply and Nerve supply .
 The coats of the eye ball - There are three coats of the eye ball .- outer coat is the cornea and sclera,
anterior 1/6 of which is the cornea and posterior 5/6 is the sclera, The junction of the cornea and
sclera is called limbus.
 Middle coat is vascular coat, the anterior part of which is iris , middle part is ciliary body and
posterior part is choroid
 The junction of the ciliary body and choroid or anterior termination of retina is called oraserrata
 Inner coat is the retina.
 The eye ball is enclosed in a fibrous capsule called Tenon’s capsule, the anterior part is attached at
surgical limbus and posterior part is fused with dura covering of the optic nerve.
 Contents of the eye ball are Cavities of the eye ball, Crystalline lens andVitreous.
 The cavities of the eye ball are – Anterior cavity and Posterior cavity.
 Anterior cavity is divided into anterior chamber and Posterior chamber.
 Anterior cavity contains aqueous and posterior cavity contains vitreous.
 The eye ball is also divided into anterior segment and Posterior segment
 Anterior segment is anterior to the posterior capsule of the crystalline lens
 Posterior segment is posterior to crystalline lens.
 Ocular adnexa- The eye lids, Lacrimal apparatus, Orbit.
 Extra ocular muscles – Four recti i.e. Superior rectus, Medial rectus, Inferior rectus, Inferior oblique,
Lateral rectus and two oblique i.e. superior oblique and inferior oblique.

-----------------------------------------------------------------

3
Chapter 2. Ocular Symptoms
(2.1., 2.2., 2.3., 2.4.,)

A “Symptom” is the complaint given by the patient regarding his/her illness while a “Sign” is that the doctor
elicits after clinical examination.

Ocular Symptoms fall into five categories

1. Disturbances of Ocular Motility
2. Disturbances of Ocular surface
3. Diminution of vision
4. Disturbances in Visual phenomena
5. Headache (ocular or non ocular)
6. Other symptoms – Drooping of the lids (Ptosis), Swelling of the lids, Mal positions of the lid
deviation of the eyes, Proptosis, are explained in appropriate chapter.

In this Chapter 2 ,
 2.1 is 2.1., Symptoms of disturbance in Ocular Motility
 2.2 is Symptoms Disturbances of Ocular surface
 2.3 is Diminution of vision

 2..4 is Disturbances in Visual phenomena

1
Chapter 2 Ocular symptoms
2. 1.Symptoms of disturbance in Ocular Motility
 Asthenopia
 Binocular Diplopia

Asthenopia
Asthenopia is a feeling of tiredness or weakness in the eye after reading or watching a distant object for a long
time or aggravated by near work.
Causes
 Dry eyes
 Uncorrected Refractive errors e.g.: Hypermetropia, Astigmatism
 Presbyopia – Physiological failure / deficiency of accommodation
 Hetero Phoria- Latent squint (Hidden squint)
 Convergence insufficiency

Asthenopia is associated with

 Congestion of the conjunctiva
 Pain in the eye
 Pain, tenderness in and around the eye and orbit
 Headache – Ocular or Non-Ocular symptoms
 Dry eyes i.e., Burning sensation, Heaviness in the eye lids, Congestion of the conjunctiva

Pain in the eye - Pain in the eye may be ocular or non-ocular referral pain
Ocular pain causes -
 Refractive errors – Hypermetropia, Astigmatism, Presbyopia
 Trauma –Blunt and penetrating injuries of the eye and orbit
 Corneal ulcer – Infection of the cornea
 Herpes zoster ophthalmicus – Varicella virus infection along the distribution of the ophthalmic division of
the fifth cranial nerve
 Episcleritis and Scleritis - Inflammation of episcleral tissues and sclera
 Iritis and Iridocyclitis – Inflammation of iris and ciliary body
 Acute and post congestive glaucoma of Primary angle closure Glaucoma
 Endophthalmitis and Pan ophthalmitis: Endophthalmitis is inflammation of the inner coats of the eye ball
and cavities of the eye ball and Pan ophthalmitis is suppurative (Pus) inflammation of all coats of the eye
ball including tenon’s capsule and cavities of the eye ball.
 Orbital cellulitis – Inflammation of the orbital elements
 Retro ocular Pain in the first two days of acute retrobulbar neuritis

1
Table 1. Causes for Pain in the eye
Figure 2.1 Figure2. 1 Figure2. 2 Figure2. 3
Refractive errors Corneal ulcer with Herpes Zoster
Blunt Trauma and
Hypopyon Ophthalmicus
Penetrating Trauma

Table 2. Figure2. 4 Figure2. 5 Figure2. 6 Figure 2.8

Acute Iridocyclitis Orbital cellulitis Pan ophthalmitis Scleritis
with Hypopyon
Figure

Pain, tenderness and discomfort in and around the eye and orbit also causes pain in the eye - Causes
 Suppurative Inflammatory conditions of the glands of eye lids like Hordeolum
externum (Zeis glands, moll glands, eye lash follicle), Hordeolum Internum
(Meibomian glands), and lid abscess, Ulcerative Blepharitis
 Orbital cellulitis – Inflammation of the orbital elements
 Acute Proptosis – Acute forward protrusion of the eye ball
 Acute dacryocystitis, - Acute inflammation of the lacrimal sac
 Fractures of the orbit and its bones
 Sinusitis - Maxillary, frontal and ethmoidal sinusitis
 Referral pain from tooth ache
 Cavernous sinus thrombosis
Non ocular causes for Referred Pain in the eye
 Viral fevers.
 Malnutrition,
 Morbidity
 Dyspepsia

2
 Constipation
 Anemia
 Prolonged illness
 Systemic illness i, e brain tumors, lung infections,

Table 3. Causes for Pain, tenderness and discomfort in and around the eye and orbit

Figure2. 7 Figure2. 8 Figure2. 9 Figure2. 10

Black line showing Hordeolum Hordeolum Internum Black line showing Acute dacryocystitis
Externum ulcerative blepharitis

Figure2. 11 Figure2. 12 Figure2. 13 Figure2. 14

Lid abscess fractures of the floor of the Acute proptosis Acute – bilateral
orbit proptosis

Headache
 It is the commonest symptom referred to the ophthalmologist.
 Headache may be Ocular or Non ocular
 Ocular causes of Headache - The ocular causes for headache are the same as pain in the eye and pain and
tenderness and discomfort in and around the eye and orbit as described above

Table 4.
Figure2. 15 Figur2. 16 Figure2. 17 Figure2. 18 Figure2. 19
Iridodialysis (Blackline Black line showing Black line showing Black line showing Restrictive squint
showing) temporal iridotomy Subluxated lens Subluxated IOL in Thyroid
orbitopathy
.

3
 Non ocular causes are – Head injuries, Tumors in the brain, meningitis, viral fevers, Constipation
,Dyspepsia etc.
 Any ill health in the body may reflect as a headache and eye pain.

Diplopia
Diplopia is Subjective impression of two images of the same object when both eyes are open.
It may be Binocular diplopia and uniocular diplopia

Causes for Binocular Diplopia

Binocular diplopia - This is due to failure of coordinated movements by the eye ball.
 Extra ocular muscle paresis, paralysis
 Restrictive squint – in thyroid orbitopathy where the muscles are enlarged and fibrosed and in fractures of
the orbit where the extra ocular muscle is trapped in the fractured bones causing restriction of ocular
movements
 . Post operative extraocular muscle surgeries

Causes for Uniocular diplopia

 Anisometropia – Difference of refractive power in both the eyes more than 4 diopters.
 Astigmatism
 Iridodialysis – Tear of the iris from the ciliary body
 Any particle coming in the way of visual axis – e.g.: a protein particle of acute Iridocyclitis, immature
cataract lens fibers, Vitreous opacities, exudates in the macula.
 Subluxated crystalline lens and Subluxated intra ocular lens.
 Displaced globe due to mass in the orbital cavity as in proptosis
 Temporal iridectomy or Iridotomy done to relieve pupillary block in Primary angle closure glaucoma
(PACG). (Making a hole surgically in the periphery of the iris is called iridectomy and making a hole with
lasers in the periphery of the iris is called Iridotomy)
 Myasthenia Gravis – Autoimmune disease characterized by abnormal fatigability of the muscles because
of deficiency of acetyl choline receptors as a result of antibodies directed against them. This causes
variable degree of ptosis and muscle imbalance
It has to be differentiated from Uniocular diplopia. Binocular diplopia disappears when either eye is closed
Uniocular diplopia disappears when the affected eye is closed

-----------------------------

4
Chapter 2. Ocular Symptoms
2.2., Symptoms of ocular surface disturbance

The ocular surface is the epithelium covering the conjunctiva, cornea, the inner side of the eye lids and tear film.
The symptoms of the disorders of ocular surface.
 Redness or Congestion of the eye
 Foreign body sensation / Irritation of the eye/ Gritty feeling
 Mild Swelling of the lids
 Watering of the eye
 Dryness of the eye
 Discharge from the eye
 Photophobia
 Itching of the eye

Redness or Congestion of the eye

Redness or congestion of the eye are of 5 types-
 Conjunctival congestion - Congestion at the bulbar and palpebral conjunctiva
 Circum ciliary congestion - Congestion around the limbus
 Mixed condition – Both Conjunctival and Circum ciliary congestion
 Circum corneal congestion – Peri limbal congestion as in Spring catarrh

Deep red or dusky red – deep conjunctival, angry looking congestion

Causes for Deep red ,
Dusky red,
 Uveal inflammation
 Scleritis – inflammation of the sclera

Causes for Mixed congestion

 Endophthalmitis,
 Pan ophthalmitis
Table 4. Difference between Conjunctival and Circumciliary congestion (CCC)

Conjunctival congestion Circum ciliary congestion (CCC)

 More pronounced in the Fornices  More pronounced Around the limbus

 Bright red in color  Pink in color

 Blood flow from fornix towards limbus  Blood flow from limbus towards fornix

 Conjunctival blood vessels are Lacrimal artery, anterior  Circum ciliary vessels are the branches of Anterior
ciliary, posterior conjunctival artery and Marginal tarsal ciliary vessels
vessels,

 Associated with mucus or mucopurulent discharge  Associated with watery discharge

 Causes: Any insult to the conjunctiva: Infective, Allergic,  Causes: Keratitis, Corneal ulcer, Corneal F.B, acute
chemical conjunctivitis. F.B in the conjunctiva, Dry eyes Iridocyclitis, acute congestive glaucoma, Phaco
morphic and phacolytic glaucoma

Differential Diagnosis of Red eye –

The Differential Diagnosis of Red eye are Conjunctivitis, Acute anterior uveitis and Acute congestive glaucoma (For
more details See examination of Conjunctiva topic)

Foreign body sensation / Irritation of the eye - Causes

 Dry eyes - The Sandy or Gritty feeling and burning sensation in the eyes which is felt worst or
aggravates in the evening associated with asthenopia, and blurred vision.
Concretions – Inspissated mucus in the Henle layers of the conjunctiva. They are minute, hard yellow dots in the
palpebral conjunctiva.
May be associated with dry eye, infections of the conjunctiva and lid. See the chapter on the examination of the
Lids.
Watering of the eye –two types i.e. Lacrimation and Epiphora
Normally one is not aware of the wetness of the eye. The person is generally aware of the wetness of the eye only
when there is Lacrimation or Epiphora.

Table 5. .Figure 20 Figure 21Circum Figure 22(CCC) Figure 23 Corneal F.B Figure 24
Conjunctival congestion ciliary congestion (CCC) Conj.Concretion
Lacrimation –
Lacrimation is increased secretions of the tears by reflex phenomena
Lacrimation may be Psychogenic reflex or Neurogenic due to reflex phenomena
Neurogenic reflex Causes – Irritation / stimulation of the ophthalmic division of 5 cranial nerve.
th

 Foreign body on the cornea or conjunctiva

 Trichiasis –Misdirected eye lashes
 Corneal ulcer

Psychogenic reflex Causes

 Excited with happiness or depression

Epiphora
Epiphora is overflowing of tears due to obstruction to the drainage of tears i.e., occlusion of the lacrimal drainage
from punctum to the inferior meatus or due to failure of physiological pump mechanism.
Causes-
 Chronic Dacryocystitis – Chronic inflammation of lacrimal sac
The causes for Chronic Dacryo cystitis -
Chronic dacryocystitis due to naso lacrimal duct block, Inferior meatus obstruction in the nasal cavity due to
nasal pathology.
 Occlusion of Punctum,
 Canalicular stenosis,
 Congenital dacryocystitis – Congenital failure or delay in the cleavage of the nasolacrimal duct
 Coloboma of the lower lid – congenital coloboma of the lid
 Eversion of the punctum - Normally the puncti aptly opposes the eye ball to drain the tears. If the puncti are
away from the eye ball which is called Eversion of the punctum. It causes epiphora.
 Ectropion of the lid - outward rolling of the lid margin
 Entropion of the lid - inward rolling of the lid margin

Dryness of the eye (scanty tears formation)

The symptoms of dryness of the eye are irritation, pain and redness of the eye.
The causes of dry eye are
 Diseases of the ocular surface, lacrimal gland, Meibomian gland dysfunction, Dry eye syndromes like vit- A
deficiency and Steven Johnson syndrome (drug reactions.)
Discharge from the eye
Discharge from the eye may be due to the diseases of the conjunctiva, cornea, Lacrimal sac, and orbital fistula.,
Hordeolum externum and Internum.
The discharge may be watery, serous. Mucoid, Mucopurulent, Purulent, ropy, Table 6.Figure2. 25
Ophthalmia neonatorum
Bloody in nature.
 Watery discharge is due to viral conjunctivitis
 Mucopurulent, Purulent discharge from conjunctiva is due to Bacterial
conjunctivitis
 Ophthalmia neonatorum -
Mucoid or mucopurulent discharge from both the eyes in the neonate (0 to
28 days). Mucopurulent /purulent Conjunctivitis is due to Neisseria
gonococcal infections
Mucus secretions are due to mild conjunctival infection
Ropy discharge from conjunctiva is seen in Spring catarrh (Allergic conjunctivitis)
Causes for blood Discharge from conjunctiva
 Trauma – blunt or penetrating trauma on the eye and orbit
 Membranous conjunctivitis is due to Corynebacterium diphtheriae, Beta hemolytic streptococci Streptococcus
pneumococci, Haemophilus Aegyptius etc.
 Hemangioma of Conjunctiva.
 Telangiectasia of conjunctival vessels

Photophobia
Photophobia is discomfort due to abnormal sensitivity to normal light due to ocular or systemic diseases. It is
associated with pain due to ciliary spasm causing constriction of the pupil
Ocular Causes
 Ocular surface disorders – Dry eye
 Corneal abrasion,
 Corneal ulcer
 Interstitial keratitis –Inflammation of the stroma of the cornea. It may be infective or allergic
 Acute iridocyclitis
 F.B on the cornea
 Welding arc keratitis
 Snow blindness
 Acute iridocyclitis – acute inflammation of the iris and ciliary body causing ciliary spasm
Systemic causes
 Meningitis, Migraine, Trigeminal neuralgia, Subarachnoid hemorrhage etc.

Itching of the eyes

Causes-
 Dry eye
 Spring catarrh
 Acute allergic conjunctivitis
 Allergic rhinitis.
Chapter 2. Ocular symptoms
2.3., Diminution of vision

Diminution of vision –
Diminution of vision –
The person (patient) is asked the following questions to characterize the diminution of vision

 Age of onset
 Duration
 Onset – Gradual or Sudden
 Progressive or stationary / improving or worsening/ constant or intermittent
 Painful or Painless
 For distance or near vision
 For day vision or night vision
 Both eyes affected simultaneously or separately
 Associated symptoms like redness, watering, photophobia floaters, diplopia, scotoma.

After detail enquiry of the symptom, the diminution of vision can be grouped as
 Gradual progressive painless diminution of distant Vision and near vision
 Sudden Painless loss / diminished Distant Vision and Near vision
 Sudden Painful loss / diminished
Figure 26
Table 7. Causes of Gradual progressive painless diminished Vision for Distant and Near

Causes of Gradual progressive painless diminution of Causes of Gradual progressive painless diminution of f
Distance Vision Near vision
 Refractive errors –Hypermetropia, Myopia,  Presbyopia
Astigmatism  Insufficiency of accommodation
Corneal causes –  Posterior capsular cataract
 Keratoconus (Conical cornea), Keratoglobus (Globular  Macular degeneration
cornea)  Nasal corneal opacities
 Corneal degenerations  Cupuliform cataract
 Corneal dystrophies

Angle of Anterior Chamber causes

 Primary glaucoma– Primary open angle glaucoma
(POAG),  Cycloplegia
 Chronic Primary angle closure glaucoma (PACG)  Internal ophthalmoplegia
(Creeping angle Glaucoma)

Uveal tissue causes

 Chronic Uveitis – Chronic inflammation of the uveal
tissue
Crystalline lens Causes –
 Cataract – Opacities of the crystalline lens
 Posterior capsular Opacification - after intra ocular
lens implantation.
Retina causes
 Retinitis pigmentosa – Pigmentary epithelial
dystrophy of the retina
 Diabetic Retinopathy – Retinal changes due to
diabetes
 Age related Macular Degeneration (ARMD)
 Chronic optic neuropathy – Optic neuropathy due to
alcohol & smoking
Figure27

Table 8. Causes of Unilateral sudden Painless/loss Causes for Unilateral sudden painless
of diminution of Distant Vision and Near Vision diminution/loss of Near vision
 Retinal vascular conditions involving macula – Central  Instillation of Cycloplegics and mydriatics like
retinal artery occlusion (CRAO), Central retinal vein Atropine1%, Homatropine2%, Tropicamide1%,
occlusion (CRVO), Branch retinal vein occlusion, Cilio cyclopentolate 1 % in the eye for refraction, corneal
retinal artery occlusion, anterior ischemic optic ulcer and uveitis.
neuropathy (AION)
 
rd
Retinal Detachment involving macular area Internal Ophthalmoplegia in 3 cranial nerve palsy
 Sub hyaloid Hemorrhage  Spasm of Accommodation
 Vitreous Hemorrhage
 Exudative ARMD
 Central serous chorioretinopathy (CSR)
Figure 28

Table 9. Bilateral Sudden painless/loss of vision – Methyl alcohol poioning, Amaurosis etc.
Causes of Unilateral sudden painful diminution /loss Causes of Bilateral sudden Painful diminution
of vision /loss of Vision
 Corneal ulcer, Keratitis  Cortical Blindness - Trauma
 Acute iridocyclitis with anterior ischemic optic  Malingering
neuropathy (AION)
 Phacomorphic Glaucoma  Uremia
 Acute congestive Stage of PACG  Methyl alcohol Poisoning
 Endophthalmitis & Pan ophthalmitis  Quinine toxicity
 Acute Retro bulbar neuritis (in first two to three days)
 Injuries of the eye ball and orbit – Blunt trauma and
Penetrating Trauma

Other causes for Diminution of vision -

a)-Amblyopia, b) Amaurosis. c) Amaurosis fugax, d) Gaze evoked amaurosis, e) Night blindness (Nyctalopia), f) Day
Blindness (Hemeralopia) g) Color Blindness (Achromatopsia), h) Word blindness – Dyslexia, I) Visual field defects. j)
Non organic or functional visual loss (Malingering)
a) Amblyopia
Amblyopia is partial loss of central vision in one eye or both eyes due to failure of binocular interaction/ binocular
single vision (BSV). No marked visible ophthalmoscopic fundus signs are found. Color vision and Peripheral vision
are Normal.
Amblyopia is one of the anomalies of Binocular single vision (BSV)
Binocular single vision is based on three components – (See in detail in the BSV chapter)
 Sensory mechanism
 Motor Mechanism
 Fusion Mechanism

rd th th
BSV develops from 3 month to 9 month (critical period) of baby’s age, however it extends to 9 year of the
child. Failure of any one of the components of BSV in that age group causes anomaly of BSV- The anomalies of
BSV are Diplopia, Confusion, Amblyopia, Squinting, Loss of stereopsis.

a) Diminution of vision due to Amblyopia –

Uniocular Amblyopia – Amblyopia ex anopsia/ Stimulus deprivation amblyopia
Obstruction to the flow of light into the eye causes sensory stimulus deprivation to the development of the
macula which causes Uniocular Amblyopia.
Causes of unilateral Amblyopia –
 Unilateral congenital cataract
 Unilateral congenital ptosis

rd th
Unilateral corneal opacities in the age group of 3 month of baby to 9 year of the child i.e. (amblyogenic age)
 Anisometropia with a unilateral high refractive error.

Bilateral Amblyopia -
Due to bilateral sensory deprivation in the childhood.
Causes
 Bilateral congenital corneal opacities
 Bilateral cataracts
 Bilateral high refractive errors and in uncorrected refractive errors
 Toxic optic neuropathies.

b) Diminution of vision due to Amaurosis

Amaurosis is Complete loss of vision in one eye or both eyes with no marked visible ophthalmoscopic fundus oculi
sign . Amaurosis due to systemic causes like
 Acute nephritis especially due to complicated pregnancy.
 After scarlet fever
 chronic Renal failure due to chronic kidney disease (CKD),
 Uremia.
Amaurosis blindness is sudden or rapid in onset (8 to24hours) which is bilateral and complete. The Fundus oculi
has no changes except in some patients with hypertension changes.
Vision improves in 10 to 18 hours, and is fully restored in 48 hours.
In uremic amaurosis the pupils are dilated but react to light showing that lower centers are intact. It is because of
the effect of toxins on the visual cortex.

c) Diminution of vision due to Amaurosis Fugax

Amaurosis Fugax is transient monocular blindness caused by temporary spasm of blood vessels which causes
reduced blood flow either to the brain or to the retina.
Causes
 Papilloedema - unilateral or bilateral increase in intracranial pressure.
 Migraine
 Optic disc edema (Unilateral)
 Atherosclerosis in the blood vessels of the brain
 Emboli from atheromatous plaques from the carotid artery
 Cardiovascular valve defects like Rheumatic Heart disease
 Arrhythmias
 Mitral valve Prolapse
 Migraine

d) Diminution of vision due to Gaze evoked Amaurosis

Gaze evoked Amaurosis is a transient monocular loss of vision in a particular direction of eccentric gaze. It is
pathognomonic of orbital disease. commonly seen in optic nerve sheath meningioma. It is due to transient optic
nerve ischemia or due to failure of axonal impulse.

e) Diminution of vision due to Night blindness (Nyctalopia)

Night blindness (Nyctalopia) is inability to see in the dark due to the dysfunction of the retinal rods.
 Familial, Congenital
 Xerophthalmia - Defined as all eye symptoms and signs of Vitamin – A deficiency
 Retinal Pigmentary dystrophy – Retinitis Pigmentosa.
 Functional nervous disorder, Neurosis or malingering.
 Cuneiform cataract
f) Diminution of vision due to Day Blindness (Hemeralopia)
Day Blindness (Hemeralopia) is a term given where the vision is better in the night or in dim illumination than in
bright light.
 Congenital deficiency / absence of cones
 Scotoma, visual field defects, tobacco optic neuropathies
 Central corneal opacities.
 Posterior sub capsular opacities due to cataract,
 Posterior Capsular Opacification (After cataract) ,a common complication of IOL surgery
 Early nuclear sclerosis cataract
 Polar cataract
 Central vitreous opacity
 Cupuliform cataract.

g) Color Blindness (Daltonism)

Color vision - It is the ability to distinguish between different colors of different wavelength of the light. Inability to
identify the primary colors is called color blindness. Color Blindness is of two types - Congenital Color blindness
and Acquired Color blindness
Congenital Color blindness - Two types –
 Total
 Partial

Achromatopsia -
Congenital total color blindness is called Achromatopsia - Congenital total color blindness is rare. Congenital total
color blindness is caused by a central defect. Generally associated with nystagmus and diminution of vision. All
colors appear grey of different brightness. The spectrum appears as a grey band.
Dichromatopsia syn: Dyschromatopsia–
Congenital partial Color blindness is called Dyschromatopsia - Congenital partial Color blindness seldom diagnosed.
Since the subjects compensate for the defects by attention to the shade, texture and combines these with
experience. Occurs in 3 to 4 % males and 0.4 % of females. Inherited, it being transmitted as X linked recessive
through females, who are usually unaffected. It is due to absence of one of the photo pigments in the foveal cones.

Normal person is called Trichromats i.e., Normal color vision. The trichromats with color defects are called
anomalous trichromats. There are three types of anomalous trichromats. They are Protanomalous.,
Deuteranomalous, tritanomalous
 Protanopia / Protanomalous – Congenital partial red color vision deficient anomaly is called Protanopia /
Protanomalous These persons Confuses red color with blue green. The red end of the spectrum is much less
bright or shortened than the normal people. These subjects are called Protanopes. This anomaly is called
Protanomaly
 Deuteranopia / Deuteranomalous – Congenital partial green deficient anomaly is called Deuteranopia /
Deuteranomalous. These subjects are called Deuteranopes. This anomaly is called Deuteranomaly

 Tritanopia/ Tritanomalous –Congenital partial blue color vision deficient anomaly is called Tritanopia/
tritanomalous. These subjects are called Tritanopes. This anomaly is called Tritanomaly.
 Dichromatic vision - These subjects will have both Protanomalous and Deuteranomalous i.e., congenital
partial red and green deficiency.
The red and green color deficiency is a source of danger for certain occupations like railway , aero plane engine
drivers and sailors.

Acquired Color blindness –

Acquired Color blindness may be partial or complete.
Acquired color blindness may be Blue – yellow deficiency and red and green deficiency.

Causes for Blue – yellow deficiency -

Central serous chorio retinopathy, Macular edema

Causes for Red and green deficiency

 Diseases of the optic nerve like optic neuritis
 Diseases of the Retina and Choroid
Blue Blindness –
 . Nuclear sclerosis – Blue color is absorbed by the pigment in the nuclear sclerosis
 Blue end of the spectrum is affected. Partial blue color blindness associated with relative scotoma
Tests for Diagnosis of color vision – Commonly – Ishihara’s isochromatic color vision charts Identifies red and
green color deficiencies.

h) Dyslexia - Diminution of vision due to Word blindness

Word blindness/Dyslexia is Inability to recognize printed or written words. Numericals and music can be read. It
may be congenital or acquired
Congenital Dyslexia
 Seen in 0.1 % of the school children. Males are more affected.
 The defect is in the association area of the Brain.
 It runs in the families
 Oral learning is good. Intelligent and good in arithmetic’s
 Gradually improves by individual tuitions and perseverance.
Acquired Dyslexia --It is part of Aphasia.

I) Diminution of vision due to visual field defects (See chapter in visual pathway defects)
 Scotoma- Reduced sensitivity of the retina as in the diseases of the retina
 Visual pathway defects

j) Diminution of vision due to non organic or functional visual loss. Malingering and Hysteria
 Malingering –
Malingering is Willful Blind behavior for personal and financial gains to get government benefits. Examination with
prisms will confirm the malingering
 Hysteria (Indifference)
Hysteria (Indifference) is Subconscious expression of non organic signs and symptoms of defective vision.
A close observation of the patient’s behavior, clinical examination, pupillary light reaction and fundus oculi
examination, and base out Prism in front of the eye and VEP will differentiate normal eye from a malingering and
Hysterical eye.

----------------------------------------
Chapter 2 Ocular symptoms
2.4 Other ocular symptoms
Symptoms due to visual disturbances in Visual phenomena
Table 9 .
 Glare  Colored halos
 Floaters  Colored vision. (Chromatopsia)
 Photopsia  Scintillating scotoma
 Polyopia  Uniocular Diplopia
 Micropsia, Macropsia, Metamorphopsia

Glare
Glare is awareness of excessive light entry into the eye
Causes
• Aniridia - absence of iris
• Lamellar separation stage of cortical cataract
• Post refractive surgeries on cornea
• Ocular Albinism – Absence of melanin pigments in the uveal tissue and pigment layer of the retina
• Drug mydriasis – Use of cycloplegics and Mydriatics
• Sub capsular cataract
• Cone dystrophy

Floaters - It may be idiopathic or Pathological

 Idiopathic
The Patient complains of small dots, rings, clusters strands or small size particles moving in front of the eye
and moving with the movement of the eye. It is due to RBC circulating in the blood vessels which cast a
shadow in the visual field. (This is due to entoptic Phenomena) These are called mucosae volitantes.

Pathological Causes
 Degenerative myopia – Due to degeneration of vitreous fibrils in Degenerative myopia
 Vitreous hemorrhages - the causes for vitreous hemorrhage are retinal tears, Diabetic retinopathy,
Hypertensive retinopathy, retinal vascular occlusions, blunt and penetrating trauma of the eye and orbit.

Photopsia
The patients perceive flashes of light or sensation of the flickering of light in the visual field.
Causes
 Traction on the vitreo retinal attachments due to pull of the collapsing vitreous
 It is due to retinal irritation and is a predisposing cause for retinal break or retinal detachment.

1
 Posterior vitreous detachment
 Migraine
 Sudden appearance of flashes and floaters indicates retinal tears

Polyopia – Many images of the same object

Causes - Typically seen in incipient cataract, immature cataract as the refractive index of lens fibers changes
causing irregular refraction and thus causing polyopia and colored halos.

Micropsia, Macropsia, Metamorphopsia

Micropsia, Macropsia, Metamorphopsia are the signs of Macular diseases
 Micropsia – Everyday seeing objects look smaller than original
 Macropsia – Everyday seeing objects looks bigger than original
 Metamorphopsia – Distortion of the shapes of the objects. E.g. – the graph paper lines when shown to the
patient are seen bent or obscured.
Causes –
 Central serous chorio retinopathy- Idiopathic Serous fluid collection between Bruch’s membrane and
pigmentary layer of the retina.
 Age related macular degeneration
Table 10..
 Diabetic maculopathy – in Macular edema Figure 29 Colored halos
 Macular hole
 Central chorio retinitis
 Choroidal neovascularization neovascularization membrane
(CNVM)

Colored halos around the bulb-

Rainbow colored rings around the bulb are known as Colored halos blue
color is observed inside and red color outside the ring. It is due to
prismatic effect of light that display the colors when passed through the fluid vacuoles in the corneal
epithelium and alteration in the refractive index of the corneal and crystalline lens lamellae.
Causes Table 11
 Primary angle closure suspect or Acute stage Figure 30 Diagram showing Fincham’s test --
Stenopeic slit
of angle closure glaucoma of PACG
 Immature Cataract – a stage of cortical
Continuous colored Broken colored
cataract rings with rotation rings with rotation
 Corneal edema stenopeic slit in PACG stenopeic slit in
cataract
 Mucus plugs at the visual axis of the cornea
Diagram showing Fincham’s test --

2
The colored halos produced by the corneal disease and immature cataract can be differentiated by Fincham
test.
Fincham test - Colored halos can be demonstrated by keeping a fine film of lycopodium powder enclosed
between two glass plates made up as a trial lens. A stenopeic slit is placed in front of the colored halo and
rotated in 360 degrees. The colored rings of immature cataract will break into segments, where as the colored
rings in the corneal disease will be seen as continuous rings and will not break.

Colored vision. (Chromatopsia)

 Chromatopsia occurs in resolution phase of optic neuritis
Erythropsia – Red vision. The objects appear red in bright light in some patients after cataract extraction
with a normal visual acuity.
 Blue vision blindness – Nuclear sclerosis cataract. This is due to blue light filtered by yellow spectrum
of light. Blue vision is also seen in snow blindness and sometimes seen post cataract surgery.
 Black print is sometimes seen as deep red print due to lateral entry of light through the sclera.

 Scintillating scotoma
A gradually increasing positive scotoma with shimmering character appears in the visual field. This gradually
increases in visual field and occupies one half of the visual field with central fixation point and then becomes
homonymous, finally total field is lost and visual field recovers after some time.
Scintillating scotoma occurs in Migraine which is a vascular instability of the occipital cortex i.e.,
vasodilatation followed by vasoconstriction.

Visual Hallucinations
In the disorders of the cerebral cortex the objects, odd shapes or lights are seen by the patients which are not
visible to other persons.
 Formed visual hallucinations - seeing animals or objects is due to specific localizing value in temporal lobe
cortex. They are seen in Temporal lobe tumors, Epilepsy. Formed visual hallucinations are also due to
misinterpretation of the information in the brain due to the disruption of the areas needed to process the
information.
 Unformed visual hallucinations - Distortion of light as in flashes or spots, lines or objects shape or
symptoms of cerebral cortex due to arterio-venous malformations and also migraine.
 Visual hallucinations frequently seen in Parkinsonism.
 Charles Bonnet syndrome – People having gross diminution of vision can see the images clearly. It is an
attempt of the brain to interpret the impulses received from the objects and form a mental picture.

--------------------------

3
Chapter 2. Ocular Symptoms

(Chapter 2. Ocular Symptoms consists of Chapter 2.1 Symptoms of ocular surface disturbances ,
Chapter 2.2 Symptoms of disturbances ocular motility, Chapter 2.3 Diminution of vision, Chapter 2.4
Disturbances in Visual phenomena )

A “Symptom” is the complaint given by the patient regarding his/her illness while a “Sign” is that the doctor
elicits after clinical examination.

Ocular Symptoms fall into five categories

1. Disturbances of Disturbances of Ocular surface
2. Ocular Motility
3. Diminution of vision
4. Disturbances in Visual phenomena
5. Headache (ocular or non ocular)
6. Other symptoms – Drooping of the lids (Ptosis), Swelling of the lids, Mal positions of the lid
deviation of the eyes, Proptosis, are explained in appropriate chapter.

In this Chapter 2 , it is categorized as ,

 Chapter 2.1., Symptoms of ocular surface disturbance
 Chapter 2.2 Symptoms of disturbance in Ocular Motility
 Chapter 2.3 is Diminution of vision
 Chapter 2..4 is Disturbances in Visual phenomena
---------------------------------------------------

2.1., Symptoms of ocular surface disturbance

4
 Itching of the eye

Redness or Congestion of the eye

Deep red or dusky red – deep conjunctival, angry looking congestion

Causes for Deep red ,
Dusky red,
 Uveal inflammation
 Scleritis – inflammation of the sclera

Causes for Mixed congestion

 Endophthalmitis,
 Pan ophthalmitis

Table 4. Difference between Conjunctival and Circumciliary congestion (CCC)

Conjunctival congestion Circum ciliary congestion (CCC)

 More pronounced in the Fornices  More pronounced Around the limbus

 Bright red in color  Pink in color

 Blood flow from fornix towards limbus  Blood flow from limbus towards fornix

 Associated with mucus or mucopurulent discharge  Associated with watery discharge

5
Differential Diagnosis of Red eye –
The Differential Diagnosis of Red eye are Conjunctivitis, Acute anterior uveitis and Acute congestive glaucoma (For
more details See examination of Conjunctiva topic)

Foreign body sensation / Irritation of the eye - Causes

 Foreign body on the cornea or conjunctiva

 Trichiasis –Misdirected eye lashes
 Corneal ulcer

Psychogenic reflex Causes

 Excited with happiness or depression

Epiphora 7
Epiphora is overflowing of tears due to obstruction to the drainage of tears i.e., occlusion of the lacrimal drainage
from punctum to the inferior meatus or due to failure of physiological pump mechanism.

Table 5. .Figure 20 Figure 21Circum Figure 22(CCC) Figure 23 Corneal F.B Figure 24
Conjunctival congestion ciliary congestion (CCC) Conj.Concretion

6
Causes-
 Chronic Dacryocystitis – Chronic inflammation of lacrimal sac
The causes for Chronic Dacryo cystitis -
Chronic dacryocystitis due to naso lacrimal duct block, Inferior meatus obstruction in the nasal cavity due to
nasal pathology.
 Occlusion of Punctum,
 Canalicular stenosis,
 Congenital dacryocystitis – Congenital failure or delay in the cleavage of the nasolacrimal duct
 Coloboma of the lower lid – congenital coloboma of the lid
 Eversion of the punctum - Normally the puncti aptly opposes the eye ball to drain the tears. If the puncti are
away from the eye ball which is called Eversion of the punctum. It causes epiphora.
 Ectropion of the lid - outward rolling of the lid margin
 Entropion of the lid - inward rolling of the lid margin

Dryness of the eye (scanty tears formation)

The symptoms of dryness of the eye are irritation, pain and redness of the eye.
The causes of dry eye are
 Diseases of the ocular surface, lacrimal gland, Meibomian gland dysfunction, Dry eye syndromes like vit- A
deficiency and Steven Johnson syndrome (drug reactions.)
Discharge from the eye
Discharge from the eye may be due to the diseases of the conjunctiva, cornea, Lacrimal sac, and orbital fistula.,
Hordeolum externum and Internum.
The discharge may be watery, serous. Mucoid, Mucopurulent, Purulent, ropy, Table 6.Figure2. 25
Ophthalmia neonatorum
Bloody in nature.
 Watery discharge is due to viral conjunctivitis
 Mucopurulent, Purulent discharge from conjunctiva is due to Bacterial
conjunctivitis
 Ophthalmia neonatorum -
Mucoid or mucopurulent discharge from both the eyes in the neonate (0 to
28 days). Mucopurulent /purulent Conjunctivitis is due to Neisseria
gonococcal infections
Mucus secretions are due to mild conjunctival infection
8
Ropy discharge from conjunctiva is seen in Spring catarrh (Allergic conjunctivitis)
Causes for blood Discharge from conjunctiva

7
 Trauma – blunt or penetrating trauma on the eye and orbit
 Membranous conjunctivitis is due to Corynebacterium diphtheriae, Beta hemolytic streptococci Streptococcus
pneumococci, Haemophilus Aegyptius etc.
 Hemangioma of Conjunctiva.
 Telangiectasia of conjunctival vessels

Systemic causes
 Meningitis, Migraine, Trigeminal neuralgia, Subarachnoid hemorrhage etc.

Itching of the eyes

Causes-
 Dry eye
 Spring catarrh
 Acute allergic conjunctivitis
 Allergic rhinitis.

8
Chapter 2 Ocular symptoms
2. 2.Symptoms of disturbance in Ocular Motility
 Asthenopia
 Binocular Diplopia

Asthenopia is associated with

9
 Retro ocular Pain in the first two days of acute retrobulbar neuritis

Table 1. Causes for Pain in the eye

Figure 2.1 Figure2. 1 Figure2. 2 Figure2. 3
Refractive errors Corneal ulcer with Herpes Zoster
Blunt Trauma and
Hypopyon Ophthalmicus
Penetrating Trauma

Table 2. Figure2. 4 Figure2. 5 Figure2. 6 Figure 2.8

Acute Iridocyclitis Orbital cellulitis Pan ophthalmitis Scleritis
with Hypopyon
Figure

10
 Dyspepsia
 Constipation
 Anemia
 Prolonged illness
 Systemic illness i, e brain tumors, lung infections,

Table 3. Causes for Pain, tenderness and discomfort in and around the eye and orbit

Figure2. 7 Figure2. 8 Figure2. 9 Figure2. 10

Black line showing Hordeolum Hordeolum Internum Black line showing Acute dacryocystitis
Externum ulcerative blepharitis

Figure2. 11 Figure2. 12 Figure2. 13 Figure2. 14

Lid abscess fractures of the floor of the Acute proptosis Acute – bilateral
orbit proptosis

Headache
 It is the commonest symptom referred to the ophthalmologist.

 Headache may be Ocular or Non ocular

11
 Ocular causes of Headache - The ocular causes for headache are the same as pain in the eye and pain and
tenderness and discomfort in and around the eye and orbit as described above
 Non ocular causes are – Head injuries, Tumors in the brain, meningitis, viral fevers, Constipation
,Dyspepsia etc.
 Any ill health in the body may reflect as a headache and eye pain.

Diplopia
Diplopia is Subjective impression of two images of the same object when both eyes are open.
It may be Binocular diplopia and uniocular diplopia

Causes for Binocular Diplopia

Causes for Uniocular diplopia

12
Chapter 2. Ocular symptoms
2.3., Diminution of vision
Diminution of vision –
Diminution of vision –
The person (patient) is asked the following questions to characterize the diminution of vision

13
Table 7. Causes of Gradual progressive painless diminished Vision for Distant and Near

Angle of Anterior Chamber causes

 Primary glaucoma– Primary open angle glaucoma
(POAG),  Cycloplegia
 Chronic Primary angle closure glaucoma (PACG)  Internal ophthalmoplegia
(Creeping angle Glaucoma)

Uveal tissue causes

14
Figure27

15
Figure 28

16
Other causes for Diminution of vision -
a)-Amblyopia, b) Amaurosis. c) Amaurosis fugax, d) Gaze evoked amaurosis, e) Night blindness (Nyctalopia), f) Day
Blindness (Hemeralopia) g) Color Blindness (Achromatopsia), h) Word blindness – Dyslexia, I) Visual field defects. j)
Non organic or functional visual loss (Malingering)
a) Amblyopia
Amblyopia is partial loss of central vision in one eye or both eyes due to failure of binocular interaction/ binocular
single vision (BSV). No marked visible ophthalmoscopic fundus signs are found. Color vision and Peripheral vision
are Normal.
Amblyopia is one of the anomalies of Binocular single vision (BSV)
Binocular single vision is based on three components – (See in detail in the BSV chapter)
 Sensory mechanism
 Motor Mechanism
 Fusion Mechanism

a) Diminution of vision due to Amblyopia –

17
 Toxic optic neuropathies.

b) Diminution of vision due to Amaurosis

c) Diminution of vision due to Amaurosis Fugax

d) Diminution of vision due to Gaze evoked Amaurosis

18
e) Diminution of vision due to Night blindness (Nyctalopia)
Night blindness (Nyctalopia) is inability to see in the dark due to the dysfunction of the retinal rods.
 Familial, Congenital
 Xerophthalmia - Defined as all eye symptoms and signs of Vitamin – A deficiency
 Retinal Pigmentary dystrophy – Retinitis Pigmentosa.
 Functional nervous disorder, Neurosis or malingering.
 Cuneiform cataract
f) Diminution of vision due to Day Blindness (Hemeralopia)
Day Blindness (Hemeralopia) is a term given where the vision is better in the night or in dim illumination than in
bright light.
 Congenital deficiency / absence of cones
 Scotoma, visual field defects, tobacco optic neuropathies
 Central corneal opacities.
 Posterior sub capsular opacities due to cataract,
 Posterior Capsular Opacification (After cataract) ,a common complication of IOL surgery
 Early nuclear sclerosis cataract
 Polar cataract
 Central vitreous opacity
 Cupuliform cataract.

g) Color Blindness (Daltonism)

19
experience. Occurs in 3 to 4 % males and 0.4 % of females. Inherited, it being transmitted as X linked recessive
through females, who are usually unaffected. It is due to absence of one of the photo pigments in the foveal cones.

Acquired Color blindness –

Acquired Color blindness may be partial or complete.
Acquired color blindness may be Blue – yellow deficiency and red and green deficiency.

Causes for Blue – yellow deficiency -

Central serous chorio retinopathy, Macular edema

Causes for Red and green deficiency

20
h)Dyslexia - Diminution of vision due to Word blindness
Word blindness/Dyslexia is Inability to recognize printed or written words. Numericals and music can be read. It
may be congenital or acquired
Congenital Dyslexia
 Seen in 0.1 % of the school children. Males are more affected.
 The defect is in the association area of the Brain.
 It runs in the families
 Oral learning is good. Intelligent and good in arithmetic’s
 Gradually improves by individual tuitions and perseverance.
Acquired Dyslexia --It is part of Aphasia.

I) Diminution of vision due to visual field defects (See chapter in visual pathway defects)
 Scotoma- Reduced sensitivity of the retina as in the diseases of the retina
 Visual pathway defects

----------------------------------------

21
Chapter 2Ocular symptoms
2.4 Other ocular symptoms
Symptoms due to visual disturbances in Visual phenomena
Table 9 .
 Glare  Colored halos
 Floaters  Colored vision. (Chromatopsia)
 Photopsia  Scintillating scotoma
 Polyopia  Uniocular Diplopia
 Micropsia, Macropsia, Metamorphopsia

Floaters - It may be idiopathic or Pathological

22
 It is due to retinal irritation and is a predisposing cause for retinal break or retinal detachment.
 Posterior vitreous detachment
 Migraine
 Sudden appearance of flashes and floaters indicates retinal tears

Polyopia – Many images of the same object

Causes - Typically seen in incipient cataract, immature cataract as the refractive index of lens fibers changes
causing irregular refraction and thus causing polyopia and colored halos.

Micropsia, Macropsia, Metamorphopsia

Colored halos around the bulb-

23
 Mucus plugs at the visual axis of the cornea
Diagram showing Fincham’s test --
The colored halos produced by the corneal disease and immature cataract can be differentiated by Fincham
test.
Fincham test - Colored halos can be demonstrated by keeping a fine film of lycopodium powder enclosed
between two glass plates made up as a trial lens. A stenopeic slit is placed in front of the colored halo and
rotated in 360 degrees. The colored rings of immature cataract will break into segments, where as the colored
rings in the corneal disease will be seen as continuous rings and will not break.

Colored vision. (Chromatopsia)

24
Chapter 3. History taking and Case Sheet writing
Introduction
 All students should cultivate the habit of talking to the patients respectfully and pleasantly. Examination
of the lady patients requires privacy and modesty.
 Patient is encouraged to narrate the complaints in their language, listen carefully to the patient while
explaining his/her illness and ask relevant questions as and when necessary.
 Patient will give information about his/her illness and helps the doctor to construct the natural course of
the disease.
 History taking directs for requesting relevant investigations for the diagnosis of the case.
 After case sheet writing student should present the cases to the faculty and should document the case
in the log book.
 It is also necessary to take a clinical Photo graph of the relevant clinical signs of the patient for
documentation and future reference.

Case sheet writing in Ophthalmology follows same methodology like any other branches of medicine i.e. bio
data , Symptom, H/o Present illness, H/o Past illness , Family history , Personal history and General
examination, Vital data , local examination and systemic examination.

Bio data - Name, Age, Sex, Occupation, Address, I.D

Symptoms: Described in symptomatology
H/O Present illness - Patient’s symptoms should be elaborated in H/o present illness

H/O Past illness/ Past continuous –The illness might have started long back and being continued.
Hence relevant past illness can be written in the H/o present illness if necessary.
 Any similar illness in the past such as uveitis, herpes simplex keratitis may have recurrent history.
• H/o Diabetes - Associated with ocular signs particularly retinopathy , POAG and Myopia. Diabetes
causes anterior ischemic optic neuropathy. Control of Diabetes is required for ocular surgeries. Intra
ocular surgeries like cataract, glaucoma or retinal surgeries done without control of diabetes may develop
post-operative endophthalmitis and Panophthalmitis. Diabetes is the risk factor for the glaucoma.

• H/o Hypertension – Causes retinopathy. Control is required for ocular Surgeries. Intra ocular Surgeries like
cataract, glaucoma or retinal surgeries done without control of hypertension may develop per - operative
expulsive hemorrhage (Choroidal hemorrhage). Use of sympathomimetic drugs like Brimonidine may
precipitate hypertension. Hypertension is also a cause for anterior ischemic optic neuropathy.
Hypertension is the risk factor for the glaucoma.

• H/o Bronchial Asthma / COPD - Treatment of Glaucoma with Beta-blockers like Timolol maleate 1% may
precipitate Bronchial asthma. Bronchial asthma is the risk factor for the glaucoma.

1
• H/o Cardiac disease – Treatment of Cardiac disease and Glaucoma with Beta-blockers may precipitate
bradycardia in heart blocks

• H/o Diseases of skin, bones, and joints – may be associated with scleritis and uveitis.

• Chronic specific infections like Hansen’s disease (Leprosy) Koch`s (Tuberculosis) may causes
hypersensitivity uveitis. HIV (immunodeficiency disease) HbsAg, should be noted for the safety of the
surgeons.

• Spectacles history - Hypermetropia and Myopia may be associated with Primary glaucoma. Myopia is
associated with degenerations in the eye and complicated cataract.

• Thyroid diseases –Clinical signs of Thyroid orbitopathy – some of the clinical signs are association with dry
eyes and may be aggravated after cataract surgery.

• Drug History – H/o drug use is necessary to rule out side effects and drug interactions. Use of
Corticosteroids for a long time causes toxic cataract, steroid induced glaucoma. Tab. Clopitab, Tab.
Aspirin which are antiplatelet medicines, are to be stopped three days before surgery to reduce per
operative bleeding. Tab. Chloroquine used for joint pains may produce maculopathy.

• Surgical History – Cataract surgery with IOL implantation in the fellow eye or any other surgical history
should be noted

• H/0 Trauma - Concussion/ Blunt Trauma, Penetrating injuries, chemical injuries. Injury with vegetative
matter with signs of inflammation, photophobia and lacrimation may suggest fungal corneal ulcer.

• Chronic constipation, retention of urine, COPD may cause post operative complications like wound
dehiscence and iris prolapse due to strain on the eye in Valsalva maneuvers.
Family History –Some diseases which run in the families may be seen in the off springs are Myopia, Corneal
dystrophy, Congenital Zonular cataract. Primary Glaucoma, Retinitis pigmentosa etc.

Personal History: H/O of Smoking, consumption of Alcohol as they cause / lead to Chronic Optic Neuropathy.
Smoking and alcohol are the risk factors for the glaucoma and cataract.
General Examination - In the general examination gross visible physical abnormalities from hair to the toe are
to be noted. Besides routine `PICKLE` (pallor, icterus, cyanosis, clubbing koilonychia, lymphadenopathy, edema
and gait which are generally examined in medical cases) the following specific observations are to be made in
the eye examination while patient is entering into the OPD.
 Abnormal Head posture

2
• Ocular posture
• Facial Symmetry
• Forehead Furrows
• Eruption of vesicles on the forehead

Table 1.
Figure 3-1Face /Head Figure 3-2 Chin Figure 3-3 Head Figure 3- 4 Figure 3-5 RE in
turned left side
Elevation tilt RE Divergent position Convergent Position

Abnormal Head posture –

Normal head posture is erect and straight Abnormal head posture is due to the paresis or paralysis of the extra
ocular muscles. Abnormal head posture is towards the direction of the action of the paralyzed muscle.
 Head/face turned to the right or left indicates paralysis or paresis of the horizontal extra ocular muscles
lateral rectus or medial rectus
 Head elevation / Chin elevation indicates Paresis or paralysis of the vertical recti i.e., superior rectus Chin
elevation is also present in blepharo Ptosis
 Head depression / Chin depression indicates Paresis or Paralysis of Inferior rectus
 Head tilt towards the right shoulder or left shoulder indicates Paresis or paralysis of the oblique muscles.
Ocular posture
Normally the two eyes are axial and parallel in position in the orbital cavity Eccentric position of the eyes in the
orbital cavity indicate that the eyes are in Divergent, Convergent, up, or Down position.

Table 2.
Figure 3-6 Right Figure 3-7 Figure 3-8 LE upper Figure 3-9 Figure 3-10
hyper tropia and Asymmetry lid Ptosis and furrows Eruptions on RE Proptosis
left hypo tropia of the face on the left fore head the eye lid and
Fore head

3
Facial symmetry – Normally the
Table 3
face is bilaterally symmetrical
Facial Asymmetry-is seen in Figure 3-11 Prominent Figure 3-12 LE Figure 3 - 13
maxillary area of the Lt Enophthalmos Duane’s Retraction
 Duane’s Retraction Syndrome-
side of face Syndrome
The affected eye.
clinical signs in type –I
Duane’s Retraction Syndrome
are unilateral Hypoplasia of the
face, restriction of the
abduction, enophthalmos and narrowing of the palpebral aperture in adduction,
 Maxillary carcinoma – Prominent maxillary area due to maxillary carcinoma.
 Proptosis – Forward protrusion of the eye ball due to space occupying lesion in the orbital cavity
 Enophthalmos – Backward retraction of the eye ball
 Uniocular blepharo Ptosis

Furrows on the forehead – Normally no forehead furrows are seen. Forehead furrows indicate over activity of
the frontalis muscle.
 Seen in Old age
 Blepharo ptosis
 Brow ptosis.

Gait – Circumduction gait indicates hemiplegia and patients may be suffering from diabetes and hypertension
or associated with cranial nerve palsy etc.

Vital data – B.P, Pulse rate, Temperature, Respiratory rate to be recorded. In patients with glaucoma and
cardiac diseases, pulse rate to be recorded before instilling beta blockers or adrenergic in the eye.

History taking is followed by

Examination of the Visual Functions of the eye- Visual acuity, Color vision, visual field sense Etc. (Some
surgeons first examine anterior segment and Posterior segment and then examine the visual functions of the
eye.)
 . Examination of the Ocular adnexa (See below)
 Examination of the Anterior segment (See below)
 Examination of the Posterior segment,
 Systemic examination – RS, CVS, Abdomen CNS,
 Diagnosis -- Anatomical diagnosis. and Pathological diagnosis.

4
Anterior segment examination should be carried out with a Slit lamp Bio microscopy.
But UG students can use a bright torch light and a binocular loupe for examination of the eye.
Clinical signs will be demonstrated to the students in a Slit lamp.
Examination of the Ocular adnexa
 Examination of the Eye brows
 Examination of the eye Lids
 Examination of the Orbit
 Examination of the Lacrimal apparatus

Examination of the Anterior Segment of the eye

 Examination of the Eye ball
 Examination of the Conjunctiva
 Examination of the Cornea
 Examination of the Sclera
 Examination of the Anterior Chamber (A.C)
 Examination of the Iris
 Examination of the Pupil
 Examination of the Crystalline lens
Up to the Crystalline lens is the anterior segment.
Behind the anterior segment is the posterior segment. Examination of the posterior segment is done with
Direct and indirect ophthalmoscope, +78 D, +90 D lens and B – scan.

Final Documentation
 Diagnosis
 Salient findings for the diagnosis to be written
 Investigations
 Plan of Treatment
 Differential Diagnosis.

5
Chapter 3. History taking and Case Sheet writing
(Chapter 3.1 Student Preparedness for History taking , Chapter 3.2 History taking, Chapter 3.3 General
examination, Vitals Etc. )

Chapter 3.1 . Student Preparedness for History taking.

 The students must carry a bright torch light , Binocular loupe , Ophthalmic clinical methods , a note
book exclusively for writing ophthalmic teachings and a log book .
 All students should cultivate the habit of talking to the patients respectfully and pleasantly.
 Examination of the lady patients requires privacy and modesty.
 Patient is encouraged to narrate the complaints in their language, listen carefully to the patient while
explaining his/her illness and ask relevant questions as and when necessary.
 Patient will give information about his/her illness and helps the doctor to construct the natural course of
the disease.
 History taking helps us for Binocular Loupe Torch light Slit Lamp

requesting a relevant
investigations for the diagnosis
of the case.
 It is also necessary to take a
clinical Photo of the patient
relevant clinical signs for documentation and future reference.
 Slit lamp findings will be demonstrated to the students by the faculty .
 Case sheet writing in Ophthalmology follows same methodology like any other branches of medicine i.e
bio data , Symptom, H/o Present illness, H/o Past illness , Family history , Personal history and
General examination, Vital data , local examination and systemic examination.

About Binocular Loupe, Torch Light , and Slit lamp :

A separate torch light lens with a binocular loupe and a slit lamp are essential instruments for examination
of the eye. Both the instruments work on the principle of focal illumination otherwise called oblique
illumination. The present day torch lights are coming with a fitted condensing lens i.e biconvex lens instead of
plane glass. .

What is focal illumination/ oblique illumination –

The diffuse light coming from a light source is passed through a condensing lens ( Biconvex lens) to form a
point of focused light at its principle focus . This point of focused light is a highly concentrated light
surrounded by a black area and the black area acts as a contrast for better visualization of the lesion.

25
Torch light examination with binocular loupe
The light rays coming from the electric bulb passes through the condensing lens i.e biconvex lens and is
focused on the area of interest and then magnified with a binocular loupe . The image magnification of the
Binocular loupe is three to four times with stereoscopic view . The torch light and binocular loupe
examination gives a comprehensive and wider area of visualization of the eye.
Slit lamp –
The slit lamp is a built up instrument with a light source ,condensing lens and binocular microscope
magnification . The slit disc is incorporated in the instrument to modify the shape of the focal point light into
slit beam. The slit beam is essential to make an optical section of the transparent tissues like cornea and
crystalline lens.
The essential methods of examination with a slit lamp are direct focal illumination , Indirect focal illumination
and retro illumination
In a direct focal illumination the optical section of cornea and crystalline lens is made to identify the depth
and position of the lesion ,
In Indirect oblique illumination the adjacent area to slit beam is examined for corneal edema
In a retro illumination – the light beam and visual axis coming through the microscope are 1to 2 degrees
apart or the light is reflected behind the lesion to identify the appearance of lesion .
Other techniques of slit lamp are specular examination for corneal endothelium study and sclerotic scatter to
identify the subtle corneal lesion.
The slit lamp examination is done for the study of aqueous flare for protein particles and cells in the
aqueous, Applanation tonomety for IOP recording , +90 D for stereoscopic examination of optic disc in
glaucoma and macular examination in diabetic retinopathy etc .
The setting of the slit lamp is necessary to examine the different lesions of the anterior and posterior
segment of the eye i.e. angulations between the slit beam and microscope, width and height of the slit beam ,
cobalt green and blue colors of the slit beam etc .
------------------------------------

25
Chapter 3.2 Case sheet writing

Bio data - Name, Age, Sex, Occupation, Address, I.D

Symptoms: Described in symptomatology

H/O Present illness - Patient’s symptoms should be elaborated in H/o present illness

H/O Past illness/ Past continuous –The illness might have started long back and being continued.

Hence relevant past illness can be written in the H/o present illness if necessary.

 Any similar illness in the past such as uveitis, herpes simplex keratitis may have recurrent history.
• H/o Diabetes - Associated with ocular signs particularly retinopathy , POAG and Myopia. Diabetes causes
anterior ischemic optic neuropathy. Control of Diabetes is required for ocular surgeries. Intra ocular
surgeries like cataract, glaucoma or retinal surgeries done without control of diabetes may develop post-
operative endophthalmitis and Panophthalmitis. Diabetes is the risk factor for the glaucoma.

• H/o Bronchial Asthma / COPD - Treatment of Glaucoma with Beta-blockers like Timolol maleate 1% may
precipitate Bronchial asthma. Bronchial asthma is the risk factor for the glaucoma.
• H/o Cardiac disease – Treatment of Cardiac disease and Glaucoma with Beta-blockers may precipitate
bradycardia in heart blocks

• H/o Diseases of skin, bones, and joints – may be associated with scleritis and uveitis.

• Chronic specific infections like Hansen’s disease (Leprosy) Koch`s (Tuberculosis) may causes hypersensitivity
uveitis. HIV (immunodeficiency disease) HbsAg, should be noted for the safety of the surgeons.

• Spectacles history - Hypermetropia and Myopia may be associated with Primary glaucoma. Myopia is
associated with degenerations in the eye and complicated cataract.

26
• Thyroid diseases –Clinical signs of Thyroid orbitopathy – some of the clinical signs are association with dry eyes
and may be aggravated after cataract surgery.

• Drug History – H/o drug use is necessary to rule out side effects and drug interactions. Use of Corticosteroids
for a long time causes toxic cataract, steroid induced glaucoma. Tab. Clopitab, Tab. Aspirin which are
antiplatelet medicines, are to be stopped three days before surgery to reduce per operative bleeding. Tab.
Chloroquine used for joint pains may produce maculopathy.

• Surgical History – Cataract surgery with IOL implantation in the fellow eye or any other surgical history should
be noted

• H/0 Trauma - Concussion/ Blunt Trauma, Penetrating injuries, chemical injuries. Injury with vegetative matter
with signs of inflammation, photophobia and lacrimation may suggest fungal corneal ulcer.

Personal History: H/O of Smoking, consumption of Alcohol as they cause / lead to Chronic Optic Neuropathy.
Smoking and alcohol are the risk factors for the glaucoma and cataract.

------------------------------------------

27
Chapter 3.3 General examination

General Examination - In the general examination gross visible physical abnormalities from hair to the toe are
to be noted. Besides routine `PICKLE` (pallor, icterus, cyanosis, clubbing koilonychia, lymphadenopathy, edema
and gait which are generally examined in medical cases) the following specific observations are to be made in
the eye examination while patient is entering into the OPD.

 Abnormal Head posture

• Ocular posture
• Facial Symmetry
• Forehead Furrows
• Eruption of vesicles on the forehead

Table 1.

Figure 3-1Face /Head Figure 3-2 Chin Figure 3-3 Head Figure 3- 4 Figure 3-5 RE in
turned left side Elevation tilt Convergent Position
RE Divergent position

Abnormal Head posture –

28
Table 2.

Figure 3-6 Right Figure 3-7 Figure 3-8 LE upper Figure 3-9 Figure 3-10
hyper tropia and Asymmetry lid Ptosis and furrows Eruptions on RE Proptosis
left hypo tropia of the face on the left fore head the eye lid and
Fore head

Facial symmetry – Normally the

Table 3
face is bilaterally symmetrical
Figure 3-11 Prominent Figure 3-12 LE Figure 3 - 13
Facial Asymmetry-is seen in maxillary area of the Lt Enophthalmos
Duane’s Retraction
 Duane’s Retraction Syndrome- side of face
Syndrome
The affected eye.
clinical signs in type –I
Duane’s Retraction Syndrome
are unilateral Hypoplasia of the
face, restriction of the
abduction, enophthalmos and
narrowing of the palpebral
aperture in adduction,

 Maxillary carcinoma – Prominent maxillary area due to maxillary carcinoma.

 Proptosis – Forward protrusion of the eye ball due to space occupying lesion in the orbital cavity
 Enophthalmos – Backward retraction of the eye ball
 Uniocular blepharo Ptosis

Furrows on the forehead – Normally no forehead furrows are seen. Forehead furrows indicate over activity of
the frontalis muscle.

 Seen in Old age

 Blepharo ptosis
 Brow ptosis.

29
Gait – Circumduction gait indicates hemiplegia and patients may be suffering from diabetes and hypertension
or associated with cranial nerve palsy etc.

History taking is followed by

Examination of the Ocular adnexa

 Examination of the Eye brows
 Examination of the eye Lids
 Examination of the Orbit
 Examination of the Lacrimal apparatus

Examination of the Anterior Segment of the eye

Behind the anterior segment is the posterior segment. Examination of the posterior segment is done with
Direct and indirect ophthalmoscope, +78 D, +90 D lens and B – scan.

Final Documentation
 Diagnosis
 Salient findings for the diagnosis to be written
 Investigations
 Plan of Treatment
 Differential Diagnosis.

30
Chapter 4 .1- Visual acuity (VA).Steps of Visual Acuity Demonstration

Competency OP-1.3
Visual acuity, color vision, light adaptations, Contrast sensitivity, Visual field sense, Stereopsis are the visual
functions of the eye. Visual acuity, color vision, Visual field sense is written in this chapter and Light
adaptations, Contrast sensitivity, Stereopsis are written in Clinical method 2.
Clinical Examination of the Visual acuity -
VA - It may be Central (Fovea)VA, or Peripheral VA -- The central VA is recorded by using the VA charts .
Peripheral VA is recorded by Visual field examination
The Visual acuity Examination is a basic clinical skill. It must be done on all patients and should be learned by
all medical graduates.
Visual acuity (VA) – Defined as the measurement of spatial resolving power of the eye at a physiological level
(Fovea and Retina) and interpretation at a psychological level (brain).

Visual acuity is also defined as the measurement of smallest image.

It is also defined as the estimation of the eye`s ability to recognize two discriminate points separately i.e., the
power to distinguish one object from the other.

Resolving power of the eye is based on the visual angle. The minimum visual angle is the angle subtended at
the nodal point of the eye by the physical dimensions of the object in the visual field.

The minimum visual angle or minimum resolving power of the eye

Table 1
is determined at the fovea. Fovea contains many cones. To see two
Figure4.1.-1
points separately, two cones must be stimulated while the cone in
between the two should remain un stimulated. The distance
between the two cones is 0.002 mm or 2 microns, (which
corresponds to the size of one cone). This is the minimum
resolvable distance. The minimum resolvable distance is the
tangent of angle that the retinal image makes at the nodal point of
the eye.

The minimum visual angle is calculated by dividing minimum resolvable Table 2. Figure4.1-2

distance by the distance from extremity of the cone to the nodal point
17.054 mm. i.e., 0.002 which is divided by 17.054 and the tan of it is= tan
24ʺ.14′). The minimum angle of resolution (MAR) is 30 seconds to 60
seconds of an arc, practically considered as 1minute of an arc.

1
Table 3. Figure4.1.-3
Minimal angle of resolution (MAR) is known in numerical
decimal form for eg VA 6/60, reduced to 0.1.The visual
angle can also be known by inverting Snellen’s acuity.Thus,
reciprocal of visual acuity is the resolving power/angle of
the eye. E.g.: 6/60 =60/6 = 10’.
The visual angle can be increased or decreased either by
increasing or decreasing the size of the object or distance
of the object from the eye.
Thus Visual acuity is based on a minimum angle of
resolution of 1 minute of arc at nodal point of the eye. To
appreciate an object, the object should have a minimum of 1 minute of an arc and to appreciate total object it
should subtend an angle of 5minutes of an arc at the nodal point.
Interpretation of VA. The visual acuity is expressed as difference/ ratio betweennormal VA and abnormal
VA.
 E.g., Based on the numerical form - Normal VA 6/6 which is reduced to1.And if VA is 6/60 which is
reduced to decimal form is =0.1. Thus, the difference /the ratio between 6/6 and 6/60 is = 1: 0.1 Thus
VA 6/60 less vision by ten times when compared to 6/6.
 E.g.,Based on visual angle - The minimum of visual angle of 6/6 is 1’ of an arc .And if VA is 6/60, the
minimum visual angle of 6/60 is 10’ of an arc. (The visual angle is calculated by reversing the VA.
 Thus the visual angle of VA 6/6 is= 1’, VA of 6/60 is 60/6 =10’). The difference/ratio between 1’ for
normal visual angle and 10’ visual angle for6/60 is 10’ of an arc. Thus VA 6/60 has 10 times has
more visual angle than the required 1’ of an arc.

Finally, the interpretation of VA is expressed in the ratio between normal visual angle and abnormal visual
angle.
Resolving power at physiological level depends on
 The Dioptric power of the eye,
 Clear aqueous and vitreous,
 Normal macula and fovea
 Minimal visible stimulus – Ideal 20 to 40 Foot candles. (Minimum required is 3 Foot candles) or 100
lumens per square ft.
Interpretation at a psychological level depends on normal functioning of central nervous system.

The central VA is recorded by using the VA charts

 Snellen’s chart - forliterates.
 ETDRs Charts (Early Treatment for Diabetic Retinopathystudy)
 Log MAR charts
 Landolt broken rings chart /C chart - for illiterates

2
 E chart - for children (2 to 3 years)
 The principle of Snellen’s chart is in conformity with the Visual acuity of minimum angle resolution of 1
minute of arc at nodal point.
 The letters / optotypes are written in black color on white opaque panels and fitted on illuminated
rectangular boxes. There is total 28 letters arranged in 7 rows. The sizes of the letter in successive rows
from top to down are gradually diminishing in size in the ratio of 1:10, 1:6, 1: 4, 1 :3,1:2,
1: 1.5, 1:1. i.e., the top letter is 10 times larger and successive row of letters are larger by 6, 4, 3 ,2,1.5, 1
when compared to the seventh-row size letter.

 The successive row of the Snellen letter lines from top to the bottom is represented by the numbers in
meters distance 60, 36, 24, 18, 12, 9, 6, The letters are so arranged that the top size letter of Snellen’s and
successive rows at 36, 24, 18,12, 9, 6 meters distance will subtend an angle of 5 minutes and each
component of optotype will subtend a minimum angle of 1 minute at the nodal point of the eye.

 In order to analyze constituent parts of an object completely, the eye must able to resolve each
constituent down to the limit of minimum angle of resolution of 1 minute of arc at nodal point.

(The degrees, minutes, seconds are the astronomical units to calculate the objects in the space. One degree
is 360 minutes. Each minute is dividesinto 60 seconds of an arc)

Clinical examination of Distant central Visual Acuity.

 The Central Visual acuity examination is done both for distant and near vision

The distant VA is examined in five stages

 The distant VA examination is done with illuminated Snellen’s chart
 Reduced distance VA examination (This stage of examination is done if the first letter of Snellen chart
is not visible).

 CF (Finger counting) - Finger counting examination (This stage of examination is done if reduced
distance VA examination is less than 1 meter)
 HM - Hand Movements examination (This stage of examination is done if Finger counting examination
is less than counting fingers close to face)
 PL - Perception of light and PR (Projection of rays) (This stage of examination is done if HM
examination is absent)

The distant Unaided VA is examined with Snellen’s chart

3
 The participant is comfortably seated in front of the illuminated Snellen’s chart at six meters distance or
20 feet distance. (If a six meters long room is not available, the participant is seated in front of a plane
mirror at 3 meters distance and the Snellen’s illuminated board is kept behind the participants head. The
plane mirror forms an image of Snellen board behind the mirror at 3 meters and thus the distance
betweenSnellen’s board and mirror is 3 meters and the distance behind the mirrorand Snellen’sboard
image is 3 meters and total6 meters distance room is made). The six meters are taken as the rays that are
coming from Six meters distance are parallel and there is no play of accommodation at that distance by
the eye.

 A trial frame is kept in front of the eyes. An occluder is preferably kept in the left eye (conventionally) to
block the vision of that eye and the participant is asked to read the optotypes on the Snellen’s board with
right eye.

Table 4 . Figure4.1.-4

The participant is asked to read the Snellen rows from the top to the seventh row. The visual acuity is
recorded in fraction. The numerator is the distance between the participant and the Snellen chart and the
denominator is the size of the Snellenchart that the participant reads. Thus, the successive rows of visual
acuity are documented as 6/60, 6/36, 6/24, 6/18, 6/12. 6/9, 6/6.

Normal central distant visual acuity is 6/6.

If the participant is not able to read 60 meters size Snellen’s letter/ opto type i.e., the top optotype of
Snellen , then the next stage of VA is reduced distance VA examination.
Reduced distance VAexamination (Unaided)
If the participant is not able to read the 60 size Snellen’s letter/ optotype i.e., the top optotype of
Snellen’s then the distance between the participant and the Snellen’s is reduced from 6 meters to 5, 4, 3,
2, and 1 meter and graduallymove the participant towards Snellen’s which is difficult to perform for
oldpeople.Instead take a first size letter of Snellen’s and the surgeon move towards the participant and
show at 5, 4-, 3-, 2-, and 1-meter distance to the participant. The farthest point at which he can recognize
is determined and recorded accordingly, i.e. 5/60, 4/60, 3/60, 2/60, 1/60.

If participant is unable to recognize even at 1-meter distance then next stage of examination is Finger
counting examination.

4
Finger counting examination (Unaided)
Finger counting examination is done at a distance of 3 meters from the participant. One eye is closed. The
stretched fingers are shown at a distance of 3, 2, 1 meter and ask the participant to count the fingers. The
farthest distance at which one counts the fingers is documented as CF 3 meters, CF 2 meters, CF 1 meters, and
CFCF (Counting fingers close to face).

Each size of the finger will subtend an angle of 1 minute at the nodal point and thus in conformity of principle
of minimum angle of resolution at the nodal point.
If the participant is not able to count fingers close to face then the next stage of examination is HM (Hand
Movements).
Table-5

HM (Hand Movements) Unaided

If participant is unable to count the fingers, Hand movements are shown close to participant face, if one
perceives the hand movements then visual acuity is recorded as HM.
If the participant is unable to recognize the Handmovements,then next stage of examination is Perception of
light (PL) and Projection of rays (PR).

PL and PR examination (Unaided)

If the participant is unable to perceive the Hand movements,then ask the person to see a distant object,then a
light is flashed in front of one eye while other eye is closed, and the patient is asked whether he/she can
perceive the light.If the participant perceives the light it is documented as PL +. If the participant is not able to
perceive light, it is recorded as PL– sign. The pupillary light reaction is also simultaneously examined. If the
participant is not able to express the perception of light, pupillary light reaction will help whether PL is
present or absent.

The Perception of light test is followed by the Projection of rays test. Light is Projected to the four quadrants
of the retina. For the upper quadrant of the retina, the light is projected from the lower side, for the lower
quadrant from the upper side, for the lateral quadrant from the medial side and for the medial quadrant

5
from the lateral side. The quadrant where he perceives light is documented as PR+ sign, the quadrant where
he is not able to perceive light is documented as PR– sign.

If the participant perceives light in all quadrants it is recorded as PR + in all quadrants

If the participant is unable to perceive PL and PR theperson is considered as blind.
 The Perception of light test is for maximum Central cone function,
 The Projection of light test is for maximum rods function at the retinalPeriphery.
Table-6

Pinhole Examination
If, at any point of time during the visual acuity examination it is found that the vision is less than normal a pin
hole is kept in the trial frame and the participant is asked to read the Snellen’s chart again. If the participant
improves reading of rows of the Snellen’s through the pinhole, it indicates that the dioptric component is
defective and requires refractive error correction. Thus, the pinhole examination differentiates refractive
errors from the diseases of the eye.

Mechanism of Pin Hole

The peripheral rays are cut off in the pin hole The light rays which pass through the pinhole passes through the
centre of cornea and centre of crystalline lens do not participate in refraction i.e., will not bend and fall
straight on the fovea which represents maximum central VA. The optical principle is that , the light rays
passing through the centre of optical medium will not participate in refraction i.e the light rays will not bend
and

6
After recording the central Distant visual acuity of right eye, the Left eye Distant Visual acuity is to be recorded
in the same way. Finally visual acuity of both eyes with out occluder is recorded. Both eyes VA is greater than
the single eye visual acuity.
Table 7 .
If the subject has a spectacle, repeat the VA recordings after wearing spectacle.

Examination ofVisual Acuity for Near (NV). (Central visual acuity for Nearby)
The central Distant visual acuity examination is followed by Visual acuity for Near

rd
Near vision is tested at a distance of 33cms (1/3 of a meter.)
 Near vision charts are called Snellen charts or Jaeger’s charts
 These charts are also prepared according to the principle of Snellen.
 Various paragraphs showing different sizes of letters are marked with different numbers in Snellen’s
N6, N8, N10, N12, N18, N24, N36. The paragraph which the person reads is recorded.
Table 8

Log MAR acuity –Bailey Lovie Chart –It is more accurate than Snellen’s chart.
Log MAR is simply the log of MAR (MAR is expressed in log).Snellen’s acuity is inverted and reduced to express
MAR and this MAR is expressed in Log units.
 At 6 meters, 6/6 letter subtends maximum angle of 5 minutes at nodal point and each limb of the letter has
an angular width of 1 minutes i.e. MAR of 1 minute is needed for resolution. And log MAR of 1 minute is
0.00.
 A 6/12 letter subtends an angle of 10 minutes of arc at the nodal point and each limb of the letter has an
angular width of 2 minutes so MAR of 2 minutes is needed for resolution and log MAR of 2 minutes is 0.301
(0.30).
The Total letter Snellen’s visual acuity is 6/60 subtends an angle of 50 minutes of arc at the nodal point MAR is
10 and log of MAR 10 is 1.

Table 9

7
Normal Visual acuity for
Table10.
Nearins N6 size letter
Thus, the chronology of Figure4.1-8

central visual acuity

documentation for distance
is as follows for each eye
Central Distant Visual acuity
 Snellen’s recording -
6/6, 6/9, 6/12, 6/18,
6/24, 6/36, 6/60
 Reduced distance visual acuity examination - 5/60, 4/60, 3/60, 2/60, 1/60. This examination should be
done only if the participant is unable to read the Snellen’s 6/60 size optotype. This examination will help
to estimate the visual acuity of 5 metres. (5/60) and 4 metres (4/60).
 Counting fingers Examination - CF 3 meters, CF 2 meters, CF 1 meter, CFCF. This examination should be
done only if the participant is unable to tell 1/60 in reduced distance visual acuity examination.
 HM - This examination should be done if the participant is unable to tell CFCF.
 PL and PR.examination - This examination should be done if HM are absent.
Visual Acuity Examination for Near vision (NV) (Central near Visual acuity)
 Near vision examination -N 6, N8, N10, N12, N18, N24, N 36.
Clinical skills to be practised
 Distant Visual Acuity examination
 Near vision Visual Acuity examination
 Pin hole Examination
OSCE -Visual acuity Charts / Near vision Charts -Snellen’s, Landolt’ s, E charts
Instruments required for VA examination – Visual acuity charts, Near vision Charts, Occluder, Pinhole,Trial
Frame, Torch light. ----------------------------

8
4.2. Visual functions of the eye - Visual Field (VF) sense /Field of Vision.
Competency --Physiology – PY 10.20. Demonstrate the testing of VF/ Field of vision in volunteer/simulated
environment.
Harry Moss Traquair (1875 – 1954) ScottishOphthalmologist defines visual field (VF) as an Island of vision in a sea
of darkness (Blindness). It is also described as the visible area
surrounding the fixing target. Figure 16.1 Figure 1.6 .2

The normal configuration of the visual field is three- Two dimensional VF Three dimensional VF
dimensional island of hill of vision with steeper nasal slope island of hill of vision

than temporal. It is not a flat surface. The tip of the hill is

foveola where the visual acuity (VA) is sharpest at that point
and the VA decreases progressively to the periphery.

VF is measured in degrees and the unit is an isopter. An

isopter is an area of retina bounded by a contour/circle and the circles are drawn from fovea as a referral point.
Any area of the retina in a given degree of an Isopter has an equal sensitivity.
The Optic disc has no elements of photo receptors of vision and it is called physiological blind area in the visual
field. It is situated at 10 to 20 degrees isopter temporal to the fixation in the visual field.

Divisions of the visual field - The visual field is divided as

 Central field and Peripheral field
 VF is divided into Nasal half and Temporal half by a vertical meridian passing through the fovea. The
nasal field is divided into superior nasal and inferior nasal. The temporal field is divided into Superior
Temporal and inferior Temporal VF.

Figure 1.6.3 Central visual field Figure1.6. Peripheral Visual field Figure 1.6. 5
The extent of uniocular central visual The extent of Uniocular peripheral The extent of Binocular visual field is
field – 30 degrees Isopter Visual field is beyond 30 degrees 120 with 40 degrees temporal crescent
Isopter on the sides

44
VF is divided into Superior half and Inferior half by a horizontal meridian passing through the fovea.

The extent of visual field depends on the color of the target. The extent of visual field with a white target will be
more than the red and the green targets i.e. the extent of VF is lesser with red and the green targets than white
target.
The extent of Uniocular central visual field with a white Target
The extent of uniocular central visual field with a white target is 30 degrees Isopter from the fovea

The extent of uniocular Peripheral Visual field with a white Target

• The Peripheral field is beyond central 30 degrees isopter.

The extent of Uniocular peripheral Visual field

 Superiorly is 50 degrees isopter because of the limitation by the frontal eminence
 Nasally 60 degrees isopter because of the limitation by the nasal bridge ,
 Inferiorly 70 degrees Isopter because of the limitation by the maxillary bone
 Laterally 90 to 110 degrees isopter because of no limitation by the temporal bone.

Binocular Visual field -Binocular visual field is the visual field seen simultaneously with both eyes
The extent of Binocular visual field is 120 degrees with 40 degrees temporal crescent on the sides.

Perimetry-
Recording of visual field is called Perimetry.
Perimetry is finding the boundary of an area. To record the visual field, a target is required. The target must
have a color i.e. white or primary colors i.e red, green, blueand also the target must have
illumination/intensity.

Perimetry is based on two Principles

i.e. Kinetic Perimetry and Static Perimetry.

Kinetic Perimetry: It is a method of detecting a visual field defect by manual technique

Principle of Kinetic Perimetry -It involves the presentation of a moving stimulus of known luminance or intensity
from non-seeing area to a seeing area until it is perceived.

• It is a two-dimensional assessment of boundaries of a hill of vision.

45
• It is qualitative perimetry.

Figure 1.6. 6 Figure 1.6. 7 Figure 1.6. 8 Figure 1.6. 9 Figure 1.6. 10
Confrontation Method AmslerGrid Bjerrum’s screen Lister’s perimeter Goldmann’s
(Arc perimetry) perimeter
(Bowl Perimetry )

Methods of recording of Kinetic perimetry

• Confrontation Method – Bed side method of perimetry

• Central 10 degrees VF is tested by Amsler grid
• 30 degrees central VF is tested by Bjerrum’s screen which is Straight screen /Tangent screen. Recording
perimetry with a straight screen is called campimetry.
• Arc perimetry - Lister’s perimetry (Refer text Book)
• Bowl Perimetry - Goldmann perimetry (Refer text Book)
Confrontation Method –
Bedside clinical examination of visual field is recorded by Confrontation test
• Gross visual field defects can be identified by a simple bedside Confrontation test.
• Considering the visual field of the surgeon/examiner is normal, the visual field of the participant is
compared with the surgeon’s visual field.

Method of recording of Confrontation test -

• The surgeon conducting the visual field test is seated 60cms away, opposite to and at the head level of
the participant.
• The surgeon closes his right eye with the palm of the hand and the participant is asked to similarly
close the left eye, and the participant fixes the left eye on the surgeon’s right eye.

46
• The surgeon then brings his finger halfway between both of them from the periphery i.e.from non-seeing
area and the participant is asked to indicate as soon as he can see the surgeon’s finger.
• If the surgeon and the participant see the finger at same time, then the participant’s visual field is
considered to be normal.
• This is repeated in all meridians and thus the sensitivity and extent of the visual field of that eye is
recorded.
• The same procedure is repeated with the other eye.
• The visual fields of both the eyes are compared to say whether it is normal or abnormal.
• If any abnormality in visual field is noted, further Perimetry tests are done.
Static Perimetry Figure 1.6. 10 Figure 16. 11
Principle of Static Perimetry: Instruments for Static Visual field chart of
Perimetry -Humphrey’s Static perimetry
Patient’s retinal sensitivity data is compared with age automated perimeter
matched mean normal sensitivity data and
difference is calculated statistically.

• Static Perimetry is a computerized method of

recording VF.
• It is quantitative perimetry.
• In a static Perimetry the stimulus is Non- moving
• It is a three-dimensional assessment of the .
predetermined area of VF. Peak of the island of
hill of vision , is point of highest visual acuity - fovea
• Measures the threshold of light perception at a given point
• Assesses differential light sensitivity of a predetermined area of the VF
• It gives sensitivity in terms of size, shape, depth, and progression.

Advantages of Static Perimetry over Kinetic Perimetry

• Static Perimetry is Quantitative,
• It is a Computerized technique
• Previous Data can be retrieved from the hard disc of the computer for comparison of the previous VF with
the present visual field for progression of VF defect.
• Reliability of the test can be assessed by the false positives and false negatives.

47
Disadvantages of Static Perimetry

• Person must give a correct date of birth, otherwise the sensitivity data of the participant is compared to
the wrong sensitivity data present in the computer.
• Person must be literate, alert, and able to understand the computer commands.

Terms used to describe VF defect of retina

The terms used todescribe the visual field defectsof the retina is called Scotoma.

Scotoma is defined as defect in the retina

 Scotoma - The retinal sensitivity defect in in a particular isopter surrounded by a seeing area is called
Scotoma. Scotoma may be Absolute scotoma,Relative Scotoma, Positivescotoma, Negative scotoma.
 Absolute scotoma - An area of total sensitivity loss in the retina in an isopter in which even the largest
target and brightest illumination cannot be perceived.
 Relative Scotoma: A partial loss of sensitivity in a particular isopter of the retina. A scotoma is
identified in an isopter with a particular size of a target and particular illumination of a target.
Targets below that particular size and illumination cannot be identified, but targets above that particular
size and illumination can be identified.

Positive scotoma: The subject always experiences a non-seeing area in a particular isopterin the visual
field E.g.: Age related macular degeneration (ARMD)

 Negative scotoma: Even though there is a blind area (Non sensitive area) in the retina, the subject will not
see the blind area in the visual field E.g.: Optic disc.

Causes of VF defects are - Visual field defects of the retina are seen in
 Glaucoma - Follows the arrangement of nerve fibers in the retina (Nerve bundle defect)
 Retinitis pigmentosa
 Retinal detachment
 Optic Nerve diseases – .Visual field defects of Optic nerve in retina

Terms used to describe VF defects of the visual pathway

 Anopia – Complete loss of vision in the VF
 Hemianopia – Complete loss of half vision in the VF
 Altitudinal Hemianopia - Complete loss of half vision above or below the horizontal raphe of the VF

48
Visual fields in Cataract –In immature cataract the extent of peripheral field is reduced and in total cataract the
extent of both central and peripheral fields are absent ,because the opacity masks the retina, however the
sensitivity of retina is normal.

For the details of the instrumentation, methodof recording and interpretation, please refer the standard text
books.

Diagrams - Charts
 Central visual field charts
 Peripheral visual field Charts
 Binocular visual field Charts

Clinical skills – Recording of VF by confrontation Method, Bjerrum’ method, Humphrey’s method.

-------------------------------------------

49
4.3 Clinical examinations of Visual functions of the Eye -- Colour vision

Competency OP 1 .3

The theory part of colour vision is explained in symptomatology chapter.

Tests for Diagnosis of color vision –Commonly – Ishihara’s isochromatic color vision charts Identifies red and
green color deficiencies.

Color appreciation is the function of cones, hence clinical examination of the color sense is to be done in
photopic vision.

Ishihara’s isochromatic color vision Plates - Table 1.

The color vision book consists of 38 plates. Figure 4.2-1 Figure 4.2-2

The chart is kept at a distance of 33cms and the

person is asked to identify the
numbers in with one eye closed.
Normal persons areTrichromatic and
will identify the numbers written in
primary colors. The persons with red
deficiency will not be able to identify
red numbers/color and green deficiency persons will not be able to identify greennumbers. Both red
and green deficient persons will not identify red and green colors. These charts are used to screen
congenital and acquired red and green deficiency.

Table 2 . Interpretation of six screening Plates

Persons with normal Color vision Persons with red and green CV Persons with total CV blindness
read as blindness read as read as

Plate 1 12 12 12

Plate 2 29 70 x

Plate 3 5 2 x

Plate 4 6 x x

Plate 5 7 x x

Plate 6 x x

In this chapter Visual acuity, color vision is discussed. The visual field sense is discussed in chapter 1(Anatomy
and Physiology topic) Light adaptations, Contrast sensitivity of the visual functions of the eye see in Clinical
module 2 --------------

50
Chaper 5 Practical refraction of the eye
5.1 Clinical Refraction of the eye – Basic Class

Basic class –

It is necessary to know the basic optical instruments to understand the refraction of the eye

Optical instruments used for refraction of the eye and elementary optic principles , physical characters,
identification and uses of each is described in this chapter.

The basic instruments required for refraction are present in a trial box which contains Spherical lenses –
biconvex and Biconcave lenses , Cylindrical lenses – biconvex and biconcave cylinders , Mirrors -Plane and
concave mirrors,Occluder, pinhole ,Stenopic slit, red and green glasses , Prisms and trial frame .

Spherical lenses:
The spherical lens is part of a sphere , hence it has equal power in all meridians and parallel rays are brought to
a pin point focus at focal point.The unit of spherical lens is Diopter (D) . D =1 meter(100 cm ) ÷ f
The commonly used spherical lenses for ophthalmic practices are convex and concave lenses. On rotating the
lens there is no distortion of the image of the object, indicating the sphere. The optical center is on the curved
surface where optical axis cuts it. The lenses are combination of
multiple prisms
Table -1 .Figure 5-1

The convex lenses -

The types of convex lenses are biconvex,Plano convex or Meniscus
lenses .The biconvex lens is a combination of two prisms with its
bases against each other. The light rays emerging out of convex lens
will converge towards the base of the prism . Hence the biconvex lenses are called converging lenses
.Spherical convex lenses are indicated with the prefix + .
The concave lenses–
Table-2. Figure 5-2
Types of concave lenses are biconcave, Plano concave or meniscus
lenses The bi concave lens is combination of two prisms with it
apexes against each other. The light rays emerging out of concave
lens will be divergent towards the base of the prism . Hence the
biconcave lenses are called diverging lenses .The spherical concave
lenses are indicated with the prefix– sign (Negative sign).

Meniscus lenses also act as Biconvex, Biconcave lenses but the lens is considered as Convex, Concave based
on which surface is more curved. In Meniscus lenses the optical center is out side of the lens.

1
Table -3 . Biconvex Lenses --How to identify the biconvex lens.
 Hold the lens close to the eye ball
 Select the distant object
 Move the lens side to side and up and down and rotate the lens
 Observe the movement of the image of the object - i.e
whether the image is moving with or against the movement of
the lens
 In the convex lens the image moves against the movement of
the lens because the image formed is inverted image
The image is magnified
 The central part of Convex lens is thick and peripheral part is Figure 5-3
thin.
 On rotation of the lens
there is no distortion of
the image

Table -4 . Uses of Spherical Biconvex lens

Figure 5-5 Abraham Lens - +64 D
Abraham Lens(with slit lamp) used for YAG
capsulotomy for after cataract (PCO), laser
Figure 5-4
Iridotomy for pupillary block in PACG .
 For the correction of Hypermetropia
 For correction of Presbyopia
 For correction of Aphakia.
 Most of the IOLs are Biconvex LenseFor correction of Compound
hypermetropic astigmatism, Mixed astigmatism
Used as Objective lens in Slit Lamp and
 Used in Low vision correction. surgical Microscope ,
 + 20 D, + 30 D lens used as an objective lens in indirect Figure 5-6 Direct Ophthalmoscope .
ophthalmoscopy procedure
 + 78, +90 lens used with slit lamp for stereoscopic view of optic
disc in glaucoma and disc edema in papilloedema and
Maculopathy in diabetic retinopathy.

2
Table -5 . Concave lens - How to identify the concave lens.
 Hold the lens close to the eye ball
 Select the distant object
 Move the lens side to side and up and down
and rotate the lens
 Observe the movement of the image of the Figure 5-7

object i.e whether the image is moving  Magnification – the image is minified

with or against the movement of the lens  The central part of Concave lens is thin and peripheral

 In the concave lens the object moves with part is thick.

the movement of the lens because the

image formed is erect image

Table -6 Uses of concave lens

For correction of Myopia Figure 5-8 - 55D lens is called Hruby’s lens. Used with slit lamp to examine
the posterior vitreous phase and posterior pole of the retina .
-55 D lens is used as contact lens with surgical microscope in the
vitreo retinal surgeries

• For correction of Compound Myopic

In the Gonioscope and in Goldmann three mirror contact lens
astigmatism
the lens is – 55 D .
• For correction of Mixed astigmatism
•

Table -7 . Comparison of Spherical lenses

Character of the lens Spherical – Convex Spherical –Concave

Movement of the lens with the The image moves against the The image moves with the movement
image of the object movement of lens of the lens.

Size of the image Magnified Minified

Edge of the lens Thin Thick

Thickness of the lens Thick at the center Thin at the center

Image Inverted image Erect image

3
Cylindrical Lenses
Cylindrical lens is a part of the cylinder and has power in one meridianand parallel rays are brought to focus as
a line focus
How to identify the cylindrical lens Table -8.
 The lens has two axis marks at the edge of the lens Figure 5-9
 Draw an imaginary line connecting the two axis marks
 Hold the imaginary line of the lens close to the eye , select a
distant object and move the lens along the imaginary line and
perpendicular to the imaginary line
 The image will not move along the imaginary line but image
Axis
moves perpendicular to the imaginary line.
Mark
 If the perpendicular movement of the image is with the movement
of lens it is biconcave cylinder and if it is against the movement of
lens it is Biconvex cylinder.
 On the rotation of the lens image is distorted

Table -9. Uses of Biconvex cylindrical and Biconcave cylindrical lens

Uses of Biconvex cylindrical lens Uses of Biconcave cylindrical lens

• For correction of Simple Hypermetropic • For correction of Simple Myopic

astigmatism astigmatism
• For correction of Compound • For correction of Compound Myopic
hypermetropic astigmatism astigmatism
• For correction of Mixed astigmatism • For correction of Mixed astigmatism

Plane mirror -How to identify a plane mirror – Table -10.

One side of the plane mirror has a reflecting surface and other side is non reflecting Figure 5-10
surface . Plane mirror
The plane mirror optical characters of the image :

 The size of the image is equal to the size of the object

 Erect image
 Laterally reversed image – i.e. if one is combing their hair with right hand the
observer sees as if the subject is combing with left hand.
 The rays that are coming from the image of a plane mirror are far behind the mirror and are virtual.
When the plane mirror moves up the image moves against to the movement of the plane mirror ,
i.e the image moves down .

4
 The rays reflected from the plane mirror are divergent
 The distance between object and the mirror is equal to the distance between the mirror and the
image . This principle is used to convert the room distance from 3 meters to six meters when 6 meters
room is not available for visual acuity assessment by Snellen’s chart.
 For retinoscopy procedure – Plane mirror is commonly used as retinoscope
 The plain mirror is used to reflect the light from a light source on to the area interest i.e in a
retinoscopy procedure the light is reflected from a light source to the dilated pupil, same in a slit
lamp, Gonioscope, Goldmann three mirror contact lens , direct and indirect ophthalmoscope.
 Plain mirror examination at 1 meter distance is one of the techniques to confirm the diagnosis of
cataract.

Concave mirror:
If the object is farther away from the mirror than the focal distance, the image formed is real ,
inverted and situated in front of the mirror
 It is important to know that , if the concave mirror is further away from its focal distance
, the image fomed is real , inverted and situated in front the mirror. The focal length of the
concave mirror used In the concave retinoscope is 25 cms and commonly used distance for
retinoscopy is 1 meter.
 The rays that are coming from the image of a concave mirror are in front of the mirror
and the image is real and inverted . When the concave mirror moves up the image moves
with the movement of the concave mirror i.e image moves up.
 The real and inverted rays move against to the movement of the plain mirror.

Prisms :
The lens is a combination of multiple prisms .The two prisms with base against each other will act as a
convex lens and the light rays which exits through it , will converge towards the base of the prism.
The two prisms with apex against each other will act as concave lens and the light rays which exits through it
will diverge towards the base of the prism.

Unit of Prism is Prism Diopter

One cm displacement of an image towards the apex when the object is kept at a distance of 1meter away
from the prism is called Prism Diopter .
• Two prism diopters of displacement is equal to one degree of arc
Calculation of prism Diopter - The power of the prism is equal to apparent displacement in centimeter
divided by object distance in meters.

• Eg - Object distance=25cm; deviated by 3cm

Power=3/0.25m=12prism diopters.

5
Table -11. Description of the Prism
• Prism has two plane surfaces inclined to Figure 5-11
each other
• The line at which the two surfaces meet
together is called apex, while the surface
opposite to the apex is called base.
• Refracting angle of a prism is the angle
• The total amount of deviation is called ANGLE OF
between two surfaces.
DEVIATION.
• Axis of prism is line bisecting the apical
• Image formed by prism is erect, virtual
angle.
• When prescribing prism orientation is indicated
• The light passing through the prism is
by the position of base, e.g. base-in /base-
deviated towards the base and the object
out/base-up/base-down.
seems to move towards the apex.

Table -12 . Identification of the Prism (To find out the lens has a prismatic value or not )
• Hold the lens near to the eye and select a distant straight Figure 5-12
line and see the selected line through the lens. If the lens has
a prism, the image of the line will move towards the apex
and parallel to the base. (Continuity of the line is broken) .
• Now rotate the prism by 90 degrees , there is no deviation of
the image
• Since the line appears to be deviated towards the apex,we
will get to know the direction in which side the apex of
prism lies.

Guidelines for prescribing the prisms

The apex of the prism is kept towards deviation of the eye is the key to remember . i.e . base of the
prism is kept opposite to the deviation of the eye .
In eso deviation – the apex of prism is towards eso deviation i.e base out prism for correcting the eso
deviation

In exo deviation – the apex of the prism is towards exo deviation i.e base in prism for correcting the exo
deviation.

Split the amount of correcting prism equally between both eyes.

6
Table -13 . Uses of Prisms in Ophthalmology

Diagnostic uses Therapeutic uses Optical use in instruments

Objective measurement of the To improve fusional reserve in Used as reflectors of light in

angle of squint by prism bar cover patients with convergence ophthalmic instruments like slit
test, Krimsky test insufficiency lamp. Surgical microscope,
Gonioscope, Keratometer,
applanation Tonometer and
Synaptophore , etc.

Subjective measurement of the Used in the treatment of diplopia in

angle of squint by Maddox rod phorias

Measurement of fusional reserve

4 D prism test for diagnosis of

Microtropia

For Diagnosing malingering

Table -14 . Prisms available for clinical use
Prism bars – Figure 5-13
Available as horizontal prism bars and vertical prism
bars
Horizontal prism bars are used for Horizontal
squints and vertical Prism bars are used for vertical
squint
Loose prisms – Figure 5-14
If the angle of the squint measurement exceeds the
prism strengths available in prism bar then loose
prisms are added over and above the prism bar
strength

Mounted prisms – Fresnel Prisms –

Prisms available in the trial set These are thin sheets of plastic prisms which can be stuck
to the patient glasses
Decentering of the spectacle lens acts as a prism Spectacle mounting of Prisms –
The decentering distance from the optical center X When the patient does not require spectacle correction,
dioptric power of the lens = strength of the prism prisms can be mounted in the spectacle.

7
Trial frame  The trial frame is adjustable anteriorly
There are three slots in trial frame . posteriorly , and lateral positions.
 The slot nearer to the eye is for spherical  It has nose pad to sit comfortably on the nose.
lenses for presbyopia correction. Figure 5-15
 The middle slot is for spherical lenses for
correction of distance vision , to keep
occluder, pinhole, to keep lenses for
retinoscopy, PMT.
 The outer slot is for cylindrical correction

Table -15 . Trial set / Box

Trial set / box – Consists of
 Two rows of Biconvex spherical Figure 5-16
lenses
 Two rows of Biconvex Cylindrical
lenses
 Two rows of Biconcave spherical
lenses
 Two rows of Biconcave Cylindrical
lenses
 Trial frame
 Occluder
 Pin hole
 Stenopic Slit
 Maddox rod
 Red and Green glasses
 Prisms

8
Table -16. Figure 5-17 Pin hole Figure 5-18 Figure 5-19
Occluder Pin hole
Occluder Pin hole Stenopic Slit – uses
Uses of occluder - examination To identify the axis
In visual acuity Differentiate the of the cylinder
examination to block refractive errors
the vision of the eye. from the diseases
of the eye

Table -17. Figure 5-21

Figure 5-20
Red and Green glasses –
Maddox Rod uses
• Macular function Uses of Red and Green glasses - Used to

• To find phorias know the anomalies of binocular single

vision like diplopia, suppression,
stereopsis, FRIEND test, Worth four dot
test

Table -18 RED FIN

The person able to see RED in red The person able to see FIN in green
colors Indicates LE suppression color Indicates RE suppression
Test
Keep the red and green glasses in
front of the eye, Red in front of the
right eye and green in front of the
left eye and the person is asked to
read FRIEND which is present at the
bottom of the illuminated
Snellen’sdrum. If the person read
FRIEND at a time then binocular
single vision is present

9
Worth four dot test.
 Worth four dots present at the bottom of the illuminated snellen’s drum . The four dots are – One
Red,Two green and one white / Amber color /mix of red and green
 The person has to wear red and green glasses in front of the eye, Red in front of the right eye and
green in front of the left eye and the person is asked to identify the colors of worth four dots
 If the person says more than four dots it indicates Diplopia
 If the person sees green colors only it indicates RE suppression
 If the person sees red colors only it indicates LE suppression

Table -19
Red and green Worth four Wearing red More than four Three green Two red colors
glasses dots and green colors Indicates colors indicate indicate LE
diplopia RE suppression suppression

Bagolini striated glasses

Two glasses has scratched striations which are placed at 45 degrees in RE and 135 degrees in left eye . These
glasses are kept in front of an eye . Each eye will perceive an oblique streak of light perpendicular to axis of
striations.
Interpretation of Bagolini striated glasses

Table -20

-------------------

10
Chaper 5 Practical refraction of the eye
(Chapter 5 consists of 5.1 Clinical Refraction of the eye – Basic Class . 5.2 Clinical examination of Refraction ,
5.3 Post Mydriatic test)

5.1 Clinical Refraction of the eye– Basic Class

Basic class –

It is necessary to know the basic optical instruments to understand the refraction of the eye

Optical instruments used for refraction of the eye and elementary optic principles , physical characters,
identification and uses of each is described in this chapter.

The convex lenses -

51
Table -3 . Biconvex Lenses --How to identify the biconvex lens.
 Hold the lens close to the eye ball
 Select the distant object
 Move the lens side to side and up and down and rotate the lens
 Observe the movement of the image of the object - i.e
whether the image is moving with or against the movement of
the lens
 In the convex lens the image moves against the movement of
the lens because the image formed is inverted image
The image is magnified
 The central part of Convex lens is thick and peripheral part is Figure 5-3
thin.
 On rotation of the lens
there is no distortion of
the image

Table -4 . Uses of Spherical Biconvex lens

52
Table -5 . Concave lens - How to identify the concave lens.
 Hold the lens close to the eye ball
 Select the distant object
 Move the lens side to side and up and down
and rotate the lens
 Observe the movement of the image of the Figure 5-7

object i.e whether the image is moving  Magnification – the image is minified

with or against the movement of the lens  The central part of Concave lens is thin and peripheral

 In the concave lens the object moves with part is thick.

the movement of the lens because the

image formed is erect image

Table -6 Uses of concave lens

• For correction of Compound Myopic

In the Gonioscope and in Goldmann three mirror contact lens
astigmatism
the lens is – 55 D .
• For correction of Mixed astigmatism
•

Table -7 . Comparison of Spherical lenses

Character of the lens Spherical – Convex Spherical –Concave

Movement of the lens with the The image moves against the The image moves with the movement
image of the object movement of lens of the lens.

Size of the image Magnified Minified

Edge of the lens Thin Thick

Thickness of the lens Thick at the center Thin at the center

Image Inverted image Erect image

53
Cylindrical Lenses
Cylindrical lens is a part of the cylinder and has power in one meridianand parallel rays are brought to focus as
a line focus
How to identify the cylindrical lens Table -8.
 The lens has two axis marks at the edge of the lens Figure 5-9
 Draw an imaginary line connecting the two axis marks
 Hold the imaginary line of the lens close to the eye , select a
distant object and move the lens along the imaginary line and
perpendicular to the imaginary line
 The image will not move along the imaginary line but image
Axis
moves perpendicular to the imaginary line.
Mark
 If the perpendicular movement of the image is with the movement
of lens it is biconcave cylinder and if it is against the movement of
lens it is Biconvex cylinder.
 On the rotation of the lens image is distorted

Table -9. Uses of Biconvex cylindrical and Biconcave cylindrical lens

Uses of Biconvex cylindrical lens Uses of Biconcave cylindrical lens

• For correction of Simple Hypermetropic • For correction of Simple Myopic

Plane mirror -How to identify a plane mirror – Table -10.

One side of the plane mirror has a reflecting surface and other side is non reflecting Figure 5-10
surface . Plane mirror
The plane mirror optical characters of the image :

 The size of the image is equal to the size of the object

 Erect image
 Laterally reversed image – i.e. if one is combing their hair with right hand the
observer sees as if the subject is combing with left hand.

54
 The rays that are coming from the image of a plane mirror are far behind the mirror and are virtual.
When the plane mirror moves up the image moves against to the movement of the plane mirror ,
i.e the image moves down .
 The rays reflected from the plane mirror are divergent
 The distance between object and the mirror is equal to the distance between the mirror and the
image . This principle is used to convert the room distance from 3 meters to six meters when 6 meters
room is not available for visual acuity assessment by Snellen’s chart.
 For retinoscopy procedure – Plane mirror is commonly used as retinoscope
 The plain mirror is used to reflect the light from a light source on to the area interest i.e in a
retinoscopy procedure the light is reflected from a light source to the dilated pupil, same in a slit
lamp, Gonioscope, Goldmann three mirror contact lens , direct and indirect ophthalmoscope.
 Plain mirror examination at 1 meter distance is one of the techniques to confirm the diagnosis of
cataract.

Unit of Prism is Prism Diopter

55
Calculation of prism Diopter - The power of the prism is equal to apparent displacement in centimeter
divided by object distance in meters.

• Eg - Object distance=25cm; deviated by 3cm

Power=3/0.25m=12prism diopters.

Table -11. Description of the Prism

• Prism has two plane surfaces inclined to Figure 5-11
each other
• The line at which the two surfaces meet
together is called apex, while the surface
opposite to the apex is called base.
• Refracting angle of a prism is the angle
• The total amount of deviation is called ANGLE OF
between two surfaces.
DEVIATION.
• Axis of prism is line bisecting the apical
• Image formed by prism is erect, virtual
angle.
• When prescribing prism orientation is indicated
• The light passing through the prism is
by the position of base, e.g. base-in /base-
deviated towards the base and the object
out/base-up/base-down.
seems to move towards the apex.

Table -12 . Identification of the Prism (To find out the lens has a prismatic value or not )
• Hold the lens near to the eye and select a distant Figure 5-12
straight line and see the selected line through the
lens. If the lens has a prism, the image of the line
will move towards the apex and parallel to the base.
(Continuity of the line is broken) .
• Now rotate the prism by 90 degrees , there is no
deviation of the image
• Since the line appears to be deviated towards the
apex,we will get to know the direction in which
side the apex of prism lies.

Guidelines for prescribing the prisms

In exo deviation – the apex of the prism is towards exo deviation i.e base in prism for correcting the exo
deviation.

Split the amount of correcting prism equally between both eyes.

56
Table -13 . Uses of Prisms in Ophthalmology
Diagnostic uses Therapeutic uses Optical use in instruments
Objective measurement of the To improve fusional reserve in Used as reflectors of light in
angle of squint by prism bar cover patients with convergence ophthalmic instruments like slit
test, Krimsky test insufficiency lamp. Surgical microscope,
Gonioscope, Keratometer,
applanation Tonometer and
Synaptophore , etc.
Subjective measurement of the Used in the treatment of diplopia in
angle of squint by Maddox rod phorias
Measurement of fusional reserve
4 D prism test for diagnosis of
Microtropia
For Diagnosing malingering

Table -14 . Prisms available for clinical use

Prism bars – Figure 5-13
Available as horizontal prism bars and vertical prism
bars
Horizontal prism bars are used for Horizontal
squints and vertical Prism bars are used for vertical
squint

Loose prisms – Figure 5-14

If the angle of the squint measurement exceeds the
prism strengths available in prism bar then loose
prisms are added over and above the prism bar
strength

Mounted prisms – Fresnel Prisms –

Trial frame  The trial frame is adjustable anteriorly

There are three slots in trial frame . posteriorly , and lateral positions.
 The slot nearer to the eye is for spherical  It has nose pad to sit comfortably on the nose.
lenses for presbyopia correction. Figure 5-15
 The middle slot is for spherical lenses for
correction of distance vision , to keep
occluder, pinhole, to keep lenses for
retinoscopy, PMT.
 The outer slot is for cylindrical correction

57
Table -15 . Trial set / Box
Trial set / box – Consists of Figure 5-16  Occluder
 Two rows of Biconvex spherical  Pin hole
lenses  Stenopic
 Two rows of Biconvex Cylindrical Slit
lenses  Maddox
 Two rows of Biconcave spherical rod
lenses  Red and
 Two rows of Biconcave Cylindrical Green
lenses glasses
 Trial frame  Prisms

Table -16. Figure 5-17 Pin hole Figure 5-18 Figure 5-19
Occluder Pin hole
Uses of occluder - Occluder examination Pin hole Stenopic Slit – uses
In visual acuity Differentiate the To identify the axis
examination to block refractive errors of the cylinder
the vision of the eye. from the diseases
of the eye

Table -17. Figure 5-20 Figure 5-21 Red and Green glasses –
Maddox Rod uses -- Macular function, To find phorias
Uses of Red and Green glasses - Used to
know the anomalies of binocular single
vision like diplopia, suppression,
stereopsis, FRIEND test, Worth four dot
test

Table -18 Worth four dot test. RED FIN

The person able to see RED in The person able to see FIN in green
red colors Indicates LE color Indicates RE suppression
suppression
Test
Keep the red and green glasses in
front of the eye, Red in front of the
right eye and green in front of the
left eye and the person is asked to
read FRIEND which is present at
the bottom of the illuminated
Snellen’sdrum. If the person read
FRIEND at a time then binocular
single vision is present

58
Worth four dot test.
Worth four dots present at the bottom of the illuminated snellen’s drum . The four dots are – One Red,Two
green and one white / Amber color /mix of red and green
 The person has to wear red and green glasses in front of the eye, Red in front of the right eye and
green in front of the left eye and the person is asked to identify the colors of worth four dots
 If the person says more than four dots it indicates Diplopia
 If the person sees green colors only it indicates RE suppression
 If the person sees red colors only it indicates LE suppression

Bagolini striated glasses

Table -19
Red and green Worth four Wearing red More than four Three green Two red colors
glasses dots and green colors Indicates colors indicate indicate LE
diplopia RE suppression
suppression

Table -20 Bagolini striated glasses

-------------------------------------

59
5.2 Clinical examination of Refractive Error

(Relevant History Taking, Clinical examination of the eye, Retinoscopy and Post Mydriatic Test (PMT)

Clinical examination of refractive error follows the same methodology as any other case sheet writing.

Bio data, symptoms , H/o present illness, Past history , H/o using spectacles, family history, personal history,
General examination, anterior segment examination , Dilatation of the pupil with appropriate cycloplegics and
Mydriatics for retinoscopy and Fundus oculi exam, Retinoscopy, Post mydriatic test and Spectacle prescription

. Bio Data –
• Name /ID.
• Age – Secondary School children commonly complain of inability to see the black board . At birth the
eye is Hypermetropic of 2 Dioptre . Eye ball grows with the age , the growth of the eye will stabilize at
the age of about 10 years and Emmetropia is achieved . Over growth of the eye against the age norms
will causes myopia and Under growth of the eyeagainst the age norms causes hypermetropia .
Because of the over growth of the eyes against its norms , Children come to the eye surgeon for
spectacles and usually they are myopics.

Presbyopia – at the age of 40 years physiological failure of accommodation i.e. presbyopia occurs which
causes recession of near vision In hypermetropics presbyopia sets in early than emmetropics .

At the age of 40 years the nuclear sclerosis cataract occurs and there is shift of emmtropia to index
myopia and which makes the presbiopics to do away with their presbyopia glasses (Second sight)

At the age of 50 years cortical cataract starts which causes index hypermetropia

Age is also important to select cycloplegic or mydriatic drugs for refraction

 Sex - Sex has no predilection for refractive errors

• Occupation - The refractive errors are to be corrected to suit to the needs of the profession

Symptoms of refractive errors –

• Gradual progressive painless diminution of vision for distance and Near
• Recession of the near vision
• Asthenopia – feeling weakness in the eye . This symptom constitute pain, congestion in the eye and head
ache due to accommodation and convergence inaccuracy.

60
• Eye strain – Astigmatism Hypermetropia, Phorias are an important cause for eye strain and precipitated
in general ill health
• Headache - Frontal/Occipital area aggravated after long hours of work.
• Symptoms of Muscle imbalance – phoria or tropia – the letters are running in between two lines
• History of diabetes – Hyperglycemia induces myopia, and hypoglycemia induces hypermetropia.
• H/o Past History – History of using spectacles and verification of using spectacles will give a quick assessment of
refractive error and how to address the problem.
• Family History –Refractive errors like Myopia, particularly degenerative myopia and Hypermetropia has hereditary
predisposition .
• Personal history – Some people refuse to wear spectacles for cosmetic reasons.
• General examination -Chin elevation seen in congenital ptosis and ocular deviations i.e squints

Plan of clinical examination of the eye for refraction

• Visual acuity - Distant Visual acuity (VA)– examination for Distant VA-un aided, pin hole, aided (spectacle)
. If the person has diminution of vision, pinhole examination has to be done . Pin hole examination will
differentiate the refractive errors from the diseases of the eye (Described in the visual acuity examination
– Refer to that chapter)
• Near vision VA
Anterior segment examination –
• Anterior segment examination is for noting any pathological causes which reduces VA other than
refractive errors.
• Hirschberg’s corneal reflection test ,Examination of ocular movements and cover test to rule out
phoria and tropia.
• The angle of AC should be assessed prior to the instillation of the Mydriatic and cycloplegic drugs for
refraction. Shallow anterior chamber and narrow angles are contra indicated for instillation of
Mydriatics and cycloplegics,as dilatation may precipitate closure of the angle of AC.

Dilatation of the pupil -

After Anterior segment examination ,dilatation of the pupil with appropriate cycloplegic and Mydriatic drugs
for fundoscopy and followed byRetinoscopy.

Appropriate cycloplegic and Mydriatic drugs used for refraction

The drugs used for refraction are Para sympatholytic drugs likeAtropinesulphate 1%, Cyclopentolate -1%,
Homatropine -2% , and sympathomimetic drugs like phenyl ephrine hydrochloride 10%..

61
The drug characters that are to be noted -
Drug action, at what age the drug is an indication, drug Instillation interval, Peak action of the drug and at what
time the retinoscopy to be done , Duration of action of the drug ,After PMT, How much drug causes myopia

Table -1
Drug and % Drug Age Instillation Peak Time of Duration PMT Drug
Action Indication interval action Retinosc of action done induced
opy Myopia
done
th
1).Atropine Complete Children < 5 Thrice a 2 to 3 4 day 2 to After - 1 DSP
sulphate 1% Cycloplegic yrs and day for 3 days 3weeks three
ointment and All Children consecutive weeks
Mydriatic with squint days
2).Cyclopentolate Short acting Children 5 to one drop 60 After 3 days After 3 - 1 DSP
1% drops complete 15 yrs. every 15mts minutes 60mts days
Cycloplegic for 1hour
and
Mydriatic
3).Hom Atropine Partial 16 to 40 yrs. One drop 60-90 After 3 days After 3 -
2%drops Cycloplegic every 10mts minutes 90mts days 0.50DSP
and for 1hour
Mydriatic
4).Tropicamide Mydriatic 16 to 40 yrs. One drop 30 - 60 After one 3 to 4 After 0
1% drops every 15mts minutes hour Hours 6 to 8
for ½ hour hours
5).Phenylephrine Mydriatic Above 40 yrs. One drop 30 - 45 After 20 3 to 4 After 6 0
10 % drops every 15mts minutes to 30 hours to 8
for ½ hour minutes hours

Side effects and Disadvantages of the Appropriate cycloplegic and Mydriatic drugs used for refraction
 Atropine sulphate 1% and Homoatropine-Local side effects are contact dermatitis ,risk of angle closure,
raised IOP and Systemic side effects - All the side effects of Para sympatholytic drugs i.e Hyper pyrexia,
Tachycardia must be informed to the mother and if noted inform to discontinue the drug immediately
and other side effects are Dryness of mouth , constipation , retention of urine etc.
The disadvantage of Atropine 1% drug is loss of accommodation for three weeks.

62
 Cyclopentolate 1% -Local side effects are Transient stinging, allergic reaction, irritation, diffuse redness.
The systemic side effects of the drug are hallucinations, Drowsiness, Ataxia, Disorientation.

 Tropicamide 1% – Local side effects are – raised IOP, Hypersensitivity ,Transient stinging and systemic
side effects are confusion, skin rash, dryness of mouth.
 Phenylephrine 10 % - Local side effects are transient pain, lacrimation, Rebound miosis .
Systemic side effects are increased blood pressure Contraindicated in hypertension as it precipitates the high
bloodpressure, Tachycardia, ventricular arrhythmia . These days Tropicamide 1% is used instead of
Phenylephrine 10 %.

After dilatation of the pupil ,Ophthalmoscopy and retinoscopy is done

 Ophthalmoscopy -Ophthalmoscopy is done to rule out fundus pathology which may be also a cause for
diminution of vision .
 Retinoscopy (described below) to determine the refractive error of the eye.
After retinoscopy Post Mydriatictest (PMT) - The time schedule for PMT depends on the drug used for

retinoscopy as mentioned above in the drug table.

 Post Mydriatic test (PMT) - After Retinoscopy , Post Mydriatic test (PMT) is done to prescribe the
spectacle for distance and near . This is done by noting the neutralization spherical power
andconverting it into a spectacle power .
 Muscle Balance -With full spectacle correction in place assess the muscle balance for distance and near
and determining the near point of accommodation and convergence .
 Correction of near vision (NV) -Based on the age of the person NV correction has to be done .

Retinoscopy (Synonyms - Shadow test, Skiascopy, Pupilloscopy, Koreoscopy)

Retinoscopy is defined as the Objective estimation of the refractive error of the eye by neutralization
technique .
• The terms objective and neutralization are important terms in the definition without which the
definition has no meaning
• The term objective means the surgeon physically estimate the refractive error.
• The term neutralization is used for the technique of estimation of refractive error.
(The details of the neutralization technique will be explained in this chapter)

63
What is the purpose/objective of Retinoscopy?
 The objective of retinoscopy is to find out the position of the image at far point which is formed by
the refractive apparatus of the person’s eye. The eye is a refractive apparatus with 64 Diopters
( Cornea 44 D and Lens 17 to 19 D) and when light rays pass through this dioptric power it will form
an image . The formation and position of the image depends upon the refractive condition of the
eye.
 The Second objective of retinoscopy is to bring the image at far point on to the nodal point of the
surgeon by neutralization technique.
How to bring the image at far point to the nodal point of the surgeon is based on the principle of
retinoscopy.

What is the principle of retinoscopy?

The principle of retinoscopy is that ,Irrespective of the refractive power of the eye, the eye is made a myopic
eye by keeping appropriate spherical lenses and the rays coming from the myopic eye are made to focus at
the nodal point of the surgeon by neutralization technique.
Image formation at far point in various refractive conditions of the eye
Table -2
 Emmetropia - In Emmetropia the image is formed at far pointi.e
infinity Explanation– When accommodation is at rest the parallel
rays of light coming from the infinity after making refraction with
cornea and crystalline lens makes a focus on the fovea . The
emerging rays from thefocusagain makes refraction with the
crystalline lens and corneaandleaves the eye as parallel rays to
form the image at far point at infinity.

 Hypermetropia - In Hypermetropia the image is formed at far point behind the Sentient layer of retina
, (i.e layer of rods and cones is called sentient layer of retina ) .
Table -3
Explanation -When accommodation is at rest the parallel rays of
light coming from infinity refract with cornea and crystalline lens
makes a focus behind the sentient layer of retina . The emerging
rays from the focus again refract with the crystalline lens and
cornea and leave the eye as divergent rays as if they are coming
from a far point behind the retina .

64
Table -4

 Myopic eye of more than 1 D - In Myopia the image is formed at

far point i.ein front of the observer .Explanation - When
accommodation is at rest the parallel rays of light coming from
infinity after refracting at cornea and crystalline lens focus in front of
the retina.The emerging raysfromthe focus again refract with the
crystalline lens and cornea and leaves the eye and forms the image at far point in front of the persons
eye i.e in front of the surgeon/observer or in front of the retinoscopy mirror.

 Myopia of less than1 diopter -- Table -5

in Myopia of less than 1 dioptertheimage is formed at far point
beyond the observer . Explanation - When accommodation is at
rest the parallel rays of light coming from infinity after
refracting with cornea and crystalline lens focus in front of the
retina. The emerging raysfrom the focus refract with the
crystalline lens and cornea and leaves the eye and forms the
image at far point beyond the surgeon’s eye/ observer.

Requirements for retinoscopy.

• Dark Room
• Source of light – may be separate source of light which is kept behind the patient head or light emanating
from a bulb with inbuilt battery source ( Electric retinoscopes). . These light source is called original
source of light . If the retinoscopy is done with a separate source of light , it is called spot retinoscopy
and if it is done with electric retinoscope it is called streak retinoscopy . The spot retinoscopy gives wide
luminous reflex at the pupil and where as streak retinoscpy gives streak luminous reflex at the pupil.
Examination with Spot retinoscope also confirms the opacities in the crystalline lens.
• Mirrors- Plane mirror, or concave mirror. The mirrors are called retinoscopes. Most of the surgeons will
practice retinoscopy with a planemirror .(Detailed below)
• Trial set –- consisting of Trial frame ,Spherical lenses . cylindrical lenses, etc
• Direct Ophthalmoscope to see the fundus oculi to exclude the causes for reduced vision other than the
refractive error.

65
Table -6
Priestley smith mirror

Plane mirror Electric Appearance of

One end Plane mirror
retinoscope Appearance of Luminous Luminous reflex
and another end in Streak
Concave mirror /Streak reflex in Spot retinoscopy
retinoscope retinoscopy

Practice of retinoscopy procedure

 From the original source of light , the light is taken onto the plane mirror/ concave mirror and projected
into the eye at a distance of 1 meter .(Retinoscopy is commonly done at a distance of 1 meter as a
matter of convenience for calculations and to handle the lenses in the trial frame for neutralization )
and reflected on to the dilated pupil of the subjects eye.( The subject is the person who is under going
Retinoscopy test) .
• The projected light illuminates a small area of the retina of the subject. This is called immediate source of
light.
• As the sclera is non transparent, the light is reflected back from the illuminated area of the retina , and
after refracting with crystalline lens and cornea, the rays exit from the subjects eye.
• The exiting rays forms an image at the pupil which is visible for the surgeon as luminous reflex
surrounded by a shadow which corresponds to the image at the far point of the subjects eye.
.Because of this shadow the retinoscopy is called as skiascopy or shadow test.
• The surgeon will observe the luminous reflex with a peep hole of a plane mirror at a distance of 1 meter
as a blurred luminous reflex because of his in accurate accommodation .
• The luminous reflex corresponds to the image at far point of the eye seen as wide reflex in spot
retinoscopy or a linear reflex in streak retinoscopy

Table -7
1. F
r
o
m

66
• From a distance of 1 meter the surgeon movestheilluminated reflex at the pupil with a plane mirror/
concave mirror and observe the movement of reflex, color , & speed of luminous reflex . The
movement with a plane mirror is done in two meridians i.e. vertically, horizontally or obliquely and
observe whether the luminous reflex is moving with or against the movement of the mirror .
• The rays that exit from the eyes of hypermetropia, myopia of less than 1 Diopter are divergent and in
emmetropia are parallel , and the image is erect and virtual .
• The rays that exit from the eyes of myopia of more than one Diopter are convergent and the image is
inverted and real..

 It is the axiom of the optics , the image formation depends on the position of the object on the principle
axis , ie. On the principle focus, in front , or behind the principle focus . This is an important fact to
remember to explain whether the image is virtual or real.
Optic principles of the Plane mirror –
The image of an object formed by reflection at a plane mirror is characterized by

 Erect image

 Virtual image

 Laterally inverted image

 The size of the image is equal to the size of object.

 The image is situated behind the mirror

 The distance between the object and mirror is equal to the mirror and image

Optic principles of the Concave mirror–

 If the object is farther away from the mirror than its focal distance i.e more than Half of its radius of
curvature , the image is real, inverted, and situated in front of the mirror. .

Inferences made based on the movement of the luminous reflex with the plane mirror
• If the luminous reflex moves with the movement of plane mirror the inferences are that the
subject may be hypermetropic, emmetropic or myopic of less than 1 D.
• If theluminous reflex moves against to the movement of the plane mirror the inference is thatthe
subject is myopic of more than 1 D.
• In high refractive errors the luminous reflex moves slowly with the movement of the mirror . The
color of the luminous reflex is bright red in low and moderate refractive errors, and dull red or faint
red in high refractive errors.

67
Inferences made based on the movement of the luminous reflex with the concave mirror
The movement of luminous reflex with concave mirror is quite against that in the plane mirror.
• If the luminous reflex moves with the movement of concave mirror the inference is that the
subject is myopic of more than 1 D.
• If the luminous reflex moves against to the movement of concave mirror the inferences are that
the subject may be hypermetropic, emmetropic or myopic of less than 1 D.

How does the red reflex at the pupil moves with plain mirror
 The exit rays which are coming from the hypermetropic eye, emmetropic eye and Myopic eye of less
than one diopter forms virtual , erect image which will match with the principles of plane mirror
and moves with the movement of Plane mirror.
 The exit rays which are coming from the myopic of more than 1 Diopter are real and form an
inverted image which will mismatch with the principles of plane mirror , hence moves against to
the movement of the plane mirror.

How does the red reflex at the pupil moves with Concave mirror
 The exit rays which are coming from Myopic eye of more than one diopter are real and form
inverted image which will match with the principles of concave mirror and moves with the
movement of Plane mirror.
 The exit rays which are coming from the hypermetropic eye, emmetropic eye and Myopic eye of less
than one diopter are virtual and form erect image which will mismatch with the principles of
concave mirror , hence moves against to the movement of the concave mirror.
 If the person is myopia of 1D there is no reflex shadow at the pupil as the luminous reflex is in a
state of neutralization at 1 meter retinoscopy distance .

Thus the type of mirrors used is of subsidiary matter. It merely determines the direction of movement of
the image formed by refractive state of the eye

68
How luminous reflexes moves with the Plane mirrorare explained diagrammatically below.
Table -8
Person is Hypermetropic ,Emmetropic and
Myopic of less than 1 diopter –
L is the original source of light. 1 is the
immediate source of light on the plane mirror
and its image is formed behind the retina.

If the plane mirror is moved down i.e. 1 is

shifted towards the tilted plane mirror and the
image 1’ is moved down.

 In the plane mirror mirror the image moves with the

movement of the mirror .
(When the plane mirror is tilted downwards , the image
of the retina formed by the lens ----- moves downwards ,
because the Hypermetropic eye lens form virtual &erect
image , which is towards same axis to which plane mirror
tilted.)

Table -9
Person is Myopic of more than 1 Diopter Myopia of more than 1 Diopter - Diagram of
L is the original source of light, 1 is the luminous reflexes at the pupil moves against
immediate source of light on the plane mirror the movement of plane mirror
and its image is formed in front of the retina.

If the plane mirror is moved down i.e. 1 is

shifted towards the tilted plane mirror and the
image 1’ is moved up .

 In the plane mirror the image moves against the

movement of the plane mirror
(When plane mirror is tilted downwards , the image of
retina formed by the lens moves upwards as it forms real
& inverted image and it formed opposite to the axis of
the tilted.)

69
Person is myopic of 1 Diopter
If the person is myopia of 1 Diopter and the surgeon is In myopic of 1 Diopter the luminous reflex is static
doing retinoscopyat 1 meter distance the far point of with the movement of plane mirror
the patient will be at the nodal point of the surgeon .

• Here the illuminated retina will have a limited

movement/ no movement as the far point of
the patient is at the nodal point of surgeon .

The shadow of the pupil of the patient is bright and will

not move with the movement of plane mirror.

Table 10

How to bring the far point to the nodal point of the surgeon in hypermetropia , myopia of less than 1D and
emmetropia and myopia of more than 1D.

 It is evident that the rays that exit from the eyes of hypermetropia and myopia of less than 1D are
divergent and from the emetropia are parallel and these rays are made to convergeby keeping
appropriate biconvex lenses (Biconvex lens is a Converging Lens) till the moving luminous reflex is
made static reflex at a retinoscopy working distance which is called neutralization.

70
Table 11
How to bring the far point to the nodal point of the surgeon in myopia of less than 1D and emmetropia and
myopia of more than 1D.

 It is evident that the rays that exit from the eyes of myopia of more than 1D are convergent and these rays are
made divergent by keeping appropriate biconcave lenses ( Biconcave lens is diverging lens) till the moving
luminous reflex is made static reflex at a retinoscopy working distance . This is called neutralization.

In all refractive errors ,at neutralization the far point of the subject is at the nodal point of the
surgeon.
Then the neutralization spherical lenses power is converted to spectacle power by deducting the myopia
that has been induced by the drugs and to the retinoscopy distance at neutralization state . This is
called Post Mydriatic Test (PMT) , which is described in the next chapter.

Automated / Computerized refractometer - The Automatedrefractometer is computerized method of

estimating refractive error. It utilizes the principle of indirect ophthalmoscope . The light rays which
enters the eye of a person from an identified object is focused on the retina . The emerging rays from the
retina of the eye , passes through the condensing lens which are focused at convenient distance to the
identified object and the computer converts the focused rays into spectacle lenses .

In other words , it follows the same principle of retinoscopy . The disadvantage is that the eyes are kept near to
the refractometer which causes the change in the refractive condition of the eye due to accommodation. This
causes display of erratic refractive powers by the computer.

--------------------------------------------------------------------

71
5.3 Post Mydriatic test (PMT)

After Retinoscopy and Neutralization the next step of examination is Post mydriatic test (PMT)
Post mydriatic test (PMT )is to convert the neutralization spherical lenses (the lenses which made the
moving luminous reflex into static reflex ) into spectacle lenses
PMT is to examine the person for spectacle prescription based on the neutralization .
PMT examination is done after the cycloplegic effect is passed off .
The duration of the cycloplegic drug effect in the eye is described in the clinical examination topic .
Three parameters are to be considered for converting neutralization spherical lenses into spectacle
lenses.
 The first parameter is the age of the person - The age of the person is important to know the
type of cycloplegic and mydriatic drug to be used for retinoscopy and for the correction of
presbyopia.

 The second parameter is to know how muchis the myopia produced by the each
cycloplegicdrug.Cycloplegic drug causes paralysis of accommodation which causes myopic shift . This
is explained like this - Instillation of Atropine sulphate 1% or cyclopentolate1%, paralyzes the ciliary
muscles. The paralysis of ciliary muscles causes the zonules to relax. Once the zonules are relaxed the
anterior curvature of the crystalline lens increases which causes the increase of anterioposterior
diameter of the crystalline lens there by the crystalline lens becomes more converging lens, thus
causing myopia shift.. Atropine sulphate 1 % and cyclopentolate 1% causes myopia of minus 1D.
Homatropine 2% causes myopia of 0.5D.Tropicamide 1% Phenylephrine 10% does not produces
myopia.

 Third parameter is the distance at which retinoscopy is done , In retinoscopy neutralization is

done at various distances i.e 66 cms , 1meter , 1.50 meter.At neutralization distancesome amount of
myopia is retained in the eye . This myopia is calculated by formula D =1/ F .D= diopter ,( 1 means 1
meter i.e. 100cm , F is Focal length)
 If the retinoscopy is done at 1 meter (100cm) distance, i.e D = 100cms / 100 cms = 1D. that
means doing retinoscopy at a distance of 1 meter myopia of minus 1D is retained in the eye at
neutralization point .

72
 If the retinoscopy is done at a distance of 1.5 meter (150cm) , i.e. D = 100 cms / 150 cms =
0.66 D.that means doing retinoscopy at a distance of 1.5 meter(150cms), myopia of 0.66D is retained
in the eye at neutralization distance .
 If the retinoscopy is done at a distance of 66cms i.e. D = 100cms / 66 cms = 1.5 D. that means
doing retinoscopy at a distance of 66cms myopia of 1.5D is retained in the eye at neutralization
distance.
 The total amount of myopia present in the eye at neutralization is calculated by adding together
the cycloplegic induced myopia and the myopia retained in the eye at neutralization distance. The
total myopia is“deducted” from the neutralization biconvex spherical lenses and“added” to the
distance neutralization biconcave spherical lenses .
 After addition or deduction of the induced myopia in the eye from the neutralization spherical
lenses the remaining is the spherical power which is prescribed as spectacle power.

Examples to explain PMT

Table 1
Eg 1: Parameters Spectacle Power
 Age of the person is 5  Add (Deduct ) myopia –
years 2D present in the eye
 Atropinesulphate 1% is to the neutralization
instilled for retinoscopy spherical power +4D.
which causes myopia of  The power after
minus 1D. deduction +4 – 2 is
 The distance at which the =+2D.
retinoscopy done is 1  Thus the person
meter which retains requires +2D of
myopia in the eye at spectacle power for
neutralization distance . distance vision.
 Total myopia retained in
the eye is minus 2D (-1D
and -1D) .

73
Eg 2: Parameters Spectacle Power
 Age of the person is 10  Add (Deduct) myopia
years. of minus 2D present in
 Cyclopentolate 1% is the eye to the
instilled for retinoscopy neutralization spherical
which causes myopia - power - 4D.
1D.  The power after adding
 The distance at which the is minus 6 D (-1D and –
retinoscopy done is 1 1 = -2D) ( -2 and – 4= -
meter which retains 6D) .
myopia in the eye is 1D  Thus the person
at neutralization distance equires minus 6D of
 Total myopia retained in spectacle power for
the eye is minus 2D (-1D distance vision .
and -1D) . The two meridians will focus on
the fovea
Eg 3 :Parameters Spectacle Power
 Age of the person is 30  Add retained myopia
years – 1D in the eye to the
 Tropicamide 1% is neutralization spherical
instilled for retinoscopy power +3D
which causes no myopia  The remaining power
after adding is 2D
 The distance at which the (+3D – 1 D) = +2 D .
retinoscopy done is 1  Thus the person
meter which retains 1D requires + 2D
myopia in the eye at spectacle power for
neutralization distance. distance vision .
The two meridians will focus on
 Total myopia retained in the fovea
the eye is minus 1D .

74
Eg 4: Parameters Spectacle Power
 Age of the person is 45  Add( Deduct) retained
years. myopia – 1D in the eye
 Phenylephrine 10% is to the neutralization
instilled for retinoscopy spherical power 3D
which causes no myopia  The remaining power
 The distance at which the after adding is +2D
retinoscopy done is 1 (3D - minus 1 D = 2 D )
meter which retains 1D .
of myopia in the eye at  Thus the person
neutralization distance . requires 2D spectacle
 Total myopia retained in power for distance
the eye is minus 1D vision
The two meridians will focus on
the fovea
Eg5: A person aged 45 years is having a difficulty in seeing near objects due to presbyopia. His near vision
difficulty is to be corrected . There is a rule of thumb i.e. for 40 years person approximately requires 1D , 45 years
1.5 D, 50 Years 2D, 55 years 2.5D, and 60 years 3D. These near vision requirement is added to the distant power.
Thus 40 years and above person requires two lenses one lens for distance and another lens for near. These two
lenses are incorporated in one single piece of lens which is called bifocals

Table 2 Types of Bifocals /Trifocals

Fused Bifocal Split Bifocal Executive Bifocal Inverted Trifocal Multi focal
D - Bifocal

75
Table 3 . Spectacle Power calculation - if the neutralization power is different in the two meridians
Eg 6 :Parameters Retinoscopy neutralization power Spectacle Power
 Age of the person is 25 years.  Add (Deduct)retained
Tropicamide 1% is instilled Let us say the neutralization myopia – 1D to the
for retinoscopy which causes spherical power in vertical and neutralization spherical
no myopia horizontal meridians are different. power in both the
 The distance at which the meridians.
retinoscopy done is 1 meter  Then the vertical meridian
which retains 1D of myopia requires + 2D and
in the eye at neutralization horizontal requires +4D.
distance.
 Total myopia retained in the In vertical meridian the The two meridians will not focus
eye is minus 1D . neutralization power is 3D, in on the fovea instead form focal

horizontal meridian the lines called astigmatism.

neutralization power is 5D.

Table 4.
Spectacle power calculation if the neutralization power is different in the two meridians
 Select least refractive power in the two meridians i.e 2D . if spherical lens 2D is kept in the trial frame it not
only correct the vertical meridian , it corrects the power in 360 meridians , i.e it corrects horizontal
meridian 2D also.
 In the horizontal meridian the power required is 4 D , In this 4D , 2D is corrected by the vertical meridian
power and the remaining 2D power is corrected by keeping cylindrical power in vertical meridian (90
degrees) so that the cylinder which is kept in 90 degrees will act perpendicular to its position thus brings
required 2D power in horizontal meridian.
 The prescription will be 2.00 DSph and 2.00 Dcyl in 90degrees. Thus the power in two meridians are
corrected by spherocylindrical lens . This is the power required for the patient for distant vision.

 By looking at the neutralization power of the two meridians one can infer that the person is having
astigmatic error and can construct and draw the diagrams of the type of astigmatic refractive error.

76
For cross checking the correctness of the PMT/ refinement of of cylinder and sphere , the subjective tests like
Jackson’s cross cylinder test, Duochrome test, Astigmatic fan , are carried out with the lenses in the frame .

Jackson’s cross cylinder : This is a toric lens i.esphero cylindrical lens . Sphere is half of the cylinder with opposite
sign with axis at right angles . Most commonly used Jackson’s cross cylinder is --0.5D sphere and +1D cylinder.It
creates an affect of two cylinders -- 0.5D cylinder and + 0.5D cylinder when placed at right angles.

Table 5.

Duochrome Test– it is for refinement of sphere . Patient is asked to compare the colors of red and green alphabets

Interpretation of Duochrome Test

 If the alphabets on RED and Green background are equally sharp then patient is emmetropic.
 If the alphabets on RED background are more clear than the alphabets on green background ,then
patient is Myopic.
If the alphabet on Green background are more clear than the alphabets on RED background ,then
patient is Hypermetropic..
Astigmatic fan / Dial
The astigmatic fan is used to find out the correct axis and the power of the cylinder. The astigmatic fan
consists of radiating lines emanating from a common point above horizontal line . All these lines are separated by
15 degrees with same width height/length and brightness. The test is done at 6meters distance .
Interpretation : If the person says , all the lines are of same width , height / length , and brightness , the cylinder
kept in the trial fame is correct if not the power or axis position may be wrong.

------------------------------

77
Chapter 6. Clinical examination of the Eye Brow

Eye brows are the lentils of the eye which protect the eye

Clinical points to be examined in the eye brow

 Position of the eye brows
 Density of the eye brow

Position of the eye brows

• Normally situated on the upper margin of the orbit.
• If seen below its normal position it is called ‘Brow ptosis which occurs in old age.
If seen above the normal position i.e. Peaking of the eye brow and is seen in Blepharoptosis. It is due to the effort
of frontalis to elevate the lid.

Figure6. 1
Density of the eye brows
Loss of density of the eye brows is calledMadarosis
causes
• Old age
• Hansen’s – particularly lateral 1/3 of the eye brow.
• Myxedema
• Alopecia totalis

Format for examination of the eye Brow

Clinical Points for examination Right eye Left eye
Position of the eye brow
Density of the eye brow hair

--------------------------

78
Chapter 7. The clinical anatomy the Eye Lid

Num COMPETENCY Domai LevelK Cor Suggested SuggestedAsse Number Verti Horiz
ber The student should be able to nK/S/A /KH/S e(Y TeachingLea ssmentmetho require cal ontal
Integ integ
/C H/P /N) rningmetho d dto ratio ratio
d certifyP n n

Topic:Lids and Adnexa ,Orbit NumberofCompetencies:(08) Numberofproceduresthatrequirecertification:(NIL)

OP2.1 Enumerate the causes, describe and discuss the K KH Y Lecture, Written/Viva Hum
aetiology, clinical presentations and diagnostic Small voce an
Anat
features of common conditions of the lid and groupdiscu
omy
adnexa including Hordeolum externum/internum, ssion
blepharitis,preseptalcellulitis,dacryocystitis,hema
ngioma,dermoid,ptosis,entropion,lidlag,
lagopthalmos
OP2.2 Demonstrate the symptoms & clinica S S Y DOAP Skill
signs of conditions enumerated session assessment
inOP2.1
OP2.3 Demonstrate under supervision clinical S S Y DOA Skill
procedures performed in the lid including: bells H P assessment
phenomenon, assessment of sessi
entropion/ectropion, performthe regurgitation on,Le
test of lacrimal sac. Massage technique in cong. cture
dacryocystitis, and trichiatic cilia removal
byepilation
OP2.4 Describe the aetiology, clinical s K K Y Lecture, Written/V
presentation . Discus complications and H Small group iva voce
management of orbital cellulitis discussion
OP2.5 Describe the clinical features on ocular K K Y Lecture, Written/Viva
examination and managementofa patien twith H Small voce
cavernous sinus thrombosis groupdiscu
ssion
OP2.6 Enumeratethecausesanddescribethedifferentiatin K K Y Lecture, Written/Viva
gfeatures,andclinicalfeatures and management H Small voce
ofproptosis groupdiscu
ssion
OP2.7 Classifythevarioustypesoforbitaltumours.Different K K Y Lecture, Written/Viva
iatethesymptoms and signs of the presentation of H Small voce
various types of ocular tumours groupdiscu
ssion
OP2.8 Listtheinvestigationshelpfulindiagnosisoforbitaltu K K Y Lecture, Written/Viva
mors.Enumerate the indications for appropriate H Small voce
referral groupdiscu
ssion

1
Chapter 7. The clinical anatomy the Eye Lid
2. Topic : Lids , Adnexa, Orbit and (Clinical examination of Eye brow and pre septal cellulitis and Clinical examination of Lacrimal
apparatus )
.No Topic Clinical skills Domain Level Core Suggested No Vertical Grade Sign of
K/S/A/C K/KH/ Y/N Suggested assessment Required integration /Marks Faculty.
SH/P Teaching Method to certify Date
and
learning
method
Demonstrate the S S Y DOAP Skill 1
OP2.1 symptoms & clinical session Assessment
sign of conditions Lecture
presepta cellulitis,
Demonstrate the S S Y DOAP Skill
OP2.1 symptoms & clinical session Assessment
sign of conditions Lecture
Perform the
regurgitation test of
lacrimal sac. Massage
technique in cong.
dacryocystitis
OP2.2 Demonstrate the S S Y DOAP Skill
symptoms & clinical session Assessment
sign of conditions Lecture
Hordeolumexternum/
internum, blepharitis
hemangioma,
dermoid, ptosis,
entropion, lidlag,
lagopthalmos
OP2.3 Demonstrate under S S Y DOAP Skill
supervision clinical session Assessment
procedures Lecture
performed in the lid
including: bells
phenomenon,
assessment of
entropion/ectropion,
, trichiatic cilia
removal by epilation

2
Chapter 7. The clinical anatomy of the Eye Lid
The lids are a pair of multi layered fibromuscular cutaneous folds in front of each eye. The upper lid is mobile
where as the lower one is immobile.

Clinical Anatomy of theLid

The layers of the lid from out to in Figure 7-1 Structure of the lid Diagram 7-2 Layers of the lid
 Skin and subcutaneous
tissue
 Muscular layer
 Sub muscular areolar
tissue
 Fibrous layer I,e Orbital
septum ,
Tarsal plate and others
 Orbital fat
 Palpebral conjunctiva

Skin and subcutaneous tissue –

 Thinnest area of the skin
in the body .
 The preseptal area of the skin is loosely attached to the underlying tissue as against the remaining
area of the eye lid , which creates a potential space for fluid collection leading to edema
 The eye lid skin creases are formed by the attachment of few of Levatorpalpebrae superioris
aponeurotic fibers on to the backside of skin
 Contains sebaceous and sweat glands.
 Skin of lid consists of 7 layers of stratified squamous epithelium

Muscles of the eye lid and its actions

 Orbicularis oculi– Function is Closure of the eye , the medial preseptal part of the Orbicularis oculi is
called Horner’s muscle , covers the canaliculi and active in the physiology of lacrimal pump
mechanism
 Levatorpalpebrae superioris(LPS)– Function is Retraction(Elevation) of the lid,
 Mullers muscle – Function is Elevation of the lid involuntarily and the medial part of it is active in
the physiology of lacrimal pump mechanism.
 Riolan muscle – The orbicularis oculi at the edge of the lid margin is called Riolan muscle which
creates a grey line. The function of the Riolan muscle is to express secretions of meibomian gland ,
blinking and keeps cilia in position
 The other movement of the lid is blinking which is a reflex phenomena. The blinking reflex is
described in the last page of this chapter.

Sub muscular areolar tissue

 Lies in a potential space in front of the tarsal plate
 It contains sensory nerve plexus which supplies the lid
 Entry through the grey line of the lid margin , divides the lid into two laminae , the anterior
lamina contains skin and orbicularis , and posterior lamina contains tarsal plate and
Palpebralconjunctiva.

Fibrous tissues of the lid

3
 Orbital septum – arises from the upper and lower orbital rim and fuses with the levator palpebrae
aponeurosis at 2.5 mm above the upper lid crease and in the lower lid margin it fuses with
capsulopalpebral ligament very close to the lower border of the lower tarsal plate. Orbital septum
divides the orbit into two compartments – preseptal compartment and post septal compartment
called orbital cavity.

 Tarsal plate –present one in each lid made of connective Figure 7-3 Tarsal Plates
tissues and gives structural support. The upper orbital
septum is attached to the superior tarsal plate and
laterally attached firmly to the periosteum of the orbit
by the canthal ligaments. Tarsal plate Contain
meibomian glands which secretes the lipid layer of the
tear film.

 Aponeurosis part of the levator palpebrae

superiors(LPS)- The levator palpebrae superioris muscle
at 40 mm of its length from its origin (at common
tendinous ring of the roof of the orbit) transforms
into10 to 12 mm aponeurosis and the junction is marked by thickened fibrous band called Whitnall’s
ligament . Lower part of aponeurosis expands and forms the lateral and medial horns .The medial
horn fuses with medial palpebral ligament and posterior lacrimal crest. The lateral horn divides
the lacrimal gland into orbital and palpebral part and firmly attached to the orbital tubercle. Some
fibers of the aponeurosis is inserted into the skin forming the creases of the upper lid.

 Whitnall’s ligament – The junction of the muscular part of the levator palpebrae superioris and
aponeurosis is thickened as fibrous band called Whitnall’s ligament. It acts as a suspensory
ligament of the upper lid. The lateral part of the ligament which forms the septa enters the lacrimal
gland and gets attached to the orbit and medially attaches to the pully of the superior oblique
tendon.

 Capsulo palpeabral fascia - Lower lid retractors are similar to Muller’s muscle of the upper lid .This is
formed by terminal fibers of the inferior rectus which is attached to the lower part of the lower lid
tarsal plate encompassing the inferior oblique muscle .
It is thickened to form Lockwood’s ligament analogous to Whitnall’s ligament. This Lockwood’s
ligament supports the globe, retracts the lower lid down on down gaze, keeps the lower lid margin in
apposition to the globe.
Medial and Lateral palpebral ligaments – attaches to the sides of tarsal plate and keep them
anchored to the orbital rims. The medial palpebral ligament is attached to the anterior lacrimal crest
and lateral palpebral ligament is attached to the orbital tubercle .These keep the lids close

4
 Sub orbicularis oculi fat pad (SOOF)– overlying the maxillary and zygomatic periosteum , It is
analogous to superiorly located retro orbicularis oculi fat .Situated deep to the eye brows and
extends into the eye lids to the globe and puncti.
Figure 7- 4 Lid Margin
Lid Margin –.
 Two margins – Outer lid margin and inner lid margin .
 In between the two lid margins is a 2mm of tissue called
intermarginal strip.
 The intermarginal strip is one of the junctional areas in the
body which is prone to squamous cell carcinoma.
 It is a mucocutaneous junction , the upper zone is skin of
the lid, the muscle of Riolan , which forms the grey line
and inner zone is the conjunctiva where the openings of
meibomian glands are seen as pits.
 The outer margin contains two or three rows of eye lashes which arises from eye lash follicles and
glands of zeis and molls which supplies to the eye lash follicle.
 The upper eye lashesare concave upwards and lower eye lashes are concave downwards .
 The medial part of the each lid contains punctum which is directed to the eye ball.

The glands of the lid

 The Meibomian glands (Tarsal glands) situated in the tarsal plate about 30 in the upper lid and 12 to
14 in the lower lid are arranged vertically in the substance of tarsal plate..
 Zeis glands– Modified sebaceous glands associated with eye lash follicle which are present in the lid
Margin .
 Moll glands – Modified sweat glands , Present in the lid Margin , opens into eye lash follicle

Palpebral part of the Conjunctiva

 Lies on the back of the lid , very adherent to the tarsal plate , contains glands of globlet cells and at
the upper margin of the tarsal plate the Palpebral part of the Conjunctiva contains glands of
wolfring .

The Nerve Supply - Figure 7-5 Nerve supply to the lid

Sensory supply –
 The upper lid is supplied by the ophthalmic
division of trigeminal nerve through the supra
orbital , supra trochlear, and lacrimal nerves .
 The lower lid is supplied by maxillary division of
trigeminal nerve through the infra orbital part
and medial part is supplied by infra trochlear
nerve.
Motor supply –
 Third nerve supplies the Levator palpebrae
superioris
 Seventh Nerve supplies the Orbicularis oculi
muscle
 The oculosympathetic nerve supplies the Muller’s muscle

5
Blood Supply to the lid
Extensive vascularity of the lids promotes the healing and Figure 7- 6 Blood supply to the lid
protects from infection.
The vascular supply of lid is from two sources –
The ophthalmic artery which is a branch of Internal carotid
artery gives branches i,e,suprapalpebral and Lacrimal
arteries.
These two arteries make a plexus 2 mm above the lower
border of the upper lid with the lateral
palpebral branch of lacrimal artery on the temporal side
and medial palpebral artery on medial side.
 The external carotid gives branches – i.e. Angular and
temporal arteries.
The lower lid has only one arterial arcade close to the
inner tarsal border.
Venous Drainage –
 Pretarsal - Medial Pretarsal drains to angular vein and Figure 7 -7 Lymphatic drainage of
lateral part drains to superficial temporal vein. the
 Post Tarsal – Orbital veins , deeper branches of facial vein
and pterygoid plexus.
 Finally both preseptal and post septal drains to tributeries
superior and inferior ophthalmic vein and cavernous
sinus.
Lymphatic drainage of the lid
Lateral parts of both lids drains into the superficial
preauricular group, parotid,and then into deep cervical
nodes
Medial part of both lids drain into submandibularlymph lid
nodes.

Functions of the Lid –

 The lids will close and covers the eye ball , thus giving protection to the eye .
 The meibomian gland of the lid will secre oily layer of the tear film
Figure 7 - 8 Measurement
there by preventing the evaporation of the tears thus prevents
of the interpalpebral
dry eye.
aperture
 The movements of the eye lid will spread the tear film on the ocular
surface and prevents dry eyes
 Helps the drainage of the tears into the lacrimal sac.

Inter Palpebral aperture

The area between upper and lower lid margin is called Inter Palpebral
aperture . The shape of it is elliptical . The dimensions are vertical 9 to 10mm
and horizontal 28 to 30mm.

For the purpose of Clinical examination of the lid it is convenient to discuss

under four headings
 Clinical examination of the Preseptal area ,
 Clinical examination of tarsal area ,

6
 Clinical examination of the lid margin.
 Examination of the Palpebral aperture
The lesion in the tarsal and preseptal portion of the lid are same . The Figure 7-9 Preseptal cellulitis
division is made to emphasize the preseptal cellulitis of the lid

I. Clinical examination of the Preseptal area

The preseptal area is clinically considered below the eye brow .The orbital
septum which is attached to the superior and inferior orbital rims , to the
respective superior and inferior margin of the tarsal plate of the eye lids
divides the orbital cavity into preseptal area and Post septal area . The area
in front of the orbital septum is called Preseptal area and behind to it is
post septal area called the orbital cavity. The preseptal area is examined
between the brows and superior palpebral border,

The points to be examined clinically in the Preseptal area

• Fullness of the Preseptal area - Preseptal fullness is
Figure 7- 11 Figure 7-10 Retraction
present in front of the orbital septum.
of the preseptal area
Preseptal fullness may be Uniocular or Binocular
 Retraction of the upper lid

Unilateral Preseptal fullness Causes –

 Infection /inflammation of the preseptal area –
Preseptal cellulitis Preseptal inflammation resolves
into lid abscess.
 Diseases of the periorbita causing proptosis i.e mass in the orbital cavity , Pseudo tumor, or infection of
the orbital elements i.e orbital cellulitis
 Injuries to the orbit causing retrobulbar hemorrhage
 Diseases of the eye like pan ophthalmitis , tumors of eye extending into the orbit, Staphyloma
 Inflammations of the adnexa i.e lid inflammation , lid edema, inflammation of the glands of the lid like
Hordeolum externum. Internum , acute dacryocystitis .
Bilateral Preseptal fullness - Non-inflammatory
Causes
• Myxedema
• Nephrotic syndrome
• Acute nephritis
• Congestive heart failure
• Protein malnutrition

Retraction of the Preseptal area Clinically identified by deep groove in the preseptal area above the
superior border of tarsal plate of the upper eye lid
.Causes
 Atrophy of the orbital fat
 Aponeurotic ptosis
 Phthisis bulbi
 Marasmic child

Points to be noted in the lid

 Color of the skin.
 Surface of the skin

7
 Edema
 Injuries. - Contusion or Ecchymosis, lacerations
 Abscess .
Figure 7- 12 Figure 7-13 Absence of
 Inflammation of the glands of the lid Eruptions on the skin skin crease in Ptosis
 Movements of the upper eye lid. of the lid due to
 Position of the eyelid . Herpes Zoster
 Congenital malformations of the lid.

Color of the skin

 May be Normal, Hyper pigmented, Hypo pigmented.
 Hyper pigmentation is seen in moles , thyroid orbitopathy.
 Hypo pigmentation is seen in Hansen’s disease, xanthelasma and vitiligo

Surface of the skin

 Lid crease - absence of lid crease indicates Blepharo ptosis
 Eruption / vesicles - Due to Chicken pox, measles, herpes zoster ophthalmicus infections, molluscum
 Contact dermatitis - Due to Drug allergies to Atropine, antibiotic ointments or drops.

Edema
 The causes of Uniocular and Binocular edema of the lid are similar to the preseptal area lesions
Contusion or Ecchymosis of the lids due to Injuries of the lid
 Contusion or Ecchymosis –- Blood in the layers of the lid –
Blunt trauma, penetrating trauma causing contusions or Ecchymosis and Lacerated injuries etc.

Figure 7-14 Lid Edema Figure 7-15 Lid Abscess Figure 7– 16 Contusion of
the Lid

Abscess
 Suppurative infections of the lid leading to abscess formation.

Inflammation of the glands of the lid

 Hordeolum externum - Acute suppurative infection of the Zeis ,Moll glands of the lid margin and eye lash
follicles . It is present on the outer lid margin of the lid on the base of eye lash.

 Hordeolum internum- Acute suppurative infection of the Meibomian gland ( tarsal gland) is called
Hordeolum internum. It is present in the substance of the tarsal plate away from the lid margin and
painful
.

8
 Chalazion or Tarsal cyst – Chronic inflammatory granuloma of the Meibomian gland, Painless, one or
multiple nodular swellings present in the substance of the tarsal plate away from the lid margin.Some
times chalazion ruptures causing granuloma
Figure 7– 17 Hordeolum Figure 7- 18 Hordeolum Figure 7-19 Chalazion
externum Internum

Examination of movements of the upper eye lid

a)Closure of the lid
b)Elevation of the lid
c)Blinking and Winking
d)Abnormal lid movements

a) Closure of the lid –

Function of the closure of the lid is done by the orbicularis oculi.muscle It is supplied by the lower motor
neuron of the seventh cranial nerve .
Evaluation of the orbicularis oculi
The strength is measured by asking the patient to close the lids tightly against the resistance offered by the
examiner’s index finger and thumb. The power is graded from 1 to 4.
The dysfunction of orbicularis oculi or seventh cranial nerve which supplies it causes
 Lagophthalmos
 Spasm of orbicularis

What is Lagophthalmos?
• Normally when the lids are closed the two eye lid margins will be approximated.
• Inability to approximate the two lid margins is called Lagophthalmos.
Causes for Lagophthalmos Figure 7-20 Lagophthalmos
 Lower motor neuron type of facial palsy. Lesions of the Facial nerve at
the neck of the mandible, stylomastoid foramen like Bell’s palsy, parotid
tumors, chronic systemic infections like Hansen’s disease or fibrosis of
the tarsal plate due to chemical or mechanical injuries.
 Bilateral Lagophthalmos is seen in Hansen’s disease.

Spasm of orbicularis – called Blepharospasm

Types of Blepharospasm
 Simple Blepharospasm is due to ocular causes like corneal ulcer
 Essential Blepharospasm – idiopathic due to neurological diseases.

What is Lid lag?

 Normally the upper eye lid will follow the downward movement of the eyeball
 Inability of the upper lid to follow the downward movement of the eyeball is called lid lag - Seen in Thyroid
orbitopathy, symblepharon.

9
b)Elevation of the upper eye lid –
Elevation of the upper eye lid is done by the levator palpebrae superioris (LPS) which is supplied by a branch
rd
of 3 cranial nerve and Muller’s muscle, a small strip of smooth muscle situated on the superior border of
tarsal plate which is supplied by oculo sympathetic .

Assessment of the function of the LPS – The patient is asked to look in the downward direction and keep the
thumb on the upper orbital margin to lock away the function of the frontalis. A transparent scale is placed in
the middle of the upper lid margin and the patient is asked to look up. Excursion of the upper lid is noted on
the transparent scale. Normal range is 8 to 12 mm.
rd
Reduced elevation is due to abnormal function of LPS or 3 cranial nerve which supplies it causing drooping of
the upper lid and it is called Blepharo Ptosis
The causes for Blepharo ptosis are
 Congenital ,
 True ptosis may be due to LPS muscle dysfunction i.e. neurogenic – 3 nerve palsy, Horner’s syndrome
rd

(Oculo sympathetic paralysis to the Muller’s muscle).

 Myogenic – Myasthenia, Thyroid orbitopathy,
 Aponeurotic causes – Congenital, Senile, trauma on the levator muscle Aponeurosis.
 Mechanical – Due to lid edema, inflammations , tumors ,plexiform Neuromatosis of the lid,
 Pseudo ptosis i.e. Mechanical due to tumors, phthisis, empty socket.

Action of the Muller’s muscle

The function of Muller’s muscle is to elevate the lid. Under action of the Muller’s muscle causes mild ptosis.
Muller’s muscle is supplied by oculo sympathetic. Paralysis of oculo sympathetic causes Horner’s syndrome i.e.
Lid retraction, Miosis, apparent enophthalmos, anhidrosis.

Lid retraction – Gap is seen between inner lid margin and limbus.
 Present in Proptosis, , Exaggeration of the Muller’s action as in Thyrotoxicosis / Thyroid orbitopathy and
Pseudo Proptosis conditions.

c) Blinking is a reflex phenomena.

Blinking is a bilateral simultaneous movement of the upper eye lids

Blink rate –Normal Blink rate 18 to 20 /minute. Increased in Psychological disturbances like apprehension,
Thyrotoxicosis and decreased in Coma, Drowsiness
Winking is the unilateral movement of the upper lid.

d)Abnormal lid movements

Synkinetic movements of the lid with movements of the jaw from side to side / opening or closing of the
mouth is called jaw winking phenomena. There is widening of the palpebral aperture and associated lid
movement

Position of the eyelids – Normal anatomical position of the upper lid is the inner margin of the upper lid
lying 1to 2 mm below the upper limbus.
Normal anatomical position of the lower lid is the inner lid margin aptly touches the lower limbus
The position of the upper lid is measured by MRD-1 (Margin Reflex Distance -I) The position of the Lower lid
is measured by MRD-II: (Margin Reflex Distance- II)

 MRD- 1 (Margin Reflex Distance-I) it is measurement of distance between the corneal light reflex and
centre of the upper lid margin in the primary position . Normal MRD-I is 1 to 5mm

10
 MRD. II - (Margin Reflex Distance-II). it is measurement of distance between the corneal light reflex
and centre of the lower lid margin in the primary position
. Normal MRD-II is 4mm

Measurement of MRD- I:
Figure 7-21 Figure 7-22
 The patient eyes and observer eyes are kept at same
Measurement of Measurement of
level
MRD - 1 MRD - II
 The patient is asked to fix a distant object.
 A fixation light is brought between the patient and the
observer.
 The position of the corneal light reflexis noted .The
distance between the corneal light reflex and the centre
of the upper lid margin is measured.
 If the corneal light reflex is obstructed by the drooping lid,
the drooped lid is elevated until the corneal light reflex
is visible and this is measured in negative mm

Measurement of MRD-II: (Margin Reflex Distance- II)

 Measurement of MRD- II is Same as MRD – I but for the lower lid.
MRD - 1 -- Decreased MRD- 1 - Increased
 Blepharo Ptosis  Lid retraction -Thyrotoxicosis
 Blepharo phimosis Syndrome  Proptosis
 Phthisis and atropic bulbi.
 Anophthalmos

MRD-2 -- Decreased MRD-2 -- Increased

 Blepharo phimosis syndrome  Proptosis
 Fractures of the orbit  Thyrotoxicosis
 Fractures of the maxilla

Growths of the lid margin

• The benign tumours are – Papilloma, Molluscum.
• Squamous cell carcinoma - Commonly arises from an intermarginal strip of Lid margin which is a
junctional area where conjunctiva joins the skin. Squamous cell carcinoma arises from this area like
any junctional areas in the body.
• Other malignant tumors arising from the lid are Basal cell carcinoma, Meibomian gland carcinoma,
Malignant melanoma.
Figure 7-23 Squamous cell Figure 7-24 Meibomian gland Figure 7-25 Basal cell
carcinoma carcinoma Carcinoma

11
Congenital mal formations of the lid –
 Coloboma, - Commonly present in the upper lid . Embryological cleft that usually occurs as an
isolated anomaly in the medial part of the upper lid
 Blepharophimosis - Both horizontal and vertical narrowing of palpebral aperture .
Fusion of the lid margins over portion of their length producing shortening of palpebral fissure.
 Congenital Blepharo Ptosis – Mal development of levator palpebrae superioris
 Ankyloblepharon – congenital Adherence of the two lid margins due to faulty or incomplete lid
th th
separation in 6 or 7 month of foetal development causes ankyloblepharon

Figure 7-26 Coloboma of the Figure 7-27 Figure 7-28 Figure 7- 28

lid Blepharophimosis Blepharoptosis Ankyloblepharon

. III - Examination of the Eye Lid margin –Points to be noted.

 Outer margin
 Inner margin
 Eye lashes
 Thickening of the lid margin – Tylosis
 Crusting of the margins
 Intermarginal strip
 Abnormal position of lid margin
 Inflammation of Glands of the lid margin
 Adhesions of the lid margin
 Parasites in the lid margin

Outer margin
Contains two or three rows of eye lashes
Normally there are about two to three rows of eyelashes on the outer margin of the lid. If there are more than
three rows then it is called Dystrichiasis – it may be congenital or acquired.

Inner margin
Acute angled and aptly opposes the globe and maintains the tear film. If the inner margin is irregular the
integrity of tear film is lost and it results in dry eye.
This is seen in
• Trachoma Figure 7-29 Trichiasis
• Chemical and mechanical injuries of the lid margin of the lid

Eye lashes - Normally the upper eye lashes are concave upwards and the lower
eye lashes are concave downwards .The abnormalities seen in eye lashes are
Trichiasis , Madarosis, Poliosis.

Trichiasis - Misdirection of eye lashes - The lashes rubs constantly on the cornea
and conjunctiva leading to chronic conjunctivitis, keratitis and corneal ulcer.

12
causes
• Trachoma
• Hansen’s disease.
• Mechanical injuries
• Chemical injuries of the eye
• Ulcerative Blepharitis

Madarosis -Loss of eye lashes or eye brows is called Madarosis . Figure 7-30 Madarosis
Normally the life span of eye lash is about 120 days – same as that of R.B.Cs life of the lid and lashes
span. After that eyelashes regrow .
• Myxoedema
• Hansen`s disease.
• Trachoma
• Meibomian gland carcinoma – corresponding eye lash loss is present
• Ulcerative Blepharitis

Poliosis –
• Grey color of the eye lashes is called poliosis.
• Commonly seen in old age, vitiligo, Harada disease (Exudative RD, Poliosis).

Thickening of the lid margin is called Tylosis

Causes
• Myxoedema
• Trachoma
• Ulcerative and Squamous Blepharitis

Crusting of the margins of the lid

Figure 7-31
Crusting of the margin and eye lashes is seen in catarrhal, purulent, and
Crusting of the
mucopurulent conjunctivitis, Squamous Blepharitis , Ulcerative Blepharitis
margins of the
lids
Inter marginal strip of the lid Margin
• An area of about 2to 3 mm between the outer and inner margin of the lid is
called intermarginal strip. It is a junctional area of the skin and conjunctiva, and is
prone to squamous cell carcinoma.
• There is a fine grey line on intermarginal strip. through this the lid can be split
into two layers , The outer lamellae which contains skin and orbicularis oculi and
the inner lamellae which contain the tarsal plate and its structures
• Below the grey line about 18 to 24 in the upper lid and about 12 to 14 in the lower lid are openings of
the meibomian glands. These glands produce oily layer which constitutes outer layer of the tear film.
• In chronic meibomitis the openings of meibomian glands are prominent and is seen with Mucus or
mucopurulent discharge.
Punctum in the intermarginal strip
• On the inner side of the intermarginal strip there is a opening called puncta one in the upper lid and one
in the lower lid ,which are inverted and aptly opposes the eye ball to suck the excessive tears by capillary
action. These are the openings of the lacrimal drainage system.
Clinical point to be noted in the punctum
• Atresia – Congenital absence of the punctum
• Eversion of the punctum – Eversion of the punctum is seen in ectropion of the lower lid and scarring of
the lower lid

13
Abnormal position of lid margin – Ectropion and
Figure 7-32 Ectropion Figure 7-33 Entropion
Entropion
of the lower lid
Ectropion – Outward rolling of the lid margin is called
ectropion
 Symptoms are Epiphora, F.B sensation.
 Signs are –eversion of the upper lid, corneal haze /
ulcer, chronic conjunctivitis.
 Causes of Ectropion of the lower lid- are Cicatricial
and Paralysis of orbicularis like Hansen’s
disease, Facial palsy, Senile, Idiopathic
 Causes of Ectropion of the upper lid – Mechanical
and chemical, thermal burns
Entropion –
 Inward rolling of the lid margin is called Entropion .
Symptoms are epiphora, or lacrimation, F.B sensation.
 Signs are Inward rolling of the lid margin, Chronic conjunctivitis , corneal haze / ulcer
 Entropion may be congenital or acquired. .
Acquired Entropion can be
 cicatricial as in Trachoma, Hansen’s disease, conjunctival scarring conditions like stevens Johnson
syndrome, membranous conjunctivitis or
 Spastic as in Senility, empty socket, phthisis bulbi, enophthalmos.

Inflammation of the lid margin

Inflammation of the lid margin is called Blepharitis. Figure 7-34 Squamous Figure 7-35 Ulcerative
There are two types. Squamous and ulcerative Blepharitis Blepharitis
Blepharitis.

In Squamous Blepharitis dandruff like white flakes seen

at the base of the eye lash.
In Ulcerative Blepharitis – Yellowish wet scabs
present.On removal of which there will be bleeding
ulcers and associated with trichiasis and chronic
conjunctivitis.

Adhesions of the lid margin - Symblepharon

Figure 7-36 Symblepharon
Symblepharon - Adherence of lid to the eye ball is called
Symblepharon. It may be anterior, Posterior or Total.
Causes
• Infections like trachoma
• Chemical injuries or burns
• Stevens-johnson syndrome

Parasites in the lid margin -

Commonly body lice (phthiriasis) cling to the skin of lid margin and their
nits are in the eye lashes causing itching . This is called phthiriasis.

IV . Examination of the Palpebral aperture

The area in between two lid margins which is elliptical in shape
 Normal dimensions – 28 mm horizontally and 9 mm vertically.

14
 Reduced dimensions – seen in Blepharo ptosis and blepharophimosis
 Increased dimensions – seen in Exophthalmos , Proptosis
Normally when the lids are closed the two eye lid margins will be approximated.
• Inability to approximate the two lids margins is called Lagophthalmos

Format for the Examination of the Eye Lids

Examination of the Preseptal area Right eye Left eye

• Fullness of the Preseptal area- either Uniocular or
Binocular
• Palpation of the Preseptal area
Any swellings if present to be palpated and describe
the swelling in detail.

Examination of the Eye Lids Right Eye Left Eye

Color of the skin
Creases of the lid
Eruption of vesicles
Diffuse Edema.
Localized swellings
Hordeolum internum
Chalazion or Tarsal cyst
Contusion or Ecchymosis
Contact dermatitis
Injuries
Abscess
Movements of the eye lid
Closure of the lid
Elevation of the lid
Blinking and Winking
Abnormal lid movements
Position of the eyelid
MRD – I& MRD-II
Congenital malformations of the lid

Format for the Examination of the Eye Lid margin

Examination of the Eye Lid margin Right Eye Left Eye
Outer margin
Inner margin
Eye lashes
Trichiasis , Madarosis, Poliosis
Thickening of the lid margin
Crusting of the margins
Intermarginal strip
Openings of the meibomian glands
Punctum – Atresia . Eversion of the punctum
Abnormal position of lid margin

15
Ectropion
Entropion
Inflammation of the lid margin
Squamous and ulcerative
Blepharitis
Inflammation of Glands of the lid margin
Hordeolum externum
Growths of the lid margin
Adhesions of the lid margin
Parasites in the lid margin

Format for the Examination of the palpebral aperture

Examination of the palpebral aperture Right Eye Left Eye
Measurement of palpebral aperture
Reduced or Increased
Lagophthalmos

OSCE Diagrams to be practiced.

 MRD-I  Structure of the lid
 MRD- II  Layers of the lid
 Measurement of levator function  Margin of the lid
 Measurement of palpebral aperture  Lymphatic drainage of the lid

Menace reflex and Blink reflex

1.5.Menace reflex andBlink Reflex

The menace reflex - Blink reflex to visual threat
 Menace Reflex is one of the three forms of blink reflex.
 Menace Reflex is a learned reflex, not present at birth.
 This is reflex blinking that occurs in response to the rapid approach of an object. The reflex comprises
of blinking of the eye lids in order to protect the eyes from potential damage.
 Menace reflex, beside blinking reflex comprises turning of the head, neck, or even the trunk away
from the optical stimulus that triggers the reflex.
 The menace reflex is lost in cortical damage retaining the pupillary reflex.
 The neural pathway of the menace reflex comprises of optic nerve and facial nerve. It is mediated by
tecto bulbar fibers in the rostral colliculi of the midbrain passing from the optic tract to the accessory
nuclei and then to the spinal cord and lower motor neurons that innervate the head, neck, and body
muscles affecting the reflex. The facial nerve is mediated through acorticotectopontocerebellar
pathway.

16
 Medial retina → optic nerve → crossing at Optic chiasma→ Optic tract→ contra lateral geniculate
body motor cortex → pontine nucleus → to the cerebellum → both facial nerve
 Menace Reflex should be performed carefully, advancing the first towards the eye without creating
the airwave or touching the eye lashes, and
observing the blink. Figure 1.5-
 The menace reflex is not well elicited from
the lateral retina.

. Blink Reflex. syn – corneal reflex, eye

lid reflex
 Involuntary blinking reflex
 Initiated by stimulation of the cornea by
touching or
by foreign body or by peripheral stimulus or 1
initiated
by the tear film break down.
 Bilateral reflex – stimulation of one cornea normally
has a consensual response with both eyes normally closing.
 Blinking is often associated with a shift in gaze thus
linked with extra ocular muscles movement.
 The purpose of this reflex is to protect the eyes from dry eyes, foreign bodies, bright light and sound
greater than 40 to 60 db.
 The lids spreads tear film over the ocular surface

The pathway of corneal reflex –

 Afferent Pathway - The reflex is mediated by nasociliary branch of ophthalmic branch of Vth
trigeminal cranial nerve, a sensory nerve.
 Efferent Pathway - The temporal and zygomatic branches of the facial nerve initiate motor
response
 The central nucleus is located in the pons- globus pallidus of the basal ganglia contains a blinking
center that controls blinking
Corneal touch→ through the ophthalmic division of fifth cranial nerve →nucleus of trigeminal
nerve i.e. Vth cranial nerve → to the facial motor nucleus (on both sides) → temporal branch of
facial nerve or VII cranial nerve → orbicularis oculi muscle →Blink.
 Causes for Absence of Corneal reflex--- Coma, damage to the ophthalmic branch of the trigeminal
nerve
-----------------------------------------------

17
Chapter 7. The clinical anatomy the Eye Lid

Num COMPETENCY Domai LevelK Cor Suggested SuggestedAsse Number Verti Horiz
ber The student should be able to nK/S/A /KH/S e(Y TeachingLea ssmentmetho require cal ontal
/C H/P /N) rningmetho d dto Integ integ
d certifyP ratio ratio
n n
Topic:Lids and Adnexa ,Orbit NumberofCompetencies:(08) Numberofproceduresthatrequirecertification:(NIL)

OP2.1 Enumerate the causes, describe and discuss the K KH Y Lecture, Written/Viva Hum
aetiology, clinical presentations and diagnostic Small voce an
features of common conditions of the lid and groupdiscu Anat
adnexa including Hordeolum externum/internum, ssion omy
blepharitis,preseptalcellulitis,dacryocystitis,hema
ngioma,dermoid,ptosis,entropion,lidlag,
lagopthalmos
OP2.2 Demonstrate the symptoms & clinica S S Y DOAP Skill
signs of conditions enumerated session assessment
inOP2.1
OP2.3 Demonstrate under supervision clinical S S Y DOA Skill
procedures performed in the lid including: bells H P assessment
phenomenon, assessment of sessi
entropion/ectropion, performthe regurgitation on,Le
test of lacrimal sac. Massage technique in cong. cture
dacryocystitis, and trichiatic cilia removal
byepilation
OP2.4 Describe the aetiology, clinical s K K Y Lecture, Written/V
presentation . Discus complications and H Small group iva voce
management of orbital cellulitis discussion
OP2.5 Describe the clinical features on ocular K K Y Lecture, Written/Viva
examination and managementofa patien twith H Small voce
cavernous sinus thrombosis groupdiscu
ssion
OP2.6 Enumeratethecausesanddescribethedifferentiatin K K Y Lecture, Written/Viva
gfeatures,andclinicalfeatures and management H Small voce
ofproptosis groupdiscu
ssion

79
OP2.7 Classifythevarioustypesoforbitaltumours.Different K K Y Lecture, Written/Viva
iatethesymptoms and signs of the presentation of H Small voce
various types of ocular tumours groupdiscu
ssion
OP2.8 Listtheinvestigationshelpfulindiagnosisoforbitaltu K K Y Lecture, Written/Viva
mors.Enumerate the indications for appropriate H Small voce
referral groupdiscu
ssion

80
Chapter 7. The clinical anatomy the Eye Lid
2. Topic : Lids , Adnexa, Orbit and (Clinical examination of Eye brow and pre septal cellulitis and Clinical examination of Lacrimal
apparatus )
.No Topic Clinical skills Domain Level Core Suggested No Vertical Grade Sign of
K/S/A/C K/KH/ Y/N Suggested assessment Required integration /Marks Faculty.
SH/P Teaching Method to certify Date
and
learning
method
Demonstrate the S S Y DOAP Skill 1
OP2.1 symptoms & clinical session Assessment
sign of conditions Lecture
presepta cellulitis,
Demonstrate the S S Y DOAP Skill
OP2.1 symptoms & clinical session Assessment
sign of conditions Lecture
Perform the
regurgitation test of
lacrimal sac. Massage
technique in cong.
dacryocystitis
OP2.2 Demonstrate the S S Y DOAP Skill
symptoms & clinical session Assessment
sign of conditions Lecture
Hordeolumexternum/
internum, blepharitis
hemangioma,
dermoid, ptosis,
entropion, lidlag,
lagopthalmos
OP2.3 Demonstrate under S S Y DOAP Skill
supervision clinical session Assessment
procedures Lecture
performed in the lid
including: bells
phenomenon,
assessment of
entropion/ectropion,
, trichiatic cilia
removal by epilation

81
Chapter 7. Clinical examination of the eye lids
(Chapter 7.1 The clinical anatomy of the Eye Lid , Chapter 7.2 clinical examination of preseptal area, Chapter
7.3 Clinical examination of the tarsal part of the eye lid, Chapter 7.4 Clinical examination of Lid Margin,
Chapter 7.5 Clinical examination of Interpalpebral aperture, Chapter 7.6 Menace reflex and Blink reflex
Chapter 7.7 Format for examination of eye lids )
The lids are a pair of multi layered fibromuscular cutaneous folds in front of each eye. The upper lid is mobile
where as the lower one is immobile.

Chapter 7.1 Clinical Anatomy of

the eye Lid Figure 7-1 Structure of the lid Diagram 7-2 Layers of the lid

The layers of the lid from out to in

 Skin and subcutaneous
tissue
 Muscular layer
 Sub muscular areolar
tissue
 Fibrous layer I,e Orbital
septum ,
Tarsal plate and others
 Orbital fat
 Palpebral conjunctiva

Skin and subcutaneous tissue –

 Thinnest area of the skin in the body .
 The preseptal area of the skin is loosely attached to the underlying tissue as against the remaining
area of the eye lid , which creates a potential space for fluid collection leading to edema
 The eye lid skin creases are formed by the attachment of few of Levatorpalpebrae superioris
aponeurotic fibers on to the backside of skin
 Contains sebaceous and sweat glands.
 Skin of lid consists of 7 layers of stratified squamous epithelium

Muscles of the eye lid and its actions

82
 Mullers muscle – Function is Elevation of the lid involuntarily and the medial part of it is active in
the physiology of lacrimal pump mechanism.
 Riolan muscle – The orbicularis oculi at the edge of the lid margin is called Riolan muscle which
creates a grey line. The function of the Riolan muscle is to express secretions of meibomian gland ,
blinking and keeps cilia in position
 The other movement of the lid is blinking which is a reflex phenomena. The blinking reflex is
described in the last page of this chapter.

Sub muscular areolar tissue

Fibrous tissues of the lid

 Orbital septum – arises from the upper and lower orbital rim and fuses with the levator palpebrae
aponeurosis at 2.5 mm above the upper lid crease and in the lower lid margin it fuses with
capsulopalpebral ligament very close to the lower border of the lower tarsal plate. Orbital septum
divides the orbit into two compartments – preseptal compartment and post septal compartment
called orbital cavity.

 Tarsal plate –present one in each lid made of connective Figure 7-3 Tarsal Plates

tissues and gives structural support. The upper orbital

septum is attached to the superior tarsal plate and
laterally attached firmly to the periosteum of the orbit
by the canthal ligaments. Tarsal plate Contain
meibomian glands which secretes the lipid layer of the
tear film.

 Aponeurosis part of the levator palpebrae

superiors(LPS)- The levator palpebrae superioris muscle
at 40 mm of its length from its origin (at common tendinous ring of the roof of the orbit) transforms
into10 to 12 mm aponeurosis and the junction is marked by thickened fibrous band called Whitnall’s
ligament . Lower part of aponeurosis expands and forms the lateral and medial horns .The medial
horn fuses with medial palpebral ligament and posterior lacrimal crest. The lateral horn divides

83
the lacrimal gland into orbital and palpebral part and firmly attached to the orbital tubercle. Some
fibers of the aponeurosis is inserted into the skin forming the creases of the upper lid.

Orbital Fat
 It lies in between a space anteriorly bounded by orbital septum and posteriorly by the
Levatorpalpebraesuperioris in the upper lid , and capsulopalpebral ligament in the lower lid
 In upper lid there are two nasal and central , In the Lower lid three Nasal, central and Temporal
pockets of fat .
Figure 7- 4 Lid Margin
 Central pad of fat is the land mark for identification of LPS
muscle on the back and orbital septum in front.
 Sub orbicularis oculi fat pad (SOOF)– overlying the maxillary
and zygomatic periosteum , It is analogous to superiorly
located retro orbicularis oculi fat .Situated deep to the eye
brows and extends into the eye lids to the globe and puncti.

Lid Margin –.
 Two margins – Outer lid margin and inner lid margin .
 In between the two lid margins is a 2mm of tissue called intermarginal strip.
 The intermarginal strip is one of the junctional areas in the body which is prone to squamous cell
carcinoma.

84
 It is a mucocutaneous junction , the upper zone is skin of the lid, the muscle of Riolan , which forms
the grey line and inner zone is the conjunctiva where the openings of meibomian glands are seen
as pits.
 The outer margin contains two or three rows of eye lashes which arises from eye lash follicles and
glands of zeis and molls which supplies to the eye lash follicle.
 The upper eye lashesare concave upwards and lower eye lashes are concave downwards .
 The medial part of the each lid contains punctum which is directed to the eye ball.

The glands of the lid

Figure 7-5 Nerve supply to the lid

Palpebral part of the Conjunctiva
 Lies on the back of the lid , very adherent to the
tarsal plate , contains glands of globlet cells and
at the upper margin of the tarsal plate the
Palpebral part of the Conjunctiva contains
glands of wolfring .
The Nerve Supply -
Sensory supply –
 The upper lid is supplied by the ophthalmic division of
Figure 7- 6 Blood supply to the lid
trigeminal nerve through the supra orbital , supra trochlear,
and lacrimal nerves .
 The lower lid is supplied by maxillary division of trigeminal nerve
through the infra orbital part and medial part is supplied by infra
trochlear nerve. Motor supply –
 Third nerve supplies the Levator palpebrae superioris
 Seventh Nerve supplies the Orbicularis oculi muscle
 The oculosympathetic nerve supplies the Muller’s muscle

Blood Supply to the lid

Extensive vascularity of the lids promotes the healing and protects from infection.
The vascular supply of lid is from two sources –

85
The ophthalmic artery which is a branch of Internal carotid artery gives branches i,e,suprapalpebral and
Lacrimal arteries.
These two arteries make a plexus 2 mm above the lower border of the upper lid with the lateral
palpebral branch of lacrimal artery on the temporal side and medial palpebral artery on medial side.
 The external carotid gives branches – i.e. Angular and temporal arteries.
The lower lid has only one arterial arcade close to the inner tarsal border.
Venous Drainage –
 Pretarsal - Medial Pretarsal drains to angular vein and Figure 7 -7 Lymphatic drainage of
lateral part drains to superficial temporal vein. the
 Post Tarsal – Orbital veins , deeper branches of facial vein
and pterygoid plexus.
 Finally both preseptal and post septal drains to tributeries
superior and inferior ophthalmic vein and cavernous
sinus.
Lymphatic drainage of the lid
Lateral parts of both lids drains into the superficial
preauricular group, parotid,and then into deep cervical
nodes lid
Medial part of both lids drain into submandibularlymph
nodes.
Figure 7 - 8 Measurement
of the interpalpebral
Functions of the Lid – aperture
 The lids will close and covers the eye ball , thus giving protection to
the eye .
 The meibomian gland of the lid will secre oily layer of the tear film
there by preventing the evaporation of the tears thus prevents
dry eye.
 The movements of the eye lid will spread the tear film on the ocular
surface and prevents dry eyes
 Helps the drainage of the tears into the lacrimal sac.

Inter Palpebral aperture

The area between upper and lower lid margin is called Inter Palpebral aperture . The shape of it is
elliptical . The dimensions are vertical 9 to 10mm and horizontal 28 to 30mm.

-------------------------

86
Chapter 7.2 clinical examination of the Preseptal area

For the purpose of Clinical examination of the lid it is convenient to discuss under four headings

 Clinical examination of the Preseptal area ,

 Clinical examination of tarsal area ,
 Clinical examination of the lid margin.
 Examination of the Palpebral aperture
The lesions in the tarsal and preseptal portion of the lid are same . The division is made to emphasize the
preseptal cellulites and others .

I. Clinical examination of the Preseptal area

The preseptal area is clinically considered below the eye brow .The orbital
Figure 7-9 Preseptal cellulitis
septum which is attached to the superior and inferior orbital rims , to the
of the lid
respective superior and inferior margin of the tarsal plate of the eye lids divides
the orbital cavity into preseptal area and Post septal area . The area in front of
the orbital septum is called Preseptal area and behind to it is post septal area
called the orbital cavity. The preseptal area is examined between the brows
and superior palpebral border,

The points to be examined clinically in the Preseptal area

• Fullness of the Preseptal area - Preseptal fullness is present in front of the
orbital septum.P a g e | 87
Preseptal fullness may be Uniocular or Binocular
Figure 7- 10 Figure 7-11 Retraction

 Retraction of the upper lid of the preseptal area

Unilateral Preseptal fullness Causes –

87
 Injuries to the orbit causing retrobulbar hemorrhage
 Diseases of the eye like pan ophthalmitis , tumors of eye extending into the orbit, Staphyloma
 Inflammations of the adnexa i.e lid inflammation , lid edema, inflammation of the glands of the lid like
Hordeolum externum. Internum , acute dacryocystitis .

Bilateral Preseptal fullness - Non-inflammatory

Causes
• Myxedema
• Nephrotic syndrome
• Acute nephritis
• Congestive heart failure
• Protein malnutrition

Retraction of the Preseptal area Clinically identified by deep groove in the preseptal area above the superior
border of tarsal plate of the upper eye lid

.Causes
 Atrophy of the orbital fat
 Aponeurotic ptosis
 Phthisis bulbi
 Marasmic child
---------------------------------

88
Chapter 7.3 Clinical examination of the tarsal part of the eye lid

Clinical Points to beexamined in the tarsal part of eye lid

 Color of the skin.
 Surface of the skin
 Edema
 Injuries. - Contusion or Ecchymosis, lacerations
 Abscess .
Figure 7- 12 Figure 7-13 Absence of skin
 Inflammation of the glands of the lid
Eruptions on the skin crease in Ptosis
 Movements of the upper eye lid.
of the lid due to
 Position of the eyelid . Herpes Zoster
 Congenital malformations of the lid.

Color of the skin

 May be Normal, Hyper pigmented, Hypo pigmented.
 Hyper pigmentation is seen in moles , thyroid orbitopathy.
 Hypo pigmentation is seen in Hansen’s disease, xanthelasma and vitiligo

Surface of the skin

Edema
 The causes of Uniocular and Binocular edema of the lid are similar to the preseptal area lesions

Contusion or Ecchymosis of the lids due to Injuries of the lid

 Contusion or Ecchymosis –- Blood in the layers of the lid –
Blunt trauma, penetrating trauma causing contusions or Ecchymosis and Lacerated injuries etc.

89
Figure 7-14 Lid Edema Figure 7-15 Lid Abscess Figure 7– 16 Contusion of
the Lid

Abscess
 Suppurative infections of the lid leading to abscess formation.

Inflammation of the glands of the lid

 Hordeolum externum - Acute suppurative infection of the Zeis ,Moll glands of the lid margin and eye lash
follicles . It is present on the outer lid margin of the lid on the base of eye lash.

 Hordeolum internum- Acute suppurative infection of the Meibomian gland ( tarsal gland) is called Hordeolum
internum. It is present in the substance of the tarsal plate away from the lid margin and painful
.

 Chalazion or Tarsal cyst – Chronic inflammatory granuloma of the Meibomian gland, Painless, one or multiple
nodular swellings present in the substance of the tarsal plate away from the lid margin.Some times
chalazion ruptures causing granuloma

Figure 7– 17 Hordeolum Figure 7- 18 Hordeolum Figure 7-19 Chalazion

externum Internum

90
Examination of movements of the upper eye lid
a)Closure of the lid
b)Elevation of the lid

c)Blinking and Winking

d)Abnormal lid movements

a) Closure of the lid –

Function of the closure of the lid is done by the orbicularis oculi.muscle It is supplied by the lower motor neuron
of the seventh cranial nerve .
Evaluation of the orbicularis oculi

The strength is measured by asking the patient to close the lids tightly against the resistance offered by the
examiner’s index finger and thumb. The power is graded from 1 to 4.

The dysfunction of orbicularis oculi or seventh cranial nerve which supplies it causes

 Lagophthalmos
 Spasm of orbicularis

What is Lagophthalmos?
• Normally when the lids are closed the two eye lid margins will be approximated.
• Inability to approximate the two lid margins is called Lagophthalmos.
Figure 7-20 Lagophthalmos
Causes for Lagophthalmos
 Lower motor neuron type of facial palsy. Lesions of the Facial nerve at the
neck of the mandible, stylomastoid foramen like Bell’s palsy, parotid tumors,
chronic systemic infections like Hansen’s disease or fibrosis of the tarsal plate
due to chemical or mechanical injuries.
 Bilateral Lagophthalmos is seen in Hansen’s disease.

Spasm of orbicularis – called Blepharospasm

Types of Blepharospasm
 Simple Blepharospasm is due to ocular causes like corneal ulcer
 Essential Blepharospasm – idiopathic due to neurological diseases.

91
What is Lid lag?
 Normally the upper eye lid will follow the downward movement of the eyeball
 Inability of the upper lid to follow the downward movement of the eyeball is called lid lag - Seen in Thyroid
orbitopathy, symblepharon.
b)Elevation of the upper eye lid –
rd
Elevation of the upper eye lid is done by the levator palpebrae superioris (LPS) which is supplied by a branch of 3
cranial nerve and Muller’s muscle, a small strip of smooth muscle situated on the superior border of tarsal plate
which is supplied by oculo sympathetic .

rd
Reduced elevation is due to abnormal function of LPS or 3 cranial nerve which supplies it causing drooping of the
upper lid and it is called Blepharo Ptosis

The causes for Blepharo ptosis are

 Congenital ,
 True ptosis may be due to LPS muscle dysfunction i.e. neurogenic – 3 nerve palsy, Horner’s syndrome (Oculo
rd

sympathetic paralysis to the Muller’s muscle).

Action of the Muller’s muscle

The function of Muller’s muscle is to elevate the lid. Under action of the Muller’s muscle causes mild ptosis.
Muller’s muscle is supplied by oculo sympathetic. Paralysis of oculo sympathetic causes Horner’s syndrome i.e. Lid
retraction, Miosis, apparent enophthalmos, anhidrosis.

92
c) Blinking is a reflex phenomena.
Blinking is a bilateral simultaneous movement of the upper eye lids

Blink rate –Normal Blink rate 18 to 20 /minute. Increased in Psychological disturbances like apprehension,
Thyrotoxicosis and decreased in Coma, Drowsiness

Winking is the unilateral movement of the upper lid.

d)Abnormal lid movements

Synkinetic movements of the lid with movements of the jaw from side to side / opening or closing of the mouth is
called jaw winking phenomena. There is widening of the palpebral aperture and associated lid movement

The position of the upper lid is measured by MRD-1 (Margin Reflex Distance -I) The position of the Lower lid is
measured by MRD-II: (Margin Reflex Distance- II)

 MRD- 1 (Margin Reflex Distance-I) it is measurement of distance between the corneal light reflex and
centre of the upper lid margin in the primary position . Normal MRD-I is 1 to 5mm
 MRD. II - (Margin Reflex Distance-II). it is measurement of distance between the corneal light reflex and
centre of the lower lid margin in the primary position
. Normal MRD-II is 4mm
Figure 7-21 Figure 7-22
Measurement of MRD- I: Measurement of Measurement of
MRD - 1 MRD - II
 The patient eyes and observer eyes are kept at same level
 The patient is asked to fix a distant object.
 A fixation light is brought between the patient and the
observer.
 The position of the corneal light reflexis noted .The distance
between the corneal light reflex and the centre of the upper
lid margin is measured.
 If the corneal light reflex is obstructed by the drooping lid, the
drooped lid is elevated until the corneal light reflex is visible and this is measured in negative mm
Measurement of MRD-II: (Margin Reflex Distance- II)

93
 Measurement of MRD- II is Same as MRD – I but for the lower lid.
MRD - 1 -- Decreased MRD- 1 - Increased

 Blepharo Ptosis  Lid retraction -Thyrotoxicosis

 Blepharo phimosis Syndrome  Proptosis
 Phthisis and atropic bulbi.

 Anophthalmos

MRD-2 -- Decreased MRD-2 -- Increased

 Blepharo phimosis syndrome  Proptosis

 Fractures of the orbit  Thyrotoxicosis
 Fractures of the maxilla

Growths of the lid margin

• The benign tumours are – Papilloma, Molluscum.

• Squamous cell carcinoma - Commonly arises from an intermarginal strip of Lid margin which is a junctional
area where conjunctiva joins the skin. Squamous cell carcinoma arises from this area like any junctional
areas in the body.
• Other malignant tumors arising from the lid are Basal cell carcinoma, Meibomian gland carcinoma, Malignant
melanoma.
Figure 7-23 Squamous cell Figure 7-24 Meibomian gland Figure 7-25 Basal cell Figure7-25Malignant
Melanoma of conjunctival
carcinoma carcinoma Carcinoma Nevus

94
Congenital mal formations of the lid –
 Coloboma, - Commonly present in the upper lid . Embryological cleft that usually occurs as an isolated
anomaly in the medial part of the upper lid
 Blepharophimosis - Both horizontal and vertical narrowing of palpebral aperture .
Fusion of the lid margins over portion of their length producing shortening of palpebral fissure.

 Congenital Blepharo Ptosis – Mal development of levator palpebrae superioris

 Ankyloblepharon – congenital Adherence of the two lid margins due to faulty or incomplete lid
th th
separation in 6 or 7 month of foetal development causes ankyloblepharon

Figure 7-26 Coloboma of the Figure 7-27 Figure 7-28 Figure 7- 28

lid Blepharophimosis Blepharoptosis Ankyloblepharon

95
Chapter 7.4 - Examination of the Eye Lid margin

Clinical points to be examined

Inner margin
Acute angled and aptly opposes the globe and maintains the tear film. If the inner margin is irregular the integrity
of tear film is lost and it results in dry eye.
This is seen in Figure 7-29 Trichiasis
of the lid
• Trachoma
• Chemical and mechanical injuries of the lid margin

Eye lashes - Normally the upper eye lashes are concave upwards and the lower eye
lashes are concave downwards .The abnormalities seen in eye lashes are Trichiasis ,
Madarosis, Poliosis.

Trichiasis - Misdirection of eye lashes - The lashes rubs constantly on the cornea and conjunctiva leading to
chronic conjunctivitis, keratitis and corneal ulcer.

96
causes
• Trachoma
• Hansen’s disease. Figure 7-30 Madarosis

• Mechanical injuries of the lid and lashes

• Chemical injuries of the eye

• Ulcerative Blepharitis

Madarosis -Loss of eye lashes or eye brows is called Madarosis .

Normally the life span of eye lash is about 120 days – same as that of R.B.Cs life span.
After that eyelashes regrow .

• Myxoedema
• Hansen`s disease.
• Trachoma
• Meibomian gland carcinoma – corresponding eye lash loss is present
• Ulcerative Blepharitis

Poliosis –
• Grey color of the eye lashes is called poliosis.
• Commonly seen in old age, vitiligo, Harada disease (Exudative RD, Poliosis).
Figure 7-31 Crusting of
the margins of the lids
Thickening of the lid margin is called Tylosis
Causes
• Myxoedema
• Trachoma
• Ulcerative and Squamous Blepharitis

Crusting of the margins of the lid

Crusting of the margin and eye lashes is seen in catarrhal, purulent, and
mucopurulent conjunctivitis, Squamous Blepharitis , Ulcerative Blepharitis

97
Inter marginal strip of the lid Margin
• An area of about 2to 3 mm between the outer and inner margin of the lid is called intermarginal strip. It is a
junctional area of the skin and conjunctiva, and is prone to squamous cell carcinoma.
• There is a fine grey line on intermarginal strip. through this the lid can be split into two layers , The outer
lamellae which contains skin and orbicularis oculi and the inner lamellae which contain the tarsal plate and its
structures
• Below the grey line about 18 to 24 in the upper lid and about 12 to 14 in the lower lid are openings of the
meibomian glands. These glands produce oily layer which constitutes outer layer of the tear film.
• In chronic meibomitis the openings of meibomian glands are prominent and is seen with Mucus or
mucopurulent discharge.
Punctum in the intermarginal strip

• On the inner side of the intermarginal strip there is a opening called puncta one in the upper lid and one in
the lower lid ,which are inverted and aptly opposes the eye ball to suck the excessive tears by capillary action.
These are the openings of the lacrimal drainage system.
Clinical point to be noted in the punctum

• Atresia – Congenital absence of the punctum

• Eversion of the punctum – Eversion of the punctum is seen in ectropion of the lower lid and scarring of the
lower lidP a g e | 98
Abnormal position of lid margin – Ectropion and
Figure 7-32 Ectropion Figure 7-33 Entropion
Entropion of the lower lid
Ectropion – Outward rolling of the lid margin is called
ectropion

 Symptoms are Epiphora, F.B sensation.

 Signs are –eversion of the upper lid, corneal haze /
ulcer, chronic conjunctivitis.
 Causes of Ectropion of the lower lid- are Cicatricial and Paralysis of orbicularis like Hansen’s disease, Facial
palsy, Senile, Idiopathic
 Causes of Ectropion of the upper lid – Mechanical and chemical, thermal burns
Entropion –

 Inward rolling of the lid margin is called Entropion .

Symptoms are epiphora, or lacrimation, F.B sensation.

 Signs are Inward rolling of the lid margin, Chronic conjunctivitis , corneal haze / ulcer

98
 Entropion may be congenital or acquired. .
Acquired Entropion can be

 cicatricial as in Trachoma, Hansen’s disease, conjunctival scarring conditions like stevens Johnson syndrome,
membranous conjunctivitis or
 Spastic as in Senility, empty socket, phthisis bulbi, enophthalmos.

Inflammation of the lid margin

Inflammation of the lid margin is called Blepharitis. There Figure 7-34 Squamous Figure 7-35 Ulcerative

are two types. Squamous and ulcerative Blepharitis. Blepharitis Blepharitis

In Squamous Blepharitis dandruff like white flakes seen at

the base of the eye lash.

In Ulcerative Blepharitis – Yellowish wet scabs present.On

removal of which there will be bleeding ulcers and
associated with trichiasis and chronic conjunctivitis.

Figure 7-36 Symblepharon

Adhesions of the lid margin - Symblepharon
Symblepharon - Adherence of lid to the eye ball is called Symblepharon. It
may be anterior, Posterior or Total.
Causes

• Infections like trachoma

• Chemical injuries or burns
• Stevens-johnson syndrome

Parasites in the lid margin -

Commonly body lice (phthiriasis) cling to the skin of lid margin and their nits are in the eye lashes causing itching .
This is called phthiriasis palpebrum .

99
Chapter 7.5 Examination of the inter Palpebral aperture

The area in between two lid margins is called inter palpebral aperture , which is elliptical in shape

 Normal dimensions – 28 mm horizontally and 9 mm vertically.

 Reduced dimensions – seen in Blepharo ptosis and blepharophimosis
 Increased dimensions – seen in Exophthalmos , Proptosis
Normally when the lids are closed the two eye lid margins will be
approximated.

• Inability to approximate the two lids margins is called Lagophthalmos

Details of Lagophthalmos and . lid lag is described in the previous chapters
Figure 7-20 Lagophthalmos

OSCE Diagrams to be practiced.

 MRD-I  Section of the lid

 MRD- II  Layers of the lid
 Measurement of levator function  Margin of the lid
 Measurement of palpebral aperture  Lymphatic drainage of the lid

---------------

100
Chapter 7.6 Menace reflex and Blink reflex

1.5.Menace reflex andBlink Reflex

The menace reflex - Blink reflex to visual threat

 Menace Reflex is one of the three forms of blink reflex.

 Menace Reflex is a learned reflex, not present at birth.
 This is reflex blinking that occurs in response to the rapid approach of an object. The reflex comprises
of blinking of the eye lids in order to protect the eyes from potential damage.
 Menace reflex, beside blinking reflex comprises turning of the head, neck, or even the trunk away
from the optical stimulus that triggers the reflex.
 The menace reflex is lost in cortical damage retaining the pupillary reflex.
 The neural pathway of the menace reflex comprises of optic nerve and facial nerve. It is mediated by
tecto bulbar fibers in the rostral colliculi of the midbrain passing from the optic tract to the accessory
nuclei and then to the spinal cord and lower motor neurons that innervate the head, neck, and body
muscles affecting the reflex. The facial nerve is mediated through acorticotectopontocerebellar
pathway.
 Medial retina → optic nerve → crossing at Optic chiasma→ Optic tract→ contra lateral geniculate
body motor cortex → pontine nucleus → to the cerebellum → both facial nerve
 Menace Reflex should be performed carefully, advancing the first towards the eye without creating
the airwave or touching the eye lashes, and
observing the blink. Figure 1.5-1
 The menace reflex is not well elicited from
the lateral retina.

. Blink Reflex. syn – corneal reflex, eye lid

reflex

 Involuntary blinking reflex

 Initiated by stimulation of the cornea by
touching or
by foreign body or by peripheral stimulus or
initiated
by the tear film break down.
 Bilateral reflex – stimulation of one cornea normally
has a consensual response with both eyes normally closing.
 Blinking is often associated with a shift in gaze thus
linked with extra ocular muscles movement.

101
 The purpose of this reflex is to protect the eyes from dry eyes, foreign bodies, bright light and sound
greater than 40 to 60 db.
 The lids spreads tear film over the ocular surface

The pathway of corneal reflex –

102
Chapter 7.7 Format for the Examination of the Eye Lids

Examination of the Preseptal area Right eye Left eye

• Fullness of the Preseptal area- either Uniocular or
Binocular
• Palpation of the Preseptal area
Any swellings if present to be palpated and describe
the swelling in detail.

Examination of the Eye Lids Right Eye Left Eye

Color of the skin
Creases of the lid
Eruption of vesicles
Diffuse Edema.
Localized swellings
Hordeolum internum
Chalazion or Tarsal cyst
Contusion or Ecchymosis

Movements of the eye lid

Closure of the lid
Elevation of the lid
Blinking and Winking
Abnormal lid movements
Position of the eyelid
MRD – I& MRD-II
Congenital malformations of the lid

Eye lid spatula Ectropion and Entropion

Desmarres lid retractor Epilation
clamp
forceps

103
Format for the Examination of the Eye Lid margin
Examination of the Eye Lid margin Right Eye Left Eye
Outer margin
Inner margin
Eye lashes
Trichiasis , Madarosis, Poliosis
Thickening of the lid margin
Crusting of the margins
Intermarginal strip
Openings of the meibomian glands
Punctum – Atresia . Eversion of the punctum
Abnormal position of lid margin
Ectropion
Entropion
Inflammation of the lid margin
Squamous and ulcerative
Blepharitis
Inflammation of Glands of the lid margin
Hordeolum externum
Growths of the lid margin
Adhesions of the lid margin
Parasites in the lid margin
Format for the Examination of the palpebral aperture
Examination of the palpebral aperture Right Eye Left Eye
Measurement of palpebral aperture
Reduced or Increased
Lagophthalmos

Surgical instruments for incision and drainage 1.Betadine 5% with swab

to clean the skin
2. Chalazion clamp
3. B.P Handle with 11
mm blade
4. Chalazion scoop

Chalazion clamp and

scoop in magnified view

--------------------------------

104
Chapter 8. Clinical examination of the Lacrimal apparatus
Ophthalmology - Topic:Lids and Adnexa ,Orbit

Num COMPETENCY Domai LevelK Cor Suggested SuggestedAsse Number Verti Horiz
ber Thes tudent should be able to nK/S/A /KH/S e(Y TeachingLea ssmentmetho require cal ontal
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Topic:Lids and Adnexa ,Orbit NumberofCompetencies:(08) Numberofproceduresthatrequirecertification:(NIL)

OP2.1 Enumerate the causes, describe and discuss K KH Y Lecture, Written/Viva Hum
the aetiology, clinicalpresentations and Small voce an
diagnostic features ofcommon conditions of groupdiscu Anat
the lid and adnexa including Hordeolum ssion omy
externum/internum,
blepharitis,preseptalcellulitis,dacryocystitis,h
emangioma,dermoid,ptosis,entropion,lidlag,
lagophthalmos
OP2.2 Demonstrate the symptoms & clinical S S Y DOAPsession Skill
assessment
OP2.3 Demonstrate under supervision clinical S SH Y DOA Skill
procedures performed in the lid P assessment
including:bells phenomenon, assessment of sessi
entropion/ectropion, performthe on
regurgitation test of lacrimal sac. Massage ,Lect
technique in cong. dacryocystitis, and ure
trichiatic cilia removal byepilation
OP2.4 Describe the aetiology, clinical Disc K K Y Lecture, Written/V
presentation .complications and uss H Small group iva voce
management of orbital cellulitis discussion
OP2.5 Describe the clinical features on K KH Y Lecture, Written/Viva
ocular examination Small voce
groupdiscu
ssion
OP2.6 Enumeratethecausesanddescribethedifferent K KH Y Lecture, Written/Viva
iatingfeatures,andclinicalfeatures and Small voce
management ofproptosis groupdiscu
ssion
OP2.7 Classifythevarioustypesoforbitaltumours.Diff K KH Y Lecture, Written/Viva
erentiatethesymptoms and signs of the Small voce
presentation of various types of ocular groupdiscu
tumours ssion
OP2.8 Listtheinvestigationshelpfulindiagnosisoforbit K KH Y Lecture, Written/Viva
altumors.Enumerate the indications for Small voce
appropriate referral groupdiscu
ssion

1
Chapter 8. Clinical examination of the Lacrimal apparatus
2. Topic : Lids , Adnexa, Orbit and (Clinical examination of Eye brow and pre septal cellulitis and Clinical examination of
Lacrimal apparatus )
.No Topic Clinical skills Domain Level Cor Suggested No Vertical Grade Sign
K/S/A/ K/KH e Suggeste assessmen Require integratio /Mark of
C / Y/N d t Method d to n s Fac
SH/P Teaching certify ulty
and .
learning Dat
method e
Demonstrate the S S Y DOAP Skill 1
OP2. symptoms & clinical session Assessmen
1 sign of conditions Lecture t
presepta cellulitis,
Demonstrate the S S Y DOAP Skill
OP2. symptoms & clinical session Assessmen
1 sign of conditions Lecture t
Perform the
regurgitation test of
lacrimal sac.
Massage technique
in cong.
dacryocystitis
OP2. Demonstrate the S S Y DOAP Skill
2 symptoms & clinical session Assessmen
sign of conditions Lecture t
Hordeolumexternum
/ internum,
blepharitis
hemangioma,
dermoid, ptosis,
entropion, lidlag,
lagophthalmos
OP2. Demonstrate under S S Y DOAP Skill
3 supervision clinical session Assessmen
procedures Lecture t
performed in the lid
including: bells
phenomenon,
assessment of
entropion/ectropion
, , trichiatic cilia
removal by
epilation

2
Chapter 8. Clinical examination of the Lacrimal apparatus

Competency 2.1 ---- Demonstrate the symptoms & clinical signs of conditions Perform the regurgitation
test of lacrimal sac. Massage technique in cong. dacryocystitis

Clinical anatomy and physiology of Lacrimal apparatus

Table -1

Figure 8-1 Figure 8-2 Figure 8-3 Figure 8-4

Tear Film Lacrimal Drainage system

Accessory Lacrimal glands

The lacrimal apparatus consists of

 Tear secreting glands i.e. lacrimal gland , accessory lacrimal glands which are glands of Krause and
wolfring ,
 Tear film and
 Lacrimal drainage system.

Tear secreting glands

Lacrimal gland –
Lacrimal gland is situated deep in the superior and anterio lateral part of the orbit in lacrimal fossa.
It is neither visible nor palpable.

The levator aponeurosis divides the lacrimal gland into two lobes , the outer orbital part situated in
the lacrimal fossa in the upper and anterior part of the orbital fossa and lower part is palpebral part lying
below the levator aponeurosis
The ducts of the lacrimal gland are 10 to 12 which opens in to the superior fornix

3
Accessory lacrimal glands
 Glands of Krause - The glands approximately 42 in the upper lid and 6 to 8 in the lower lid ,
which lie underneath the conjunctival fornix at the outer edge of the tarsal plate . These open
into the fornix through a common duct.
 Glands of wolfring - These are present at the upper border of the upper lid tarsal plate and
lower border of the lower tarsal plate and opens into the fornix.

Nerve supply to Lacrimal glands

Afferent and efferent Pathway to the lacrimal gland
 Afferent pathway ( Sensory nerve )- Lacrimal nerve , a branch of Vth cranial nerve ..
 The efferent pathway (Parasympathetic Nerve) – Secretomotor fibers
Starts from superior salivary nucleus in pons and travels through the facial and greater
superficial petrosal nerve and synapse in the pterygo palatine ganglion
nd
The post ganglionic fibers pass through the zygomatic nerve which is the branch of 2 division
of trigeminal nerve and lacrimal nerve which is the branch of first division of trigeminal nerve .

Sympathetic Innervation– Vaso motor function

Superior cervical Post ganglionic fibers travel along the internal carotid plexus and then through the
deep petrosal nerve and zygomatic nerve and supply to the lacrimal gland.

Blood supplyto lacrimal gland– Lacrimal artery, a branch of ophthalmic artery

Tear film –
Properties of tear film
 The rate of secretions 1.2microliters /min.
 The thickness of tear film is 8 micrometers.
 Refractive index is 1.336,
 Osmolarity is 309mosm/ L,
 Average PH is 7.25 Slightly alkaline.

Tear filmConsists of three layers

 Outer layer - Lipid layer / oily layer
Consists of phospholipids , Cholesterol esters and triglycerides . It reduces evaporation of
underlying aqueous layer and helps spread of the tear film.

 Middle layer – Aqueous layer

Consists of electrolytes –HCO3 , Na, K, Cl and Glucose, Proteins - Albumins , Globulins, immuno
Globulins (Ig) like IgA present abundant , IgG, IgM, and others like Lactoferrin, Urea,

4
Glycoproteins and Lysozyme. Lysozyme is a proteolytic enzyme which dissolves the bacterial wall
at PH 6 to 7.4. there by has antibacterial function.

Function of the aqueous layer –

It provides atmospheric oxygen to the cornea.
Antibacterial activity due to lysozyme and IgA
It washes away the debris.

 Inner layer - Mucin Layer.

Secreted by thGoblet cells of conjunctiva and glands.ofManz . Contains high molecular weight
glycoproteins , and forms a smooth bed that allows the tears to spread over the ocular surface.

Lacrimal drainage system –

 Drains tears into lacrimal sac
 Puncta - Each eye lid Consists of Puncta which is present in the medial end of intermarginal strip ,
 Canaliculus - Puncti leads to vertical canaliculus 2mm and horizontal canaliculus 8mm , both
upper and lower canaliculi join to form common canaliculus (90%) and joins Lacrimal sac.
Canaliculus is lined by stratified squamous epithelium
 Valve of Rosenmuller – a small mucus fold over hangs at the entrance of common canaliculus into
lacrimal sac which prevents the reflex of tears from the lacrimal sac into canaliculi.
 Lacrimal sac- present in the lacrimal fossa, 10 mm in length , the upper most part of superior
fundus lies underneath the medial palpebral ligament and also surrounded by the lacrimal
fascia. Horner’s muscle (Fibers of the medial preseptal orbicularis oculi muscle) is attached to the
lacrimal fascia. Lower end of the lacrimal sac leads to Naso lacrimal duct. , lined by columnar
epithelium
 Naso lacrimal duct(NLD) – From the lower end of the lacrimal sac extends as NLD, 12mm in
length and opens into medial nasal meatus below the inferior turbinate..
 Valve of Hasner - a small mucus fold over hangs at the opening of NLD.
 Surface marking of NLD - A line joining from the inner canthus to nasolabial fold at ala nasi.

Physiology of tear film -

Functions of tear film –
 it maintains uniform corneal surface for optical function.
 It provides oxygen to the metabolic function of cornea
 Lysozyme, IgA , lactoferrin have antibacterial function
 It prevents drying of the ocular surface by constantly wetting the ocular surface by blinking
 It flushes out the epithelial debris

5
The tear secretions
 The tear secretions are two types – Basic secretion and Reflex secretions
 Basic secretions of tears are produced by accessory lacrimal glands, of Krause, Wolfring, mucus
glands and sebaceous glands . These structures will provide the three layers of the tear film.
Extirpation of lacrimal gland does not produce dry eye as the accessory and other glands forms
the tear film.
 Reflex secretion of tears are produced by Lacrimal gland which produce aqueous part only.
Reflex secretions of tears are produced by irritation of the trigeminal sensory nerve which
supplies the cornea ,the conjunctiva , the nasal mucosa or psychogenic (Central) reflex
secretions by emotional states like weeping or excitement or some times intense light exposure
of the retina.

st
Paralysis of 1 division of the trigeminal sensory nerve does not abolish the psychogenic reflex.
 Psychogenic reflex can be abolished by blocking pterygopalatine ganglion.
 Reflex secretions are controlled by parasympathetic supply , parasympathomimetic drugs such
aspilocarpine produces an increased lacrimal flow and parasympatholytic drugs such as
atropine causes dry eye.
 Sympathetic fibers will control basic secretions.

Physiology of tears drainage -

 The tears are spread on the ocular surface by blinking of the lids , force produced by moving lids ,
contact between lid and globe and normal ocular surface . Blinking also moves the tears from
temporal to the nasal side towards the punctum.
 Some part of tears is drained by evaporation , some tears are drained by lacrimal drainage
system 70% is drained through the lower punctum and remainder through the upper punctum.

Lacrimal pump mechanism

 Medial pre septal muscle of orbicularis oculi called Horner’s muscle covers the punctum,
canaliculi and also inserted into lacrimal fascia which covers the lacrimal sac.
 In the act of each blink Horner’s muscle contract causing ampulla of the punctum compression ,
canaliculi shortening and , the lacrimal fascia draws the lacrimal sac laterally which causes
expansion of the sac thus creating a negative pressure . The negative pressure suck the tears
into canaliculi and then to lacrimal sac.
 When the lid is opened Horner’s muscle relaxes , the sac collapse and positive pressure is
created which forces the tears down the NLD into the nose .

6
Clinical examination oflacrimal apparatus
Lacrimal gland
Lacrimal gland is situated deep in the superior and anterio lateral part of the orbit in lacrimal fossa. It
is neither visible nor palpable.

Thc clinical signs of lacrimal gland swelling

 Swelling of the lacrimal gland due to infections, acute and chronic inflammations, neoplasms,
Cysts. Acute conditions are painful.
 Mild proptosis ,Down and in position of the eye ball.
 ‘S’ shaped curvature of the upper lid margin with ptosis.

Accessory Lacrimal gland

Sometimes visible on everting the upper lid at the lateral side of the superior fornix

Tear film –
Consists of three layers. outer lipid layer, middle aqueous layer,and inner mucus layer. The integrity of
the tear filmdepends on blinking mechanism, the margin of the lid, palpebral aperture dimensions,
smooth ocular surface of conjunctiva and cornea, lacrimal and accessory lacrimal
glands,meibomian glands, zeis and moll glands and lacrimal drainageall must be normal. Failure on
the part of any of these structures leads to tear film break downcausing dry eye.

Examination for the clinical signs of dry eye,

Figure 8-5
Clinical investigations for Dry eye.
 Schirmer’s test -I
 Schirmer’s test –II
 Tear Breakup Time (TBUT)

Schirmer’s test –I.

7
of the filter paper.15 to 20 mm wetting of filter Paper is normal, 8to 10 mm wetting of filter Paper
indicates moderate dry eye and less than 8 mm wetting of filter Paper indicates defiantly a dry eye.

Schirmer’s test –II.

 The test is to record the reflex secretions of tears . The procedure is the same except that the
conjunctiva is anaesthetized and ipsilateral nasal mucosa is irritated with a cotton swab.The filter
paper is observed for wetting after 2 minutes. Wetting less than 15 mm indicates failure of reflex
secretions of tears.

Tear Breakup Time ( T BUT)

 To study mucin and lipid layer deficiency in a dry eye.Tear film is stained with 2% fluorescein and
Patient is seated comfortably in front of slit lamp for cornea examination with cobalt blue filter and a
wide beam . After a few seconds black spots appear in the fluorescein tear film over on the cornea.
The time taken between last blink and black spot is noted by a stop clock .Normal tear break up time
is 10 seconds. Less than 10 seconds indicates mucin and lipid layer deficiency in a dry eye.

Lacrimal drainage system

Figure 8-6
 The common symptom of the Lacrimal drainage system is Epiphora - Regurgitation test
 Epiphora - Overflow of the tears due to the abnormality of Lacrimal drainage
system
 Clinical Examination of the punctum for atresia or occlusion
 Examination of the lacrimal area - Normally there is no fullness in the
lacrimal area or on pressure there are no abnormal contents expressed from
the punctum. Presence of fullness or swelling or regurgitation of mucus or mucopurulent discharge on
pressure over the lacrimal area suggest Chronicdacryocystitis.

ClinicalInvestigation of Lacrimal sac

 Lacrimal Regurgitation Test
 Fluorescein clearance test
 Jones dye test – 1 and 2
 Lacrimal scintillography or Dacryo scintigraphy etc

Lacrimal Regurgitation test

8
 No regurgitation frompuncti indicates a normal sac,fibrotic sac, mucocele, or encysted mucocele. In
mucocele, and encysted mucocele there is occlusion of upper and lower puncti as well as nasolacrimal
duct. Hence there is no regurgitation from the puncti.

Fluorescein clearance test

 Fluorescein 2% dye is instilled in the conjunctival sac and note the meniscus
Figure 8-7
 If normal drainage is present the dye is cleared in 5 minutes

Jones dye test – 1 and 2

To differentiate whether the watering of the eye is due to
• Hyper lacrimation
• Lacrimal Pump failure
• Partial / Total lacrimal obstruction
Jones dye test – 1
• 2% fluorescein is in the conjunctival sac and after five minutes the sterile cotton plug soaked in
anaesthetic solution is placed in the inferior meatus
• If the cotton plug is stained , there is patency of the lacrimal sac and watering is due to hyper
secretion .
• If staining is negative – There is obstruction of the lacrimal sac or lacrimal pump failure

Figure 8-7
Jones dye test – 2 Syringing Procedure
 This test is to confirm the Mechanical block in the nasolacrimal duct. It
Should be done under full aseptic precautions and with good illumination and
magnification. Anaesthetize the ocular surface with 4% xylocaine or 0.5 %
Paracaine
 Identify the lower punctum .
 Dilate the lower punctum with Nettleship Punctum dilator .
 Take lacrimal syringe fitted with lacrimal cannula (commonly 5cc syringe with lacrimal cannula)
and syringe is filled with 5 cc of distilled water .
 Negotiate the lacrimal cannula through the lower canaliculus and push the
distilled water into the lacrimal sac.
 If watery, mucus or mucopurulent discharge regurgitates from the lower
punctum it indicates nasolacrimal duct block which is the cause for chronic
dacryocystitis.

9
Criggler’s Massage technique in cong. Dacryocystitis
 Slide the finger tip in an inferior direction ,placing a moderate pressure over the lacrimal sac area and
duct using an antibiotic ointment as a lubricant to prevent the mechanical rub.
 Repeat the procedure 3 times a day , each time 10 to 15 strokes per sitting
 Topical antibiotic drops only if purulent discharge is present on pressure over the sac.

Clinical skills
 Regurgitation Test
 Schirmer’s Test -I and II
 Demonstration of Tear Breakup Time (T BUT)
 Demonstration of Syringing procedure
 Demonstrate the symptoms & clinical sign of conditions Perform the regurgitation test of lacrimal
sac. Massage technique in cong. Dacryocystitis

Format for the examination of the Lacrimal apparatus

Examination of the lacrimal Right eye Left eye
apparatus
Lacrimal gland,
Swelling
Examination for the Dry eye
 Schirmer’s test –I.
 Schirmer’s test –II
 TBUT (Tear Film Break UP
Time)
Lacrimal Regurgitation Test

OSPE
Clinical case for university examination
Any clinical form /stage or P.O lacrimal surgery with sutured wound at lacrimal area is kept as a case in the
university examination
The clinical discussion about the cases
 Draw and label a diagram of lacrimal apparatus or lacrimal drainage system
 What is the physiology of lacrimal drainage system
 What is the nerve supply of lacrimal gland – Parasympathetic secreto motor
 Layers of the tear film
 What are the glands which secretes the various layers of the tear film

10
 Schirmer test -I , Schirmer test –II ,
 Tear film break up time (TBUT)
 What is the clinical stage /form of the chronic dacryocystitis
 What are the clinical symptoms and signs of various clinical stages of chronic dacryocystitis
 What is epiphora
 What is Lacrimation
 What is the pathogenesis of chronic dacryocystitis
 What is the pathogenesis of mucocele/encysted mucocele of chronic dacryocystitis
 What is the important clinical examination for diagnosis of chronic dacryocystitis
 What are the investigations for chronic dacryocystitis
 Interpretation of Jones Dye test
 What is dacryoscintigraphy
 What are the surgeries for Chronic dacryocystitis
 What is dacryocystectomy and what is dacryocystorhinostomy.
 What is the treatment for mucocele/encysted mucocele
 Mucocele of chronic dacryocystitis
OSCE – All the images in this chapter and surgical instruments for Dacryocystectomy ,
Dacryocystorhinostomyi.e
 Images of Clinical presentations/Clinical forms of Chronic dacryocystitis
 Regurgitation Test
 Schirmer’s Test -I and II
 Demonstration of Tear Breakup Time (T BUT)
 Demonstration of Syringing procedure
 Lacrimal probes, Nettleship punctum dilator
 Dacryocystectomy , Dacryocystorhinostomy surgical instruments
Dacryocystectomy instruments Dacryocystorhinostomy

 Muller’s self retaining haemostatic  All the surgical instruments which

speculum required for dacryocystectomy and

 Lacrimal blunt dissector lacrimal bone punches , and silicone

 Nettleship punctum dilator tubes for intubation

 Lacrimal probes

-----------------------------

11
Chapter 8. Clinical examination of the Lacrimal apparatus
Ophthalmology - Topic:Lids and Adnexa ,Orbit

Num COMPETENCY Domai LevelK Cor Suggested SuggestedAsse Number Verti Horiz
ber Thes tudent should be able to nK/S/A /KH/S e(Y TeachingLea ssmentmetho require cal ontal
/C H/P /N) rningmetho d dtocerti Integ integ
d fyP ratio ratio
n n
Topic:Lids and Adnexa ,Orbit NumberofCompetencies:(08) Numberofproceduresthatrequirecertification:(NIL)

105
Chapter 8. Clinical examination of the Lacrimal apparatus
2. Topic : Lids , Adnexa, Orbit and (Clinical examination of Eye brow and pre septal cellulitis and Clinical
examination of Lacrimal apparatus )
.No Topic Clinical Domai Leve Cor Suggested No Vertic Grade Sign
skills n l e Suggest assessment Require al /Marks of
K/S/A K/K Y/ ed Method d to integr Facu
/C H/ N Teachin certify ation lty.
SH/P g and Date
learning
method
Demonstrate the S S Y DOAP Skill 1
OP2. symptoms & session Assessment
1 clinical sign of Lecture
conditions
presepta
cellulitis,
Demonstrate the S S Y DOAP Skill
OP2. symptoms & session Assessment
1 clinical sign of Lecture
conditions
Perform the
regurgitation test
of lacrimal sac.
Massage
technique in cong.
dacryocystitis
OP2. Demonstrate the S S Y DOAP Skill
2 symptoms & session Assessment
clinical sign of Lecture
conditions
Hordeolumextern
um/ internum,
blepharitis
hemangioma,
dermoid, ptosis,
entropion, lidlag,
lagophthalmos
OP2. Demonstrate S S Y DOAP Skill
3 under supervision session Assessment
clinical procedures Lecture
performed in the
lid including: bells
phenomenon,
assessment of
entropion/ectropi
on, , trichiatic cilia
removal by
epilation

106
Chapter 8. Clinical examination of Lacrimal apparatus
(Chapter 8.1 Clinical eanatomy of the Lacrimal apparatus, Chapter 8.2 .Clinical examination of
lacrimal gland, Chapter 8.3 Clinical examination of tear film, Chapter 8.4 Clinical examination of
lacrimal drinage system, Chapter 8.5 Format for clinical examination of lacrimal apparatus &
others)

Competency 2.1 ---- Demonstrate the symptoms & clinical signs of conditions Perform the
regurgitation test of lacrimal sac. Massage technique in cong. dacryocystitis

Chapter 8.1Clinical anatomy and physiology of Lacrimal apparatus

Table -1

Figure 8-1 Figure 8-2 Figure 8-3 Figure 8-4

Tear Film Lacrimal Drainage system

Accessory Lacrimal glands

The lacrimal apparatus consists of

 Tear secreting glands i.e. lacrimal gland , accessory lacrimal glands which are glands of
Krause and wolfring ,
 Tear film and
 Lacrimal drainage system.

Tear secreting glands

Lacrimal gland –
Lacrimal gland is situated deep in the superior and anterio lateral part of the orbit in lacrimal fossa.
It is neither visible nor palpable.

The levator aponeurosis divides the lacrimal gland into two lobes , the outer orbital part
situated in the lacrimal fossa in the upper and anterior part of the orbital fossa and lower part
is palpebral part lying below the levator aponeurosis
The ducts of the lacrimal gland are 10 to 12 which opens in to the superior fornix

107
Accessory lacrimal glands
 Glands of Krause - The glands approximately 42 in the upper lid and 6 to 8 in the lower
lid , which lie underneath the conjunctival fornix at the outer edge of the tarsal plate
. These open into the fornix through a common duct.
 Glands of wolfring - These are present at the upper border of the upper lid tarsal
plate and lower border of the lower tarsal plate and opens into the fornix.

Nerve supply to Lacrimal glands

Afferent and efferent Pathway to the lacrimal gland
 Afferent pathway ( Sensory nerve )- Lacrimal nerve , a branch of Vth cranial nerve ..
 The efferent pathway (Parasympathetic Nerve) – Secretomotor fibers
Starts from superior salivary nucleus in pons and travels through the facial and
greater superficial petrosal nerve and synapse in the pterygo palatine ganglion
nd
The post ganglionic fibers pass through the zygomatic nerve which is the branch of 2
division of trigeminal nerve and lacrimal nerve which is the branch of first division of
trigeminal nerve .

Sympathetic Innervation– Vaso motor function

Superior cervical Post ganglionic fibers travel along the internal carotid plexus and then
through the deep petrosal nerve and zygomatic nerve and supply to the lacrimal gland.

Blood supplyto lacrimal gland– Lacrimal artery, a branch of ophthalmic artery

Tear filmConsists of three layers

 Outer layer - Lipid layer / oily layer
Consists of phospholipids , Cholesterol esters and triglycerides . It reduces evaporation
of underlying aqueous layer and helps spread of the tear film.
 Middle layer – Aqueous layer
Consists of electrolytes –HCO3 , Na, K, Cl and Glucose, Proteins - Albumins , Globulins,
immuno Globulins (Ig) like IgA present abundant , IgG, IgM, and others like Lactoferrin,

108
Urea, Glycoproteins and Lysozyme. Lysozyme is a proteolytic enzyme which dissolves
the bacterial wall at PH 6 to 7.4. there by has antibacterial function.

Function of the aqueous layer –

It provides atmospheric oxygen to the cornea.
Antibacterial activity due to lysozyme and IgA
It washes away the debris.

 Inner layer - Mucin Layer.

Secreted by thGoblet cells of conjunctiva and glands.ofManz . Contains high molecular
weight glycoproteins , and forms a smooth bed that allows the tears to spread over
the ocular surface.

Lacrimal drainage system –

 Drains tears into lacrimal sac
 Puncta - Each eye lid Consists of Puncta which is present in the medial end of
intermarginal strip ,
 Canaliculus - Puncti leads to vertical canaliculus 2mm and horizontal canaliculus 8mm
, both upper and lower canaliculi join to form common canaliculus (90%) and joins
Lacrimal sac. Canaliculus is lined by stratified squamous epithelium
 Valve of Rosenmuller – a small mucus fold over hangs at the entrance of common
canaliculus into lacrimal sac which prevents the reflex of tears from the lacrimal sac
into canaliculi.
 Lacrimal sac- present in the lacrimal fossa, 10 mm in length , the upper most part of
superior fundus lies underneath the medial palpebral ligament and also
surrounded by the lacrimal fascia. Horner’s muscle (Fibers of the medial preseptal
orbicularis oculi muscle) is attached to the lacrimal fascia. Lower end of the lacrimal
sac leads to Naso lacrimal duct. , lined by columnar epithelium
 Naso lacrimal duct(NLD) – From the lower end of the lacrimal sac extends as NLD,
12mm in length and opens into medial nasal meatus below the inferior turbinate..
 Valve of Hasner - a small mucus fold over hangs at the opening of NLD.
 Surface marking of NLD - A line joining from the inner canthus to nasolabial fold at ala
nasi.
Physiology of tear film -
Functions of tear film –
 it maintains uniform corneal surface for optical function.
 It provides oxygen to the metabolic function of cornea
 Lysozyme, IgA , lactoferrin have antibacterial function

109
 It prevents drying of the ocular surface by constantly wetting the ocular surface by
blinking
 It flushes out the epithelial debris
The tear secretions
 The tear secretions are two types – Basic secretion and Reflex secretions
 Basic secretions of tears are produced by accessory lacrimal glands, of Krause,
Wolfring, mucus glands and sebaceous glands . These structures will provide the three
layers of the tear film. Extirpation of lacrimal gland does not produce dry eye as the
accessory and other glands forms the tear film.
 Reflex secretion of tears are produced by Lacrimal gland which produce aqueous part
only. Reflex secretions of tears are produced by irritation of the trigeminal sensory
nerve which supplies the cornea ,the conjunctiva , the nasal mucosa or psychogenic
(Central) reflex secretions by emotional states like weeping or excitement or some
times intense light exposure of the retina.

st
Paralysis of 1 division of the trigeminal sensory nerve does not abolish the
psychogenic reflex.
 Psychogenic reflex can be abolished by blocking pterygopalatine ganglion.
 Reflex secretions are controlled by parasympathetic supply , parasympathomimetic
drugs such aspilocarpine produces an increased lacrimal flow and parasympatholytic
drugs such as atropine causes dry eye.
 Sympathetic fibers will control basic secretions.
Physiology of tears drainage -
 The tears are spread on the ocular surface by blinking of the lids , force produced by
moving lids , contact between lid and globe and normal ocular surface . Blinking also
moves the tears from temporal to the nasal side towards the punctum.
 Some part of tears is drained by evaporation , some tears are drained by lacrimal
drainage system 70% is drained through the lower punctum and remainder through
the upper punctum.
Lacrimal pump mechanism
 Medial pre septal muscle of orbicularis oculi called Horner’s muscle covers the
punctum, canaliculi and also inserted into lacrimal fascia which covers the lacrimal sac.
 In the act of each blink Horner’s muscle contract causing ampulla of the punctum
compression , canaliculi shortening and , the lacrimal fascia draws the lacrimal sac
laterally which causes expansion of the sac thus creating a negative pressure . The
negative pressure suck the tears into canaliculi and then to lacrimal sac.
 When the lid is opened Horner’s muscle relaxes , the sac collapse and positive
pressure is created which forces the tears down the NLD into the nose .
-----------------------------

110
Chapter 8.2 .Clinical examination of lacrimal gland
Lacrimal gland
Lacrimal gland is situated deep in the superior and anterio lateral part of the orbit in lacrimal fossa. It is
neither visible nor palpable.

 Swelling of the lacrimal gland due to

 infections,
 acute and chronic inflammations,
 neoplasms,
 Cysts.

The clinical signs of lacrimal gland swelling

 Acute conditions are painful.
 Mild proptosis ,Down and in position of the eye ball.
 ‘S’ shaped curvature of the upper lid margin with ptosis.

‘S’ shaped curvature of the upper lid margin

with ptosis

Accessory Lacrimal gland

Sometimes visible on everting the upper lid at the lateral side of the superior fornix

111
Chapter 8.3 Clinical examination of Tear film
The tear film Consists of three layers. outer lipid layer, middle aqueous layer,and inner mucus layer. The
integrity of the tear film depends on blinking mechanism, the margin of the lid, palpebral aperture
dimensions, smooth ocular surface of conjunctiva and cornea, lacrimal and accessory lacrimal glands
,meibomian glands, zeis and moll glands and lacrimal drainage all must be normal. Failure on the part of
any of these structures leads to tear film break downcausing dry eye.

Examination for the clinical signs of dry eye,

Examination of the lacrimal apparatus structures are necessary to rule out any abnormalities causing the
dry eye . The common conjunctival signs are xerosis, Bitot’s spots, chronic Figure 8-5
conjunctivitis; while common corneal sign is punctate keratitis.
Clinical investigations for Dry eye.
 Schirmer’s test -I
 Schirmer’s test –II
 Tear Breakup Time (TBUT)

Schirmer’s test –I.

 Reliable test for establishing Dry eye. This test is for measuring the rbasic
secretions of tears.schirmer’s strip (Whatman 41 filterpaper) measuring
35mmx5mm in dimensions , and an unmeasured strip with a notch at 5
mmto bend and to keep in the unanaesthetizedouter 1/3 of the lower fornixand keep for 5 minutes and
observed for wetting of the filter paper.15 to 20 mm wetting of filter Paper is normal, 8to 10 mm wetting
of filter Paper indicates moderate dry eye and less than 8 mm wetting of filter Paper indicates defiantly
a dry eye.
Schirmer’s test –II.
 The test is to record the reflex secretions of tears . The procedure is the same except that the conjunctiva
is anaesthetized and ipsilateral nasal mucosa is irritated with a cotton swab.The filter paper is observed
for wetting after 2 minutes. Wetting less than 15 mm indicates failure of reflex secretions of tears.
Tear Breakup Time ( T BUT)
 To study mucin and lipid layer deficiency in a dry eye. Tear film is stained with 2% fluorescein and Patient
is seated comfortably in front of slit lamp for cornea examination with cobalt blue filter and a wide beam .
After a few seconds black spots appear in the fluorescein tear film over on the cornea. The time taken
between last blink and black spot is noted by a stop clock .Normal tear break up time is 10 seconds. Less
than 10 seconds indicates mucin and lipid layer deficiency in a dry eye.
---------------------------

112
8.4 Clinical examinations of Lacrimal drainage system

 The common symptom of the Lacrimal drainage system is Epiphora

 Epiphora - Overflow of the tears due to the abnormality of Lacrimal drainage system
 Clinical Examination of the punctum for atresia or occlusion
 Examination of the lacrimal area - Normally there is no fullness in the lacrimal area or on pressure there
are no abnormal contents expressed from the punctum. Presence of fullness or swelling or regurgitation
of mucus or mucopurulent discharge on pressure over the lacrimal area suggest Chronicdacryocystitis.

Clinical Investigation of Lacrimal sac

 Lacrimal Regurgitation Test
 Fluorescein clearance test
 Jones dye test – 1 and 2
 Lacrimal scintillography or Dacryo scintigraphy

Lacrimal Regurgitation test

 The lower punctum is everted by pulling the lower lid down and pressure is put with fore finger upwards
and medially on the lacrimal sac area and observe for any abnormal contents coming from the puncti.
 Any abnormal contents i.e. mucus, mucopurulent discharge, watery discharge coming from either puncti
or any fullness in the lacrimal sac area indicates Chronic dacryocystitis.
 No regurgitation frompuncti indicates a normal sac,fibrotic sac, mucocele, or encysted mucocele. In
mucocele, and encysted mucocele there is occlusion of upper and lower puncti as well as nasolacrimal
duct. Hence there is no regurgitation from the puncti.

Fluorescein clearance test

 Fluorescein 2% dye is instilled in the conjunctival sac and note the meniscus
 If normal drainage is present the dye is cleared in 5 minutes

Jones dye test – 1 and 2

To differentiate whether the watering of the eye is due to
• Hyper lacrimation
• Lacrimal Pump failure
• Partial / Total lacrimal obstruction

Jones dye test – 1

113
• 2% fluorescein is in the conjunctival sac and after five minutes the sterile cotton plug soaked in
anaesthetic solution is placed in the inferior meatus
• If the cotton plug is stained , there is patency of the lacrimal sac and watering is due to hyper secretion .
• If staining is negative – There is obstruction of the lacrimal sac or lacrimal pump failure
Jones dye test – 2 Syringing Procedure
Figure 8-7
 This test is to confirm the Mechanical block in the nasolacrimal duct. It Should be
done under full aseptic precautions and with good illumination and magnification.
Anaesthetize the ocular surface with 4% xylocaine or 0.5 % Paracaine
 Identify the lower punctum .
 Dilate the lower punctum with Nettleship Punctum dilator .
 Take lacrimal syringe fitted with lacrimal cannula (commonly 5cc syringe with
lacrimal cannula) and syringe is filled with 5 cc of distilled water .
 Negotiate the lacrimal cannula Syringing Instruments
through the lower canaliculus 1, Nettleship punctum dilator
and push the distilled water 2 ..Lacrimal Probe
into the lacrimal sac. 3 .Lacrimal cannula fitted with
 If watery, mucus or syringe
mucopurulent discharge 3 . Distilled water
regurgitates from the lower 4. Swabs
punctum it indicates
nasolacrimal duct block which
is the cause for chronic
dacryocystitis.
Lacrimal scintillography or Dacryo scintigraphy
This is used to evaluate anatomical as well as functional passage of lacrimal drainage system. .Drops
containing radio tracer TC 90 or sulpher colloid is installed and passage of this tracer is observed with gamma
camera at the interval of 5minutes for 40 minutes. In patent NLD , the tracer is visualized in the nasal cavity ,
outlining the canaliculi , sac and NLD. Retained tracer in the sac indicates NLD block.
Criggler’s Massage technique in cong. Dacryocystitis
 Slide the finger tip in an inferior direction ,placing a moderate pressure over the lacrimal sac area and
duct using an antibiotic ointment as a lubricant to prevent the mechanical rub.
 Repeat the procedure 3 times a day , each time 10 to 15 strokes per sitting
 Topical antibiotic drops only if purulent discharge is present on pressure over the sac.
--------------------------------

114
Chapter 8.5 Format Clinical examination of Lacrimal apparatus , Clinical skills , OSPE and
OACE

Format for the examination of the Lacrimal apparatus

115
 Schirmer test -I , Schirmer test –II ,
 Tear film break up time (TBUT)
 What is the clinical stage /form of the chronic dacryocystitis
 What are the clinical symptoms and signs of various clinical stages of chronic dacryocystitis
 What is epiphora
 What is Lacrimation
 What is the pathogenesis of chronic dacryocystitis
 What is the pathogenesis of mucocele/encysted mucocele of chronic dacryocystitis
 What is the important clinical examination for diagnosis of chronic dacryocystitis
 What are the investigations for chronic dacryocystitis
 Interpretation of Jones Dye test
 What is dacryoscintigraphy
 What are the surgeries for Chronic dacryocystitis
 What is dacryocystectomy and what is dacryocystorhinostomy.
 What is the treatment for mucocele/encysted mucocele
 Mucocele of chronic dacryocystitis

OSCE – All the images in this chapter and surgical instruments for Dacryocystectomy , Dacryocystorhinostomyi.e
 Images of Clinical presentations/Clinical forms of Chronic dacryocystitis
 Regurgitation Test
 Schirmer’s Test -I and II
 Demonstration of Tear Breakup Time (T BUT)
 Demonstration of Syringing procedure
 Lacrimal probes, Nettleship punctum dilator

Dacryocystectomy , Dacryocystorhinostomy surgical instruments

Dacryocystectomy instruments Dacryocystorhinostomy

 Muller’s self retaining haemostatic  All the surgical instruments which

speculum required for dacryocystectomy

 Lacrimal blunt dissector and lacrimal bone punches , and

 Nettleship punctum dilator silicone tubes for intubation

 Lacrimal probes

116
Surgical instruments for Dacryocystectomy and Dacryocystorhinostomy

1.Tilleys forceps for nasal packing 12. Fine needle holder

2.Thudicum speculum 13. Nittelship’s punctum dilator
3. Bard parker handle with 11mm blade 14. 6 zero vicryl
4. Muller’s self retaining haemostatic speculum 15. sterile pads
5. Toothed forceps 16.Sensorcain 0.5%
6. Curved artery forceps 17.Xylocain with adrenaline 2%
7. Straight artery forceps 18. Cotton swabs
8. Lacrimal blunt dissector 19. Silicon intubation tubes
9. conjunctival scissors 20.Betadine
10. claw retractor 21. Distilled water
11.Lacrimaal probe 22. Sterilization tray
23. Kerrison bone punches

117
Chapter 9. Clinical examination of the Orbit and Periorbita

Clinical anatomy of the orbit

lacrimal gland, blood vessels, nerves (Optic, Oculomotor, Trochlear, Abducent, Ophthalmic and Maxillary
nerves, Ciliary parasympathetic ganglion) Orbital fat and fascia connective tissue, Nasolacrimal apparatus.
 Height :Each orbit is about 35 mm to 40mm in height,
 Base width : 40mm
 Volume Of Orbit: 29ml
 Volume of eye ball: 6.5ml
 Ratio between Volume Of Orbit &Eyeball Is: 4.5 : 1
 Anatomical axis and visual axis are at an angle of 23 degrees with each other& makes an angle of 10
degrees with horizontal plane
 Medial wall of the orbit are parallel to one another
 Lateral walls are divergent

Table -1

1
Table 2

Table -3
The orbit has got Formed by portion of
• Medial wall 7 bones. -
• Inferior wall • Frontal
• Lateral wall • Maxilla
• Superior wall • Zygomatic
• Base • Sphenoid
• Apex • Palatine
• Ethmoidal
• Lacrimal

2
Table 3

Comparative study of the wall of the orbit

Apex of the Orbit -

Posterior end of the orbit contains two orifices
• Optic canal
• Superior orbital fissure
Optic canal
• Lies between roof and medial wall
• Formed by lesser wing and greater wing of sphenoid
• Connects orbit and middle cranial fossa
• Transmits – Ophthalmic Nerve and Ophthalmic artery

3
Table 4
Superior Orbital fissure Structures passing Superior orbital fissure
• Comma shaped aperture.
• Lies between roof and lateral wall
• Situated lateral to optic foramen at orbital
apex.
• Bounded between lesser& greater wing of
sphenoid.

Divided by the annulus of Zinn(common tendinous

ring. ) into 3 Parts.upper, middle & lower

Table 5
Ethmoidal foramen
• At the junction of frontal
and ethmoid bones,
anteriorly and posteriorly

• Connects with ethmoid

sinuses, anterior cranial
fossa, nasal cavity

4
Table 6
The importance of the surgical
spaces
The anaesthetic drugs are given
in various spaces.
The peribulbar block is given in
peripheral orbital space
The parabulbar block is given in
tenons space

Orbital fascia - Extensive sub divisions of Orbital fascia

• Periorbita i.e. Periosteum: Periorbita covers the inner walls of the orbital bones
• Orbital septum: A portion on the fascia at the orbital rim extends into the tarsal plate and to the medial
and lateral tarsal ligament.
• Prolongation of the fascia in the lid extends into the muscles of the lids and surrounds it and connect the
muscles one and the other.
• Tenon’s capsule Covers the eye ball as a capsule which separates the eye from orbital fat and connected
to the sclera by fine fibrils.
• The tendons of the recti piercethe fascia to get attached to the globe and also forms the coverings to the
recti.
• Suspensory ligament ofLockwood: Lower part of Tenon’s capsule is thickened forming a sling or Hammock
on which the eye ball rests

Clinical points to be noted in the orbit examination are Inspection, Palpation, Auscultation
Inspection–
Fullness of the Periorbita – Figure9-1
 May be Uniocular or Binocular. Fullness of periorbita is due to
space occupying lesion/mass in the orbital cavity which is called
Proptosis , defined as forward protrusion of the eye ball due to
space occupying mass in the orbitalcavity.Clinical Examination of
Proptosis is described in the eye ballchapter.

Uniocular Fullness –
 Orbital cellulitis,
 Pseudo tumors of the orbit ,
 Tumors of the orbit –Dermoid, Hemangioma,Neurofibroma,
Glioma

5
Binocular Fullness
 Orbital tumors
 Thyroid Orbitopathy

Atrophy of the periorbital area

Atrophy of the periorbital area - It is observed as deep sulcus above the superior tarsal plate
• Old people
• Aponeurotic ptosis
• Phthisis Bulbi
 Marasmic child
Palpation
 Palpate the orbital margins for fractures due to trauma and tenderness due to inflammations.
 Orbital Mass if any - Palpate the mass and describe the mass in terms of position, size, shape,
mobility,compressibility, Retropulsion, waxing and waning of the mass, palpablePulsations etc.

Auscultation -
 Observe any sounds on Auscultation.

Format for the Examination of the Orbit and Periorbita

Examination of the Orbit and periorbita Right eye Left eye
 Inspection –signs of
Fullness and atrophy
 Palpatethe margins
for fractures,tenderness.
and Mass in the Orbit
 Auscultation

Diagrams to learn
 Bony Orbit
 Structures passing through the Superior orbital fissure
 Potential spaces of the orbit

OSPE
Proptosis
 What is Proptosis
 What is Pseudo proptosis
 Clinical examination for diagnosis of proptosis
 Signs of Thyroid orbitopathy

OSCE – Image identification

 All the images in this chapter are the OSCE
-----------------

6
Chapter 9. Clinical examination of the Orbit

(Chapter 9.1 Clinical anatomy of the Orbit and Periorbita, Chapter 9.2 Clinical examination of the orbit)

Chapter 9.1 Clinical anatomy of the orbit

The Orbit is a bony space one on each side of the nose.
 The bony orbit is a quadrilateral pyramid whose base is the orbital margins.
 The apex is the optic foramen
 The walls of orbit protect the eye from the injuries.
 The Periorbital is the periosteum lining the bony orbital cavity and adjacent tissues.

th
The orbital cavity consists of periorbita , the eye ball occupying 1/5 of the orbit , Extra ocular muscles,
lacrimal gland, blood vessels, nerves (Optic, Oculomotor, Trochlear, Abducent, Ophthalmic and Maxillary
nerves, Ciliary parasympathetic ganglion) Orbital fat and fascia connective tissue, Nasolacrimal apparatus.
 Height :Each orbit is about 35 mm to 40mm in height,
 Base width : 40mm
 Volume Of Orbit: 29ml
 Volume of eye ball: 6.5ml
 Ratio between Volume Of Orbit &Eyeball Is: 4.5 : 1
 Anatomical axis and visual axis are at an angle of 23 degrees with each other& makes an angle of 10
degrees with horizontal plane
 Medial wall of the orbit are parallel to one another
 Lateral walls are divergent

Table -1

118
Table 2

119
Table 4

Comparative study of the wall of the orbit

Apex of the Orbit -

Posterior end of the orbit contains two orifices
• Optic canal
• Superior orbital fissure
Optic canal

120
• Lies between roof and medial wall
• Formed by lesser wing and greater wing of sphenoid
• Connects orbit and middle cranial fossa
• Transmits – Ophthalmic Nerve and Ophthalmic artery

Table 4
Superior Orbital fissure Structures passing Superior orbital fissure
• Comma shaped aperture.
• Lies between roof and lateral wall
• Situated lateral to optic foramen at orbital
apex.
• Bounded between lesser& greater wing of
sphenoid.

Divided by the annulus of Zinn(common tendinous

ring. ) into 3 Parts.upper, middle & lower

121
Table 5
Ethmoidal foramen
• At the junction of frontal
and ethmoid bones,
anteriorly and posteriorly

• Connects with ethmoid

sinuses, anterior cranial
fossa, nasal cavity

Table 6
The importance of the surgical
spaces
The anaesthetic drugs are given
in various spaces.
The peribulbar block is given in
peripheral orbital space
The parabulbar block is given in
tenons space

Orbital fascia - Extensive sub divisions of Orbital fascia

122
• Prolongation of the fascia in the lid extends into the muscles of the lids and surrounds it and connect the
muscles one and the other.
• Tenon’s capsule Covers the eye ball as a capsule which separates the eye from orbital fat and connected
to the sclera by fine fibrils.
• The tendons of the recti piercethe fascia to get attached to the globe and also forms the coverings to the
recti.
• Suspensory ligament ofLockwood: Lower part of Tenon’s capsule is thickened forming a sling or Hammock
on which the eye ball rests
-------------------------------------

123
Chapter 9.2 Clinical examination of the orbit

Clinical points to be noted in the orbit examination are Inspection, Palpation, Auscultation

Inspection–
Fullness of the Periorbita – Figure9-1
 May be Uniocular or Binocular. Fullness of periorbita is due to
space occupying lesion/mass in the orbital cavity which is called
Proptosis . Proptosis is defined as forward protrusion of the eye
ball due to space occupying mass in the orbital cavity. Clinical
Examination of Proptosis is described in the eye ball chapter.

Uniocular Fullness –
 Orbital cellulites,
 Pseudo tumors of the orbit ,
 Tumors of the orbit –Dermoid, Hemangioma,Neurofibroma, Glioma

Binocular Fullness
 Orbital tumors
 Thyroid Orbitopathy

Atrophy of the periorbital area

Auscultation -
 Observe any sounds on Auscultation.

123
Format for the Examination of the Orbit and Periorbita
Examination of the Orbit and periorbita Right eye Left eye
 Inspection –signs of
Fullness and atrophy
 Palpatethe margins
for fractures,tenderness.
and Mass in the Orbit
 Auscultation

Diagrams to learn
 Bony Orbit
 Structures passing through the Superior orbital fissure
 Potential spaces of the orbit

OSPE
Proptosis
 What is Proptosis
 What is Pseudo proptosis
 Clinical examination for diagnosis of proptosis
 Signs of Thyroid orbitopathy

OSCE – Image identification

 All the images in this chapter are the OSCE

-----------------

124
Chapter 10. Clinical examination of the Eye ball
Competency :
OP9.1 Demonstrate the correct technique to examine the extra ocular movements (Uniocular and
Binocular)
AN41.1 Describe and demonstrate parts and layers of the eyeball
------------------------------------------------
Clinical anatomy of the eye ball
The shape of the eye ball is Ablate spheroid and suspended in the bony orbital cabinet by the extra ocular
muscles and check ligaments. . The average anterioposterior axial length is 24mm which is slightly more than
the Horizontal due to the curvature of the cornea. The anterio posterior length is essential for IOL power
th
calculation in A scan biometry. The eye ball has three coats , the anterior 1/5 outer coat is the cornea
th
and posterior5/6 is the sclera. The corneo scleral junction is called limbus. Figure 10.1 Eye ball
Middle coat is uveal tract which is the vascular coat of eye ball . The inner coat
is the retina . The eye ball is enclosed in tenon’s capsule. The extra ocular
muscles are inserted on the sclera in spiral fashion i.e medial rectus 5.5mm,
inferior rectus 6.5mm , lateral rectus 6.9mm and superior rectus 7.7mm from
the limbus.

Clinical points to be noted in the eye ball examination.

• Whether the eye ball is present or absent in the orbit
• Fixation of the eye ball to light
• Size of the eye ball
• Shape of the eye ball
• Position of the eye ball in the orbital cavity
• Whether eye ball is protruded or retracted
• Alignment of the two eyes
Figure 10.2 Figure 10.3 Empty socket
• Ocular movements
Congenital anophthalmos
• Bell’s phenomena
• Digital tonometry.
Whether the eye ball is present or absent
Absence of the eye ball in the orbit is
called Anophthalmos
 Primary anophthalmos – Congenital
failure of development of the optic vesicle

124
 Secondary anophthalmos –Due to complete suppression or abnormality of the forebrain Consecutive or
degenerative resulting in regression of formed optic vesicle.
 Surgical removal – Empty socket
Figure 10.4
Fixation of eyes to
Fixation of the eye ball to the target
the target
• Normally the eyes fix to the looking target. The fixation of the eye ball to the
target is known by flashing light on the root of the nose and observe whether
the eyes are fixed to the light or moving. If the eyes are moving it is called
Nystagmus.
• Causes for Nystagmus - Failure of the Binocular single vision.

Size of the eye ball

Figure 10.5 Figure 10.6 Staphyloma
Increase in the size of eye ball – Macrophthalmos seen in
Buphthalmos
• High Myopia
• Buphthalmos
• Staphyloma
• Intraocular tumors extending into the coats of the
eye ball.
• Pseudotumor of the orbit Figure 10.7 RE Congenital
Microphthalmos

Decrease in the size of the eye ball –

Microphthalmos seen in
• Congenitally small eye ball- Microphthalmos
• Hypermetropia
• Atrophic bulbi
• Phthisis bulbi
• Nanophthalmos
• Perforated globe.
Figure 10.8 Figure 10.8 Figure 10.9

Phthisis bulbi Cornea Plana Keratoconus

Shape of the eye ball –
Normally eye ball is nearly
spherical (Ablate spheroid)
Causes for changes in shape
• Phthisis bulbi -- Small ,Soft ,
Shrunken, Shapeless Sightless
eye ball

125
• Cornea plana
• Keratoconus ,
• Keratoglobus
• Staphyloma

Position of the eye ball in the orbit –

• The normal position of the eye ball in the orbit is Axial
• The position of the eye ball may be Axial, Eccentric, Protruded or Retracted
To know where the position of the eye ball is axial , light is flashed on the brim of the nose from a distance
of half a meter and the light reflection on the cornea is observed. If the corneal reflection is in the center of
the cornea then the eye ball is axial.
If the corneal light reflection is not in center, the position of the eye ball is eccentric.

Figure 10.10 Axial Figure 10.11 Eccentric Figure 10.12 Protruded

position of the eye ball position of the eye ball position of the Eye ball

Eccentric position of the eyeball is due to

• Misalignment of the eyes as in the squint – Exo tropia,Eso tropia Hyper tropia,and Hypo tropia.
• Tumors in the orbital cavity as in Proptosis and Orbital cellulitis

Whether eye ball is protruded or retracted

• Protruded eye ball is called Proptosis
• Proptosis – Defined as Forward protrusion of the eyeball due to space occupying lesion in the orbital
cavity Eg Tumors of the orbital cavity,

Backward retraction of the eye ball is called Enophthalmos and is seen in

• Fracture of the floor of the orbit
• Orbital cellulitis sequelae.

126
Clinical examination for protruded / Proptosis or retracted/ Enophthalmos of the eye ball
• Rulers test –First the patient is asked to look down, then keep a ruler vertically touching the center of
the two orbital rims. In normal ( unprotruded) eyes the skin of the upper eye lid aptly touches the ruler
.In a protruded eye the ruler can not be placed vertically touching the orbital rims and in a retracted eye
gap will be present between ruler and skin of the upper lid
• Naphzeiger’s test: The patient is asked to look forward at a distant object. Standing behind the
patient, gently extend the head backwards to look down over the forehead of the patient. The
proptosed eye appears first when compared to the normal eye.
• Luedde’s exopthalmometer - It is the measurement of protrusion of the eye ball with a transparent
scale from the lateral orbital rim . A transparent scale is placed on the lateral orbital rim and the level
of the apex of the cornea is read through the transparent scale. Normal is 14 to 18 mm. Beyond 18
mm.or difference between two eyes is more than 2 mm indicates proptosis
• Other methods are .Hertel;s Exophthalmometer
Figure 10.13 Rulers test Figure 10.14 Figure 10.15 Figure 10.16 Hertel's
Naphzeiger’s test Luedde’s Exophthalmometer and
exopthalmometry exopthalmometry

Figure 10.17 Luedde's exophthalmometer Figure 10.18 Luedde's

Exophthalmometer

Pseudoproptosis – It is apparent proptosis, It is not a true proptosis as there is no space occupying mass in
the orbital cavity. It is seen in the following conditions

127
• Big eye ball- Staphylomas, Buphthalmos, High Myopia
• Lid retraction
• Intraocular tumors extending into the coats of the eye ball.
• Tower skull

Alignment of the two eyes – Figure 10.19 Hirschberg's Figure 10 . 20 Squint in

Normally the two eyes are aligned corneal light reflection test degrees

together and function as a single unit

by fusion mechanism in the brain.
Thus the two images formed by both
eyes are fused in the brain and
interpreted as one object. This is
called Binocular Single vision.

“The ability of the two eyes to see a single object by fusion” is called Binocular Single vision. Misalignment of
the two eyes is called Squint. This misalignment causes misdirected visual axis.
To know clinically whether the two eyes are aligned Hirschberg corneal light reflection test is done.
• A light is flashed on the root of the nose from a distance of half meter and a light reflection on the
corneais observed. If the corneal reflection is in the center of the cornea in both the eyes then the eyes
are aligned together. This is called Orthophoric position of the eyes.
• If the corneal light reflection is not seen in the center of the cornea it indicates total failure of the fusion
mechanism and the two eyes are not aligned. This is called manifest squint or otherwise called Tropia.
This indicates that there is failure of Binocular single vision.

Basing on the position of the corneal light reflex the angle of squint can be measured in degrees.
 If the corneal light reflection is seen nasal to the center of the cornea, the eye ball is in divergent position
and is called Exotropia. Figure 10.21 Figure 10.22 Esotropia Figure 10.22 Rt
 If the corneal light reflection is Rt Exotropia Hypotropia
seen temporal to the center of and LE Hypertropia
the cornea , the eye ball is in
convergent position and is
called Esotropia
 If the corneal light reflection is
seen above the center
of the cornea , the eye
ball is in hypo position and is called Hypotropia

128
• If the corneal light reflection is seen below the center of the cornea , the eye ball is in Hyper position and
is called Hypertropia

Sometimes due to effort of fusion, a small degree of fusion failure is masked in the Hirschberg corneal light
reflection test . i.e the corneal reflection is seen in the center of the cornea.

 To know that the two eyes are aligned Figure 10.23 -Cover Test Figure 10.24 Cover test for
with strong fusion or with weak fusion is Phoria Tropia
known by a test called Cover test

Types of the cover test

 Cover and uncover test
 Cover Test
 Alternate cover test

Cover and uncover test: For diagnosis of

Phorias / Latent squint.
A fine target is shown to the participant at a distance of half meter and one eye is Covered. After few
minutes the cover is removed. While removing the cover movements in the covered eye is observed.
Normally while removing the cover there will be no movements in the covered eye. Which indicates that
there is a Strong fusion.

While removing the cover if there is a movement in the covered eye it indicates that there is a weak fusional
mechanism which is called Heterophoria.
If the eye ball is moving from lateral to the primary position it is called Exophoria. If the eye ball is moving
from medial to primary position it is called Esophoria.
If there is no movement of the eye under cover the eyes are in orthophoria

Cover Test: For diagnosis of Tropia .

A fine target is shown to the participant at a distance of half meter and one eye is covered . The movements
of the uncovered eye is observed.. If there is a movement in the uncovered eye it indicates total failure of
the fusional mechanism of the two eyes, which is called Heterotropia.
If the eye ball is moving lateral to the primary position it is called Exotropia . If the eye ball is moving from
medial to primary position it is called Esotropia . If the eye ball is moving from below to upwards it is called
Hypotropia. If the eye ball is moving from above to downwards it is called Hypertropia.

Alternate cover test – Cover test is done by covering two eyes alternately.

129
It is for the diagnosis of alternate squint.
Alternate cover test shows alternating squint i.e either eye show squint when one eye takes up fixation.
A fine target is shown to the participant at a distance of half meter and Cover the fixing eye , let say right
eye , and after few minutes uncover that right eye. The right eye shows squint and left eye maintains
fixation.
Next cover the left eye i.e fixing eye , and now immediately right eye takes up fixation. While upon un
covering the left eye, right eye maintains fixation and left eye is seen with squint .

Cover test to be done for near, Distance, and in all ocular gazes because some squints are present for near
and absent for distance and vice versa and some squints are present in one particular ocular gaze and absent
in another ocular gaze.
Thus Cover test will establish type of squint, whether it is HeteroPhoria Or HeteroTropia.
Examination of Ocular movements – Types of ocular movements
 Duction movement and torsional movements - Uniocular movements
 Version movement , Vergence movement - Binocular Movements

Table -1
Duction movements - Binocular– Version/ gaze The torsional movements The Vergences
movements movement

 Abduction – Movement of the  Dextroversion of the eye are two types The Vergences
eye from the primary position  Dextro elevation,  Incycloduction movements are two
to lateral position  Dextro depression /Intorsion - in types
 Adduction - Movement of the  Levoversion, turning of one eye  Convergence
eye from the primary position  Levo elevation,  Excycloduction  Divergence
towards the mid line  Levo depression /Extortion – out
 Sursum duction or  Sursum version turning of one eye
Supraduction (Elevation) –  Deorsum version
Primary position to the upward
position
 Deorsum duction or
Infraduction (Depression) –
Primary position to the
downward position.

Uniocular movements – To examine the duction and Torsional movements one eye is closed and the
participant is asked to follow the target

130
To examine the version Movements the participant is asked to follow target
The other movements of the eyeball are Torsional and vergence

Table -2

Table -3

.
To examine the near point of convergence , a fine pointed target is given to the participant and
131
to keep in front of the eye at distance of 33cms and asked to slowly move the target towards the eye in
the midline. The surgeon will be observing the convergence of the two eyes, and note when the
convergences breaks to divergence. And also the participant is asked to tell when the fine pointed target

blurs and diplopia occurs. . That is the end of near point of convergence. The near point of convergence is 6
cms to 9 cms .
The amount of convergence is measured by prisms. The strongest base out prism which does not produce
diplopia , when distant object is regarded is the amount of convergence.
The strongest base in prism which doesn’t produce diplopia is the measurement of amount of divergence.
The other methods are with RAF ruler , with synoptophore.

Figure 10.25 RAF Ruler

RAF ruler : Royal air force ruler is an instrument to measure the near point
of accommodation and convergence.
The convergence constitutes, Miosis and Accommodation. In
accommodation is anterioposterior diameter of the crystalline lens
Increases. This is called Near vision complex.
Muscles Actions - One can construct muscle actions as follows
 Besides primary actions, all Recti muscles are adductors except Lateral Rectus
 Besides primary action, Obliques are abductors
 Besides primary action, Superiors (Superior Oblique & Superior Rectus) are intorters
 Besides primary action Inferi.ors (inferior Oblique & inferior Rectus )
are Extorters. Figure 10.26 Figure 10.27
Bell’s phenomena—Examination of Bell’s phenomena— Bell's phenomena Bedside digital
when an attempt is made to open the closed lids tonometry
the eye ball rolls up and out. Sometimes rolls down
and in , called reverse Bell’s phenomena. Both are
physiological and is called Bell’s phenomena Ptosis
surgery is contraindicated if bell`s phenomena is
absent.
Digital Tonometry (Tactile Tonometry) –
To know whether the eye ball approximate
intraocular pressure is normal, hard, or soft. This is measured clinically on the bed side by digital
tonometry.
To Record Digital tonometry (IOP) - The person is asked to look down . Both middle fingers are kept on
the forehead and both fore fingers are kept on lids. The eye balls are gently Pressed with one fore finger and

132
the pressure wave is felt with the other forefinger. This gives a gross idea of whether the eye ball is normal
hard, soft,

Table 3
Clinical skill to be practiced –
 Rulers test .  Cover Test .
 Naphzeiger’s sign .  Ocular Movements .
 Luedde’s exophthalmometry .  Bell’s Phenomena.

 Hirschberg’s corneal reflection test  Bed side Digital tonometry.

 Rulers test .
. OSCE –
All the images in this chapter
OSPE
Proptosis
Diagrams to practice
 Eye ball – section , Layers and Contents
 Extra ocular muscles
Format for the Examination of the eye Ball
Table 4.
Examination of the eye Ball Right eye Left eye
Whether eye ball is present or absent
Fixation of the eye ball to light
Size of the eye ball
Shape of the eye ball
Position of the eye ball
 Axial
 Eccentric
Whether eye ball is protruded or
retracted
 Rulers test
 Naphzeiger’s test
 Luedde’s exopthalmometer
 Hertel’s Exophthalmometer
Alignment of the two eyes
 Hirschberg corneal light
reflection test

133
 Cover Test , Cover and uncover
Test, Alternate cover Test
Ocular movements
 Uniocular movements - -
Duction movement
Torsional movments
 BinocularMovements
Version movement -
Vergence movement
Bell’s Phenomena
Bed side Digital tonometry

--------------------

134
Chapter 11. Clinical examination of the Conjunctiva
Ophthalmology - Topic: Conjunctiva
Number COMPETENCY Dom Lev Cor Suggested Suggested Numb Vertical Hori
The student should be able to ain el e Teaching Assessment er Integrati zont
K/S/ K/K (Y/ Learning method requir on al
A/C H/S N) method ed to integ
H/P certify ratio
n

Topic: Conjunctiva Number of Competencies (09) Number of procedures that require certification:(NIL)
OP3.1 Elicit document and present an appropriate S S Y DOAP session Skill
history in a patient presenting with a “redeye” H Assessment
including congestion, discharge, pain

OP3.2 Demonstrate document and present the correct S S Y DOAP SkillAssessment

method of examination of a “redeye” include H session
ing vision assessment, corneal lustre, pupil
abnormality, ciliary tenderness
OP3.4 Describe the etiology, patho physiology, ocular K K Y Lecture, Written/Viva
features, differential diagnosis, complications H Small group voce
and management of trachoma. discussion
OP3.5 Describe the etiology, pathophysiology, ocular K K Y Lecture, Written/Viva
features, differential diagnosis, complications H Small group voce
and management of vernal catarrh discussion
OP3.6 Describe the etiology, pathophysiology, ocular K K Y Lecture, Written/Viva
features, differential diagnosis, complications H Small group voce
and management of pterygium discussion
OP3.7 Describe the etiology, pathophysiology, ocular K K Y Lecture, Written/Viva
features, differential diagnosis, complications H Small group voce
and management of symblepharon discussion
OP3.8 Describe the etiology, pathophysiology, ocular K K Y Lecture, Written/Viva
features, differential diagnosis, complications H Small group voce
and management of pterygium discussion
OP3.9 Demonstrate the correct technique of S S Y DOAP session Skillassessment
instillation of eye drops in a simulated H
environment

Competencies
OP.3. 1 – Elicit Document and present appropriate history in a patient presenting with a “red Eye” including
congestion, discharge, and Pain.
OP3.2 - Demonstrate document and present the correct method of examination of “red Eye” including vision
assessment, Conjunctival congestion , CCC , corneal luster, Depth of anterior chamber (A.C) , Abnormal contents in A.C ,
Iris Pattern, K.P`s, Pupil, pupil abnormality , IOP, ciliary tenderness .

(Red eye
Competency OP.3. 1 -Onset, Vision, Pain, Discharge, Photophobia, Conjunctival congestion, Constitutional
symptoms for document elicitation
OP3.1 - Demonstrate document and present the correct method of examination of “red Eye” including vision
assessment, corneal luster, pupil , pupil abnormality, ciliary tenderness . )

1
Chapter 11. Clinical examination of the Conjunctiva

Clinical anatomy of the conjunctiva

The Conjunctiva is a thin, transparent membrane covering the eye. It extends from the Intermarginal
strip and covers the surface of the eyeball up to the limbus

Figure 11-1 Figure 11-2 Figure 11-3

Clinical anatomy of conjunctiva Histological section Lymphatic
(Layers) of conjunctiva drainage of the conjunctiva

The anatomical parts of the conjunctiva are

 Palpebral conjunctiva
 Bulbar conjunctiva,
 Superior fornix and Inferior fornix
 Limbal conjunctiva.
 Caruncle
 Plica semilunaris.

Palpebral conjunctiva –Present on the posterior aspect of the tarsal plate adherent to it and is divided
into marginal conjunctiva upto the subtarsal sulcus , middle part is tarsal conjunctiva and at the fornix is
the orbital conjunctiva.

The Bulbar conjunctiva - lines the anterior sclera and is loosely attached underneath with episcleral
tissue and Tenon’s capsule.

Limbal conjunctiva.
 The limbal part of bulbar conjunctiva is adherent and covers the limbus region. It is continuous
with epithelium of the cornea.
Superior and inferior Fornix
Bulbar conjunctiva connects superiorly and inferiorly with palpebral conjunctiva and forms superior fornix
and respectively inferior fornix.

2
Caruncle
 In the inner can thus, 3x3 mm pink mass is present called caruncle which is modified skin,
covered by stratified squamous epithelium with sweat glands and sebaceous glands and hair
follicles It is a vestigial organ (Third lid) however involves in the diseases of the conjunctiva.

Plica semilunaris.
 Adjacent to the caruncle there is a semilunar fold with concavity towards limbus called plica
semilunaris.

Layers/ Histology of the conjunctiva – epithelium and stroma

Epithelium –
Epithelium is two to five layered and non-keratinized . Two layered epithelium is present at palpebral
conjunctiva and gradually increases from fornix to limbus.
The epithelium contains Goblet cells which secretes mucine. Mucine forms the inner layer of tear film.

Stroma consists –
Stroma is of two layers i.e superficial adenoid layer and deep fibrous layer.
Superficial adenoid layer – Consists of Lymphocytes, mast cells and histiocytes. This layer will develop 2
to 3 months after birth. Hence conjunctival inflammation in the new born does not produce follicular
reaction.
Deep fibrous layer - Consists of collagen and elastic fibers and merges with tarsal plate.

Glands of the conjunctiva ---

 Goblet cells, glands of Henle (Crypts of Henle) and glands of Manz. in the bulbar conjunctiva are
mucin secreting glands
 The accessory glands of lacrimal glands are Glands of Krause and Glands of wolfring which open
to in the fornices of conjunctiva
 Glands of Krause - The glands are approximately 42 in the upper lid and 6 to 8 in the lower lid,
which lies underneath the conjunctival fornix at the outer edge of the tarsal plate . These open
into the fornix through the common duct.
 Glands of wolfring - These are present at the upper border of the upper lid tarsal plate and lower
border of the lower tarsal plate and opens into the fornix
Nerve supply –
The sensory nerves which supply to the conjunctiva are
 Long ciliary nerves are branch of trigeminal nerve supply the limbal conjunctiva and cornea.
 Branch of Nasociliary nerve - Infra trochlear nerve
 Branches from frontal nerve – supra trochlear and supra orbital

3
Blood supply of conjunctiva
Figure 11-4
Marginal tarsal arcade arteries Blood supply of the conjunctiva

 Peripheral tarsal arcade arteries

 Anterior ciliary arteries

Marginal tarsal arcade arteries

 Marginal tarsal arcade arteries lie 2mm away from the margin
of the eye lid, supplies the marginal conjunctiva

Peripheral tarsal arcade arteries

 Peripheral tarsal arcade arteries lie near the peripheral border
of the tarsal plate. Its perforating branches pierce the muller’s muscle to reach the conjunctiva and
gives off ascending and descending branches. The descending branches supplies the tarsal
conjunctiva and also anastomose with the vessels from the marginal arcade. Ascending branches
pass into the superior fornix and continue around the superior and inferior fornices to the bulbar
conjunctiva as posterior conjunctival arteries which supply the bulbar conjunctiva.

Anterior ciliary arteries –

 Anterior ciliary arteries run along the tendons of extra ocular muscles and give off anterior
conjunctival arteries. Anterior conjunctival arteries anastomose with terminal branches of posterior
conjunctival arteries forming peri limbal plexus.

The lymphatic drainage

 The lymphatic drainage of the conjunctiva and lids are the same. The lateral half of the conjunctiva
and the lateral half of upper and lower lids drain into the preauricular lymph nodes and the medial
half of the conjunctiva and the medial half of upper and lower lid drain into the sub mandibular
lymph nodes.

Function of the conjunctiva

 The function of the conjunctiva is to protect the eye ball through its lymphatics, rich blood supply
and mucin secretions from the conjunctiva forms the inner layer of the tear film.

The clinical examination of the conjunctiva mainly consists of inspection by diffuse light with magnification.
Palpation is limited to testing the consistency and for tenderness of the lesion.

4
Methods of examination of the conjunctiva
 The lower lid is Pulled down with fore finger to examine the lower palpebral conjunctiva, lower fornix
mid and lower part of the bulbar conjunctiva -
 The patient is asked to look down and the upper lid is raised by the examiner to examine
Upper part of the bulbar conjunctiva
 To examine the upper palpebral conjunctiva of the upper lid, it is everted.
 To examine the upper fornix the upper lid is double everted. The Conjunctiva is anaesthetized with 4%
xylocaine and first evert the upper lid with two non-toothed forceps, then the everted lid is held at two
ends and second evertion is done.
In Blepharospasm – Desmarre’s lid retractors is used to retract the lid to visualize conjunctiva and cornea.

Points to be noted in Examination of the conjunctiva

• Color and pigmentation of the conjunctiva
• Transparency /Lustre / Brightness of the conjunctiva
• Congestion- Conjunctival and CCC
• Chemosis
• Ecchymosis or sub conjunctival hemorrhage
• Discharges from the eye conjunctiva
• Inflammatory reactions –Follicle, Papillae, Phlycten, Folliculosis
• Degenerations - Pinguecula, Pterygium, Concretions
• Dryness of the eye - Bitot spots, Xerosis
• Membrane formation
• Scarring
• Cysts
• Tumors
• Limbal nodule
• Foreign bodies

Color and pigmentation of the conjunctiva

The conjunctiva is a bright tissue and has no color. The color of the conjunctiva is due to change in color of
the sclera, blood vessels and moles.
• Pale conjunctiva
Cause - Anemia
To examine the pale conjunctiva the lower lid is Pulled down for observation of the lower palpebral
conjunctiva.

Pigmentation
• Yellow color- Icterus due to infective or obstructive hepatitis.

5
• Blue color is due to cyanosis and blue sclera.
• Red color is due to congestion of the conjunctiva.
• Pigmentation - Nevus – Birth marks, Brown or Black in color, Melanosis is congenital Diffuse black
pigmentation of the conjunctiva and Keratinization

Figure 11-5 Figure 11-6 Figure 11-7

Icterus Yellow color of the Conjunctival Nevus Melanosis of
conjunctiva the conjunctiva

Transparency/ lustre / Brightness of the conjunctiva

Conjunctiva is normally transparent
The transparency is lost in all diseases of the conjunctiva.
Lustre / Brightness is lost in - muddy Conjunctiva seen in spring catarrh, xerophthalmia , Polluted
environment

Figure 11-8 Figure 11-9

Congestion Conjunctival congestion Circum ciliary congestion
Congestion may be
• Conjunctival Congestion
• Circum ciliary congestion
(CCC),
• Mixed congestion

Table 1
Causes of Conjunctival congestion Causes of Circum ciliary congestion
(CCC),
 Bacterial, and viral Conjunctivitis,  Corneal ulcer.
Epidemic kerato conjunctivitis is caused by adenovirus 8 and 19.
 Allergic Conjunctivitis  Keratitis.
 Spring catarrh  Acute congestive glaucoma.
 F.B on the conjunctiva  Acute Iridocyclitis
 Phacomorphic, Phacolytic and
malignant glaucoma

6
Table 2 Differences between Conjunctival congestion and Circum ciliary congestion

Cl.examination Conjunctival congestion Circum ciliary congestion (CCC)

Color Bright red in color Pink in color

Site More pronounced in the Fornix More pronounced around the limbus

Blood flow direction Blood flow from fornix towards limbus Blood flow from limbus towards fornix

Blood vessels are branches of --  Peripheral tarsal arcade Branches of Anterior ciliary vessels
 Marginal tarsal arcade
 Anterior ciliary arteries
Discharge Associated with mucus, Mucopurulent
discharge Associated with watery discharge.
Mixed congestion causes
• Endophthalmitis
• Panophthalmitis
Figure 11-10 Figure 11-11 Figure 11-12
Chemosis/Edema of the conjunctiva Ecchymosis/ Subconjunctival Mucopurulent Discharge
Hemorrhage

Differential Diagnosis of the Red eye

Table3 Conjunctivitis, Acute Iridocyclitis, Acute congestive glaucoma
Clinical Features Conjunctivitis Acute Iridocyclitis Acute glaucoma (Congestive)
Onset Acute Moderately Acute Sudden in the course of PACG

Vision Good Fair Poor

th
Pain Discomfort Moderate along the first Severe in all branches of v
th
division of the v cranial cranial nerve.
nerve
Discharge Mucopurulent Watery Watery
Photophobia Mild Severe Moderate
Constitutional symptoms Absent Absent Present -vomiting and sweating

7
Table 4
OP3.1 Demonstration of Red eye in slit lamp
Conjunctival congestion Severe Mild and associated with Mild and associated with CCC
CCC
CCC Absent Present Present
Tenderness on the eye ball Absent Present Present
Corneal lustre Clear. No edema Moderately edematous Severely edematous
K. P`s absent Present Pigmentary K.p may be present
Pathognomonic sign
Depth of anterior chamber (A.C) Normal Deep Shallow
Iris Pattern Normal pattern Lost due to Edema Lost due to Edema
Pupil Normal Constricted with irregular Dilated and vertically oval
margins
Abnormal contents in A.C Absent Hypopyon present Absent
IOP Normal Moderately raised Severely raised.

Chemosis or Edema of the conjunctiva

Conjunctiva is lax, prone for edema and is seen in
 Infections of the Conjunctiva, more in pneumococcal conjunctivitis
• Angioneurotic edema
• Congestive heart Failure
• Nephrotic Syndrome
• Protein malnutrition
• Orbital cellulitis

Ecchymosis of the conjunctiva and Subconjunctival Hemorrhage seen in

• Rupture of the Conjunctival blood vessels – Blood is collected in the layers of the conjunctiva and
underneath.
• Trauma – Blunt Trauma, penetrating Trauma.
• Whooping cough in children
• Blood dyscrasias. – in adults
• Pressure around the neck, on the chest, on the abdomen
• Diabetes and Hypertension - in elderly
Bleeding from the conjunctiva is seen in trauma, hemorrhagic conjunctivitis, ruptured hemangioma,
membranous conjunctivitis, conjunctiva Telangiectasia.
Acute Haemorrhagic conjunctivitis is caused by Enterovirus 70

8
Discharges from the eye
• Watery discharge- Epiphora, Lacrimation
• Mucus discharge – Catarrhal conjunctivitis
• Mucopurulent Discharge – Purulent conjunctivitis.

Inflammatory conditions of conjunctiva

Follicle
Aggregation of the lymphoid tissue of the conjunctiva. A raised 2 to 3 mms sized grayish white nodule on the
bulbar or palpebral conjunctiva
Follicle is a pathognomonic sign of Trachoma
Papillae
Hyperplasia of blood vessels of the conjunctiva, each consists of tuft of vessels covered by epithelium. Velvety,
polygonal in appearance. Seen in
• Chronic conjunctivitis, Contact lens users – Giant papillae
• Spring catarrh – Cobble stone appearance, severe papillary hyperplasia seen in upper palpebral
conjunctiva.
Phlycten-
A grayish white raised nodule of 1 or 2 mm at or near the limbus due delayed type hypersensitivity reaction
most commonly due to staphylococcal proteins , secondary to tuberculous protein and Helmenthic infection.

Figure 11-13 Figure 11-14 Figure 11-15

Follicle Papillae Phlycten

Phlyctenular conjunctivitis - The most common cause of phlyctenular conjunctivitis is Bacterial. It is a delayed
type of hypersensitivity reaction most commonly to staphylococcal proteins. (Earlier it was thought tubercular
proteins as the cause. But now staphylococcal proteins are being the most common cause)

Degenerations of conjunctiva
 Pinguecula - A raised nodule on the nasal side of the limbus, precludes the pterygium.
 Primary Pterygium-A wing shaped, triangular fold of conjunctiva apex encroaching on to the cornea. It is a
Sub conjunctival elastic degeneration. May be progressive or atrophic, true or pseudo.
 Grading of Primary Pterygium –
Grade – I Up to the limbus. Grade II – Between the centre of the cornea and limbus. Grade III – upto the
pupillary Margin. Grade IV- Beyond pupil.

9
Figure 11-16 Figure 11-17 Figure 11-18 Figure 11-19
Pinguecula Primary progressive Primary atrophic Concretions
Pterygium Pterygium

Table 5
Differences between Primary Pterygium and Pseudo Pterygium
Differences Primary Pterygium Pseudo Pterygium
Age Common in middle and old age Any age.
Site Commonly on the nasal side. rarely on the May be present anywhere in
temporal side the conjunctiva
Shape Triangular in shape and apex is towards the No fixed shape
cornea
Progression Progressive towards cornea No progression / stationary.
Infiltration cap in front of the apex Present (If progressive) Absent
on the cornea
Stockers line i.e Present Absent
Deposition of iron pigment
Probe test Can not be passed Can be passed
Etiology Ultraviolet rays exposure Chemical injuries
Pathology Degenerative Inflammatory
Common sequel after Treatment Recurrence is common No recurrence

Table 6
Differences in Clinical features of Progressive and Regressive Pterygium
Clinical feature Progressive Pterygium Regressive Pterygium
Congestion of conj Marked No congestion
Consistency Thick and Fleshy Atrophic
Infiltration cap Present in front of the apex on the cornea Absent

10
 Concretions --Epithelial debris and inspissated mucus in the Henle layers of conjunctiva. They are raised
yellowish white granules commonly seen in the tarsal conjunctiva. Also seen in atrophy of the conjunctiva.
In old age

Dry eye or Xerosis of the conjunctiva

Conjunctiva is constantly wet by the tear film. Conjunctiva not wet by tear film is called as Dry eye. Clinical
features are feeling of dryness in the
eye, Nonspecific redness, Gritty Figure 11-20 Figure 11-21 Figure 11-22
Bitot’s spots Conjunctival xerosis Keratomalacia
feeling, watering of the eye,
lustreless.

Local causes for the Dry eye

 Irregularities of Lid margin
 Blinking Failure
 Ectropion,
 Entropion,
 Lagophthalmos,
 Protrusion or retraction of the eye ball,
 Conjunctival and corneal scarring – Trachoma, chemical injuries
 Tear film break down due to mucin, lacrimal gland or Meibomian
Gland dysfunction or due to infections of the lid margins.

Figure 11-23 Schirmer’s test Figure 11-24 Tear film Break up

Dry eye syndrome - causes

 Vitamin A Deficiency – Xerophthalmia
 Sjogren syndrome,
 Steven Johnson's Syndrome
Signs of Vitamin A Deficiency
• Bitot spots - Triangular, foamy, shiny patches on the temporal limbus
• Xerosis

11
Test to examine for Dryness of the eyes –
• Schirmer’s test
• Tear film Break up time (TBUT)
Schirmer’s’ test, Tear film Break up time (described in examination of lacrimal system

Conjunctival Membrane formation

Scarring of the conjunctiva – seen in

 Trachoma
 Steven Johnson's Syndrome
 Injuries – Mechanical and Chemical injuries

Symblepharon
Al ready described (Chapter Examination of the eye lids)
 Ulcers in the conjunctiva
Figure 11-26
Causes – Phlycten, (Described below) Cysticercus cysts
 carcinomas extending into the conjunctiva,
 Steven Johnson’s, Tuberculous, Burns.

Cysts
• Cysticercus cysts (Common)
• Retention cysts from the glands of the conjunctiva.

Nodules in the conjunctiva

 Phlycten – A grayish yellow 2mm nodule seen at or near the limbus secondary to allergy reaction for
tuberculous or helminthic infection.
 Pinguecula - See degenerations of Conjunctiva
 Limbal dermoid – Usually congenital
 Foreign body granuloma
 Glaucoma filtering bleb of Trabeculectomy surgery

12
Figure 11-27 Limbal Dermoid Figure 11-28 Dermo lipoma Figure 11-29
Squamous neoplasia of conjunctiva

Tumors
Benign Tumors
• Dermoid
• Dermo lipoma – Congenital soft yellowish white mass seen at the outer canthus which. consists of fatty
tissue and dermis like connective tissue.
• Some times epibulbar dermoids may be associated with accessory auricles and other congenital anamolies
called golden Har’s syndrome.
• Hemangioma –
• Pre-cancerous condition - Bowen’s disease
Malignant Tumors
• Squamous neoplasia – Seen at the limbus and commonly associated with HIV infections.
• Lymphomas
• Epi dermoid carcinoma
• Malignant Melanoma

Figure 11-30 Figure 11-31 Figure 11-32

Conjunctival palpebral F. B Eversion of the upper lid Eversion of the upper lid

Foreign Body (F.B) on the conjunctiva

The commonest area for conjunctival F.B is the Sub tarsal sulcus, an area 1to2mm below the inner border of
the upper lid which is seen as a hood/sulcus when the lid is everted.
Sometimes F.B is embedded in granuloma and is called F.B granuloma.

13
Clinical skills
• Eversion of the upper lid to see the palpebral conjunctiva and the Subtarsal Sulcus
Method of Eversion of the upper lid – The participant is asked to look down and grasp the lateral eye
lashes of the upper lid with thumb and fore finger. Pull the upper lid down and out, keep a spatula on the
skin of the lid at the upper border of the tarsal plate and put a little pressure with the spatula while
everting the lid with thumb and forefinger.
 Removal of Conjunctival F.B
Diagrams to learn
• Draw a labeled diagram of the Clinical anatomy of the conjunctiva.
• Draw the diagram of histological section of conjunctiva.
• Draw the diagram of the Lymphatic drainage of the conjunctiva.
OSPE – Short Clinical cases for university examination
All the clinical points which are to be examined in the conjunctiva are the short cases in the university
examination.
Types of questions in the examination -
Clinical questions starts with diagrams of Clinical anatomy , Histology, functions ,lymphatic drainage of the
conjunctiva pathological changes In the lesions and Microbiological commensals in the conjunctiva ,
definitions of the lesions , methods of treatment .Etc..
OSCE – All the diagrams in this chapter are included in OSCE
Format for the examination of the conjunctiva
Table 7
Examination of the conjunctiva Right eye Left eye
Color and pigmentation
Pale, Pigments, Moles
Transparency of the conjunctiva
Congestion-
Conjunctival, CCC, Mixed.
Chemosis
Ecchymosis or sub conjunctival hemorrhage
Discharges -
Watery, Mucus Mucopurulent
Inflammatory reactions
-Follicle Papillae, Phlycten, Folliculosis
Degenerations –
Pinguecula, Pterygium, Concretions
Dryness of the eye
Bitot spots, Xerosis
Membrane formation
Scarring

Cysts

Tumors
Limbal nodule
Phlycten, Pinguecula, Limbal
dermoid, Foreign body granuloma,
Trabeculectomy bleb
Foreign bodies
----------------------------------------------------

14
Chapter 11. Clinical examination of the Conjunctiva
Ophthalmology - Topic: Conjunctiva
Number COMPETENCY Dom Lev Cor Suggested Suggested Numb Vertical Hori
The student should be able to ain el e Teaching Assessment er Integrati zont
K/S/ K/K (Y/ Learning method requir on al
A/C H/S N) method ed to integ
H/P certify ratio
n

OP3.2 Demonstrate document and present the correct S S Y DOAP SkillAssessment

135
Chapter 11. Clinical examination of the Conjunctiva
(Chapter 11.1 Clinical anatomy of the conjunctiva, Chapter 11.2 Points to be noted in Examination of the
conjunctiva )

Chapter 11.1 Clinical anatomy of the conjunctiva

The Conjunctiva is a thin, transparent membrane covering the eye. It extends from the Intermarginal
strip and covers the surface of the eyeball up to the limbus

Figure 11-1 Figure 11-2 Figure 11-3

Clinical anatomy of conjunctiva Histological section Lymphatic
(Layers) of conjunctiva drainage of the conjunctiva

The anatomical parts of the conjunctiva are

 Palpebral conjunctiva
 Bulbar conjunctiva,
 Superior fornix and Inferior fornix
 Limbal conjunctiva.
 Caruncle
 Plica semilunaris.

The Bulbar conjunctiva - lines the anterior sclera and is loosely attached underneath with episcleral
tissue and Tenon’s capsule.

Limbal conjunctiva.
 The limbal part of bulbar conjunctiva is adherent and covers the limbus region. It is continuous
with epithelium of the cornea.

Superior and inferior Fornix

136
Bulbar conjunctiva connects superiorly and inferiorly with palpebral conjunctiva and forms superior fornix
and respectively inferior fornix.

Caruncle
 In the inner can thus, 3x3 mm pink mass is present called caruncle which is modified skin,
covered by stratified squamous epithelium with sweat glands and sebaceous glands and hair
follicles It is a vestigial organ (Third lid) however involves in the diseases of the conjunctiva.

Plica semilunaris.
 Adjacent to the caruncle there is a semilunar fold with concavity towards limbus called plica
semilunaris.

Layers/ Histology of the conjunctiva – epithelium and stroma

Glands of the conjunctiva ---

137
Figure 11-4
Blood supply of conjunctiva Blood supply of the conjunctiva

Marginal tarsal arcade arteries

 Peripheral tarsal arcade arteries

 Anterior ciliary arteries

Marginal tarsal arcade arteries

 Marginal tarsal arcade arteries lie 2mm away from the margin
of the eye lid, supplies the marginal conjunctiva

Peripheral tarsal arcade arteries

 Peripheral tarsal arcade arteries lie near the peripheral border of the tarsal plate. Its perforating
branches pierce the muller’s muscle to reach the conjunctiva and gives off ascending and descending
branches. The descending branches supplies the tarsal conjunctiva and also anastomose with the
vessels from the marginal arcade. Ascending branches pass into the superior fornix and continue
around the superior and inferior fornices to the bulbar conjunctiva as posterior conjunctival arteries
which supply the bulbar conjunctiva.

Anterior ciliary arteries –

The lymphatic drainage

Function of the conjunctiva

 The function of the conjunctiva is to protect the eye ball through its lymphatics, rich blood supply
and mucin secretions from the conjunctiva forms the inner layer of the tear film.

The clinical examination of the conjunctiva mainly consists of inspection by diffuse light with magnification.
Palpation is limited to testing the consistency and for tenderness of the lesion.

138
Methods of examination of the conjunctiva
 The lower lid is Pulled down with fore finger to examine the lower palpebral conjunctiva, lower fornix
mid and lower part of the bulbar conjunctiva -
 The patient is asked to look down and the upper lid is raised by the examiner to examine
Upper part of the bulbar conjunctiva
 To examine the upper palpebral conjunctiva of the upper lid, it is everted.
 To examine the upper fornix the upper lid is double everted. The Conjunctiva is anaesthetized with 4%
xylocaine and first evert the upper lid with two non-toothed forceps, then the everted lid is held at two
ends and second evertion is done.
In Blepharospasm – Desmarre’s lid retractors is used to retract the lid to visualize conjunctiva and cornea.

139
Chapter 11.2 Points to be noted in Examination of the conjunctiva

Points to be noted in Examination of the conjunctiva

Color and pigmentation of the conjunctiva

The conjunctiva is a bright tissue and has no color. The color of the conjunctiva is due to change in color of
the sclera, blood vessels and moles.
• Pale conjunctiva
Cause - Anemia

To examine the pale conjunctiva the lower lid is Pulled down for observation of the lower palpebral
conjunctiva.

Pigmentation
• Yellow color- Icterus due to infective or obstructive hepatitis.
• Blue color is due to cyanosis and blue sclera.
• Red color is due to congestion of the conjunctiva.
• Pigmentation - Nevus – Birth marks, Brown or Black in color, Melanosis is congenital Diffuse black
pigmentation of the conjunctiva and Keratinization

140
Figure 11-5 Figure 11-6 Figure 11-7
Icterus Yellow color of the conjunctiva Conjunctival Nevus Melanosis of the conjunctiva

Transparency/ lustre / Brightness of the conjunctiva

Conjunctiva is normally transparent
The transparency is lost in all diseases of the conjunctiva.

Lustre / Brightness is lost in - muddy Conjunctiva seen in spring catarrh, xerophthalmia , Polluted
environment
Figure 11-8 Figure 11-9
Conjunctival congestion Circum ciliary congestion
Congestion
Congestion may be
• Conjunctival Congestion
• Circum ciliary congestion
(CCC),
• Mixed congestion

Table 1

Causes of Conjunctival congestion Causes of Circum ciliary congestion

(CCC),

 Bacterial, and viral Conjunctivitis,  Corneal ulcer.

Epidemic kerato conjunctivitis is caused by adenovirus 8 and 19.

 Allergic Conjunctivitis  Keratitis.

 Spring catarrh  Acute congestive glaucoma.
 F.B on the conjunctiva  Acute Iridocyclitis
 Phacomorphic, Phacolytic and
malignant glaucoma

141
Table 2 Differences between Conjunctival congestion and Circum ciliary congestion

Cl.examination Conjunctival congestion Circum ciliary congestion (CCC)

Color Bright red in color Pink in color

Site More pronounced in the Fornix More pronounced around the limbus

Blood flow direction Blood flow from fornix towards limbus Blood flow from limbus towards fornix

Mixed congestion causes

 Endophthalmitis

• Panophthalmitis
•
Figure 11-10 Figure 11-11 Figure 11-12
Chemosis/Edema of the conjunctiva Ecchymosis/ Subconjunctival Mucopurulent Discharge
Hemorrhage

142
Differential Diagnosis of the Red eye

Table3 Conjunctivitis, Acute Iridocyclitis, Acute congestive glaucoma

Clinical Features Conjunctivitis Acute Iridocyclitis Acute glaucoma (Congestive)

Onset Acute Moderately Acute Sudden in the course of PACG

Vision Good Fair Poor

th
Pain Discomfort Moderate along the first Severe in all branches of v
th
division of the v cranial cranial nerve.
nerve

Discharge Mucopurulent Watery Watery

Photophobia Mild Severe Moderate

Constitutional symptoms Absent Absent Present -vomiting and sweating

Table 4

OP3.1 Demonstration of Red eye in slit lamp

Conjunctival congestion Severe Mild and associated with Mild and associated with CCC
CCC

CCC Absent Present Present

Tenderness on the eye ball Absent Present Present

Corneal lustre Clear. No edema Moderately edematous Severely edematous

K. P`s absent Present Pigmentary K.p may be present

Pathognomonic sign

Depth of anterior chamber (A.C) Normal Deep Shallow

Iris Pattern Normal pattern Lost due to Edema Lost due to Edema

Pupil Normal Constricted with irregular Dilated and vertically oval

margins

Abnormal contents in A.C Absent Hypopyon present Absent

IOP Normal Moderately raised Severely raised.

143
Chemosis or Edema of the conjunctiva
Conjunctiva is lax, prone for edema and is seen in
 Infections of the Conjunctiva, more in pneumococcal conjunctivitis
• Angioneurotic edema
• Congestive heart Failure
• Nephrotic Syndrome
• Protein malnutrition
• Orbital cellulitis

Ecchymosis of the conjunctiva and Subconjunctival Hemorrhage seen in

Acute Haemorrhagic conjunctivitis is caused by Enterovirus 70

Discharges from the eye

• Watery discharge- Epiphora, Lacrimation
• Mucus discharge – Catarrhal conjunctivitis
• Mucopurulent Discharge – Purulent conjunctivitis.

Inflammatory conditions of conjunctiva

Follicle
Aggregation of the lymphoid tissue of the conjunctiva. A raised 2 to 3 mms sized grayish white nodule on the
bulbar or palpebral conjunctiva
Follicle is a pathognomonic sign of Trachoma

Papillae
Hyperplasia of blood vessels of the conjunctiva, each consists of tuft of vessels covered by epithelium. Velvety,
polygonal in appearance. Seen in
• Chronic conjunctivitis, Contact lens users – Giant papillae
• Spring catarrh – Cobble stone appearance, severe papillary hyperplasia seen in upper palpebral
conjunctiva.

144
Phlycten-
A grayish white raised nodule of 1 or 2 mm at or near the limbus due delayed type hypersensitivity reaction
most commonly due to staphylococcal proteins , secondary to tuberculous protein and Helmenthic infection.

Figure 11-13 Figure 11-14 Figure 11-15

Follicle Papillae Phlycten

Figure 11-16 Figure 11-17 Figure 11-18 Figure 11-19

Pinguecula Primary progressive Primary atrophic Concretions
Pterygium Pterygium

145
Table 5

Differences between Primary Pterygium and Pseudo Pterygium

Differences Primary Pterygium Pseudo Pterygium

Age Common in middle and old age Any age.

Site Commonly on the nasal side. rarely on the May be present anywhere in
temporal side the conjunctiva

Shape Triangular in shape and apex is towards the No fixed shape

cornea

Progression Progressive towards cornea No progression / stationary.

Infiltration cap in front of the apex Present (If progressive) Absent

on the cornea

Stockers line i.e Present Absent

Deposition of iron pigment

Probe test Can not be passed Can be passed

Etiology Ultraviolet rays exposure Chemical injuries

Pathology Degenerative Inflammatory

Common sequel after Treatment Recurrence is common No recurrence

Table 6

Differences in Clinical features of Progressive and Regressive Pterygium

Clinical feature Progressive Pterygium Regressive Pterygium

Congestion of conj Marked No congestion

Consistency Thick and Fleshy Atrophic

Infiltration cap Present in front of the apex on the cornea Absent

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 Concretions --Epithelial debris and inspissated mucus in the Henle layers of conjunctiva. They are raised
yellowish white granules commonly seen in the tarsal conjunctiva. Also seen in atrophy of the conjunctiva.
In old age

Dry eye or Xerosis of the conjunctiva

Local causes for the Dry eye

Figure 11-23 Schirmer’s test Figure 11-24 Tear film Break up

Dry eye syndrome - causes

 Vitamin A Deficiency – Xerophthalmia
 Sjogren syndrome,

147
 Steven Johnson's Syndrome
Signs of Vitamin A Deficiency

• Bitot spots - Triangular, foamy, shiny patches on the temporal limbus

• Xerosis
Test to examine for Dryness of the eyes –

• Schirmer’s test
• Tear film Break up time (TBUT)
Schirmer’s’ test, Tear film Break up time (described in examination of lacrimal system

Conjunctival Membrane formation

Clostridium Diphtheria causing conjunctivitis forms true membrane while Figure 11-25
streptococci and Staphylococci cause false membrane formation. True Scarring of the conjunctiva
membrane bleeds on peeling while a pseudo membrane formation does
not.
Scarring of the conjunctiva – seen in
 Trachoma
 Steven Johnson's Syndrome
 Injuries – Mechanical and Chemical injuries

Symblepharon
Al ready described (Chapter Examination of the eye lids)
 Ulcers in the conjunctiva
Figure 11-26
Causes – Phlycten, (Described below) Cysticercus cysts

 carcinomas extending into the conjunctiva,

 Steven Johnson’s, Tuberculous, Burns.
Cysts
• Cysticercus cysts (Common)
• Retention cysts from the glands of the conjunctiva.
Nodules in the conjunctiva
 Phlycten – A grayish yellow 2mm nodule seen at or near the limbus secondary to allergy reaction for
tuberculous or helminthic infection.
 Pinguecula - See degenerations of Conjunctiva
 Limbal dermoid – Usually congenital
 Foreign body granuloma
 Glaucoma filtering bleb of Trabeculectomy surgery

148
Figure 11-27 Limbal Dermoid Figure 11-28 Dermo lipoma Figure 11-29
Squamous neoplasia of conjunctiva

Figure 11-30 Figure 11-31 Figure 11-32

Conjunctival palpebral F. B Everting of the upper lid Everting of the upper lid

Foreign Body (F.B) on the conjunctiva

149
The commonest area for conjunctival F.B is the Sub tarsal sulcus, an area 1to2mm below the inner border of
the upper lid which is seen as a hood/sulcus when the lid is everted.
• Sometimes F.B is embedded in granuloma and is called F.B granuloma. Other sites are Bulbar
conjunctiva and the inner Fornix.

Clinical skills
• Eversion of the upper lid to see the palpebral conjunctiva and the Subtarsal Sulcus
Method of Eversion of the upper lid – The participant is asked to look down and grasp the lateral eye
lashes of the upper lid with thumb and fore finger. Pull the upper lid down and out, keep a spatula on the
skin of the lid at the upper border of the tarsal plate and put a little pressure with the spatula while
everting the lid with thumb and forefinger.

Removal of Conjunctival F.B - May be washed by the tears towards the Inner canthus.
 Three important points for consideration
• All F.B are to be removed under aseptic precautions
• All F.B are to be removed under good magnification and illumination , preferably under surgical
operating microscope. Under surface good anesthesia

Removal of the sub tarsal sulcus

• Evert the upper eye lid and whipping of the F.B with wisp of cotton wool . The simple technique of
everting the upper lid should be learn by all the medical graduates
If the cornea is involved -Principles of the management of corneal involvement.
• Local and systemic antiboitics
• Analgesics and anti inflammatory
• Cycloplegic and mydriatic
• Protection of the eye by pad and bandage or by shade.
Bulbar conjunctival F.B.
• If the F.B is embedded in the bulbar conjunctiva it will be picked out by a needle after local
anesthesia.
• Some times it is difficult to remove , and it may be necessary to snip off a collar of conjunctiva
containing the F.B. with scissors.
Lower fornix F.B is removed
• Removed by pulling down the lower lid and wiping the F.B with a sterile cotton swab.
Diagrams to learn
• Draw a labeled diagram of the Clinical anatomy of the conjunctiva.
• Draw the diagram of histological section of conjunctiva.
• Draw the diagram of the Lymphatic drainage of the conjunctiva.

150
OSPE – Short Clinical cases for university examination

All the clinical points which are to be examined in the conjunctiva are the short cases in the university
examination.

Types of questions in the examination -

Clinical questions starts with diagrams of Clinical anatomy , Histology, functions ,lymphatic drainage of the
conjunctiva pathological changes In the lesions and Microbiological commensals in the conjunctiva ,
definitions of the lesions , methods of treatment .Etc..
OSCE – All the diagrams in this chapter are included in OSCE

Format for the examination of the conjunctiva

Table 7
Examination of the conjunctiva Right eye Left eye
Color and pigmentation
Pale, Pigments, Moles
Transparency of the conjunctiva
Congestion-
Conjunctival, CCC, Mixed.
Chemosis
Ecchymosis or sub conjunctival hemorrhage
Discharges -
Watery, Mucus Mucopurulent
Inflammatory reactions
-Follicle Papillae, Phlycten, Folliculosis
Degenerations –
Pinguecula, Pterygium, Concretions
Dryness of the eye
Bitot spots, Xerosis
Membrane formation
Scarring

Cysts

Tumors
Limbal nodule
Phlycten, Pinguecula, Limbal
dermoid, Foreign body granuloma,
Trabeculectomy bleb
Foreign bodies

----------------------------------------------------

151
Topic: Cornea

Chapter 12. Examination of the Cornea

Number COMPETENCY Do Lev Co Suggested Suggested Numb Vertical Horizo
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Topic:Cornea NumberofCompetencies: (1 Numberofproceduresthatrequirecertification:(NIL)

OP4.1 Enumerate,describeanddiscussth K K Y Lecture, Written/Viv Human
etypesandcausesofcornealulcerat H Small a voce Anatom
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OP4.2 Enumerateanddiscussthedifferen K K Y Lecture, Written/Viv
tialdiagnosisof infectivekeratitis H Small group a voce
discussion
OP4.3 Enumeratethecausesof K KH Y Lecture, Written/Viv
cornealedema Small group a voce
discussion
OP4.4 Enumeratethecausesanddiscusst K KH Y Lecture, Written/Viv
hemanagementof dryeye Small group a voce
discussion
OP4.5 Enumeratethecausesof K KH Y Lecture, Written/Viv
cornealblindness Small group a voce
discussion
OP4.6 Enumeratetheindicationsandthet K KH Y Lecture, Written/Viv
ypesof keratoplasty Small group a voce
discussion
OP4.7 Enumerate the indications and K KH Y Lecture, Written/Viv
describe the methods of Small group a voce
tarsorrhaphy discussion
OP4.8 Demonstratetechniqueofremoval S SH Y DOAPsession Skillassess
offoreignbodyinthecorneainasim ment
ulated environment
OP4.9 Describeanddiscusstheimportanc K KH Y Lecture, Written/Viv
eandprotocolsinvolvedineyedona Small group a voce
tion andeyebanking discussion
OP4.10 Counsel patients and family A/C SH Y DOAPsession Skillassess
about eye donationin as ment
simulated environment

Competency: Op4.6
Demonstrate technique of removal of foreign body in the cornea in the simulated environment
Competency: Op4.10
Counsel patients and family about eye donation in a simulated environment

152
Chapter 12. Examination of the Cornea

The Cornea forms the anterior 1/6 of the outer coat of the eye ball. It is nearly circular in shape. The average
diameter is 11 mm and horizontal diameter is slightly more than the vertical due to the encroachment of the
upper conjunctiva on to the limbus. Limbus is a junctional area between cornea and sclera. The Vertical
diameter measures 10 to11 mm while the horizontal diameter is 11to 12 mm.

Cornea is a specialized tissue in the eye and body because

 It is transparent
 It is avascular – nutrition is partly supplied by perilimbal vessels.
 Has Refractive power of +44 Diopters
 Richly supplied with sensory nerves - Nasociliary nerves.
 Smooth
Figure 12 -1 ACorneal layers Figure12- 2 Optical section of the
 Lustrous or bright
cornea

The function of the cornea

 Refraction

The cornea consists of five layers -

 Superficial epithelium,
 Bowman’s membrane,
 Substantiapropria(stroma),
Descemet’s membrane
 Endothelium.

All Clinical Examination of the cornea starts with the Alphabet `S`
• Size of the cornea
• Shape of the cornea
• Sheen or brightness of the cornea
• Surface of the cornea – anterior and posterior surface
• Stroma
• Staining of the cornea
• Sensitivity of the cornea
• Scarring of the cornea.
• Stains and pigments of the cornea.

153
Size of the cornea –
Figure 12- 3 Micro Figure12-4 Megalocornea
Measured with a caliper after anaesthetizing the ocular
cornea
surface
Average Normal size of the corneal diameter is 11.5mm
• Horizontal - 11 mm
• Vertical is 11.5 mm.
If the corneal diameter is more than 13 mm, it is called
Megalocornea and is seen in
• Congenital
• High myopia
• Buphthalmos
If the corneal diameter is less than 10 mm, it is called Microcornea and is seen in
• Congenital conditions - Microphthalmos, Micro cornea
• Phthisis bulbi
• Atrophic Bulbi
• Nanophthalmos

Shape of the Cornea

Normally looks circular though elliptical and Convex anteriorly and concave posteriorly, like a watch glass.
The shape is lost in
Figure 12- 5 Cornea Figure12- 6 Keratoconus -
• Cornea plana – Plane corneal surface Munson's sign
Plana
• Kerato conus – Conical shape of the cornea
• Kerato globus-Globular shape of the cornea
• Phthisis bulbi –Quadrangular shapeof the
cornea

Sheen or brightness of the cornea –

The brightness/transparency is Lost in all corneal
lesions
• Corneal oedema
• Corneal ulcer
• Corneal Degenerations
• Corneal Dystrophies
• Corneal Scarring
• Chronic uveitis

Surface of the cornea - Anterior Surface and posterior surface

Anterior Corneal surface examination consistsof –

154
 Corneal curvatures,
 Smoothness of anterior Corneal surface
 Corneal ulcer
 Vascularization
 Corneal F.B
To examine corneal curvatures and smoothness the following methods are used.
Figure12- 7 Placido's disc
• Window reflex test
• Placido’s disc
• Keratoscope (Illuminated Placido’s disc )
• Keratometer
• Computerized corneal topography – used for refractive corneal procedures.
Window reflex test:
The person is to sit in front of an open window at a distance of 1 meter. The
image of the window frame and bars is to be noticed on the surface of the
cornea. If there is distortion of the window or bars on the surface of the cornea
it indicates irregular corneal surface due to corneal curvature.

Keratometer: -This is an Instrument used to study the corneal curvature as well as dioptric power of the
cornea.

Placido’s Disc – An instrument to assess the curvature of anteriorsurface of the cornea

Placido’s Disc is a circular disc measuring 10 inches in diameter with a central hole to see the cornea.
Concentric alternating white and black rings are present around the central hole. If there is distortion of these
rings it indicates irregular corneal surface due to corneal curvature.
Irregular Corneal curvature is observed withPlacido’s Disc and used for the diagnosis of
• Irregular astigmatism
 Keratoconus
 Keratoglobus
 Astigmatism caused by Anterior staphyloma and ciliary staphyloma , Limbal growth
 Corneal abrasion
 Kerato refractive procedures

Table 1
Corneal curvature is increased in Corneal curvature is decreased in
 Keratoconus • Micro cornea
• Keratoglobus • Microphthalmos
• Buphthalmos • Cornea plana
• Phthisis bulbi /Atrophic bulbi
• Perforated globe

155
b) Smoothness of anterior Corneal Figure12- 8 Corneal aberration Figure 12- 9 Corneal ulcer
surface stained with fluorescein

The anterior surface of cornea is

Smoothand Smoothness is lost in
• Astigmatism
• Corneal aberration
• Corneal ulcer
• Corneal scarring
Corneal ulcer –
Defined as the discontinuity of the corneal epithelium associated with inflammation, infection or necrosis. The
clinical features is acute pain in the eye, redness, photophobia and lacrimation. The ulcer may be bacterial,
Viral, fungal or due to blunt or penetrating trauma.
History of injury to the eye to a former by a vegetative matter with a clinical feature of an ulcer suggestive of
fungal corneal ulcer.
Figure 12- 10 Superficial Figure12- 11 Superficial
vascularization of the vascularization in
c)Vascularization – cornea leucoma cornea
Superficial or deep vascularization is due to hypoxia
of corneal tissues,
When the tissue is in Hypoxia, vascular endothelial
growth factors (VAGF) secreteVaso formative
substance which generate new vessels. This is
natures attempt to bring oxygen to the hypoxic
tissue.
Differences between Superficial vascularization and Deep vascularization
Table 2
Superficial vascularization Deep vascularization
New vessels are seen between the epithelium and Bowman’s New vessels are seen in the stroma
membrane
Limbal vessels Anterior ciliary vessels
Traced over the limbus onto the conjunctiva End abruptly at the limbus.
Bright red and well defined Ill defined and grayish red or diffuse red and brush
like.
Branch dichotomously in an arborescent fashion Deep vessels are parallel to one another in radial
direction. Branch at acute angles and their course is
determined by the lamellar structure of the stroma.
Raise the epithelium over the vessels so that the corneal surface is The surface is smooth and hazy
uneven
Trachoma, Hansen’s keratitis, Phlyctenular keratitis, Interstitial and Disc form Keratitis, Corneal graft
rejection

156
Posterior Surface of the cornea
Clinical examination of the posterior Surface
Figure12- 12 Keratic Figure 12- 13 Krukenberg's
consists of precipitates spindle
a) Descemet’s membrane
b) Corneal endothelium
c)Keratic Precipitates (K.P)
d,Krukenberg’s spindle

a) The Descemet’s membrane is examined for

Haab’s striae –Horizontal concentric
Breaks or Rupture in Descemet’smembrane seen in
 Congenital glaucoma,
 Blunt Trauma,
 Keratoconus.
 Surgical manipulation of the cornea in IOL implantation.
 Folds also seen in soft eye.
Vertical or oblique lines represents tears in Descemet’s membrane seen in birth trauma.

b) The Endothelium is studied

• By Slit lamp examination and Specular Microscopy
• Endothelial count is done by Specular Microscope. The normal density of the endothelium is 3000 cells per
square mm.
• The Keratic precipitates are studied by Slit lamp examination
Keratic precipitate (K. Ps) are the attachment of inflammatory cells to the endothelium. K. Psare the hall mark
of Cyclitis.

Types of K.Ps
• Fine dust like opacities – Allergic inflammation of Uvea
• Coarse and granular K. Ps are seen in non-granulomatous uveitis.
• Mutton fat - Granulomatous uveitis, Corneal graft rejection. Mutton fat K.P are composed of epithelioid
cells and macrophages
• Pigmented K. Ps and red Keratic precipitates are seen in hemorrhagic uveitis.
• Fresh and Old K. Ps- Fresh K. P’s are grey and in shape, old K. Ps are pale and margins are crenated.

Stroma of the cornea

The Stroma constitutes the major part of the thickness of the cornea. The central axial /optical zone is 3mm in
diameter, 0.6mm (600 microns) in thickness while 0.9 mm (900 microns) thickness at periphery.
Thickness of the cornea is measured byPachometer/ Pachymetryor by ultra sound pachometer.

157
The stroma is examined for
• Edema – due to accumulation of fluid, S/L exam shows as fluid vacuoles.
• Infiltrates – These are inflammatory cells which enter the stroma through limbal vessels, and breaks
the Bowman’s membrane. Infiltrates indicates active inflammation.
• Deep Vascularization
• Thickness of the cornea is due to Edema, Infiltrates, Vascularization,
• Thinness of the cornea is due to Keratoconus, Keratoglobus, Buphthalmos.
• Peripheral stromal corneal opacity – seen in aged people called arcus senilis, or in young people called
arcus Juvenilis.

Figure 12- 14
Staining of the cornea –By Vital stains
Three vital stains
• Fluorescein – 2 %
• Rose Bengal- 1%
• Methylene blue
• Alcian blue Figure12- 15 - Corneal aberration stained with
fluorescein

Fluorescein – 2% Sodium fluorescein

As long as corneal epithelium is intact,cornea will
not take a stain
When epithelium is lost the stroma takes up the
stain and under the background of stromal fluorescence the staining is seen as a brilliant green. Fluorescein
staining is viewed with cobalt blue filters so as to enhance the wave length of fluorescein.

Fluorescein Staining is positive in

• Corneal aberration
• Corneal ulcer

Other clinical uses of Fluorescein

• Contact lens fitting
• Applanation Tonometry
• Seidel’s test – leaking aqueous
• Lacrimal passage investigations
• Fluorescein Retinal vessels angiography.

Rose Bengal Staining – 1%.

Rose Bengal Staining is taken up by Devitalized tissues of the conjunctiva and Cornea and staining is seen as
pink

158
Rose Bengal staining is Positive in Figure 12- 16

• Margins of corneal ulcer

• Dry eyes
• Herpes simplex Keratitis
• Herpes Zoster Keratitis
• Chemical burns.

Methylene blue Staining

Methylene blue Staining is taken up by exposed nerve endings of the cornea
Methylene blue Staining is seen in
• Hansen’s Disease Figure12- 17 Examination of
corneal sensitivity
 Neuroparalytic Keratitis

Alcian Blue
Selectively stains excess in Mucus in Dry eye.

Sensitivity of the cornea

The Sensitivity of the cornea is tested by touching the corneal lesion
with a sterile wisp of cotton.
Absolute loss of corneal sensations is seen in
• Viral keratitis – Herpes simplex keratitis & Zoster keratitis.
• Hansen’s Disease
• Neuro paralytic Keratitis

Relative loss of corneal sensation is seen in all corneal lesions

• Bacterial , Fungal corneal ulcer
• Corneal edema
• Scarring
• Degenerations
• Dystrophies
• Absolute glaucoma.

Scarring of the cornea

Fibrosis /degeneration of the stroma of cornea causes scarring otherwise called opacity of the cornea.
• Any insult to the cornea heals by fibrosis causes scarring which is seen as chalky white appearance
without any signs of inflammation and does not take stains.

159
Corneal opacity is described as unilateral or bilateral, Size, shape, grade, position, Number, Staining,
Sensitivity, vascularization.

Figure12- 18 Nebula Figure12- B9 Macula cornea Figure 12- 20 Figure 12- 21 Bilateral
cornea Leucoma cornea
Leucoma cornea

Corneal scars are Graded as follows.

• Nebula cornea
• Macula cornea
• Leucoma cornea
• Adherent Leucoma
Nebula cornea
• 1/3 of Superficial layers of corneal stromal scarring ,underneath which the details of anterior chamber or
iris or pupil are seen clearly
Macula cornea
• 1/3 to ½ of the layers of the corneal stromal scarring, underneath which the details of anterior chamber
or iris or pupil are seenhazily.

Leucoma Cornea
• Total corneal stromal scarring underneath which the details of anterior chamber or iris or pupil are not
seen.
Adherent Leucoma
Corneal opacity of any grade with iris or iris pigment attached to it

Shapes of the opacities

• Dendritic pattern - In herpes Zoster keratitis
• Phlycten – Dome shape, with base towards the limbus
• Tongue shaped opacity - Sclerosing keratitis
• Arcus opacities – in arcus senilis
• Haab’s striations- in rupture of Descemet’s membrane

160
Figure12- 22 Dendritic Figure 12- 23 Arcus Figure 12- 24
Pattern senilis Haab’s striations

Stains and Pigments of the cornea

 Blood staining of the cornea – Seen in blunt trauma with hyphema and raised IOP, the cornea is
brown in color, due to deposits of hemosiderin in the stroma.
Melanin Pigments are seen in the corneal epithelium in melanosis and malignant melanoma and
 Krukenberg’s spindle is seen in endothelium in pigmentary glaucoma (Pigment deposition on the
endothelium
 Kayser-Fleischer ring –yellow pigment is seen in in the Descemet’s and endothelium in Wilson’s
diseases Figure12- 25 F.B Cornea Figure12- 26 Blood
 Fleischer ring - Deposits of hemosiderin are found stained cornea

in Bowman’s membrane in long standing of

pterygium and around the base of the cone in
keratoconus
 Siderosis – Iron F.B’s in the cornea gives staining.

F. B cornea -causes severe F. B. sensation. Describe F.B

position, type of material etc.

161
Figure 12-27 , fine corneal F.B Figure 12-28 ,F.B staining on Figure 12-28, S/L Figure 12 -29 A leash of
the cornea section showing blood vessels will point
the depth of F.B towards F.B

Diagnosis of the corneal F.B.

• Diagnosis of F.B requires good illumination , good magnification and some times with S/L.
• But smaller F.B can require S/L examination.
• A leash of blood vessels will point towards F.B
• Fluoreciene stain some times reveals its position
S/L - Optical section Shows the depth of the F.B.

Removal of the corneal F.B.

• Removal should be under aseptic conditions and Under magnification i.e binocular loupe/
microscope.
• Eye is anesthetized with 4% xylocain , Figure 12 -30 Instruments 1. F.B Needle
for corneal F.B removal 2. F.B Spud
• Wire speculum is kept to separate the lids
3. Wire speculum
• First an attempt is made to remove with a
sterile cotton swab.
• If it fails foreign body spud is used to
F.B spud in
remove F.B magnified view
• Deep F.B is carefully picked out with a
needle
• And if necessary with little keratotomy.
• Foreign body staining is removed after next day to four days.

Deep corneal F.B

• Care should be taken to prevent the F.B slipping into A.C
• By making Keratotomy
• If F.B is magnitizable use magnets
• If it slips into A.C it should be removed by opening the A.C.

If the corneal ulceration is present

• Treat the ulcer according its principles of treatment of corneal ulcer

Principles of the management of corneal involvement.

162
• Local and systemic antiboitics
• Analgesics and anti inflammatory
• Cycloplegic and mydriatic
• Protection of the eye by pad and bandage or by shade.
Prophylactic measures
• Banning of the tools with overhanging edges
• Fitting of the guards to the grinding machines
• Use of goggles
• Educative measures

OSCE
Figure12- 31 Slit Figure 12-32
 Diagram of the layers of the cornea
Keratometer
lamp
 Window reflex test –
 Placido’s disc examination
 Corneal sensitivity examination
 Staining of the cornea
 Sensitivity of the Cornea

Diagrams to learn
Diagram of the layers of cornea,
Slit lamp optical section of cornea.
Diagnostic instruments used in corneal examination.
 Slit lamp
 Placido disk and. Keratoscope (Illuminated Placido’s disc)- This instrument is a illuminated Placido`s disc
which consists of alternate black and white circles painted on a disc. The observer looks the cornea for
the images of the Placido’s disc through a central hole. This is to assess the corneal surface irregularity
 Automated (computerized) corneal topography analyzer – for corneal curvature study with computers.
 Keratometer to study corneal curvature/ corneal dioptric power
 Specular Microscope - To study the endothelium of the cornea

Figure 12- 27 Cup and saucer model to

explain any ulcer i.e. margin, edge ,floor,
base of an ulcer

163
Table 3
Format for the Examination of the Cornea
Examination of the Cornea Right Eye Left Eye
Size of the cornea Megalocornea,Microcornea
Shape of the cornea
Sheen or brightness of the cornea
Surface of the cornea
Anterior surface –
Corneal curvatures
Smoothness,
Vascularization
Posterior surface
Descemet’s membrane - Breaks,
and Folds
Corneal endothelium and KPs
Stroma
Edema, Infiltrates, Deep Vascularization ,
Thickness Thinness
Staining of the cornea
Fluorescein – 2 %
Rose Bengal- 1%
Methylene blue
Sensitivity of the cornea
Scarring of the cornea.
Nebula cornea
Macula cornea
Leucoma cornea
Adherent Leucoma
Stains and pigments of the cornea
Corneal F.B

---------------------------------------------------

164
Chapter 13 Examination of the Sclera
th
The Sclera is a white opaque tissue that forms the 5/6 of the outer coat of the eye. It protects the inner
tissues of the eye ball. The junction of the cornea and sclera is called limbus. Limbus contains stem cells
(Pluripotent cells)
Sclera is thickest around the optic nerve and thinnest at the insertion of the
Figure 13-1
extra ocular muscles.

Layers of the sclera

 Episclera – outer layer
 Sclera Proper – inner layer
 Lamina fusca – innermost layer

Openings in the sclera

 Lamina Cribrosa – Sieve like structure through which passes the optic
nerve fibers
 Anterior ciliary artery, veins and nerves
 For vortex veins
Clinical points to be noted in the examination of the sclera.
 Color of the Sclera
 Inflammations
 Ectasia of the sclera. -Staphyloma
Color of the Sclera
 Blue sclera – Blue sclera is due to thinning of the sclera through which underlying uveal tissue shine
 Yellow in jaundice
 Localized redness in the Episcleritis and Scleritis
 Black sclera in melanosis
Blue sclera Figure 13-2 Yellow sclera Figure 13-3 Black sclera
• First few months in new • In infective or obstructive • In Ocular melanosis.
born, Jaundice
• Marfan’s syndrome,
• Osteogenesis imperfecta
• Pseudoxanthoma elasticum,
• Buphthalmos,
• Ehlers Danlos syndrome,
• Ciliary Staphylomas
• Nevus of OTA
• High myopia,
• Healed scleritis.

165
Inflammations of the sclera
• Episcleritis Figure 13-4 Figure 13-5
• Scleritis Episcleritis Scleritis

Episcleritis - Idiopathic
Seen as raised reddish hue lesion, painless, not tender
commonly on the temporal side of the eye ball away from the
limbus due to localized inflammation of the Episcleral tissue.
Blanching of redness occurs using 2.5% phenylephrine

Scleritis
Seen as deep red or dusky red color of the conjunctiva, associated with peripheral keratitis, Sclerokeratitis,
sclerosing keratitis and uveitis. Tenderness present. Scleritis Commonly associated with systemic diseases like
rheumatoid arthritis. Other associated causes are SLE, ankylosing spondylitis, Wegener’s granuloma , ptosis
dermatomycosis, Reiter’s syndrome, nonspecific arteritis, polychondritis and gout

Ectasia
Ectasia of the outer coat of the eye ball with herniation or incarceration of uveal tissue is called Staphyloma
Cause of staphyloma – weak sclera due to injury, Scleritis, Raised IOP.

Figure 13-6 Figure 13-7 Anterior Figure 13-8 Figure 13-9 Figure 13-10
Staphyloma Anterior Staphyloma Ciliary Posterior
Staphyloma Staphyloma

Types of Staphyloma
Anterior Staphyloma
 Ectatic corneal cicatrix with incarceration of iris is called Anterior Staphyloma
 Total corneal ulcer is healed by weak fibrosis and can not withstand normal intraocular pressure. And
weak fibrosis becomes ectatic and iris gets incarcerated in it.
Intercalary Staphyloma
 Ectasia of the limbus with incarceration of the root of iris.
 Seen in Absolute glaucoma, penetrating injuries in the limbus.
Ciliary Staphyloma
 Ectasia of the Ciliary region of the Sclera with incarceration of the ciliary body. Seen in Absolute glaucoma,
Buphthalmos, trauma.

166
Equatorial Staphyloma
• Equatorial Scleral ectasia with uveal tissue incarceration seen in Absolute glaucoma

Posterior Staphyloma.
• Ectasia of the Sclera posterior to the equator of the globe. The most common cause for posterior
staphyloma is in High axial myopia. In I.O examination a depression is seen in the posterior pole of the
eye

OSCE and OSPE

• Episcleritis
• Staphylomas

Format for Examination of the Sclera

Table 1
Examination of the Sclera Right Eye Left Eye
Color of the Sclera
Inflammation
 Episcleritis
 Scleritis
Ectasia of the sclera. –
Staphyloma

----------------------------------------

167
Chapter 14. Clinical Examination of the Anterior Chamber (A.C)
Competency – OP 6.6
Identify and Demonstrate the clinical features and distinguish and diagnose common clinical conditions
affecting the anterior chamber.
Competency – OP 6.10
Counsel patients with the conditions of the iris and anterior chamber about their diagnosis , therapy and
prognosis in an emphatic manner in a simulated environment
-----------------------------------------------------------
The cavities of the eye ball are anterior aqueous cavity and Posterior Vitreous cavity
The anterior cavity is divided into anterior chamber and posterior chamber by the iris diaphragm and pupil .
The space in front of the iris is anterior chamber while the space behind the iris is posterior chamber.

The anterior chamber is a plano convex space formed by the posterior surface of the cornea and posteriorly
by, the anterior surface of the iris , and pupil . The junction of Plano convex is the angle of the anterior
chamber The contents of the anterior chamber is aqueous which maintains IOP and there by shape of the
eye ball.

Figure 1Cavities of the eye ball Figure -14-1 Cavities of the eye ball
The posterior chamber is a trianglular space bounded anteriorly by
the posterior surface of the iris, pupillary margin and posteriorly by
the anterior surface of the crystalline lens, laterally it is bounded by
the part of the ciliary body while the apex is formed by the
iridoletecular apposition.
The angle of the anterior chamber examination requires a
Gonioscope and a Slit lamp (See Clinical examination of Glaucoma
written in this chapter )
Clinical points to be noted in the examination of
Figure14- 2Torch light Figure14- 3 Showing nasal
A.C exam for assessment of iris is not illuminated
 Depth of the anterior chamber (A.C) – Increased, anterior chamber

Decreased, Variable depth

 Abnormal contents in the A.C

Depth of the anterior chamber

The axial depth of the A.C is 2.5 mm (From Posterior
surface of the center of the cornea to the Anterior
surface of the crystalline lens). The A.C is peripherally shallow and forms the angle of the anterior chamber.
The anterior chamber appears deep than the actual depth due to magnification produced by the cornea.
Bed side method to assess the depth of the anterior chamber

1
• A beam of light is focused with a pen torch on the temporal limbus parallel to the iris and illumination
of the nasal limbus and iris is observed.
• If the nasal limbus and nasal iris are illuminated the chamber depth is normal or deep.
• If the nasal part of the iris near the pupil is not illuminated the anterior
chamber is shallow-This is called Eclipse sign or Crescent sign. Figure14- 4 Van Herick's sign

• Van Herick Method of assessing the depth of A.C –

• Comparison of the depth of the periphery of the A.C to the
peripheral corneal thickness with a thin slit beam of oblique
illumination technique to measure the degree of the depth of the
anterior chamber .
• Examination of the angle of the anterior chamber requires
Gonioscope with slit lamp.
Table 1
Depth of the anterior chamber (A.C) – Increased, Decreased, Variable
Causes of Increased depth of the Causes of Decreased depth of the Causes of Variable depth of the
A.C A.C A.C
 Young individual  Old individual  Subluxated lens
 High Myopia  Hypermetropia  Iris bombe – Funnel shaped
 Megalo cornea  Cornea plana  Chronic uveitis
 Keratoglobus  PACG (Primary angle closure  Angle recession after trauma.
 Keratoconus Glaucoma)
 Buphthalmos
 Acute Iridocyclitis  Intumescent Cataract  Adherent leucoma
 Hyper mature cataract  Pseudophakia - IOL fixation in  Ante and retro flexion of the
the sulcus iris
 Morgagnian cataract  Malignant glaucoma.  Iris prolapse
 Hyper mature – sclerotic - -
 Aphakia  Perforated Corneal wound  Iris tumors
 Pseudophakia – IOL in the  Excess drainage through the  -
capsular Bag Fixation filtering bleb
 Dislocated lens into the A.C or  -  -
into the posterior cavity .

Table 2
Abnormal contents in the A.C --Causes
 Protein Particles  Ruptured lens particles in blunt injury
 Hypopyon  Liquefied lens matter in Morgagnian cataract
 Cells  Lens matter after ECCE procedure.
 Blood in the A.C - Hyphema  A.C IOL
 Larvae or cyst  Iris clip IOLS

 F.B  Vitreous

2
Abnormal contents in the A.C - Protein Particles, Hypopyon, cells, Hyphema, cysts, Larvae, F.Bs ( Metallic, or
wooden et)
Protein Particles
• Normally no proteins are present in the aqueous . Leak of protein particles from iris vessels into the
aqueous is pathological and is the earliest sign of uveal inflammation. The leak of proteins are due to
failure of blood aqueous barrier and the causes for proteins in the aqueous are irido cyclitis, pan
uveitis and trauma.
• The protein particle which is suspended as refractile bodies in the aqueous scatters light causing a flare
when a 0.2 mm light beam from slit lamp strikes it. This is what makes the slit lamp beam of light
visible as opalescent . This is called Aqueous flare due to Tyndall’s phenomena.
• Examination for protein particles is done by passing a 0.2mm beam of light of slit lamp (Smallest beam of
slit lamp ) oblique illumination into anterior chamber .Normally the aqueous is optically empty. If the
beam of light is seen as an opalescence, it indicates leak of protein particles
• The movement of the protein particles in the beam of light is called Brownian movement.

Table 3
Grading of Flare - 0 to + 4
Setting of the slit lamp beam for grading of flare Grading of flare
Slit lamp Oblique illumination technique No proteins = 0
The slit lamp beam of light is oblique to the plane of Faint = + 1
iris in order to evaluate the degree of obstruction of
iris details
The slit lamp intensity and magnification must be Moderate = +2
maximum
The slit lamp beam height is 3 mm Marked = +3
The slit lamp beam width of 1 mm Intense with severe fibrinous exudates = +4

Hypopyon
Pus in the anterior chamber is called hypopyon.
The aqueous with raised proteins is called plasmoid aqueous. The plasmoid aqueous is turbid. If uveal
inflammation increases, more exudation with Proteins, inflammatory cells and fibrin in the A.C forms a
sediment which gravitates down and settles at the bottom of the A.C with a horizontal level .This is
called`Hypopyon`.

Pathogenesis of Hypopyon in corneal ulcer -

In an imperforated corneal ulcer the toxins produced by the bacteria percolates through the corneal tissue
and enters into the anterior chamber and initiates the inflammatory process in the vessels of the iris. These
inflammatory exudates enter in to the anterior chamber to form `Hypopyon

3
Types of Hypopyon Table 4
• Sterile Hypopyon Causes for Hypopyon
• Unsterile Hypopyon Causes of Unsterile Hypopyon Causes of Sterile Hypopyon
• Pseudo Hypopyon
 Fungal corneal ulcer.  Unperforated corneal ulcer
• Inverse Hypopyon
 Perforated corneal ulcer  Acute Uveitis
 Penetrating injuries  Toxic anterior segment
syndrome (TASS)
 Endophthalmitis
 Panophthalmitis
 Septicemia
Figure14- 5 Hypopyon Figure14- 6 Inverse Hypopyon Figure14- 7 Hyphaema

Pseudo Hypopyon
When Hypopyon is caused by non inflammatory exudates it is Called Pseudo Hypopyon.

Causes of Pseudo Hypopyon

 Collection of tumor cells of Retinoblastoma
 Liquefied lens matter leaking into aqueous in phacolytic glaucoma
 Traumatic ruptured Lens matter in A.C.
Inverse Hypopyon
The silicon oil in the A.C which is lighter than the aqueous floats upwards with a horizontal lower border. This
is called Inverse Hypopyon
Aqueous Cells in the A.C
In the inflammation of the uvea the inflammatory cells pour into the aqueous and are larger than the protein
particles. And in 2 x 5 mm slit beam , the cells are graded 1 to 4. 5 to 10 cells are graded +1 , and more
than 50 grade +4
Grading of cells - 0 to + 4
Table 5
Setting of the slit lamp beam for grading of cells Number of cells Grade
Direct Oblique illumination technique 5 to 10 cells +1
Intensity and magnification must be maximum 11 to 20 +2
Beam height is 3 mm 21 to 50 +3
Beam width of 1 mm 50 cells +4

4
Hyphaema : Blood in the A.C - Causes
 Blunt and penetrating injuries of the eye ball.
 Post operative Ocular surgeries
 Herpes zoster uveitis,
 Gonococcal iridocyclitis
 Blood dyscrasias
 Clotting disorders
Table 6
 Intraocular tumors
Format for the Examination of the Anterior Chamber (A.C)
 Rubeosis iridis
Examination of the Anterior Chamber (A.C) Right Eye Left Eye
Cysts
 Cysticercosis cysts Depth of the anterior chamber (A.C) –
 Hydatid cysts. Increased,
Larvae - Micro filarial Decreased,
F.Bs-- Metallic or wooden Variable depth
foreign bodies are commonly Abnormal contents in the A.C
seen. Protein Particles
OSCE Cells
 Assessment of the
Hypopyon –Sterile and Unsterile
anterior chamber with a
Hyphema
torch light.
Cysts
 Hypopyon Larvae
 Hyphema Ruptured Lens particles
 Aqueous flare Liquefied lens
Diagrams to learn A.C IOL
 Draw the diagram of the
Iris Clip IOLs
angle of anterior
Vitreous
chamber and diagram of
F.Bs
the drainage of aqueous .
Clinical skills
 Assessment of anterior chamber

OSCE and OSPE

 Hypopyon
 Hyphema
 Aqueous flare
-------------------------

5
14-A Clinical examination ( Investigations) of the eye for the diagnosis of Glaucoma

Definition – Defined as group of ocular diseases with diverse clinical features, patho physiology resulting in
characteristic optic disc and visual field changes which causes progressive optic neuropathy subsequently
glaucomatous optic atrophy in which Intraocular pressure is a risk factor .

General considerations
 Primary glaucoma is bilateral disease
 Causes irreversible blindness if not diagnosed and treated at the earliest.
 It is a hereditary disease

Clinical examination for Diagnosis of glaucoma

Age – POAG in more than 40 years
Sex-Females are more affected in PACG

Symptoms
 Gradual progressive painless dimness of vision present in Primary open angle glaucoma (POAG) and
chronic primary angle closure glaucoma . In PACS ( Primary angle closure suspect) , there may be
pain in the eye which is relieved on taking rest which becomes periodical over period of time ,
 Headache, .
Figure14A -1 Colored
 Colored halos around the bulb, halos around the bulb
 Light minimum raised i.e Glaucoma patients require a maximum
illumination to appreciate an object ,
 Delayed dark adaptation,
 Change in color sense .
 Frequent change of presbyopic glasses

Risk factors for glaucoma

 Refractive errors – Hypermetropia in PACG and Myopia In POAG
 Diabetes
 Hypertension
 Bronchial asthma
 Association of vasomotor instability, emotional crisis , highly strung, Anxious in disposition , State of
fatigue
 Family history of glaucoma

6
Figure14 A -2 Van Herick's Figure14 A - 3 Iris Figure14-A 4 Torch light Figure14A -5 Rubeosis
sign atrophy assessment of depth of anterior iridis
chamber

Basic evaluation
Visual acuity for distance and near vision , examination of color sense by ishihara charts and
contrast sensitivity , light sense are also to be examined .

Slit examination
 CCC
 Corneal edema,
 VanHerick`s sign
 Gonioscopy (See below)
Figure 14A - 6 Schiotz
 Rubeosis iridis,
 Iris atrophy,
 Pupil reaction – RAPD /TAPD
 Glaucom flecken
 Optic disc evaluation with +90 D lens (See below)

Clinical Methods of examination for the diagnosis of Glaucoma

tonometer
 Tonometry – Intra ocular pressure (IOP)
 Measurement of Corneal thickness
 Assessment of depth of anterior chamber
 Gonioscopy – assessment of angle of anterior chamber
 Study of nerve fiber layer of retina with red free light of direct ophthalmoscope
 Study of optic disc changes with +90 D
 Study of visual field changes

Tonometry –
It is measurement of Intra ocular pressure (IOP).
Normal IOP is 11 to 21mm Hg (16 plus or minus 5 mm).

7
Normally the IOP is more in the morning between 8 to 12 noon and also in the evening .
The diurnal variations varies upto 5 mm Hg.
The bed side method of recording IOP is digital (the digits of hand )
Figure14A - 7 Digital
tonometry see examination of the eye ball tonometry

Measurement of Intra ocular pressure based on two principles –

 Indentation tonometry
 Applanation tonometry

Indentation tonometry –
The principle is that the fluid filled eye ball (sphere) is indented by known weight plunger , the plunger will
indent the Cornea of eyeball till the pressure of the plunger is equal to the pressure inside the globe. .The
depth of indentation is proportion to the pressure inside the eyeball

The instrument required for indentation tonometry is Schiotz tonometer

Practice of Schiotz tonometry :

The person is anaesthetized with 1% Proparacaine or 4% xylocaine , should lie on supine position and sterile
plunger of schiotz tonometer either 5.5,7.5,10 grams weight and observed the deflection of pointer on a scale
of the tonometer instrument. . The deflected scale reading is converted to pressures with the use of
Friedenwald nomogram conversion tables which is supplied with the instrument. .

Advantage of this instrument is simple to practice .

The disadvantage of this instrument is the pressure reading
include ocular/sclera rigidity. Hence the border line pressure Figure14A - 8 Applanation
tonometry
changes is not reliable and not validated .

Applanation tonometry –
Applanation tonometry is based on Imbert Fick principle. i.e.
P= F/A i.e the force required to flatten the known surface of
the cornea is equivalent to the IOP..
The instruments necessary for practice of applanation
tonometry are Goldmann tonometer and slit lamp.

Practice of applanation tonometry - The person is comfortably seated and the chin is kept on the chin rest of
slit lamp. The cornea is anaesthetized with 1% proparacaine or 4% xylocaine and cornea is stained with 2%

8
fluorescein , the biprism is illuminated with cobalt blue filter ,and gently the biprism is brought onto the
anaesthetized cornea. Slowly put a force to flatten the cornea and the end point of flattening is known by
touching of the internal margins of the two hemi circles . The IOP is calculated with dial reading.
Advantage of Goldmann tonometry is that ocular/sclera rigidity is not included in the IOP. Thus applanation
tonometry is the gold standard in the IOP measurement .

The other instruments which work on the principle of applanation are Perkins tonometer, Rebound
tonometer,, Maclakov tonometer of Barraquer, Mackay Marg tonometer , Tonopen .Pneumo tonometer ,
Pascal Tonometer (Dynamic contour testing) non contact Pulse air tonometer Etc.

Measurement of Thickness of cornea. –

Measurement of corneal thickness is called pachymetry. The IOP depends on central corneal thickness (CCT)..
If the axial corneal thickness is more than normal , the IOP recording is erroneously high and vice versa.
Hence the IOP is to be calibrated with corneal thickness. This CCT is measured before recording of tonometry.

Assessment of angle of Anterior chamber

Assessment of angle of Anterior chamber is necessary to classify glaucoma into open angle closed angle .
 Van Herick’s Method
 Torch light examination to assess the depth of anterior chamber (AC)
 Gonioscopy

Van Herick’s Method –

It is a comparison between the peripheral anterior chamber depth(PACD) with corneal thickness (CT )

Table 1
PACD/ CT Figure14A - 9 Van Herick's
PACD/ CT Grade sign
4 Wide open angle
3 Open angle – Incapable of
closure
2 Moderately narrow – requires
gonioscope
1 Very narrow angle
( Potentially occlude)

Torch light examination to assess the depth of anterior Figure14A - 10 Torch light assessment of depth
of anterior chamber
chamber (AC)
Torch light is flashed on the temporal side of the eyeball
parallel to the iris and illumination of the nasal part of iris
and nasal limbus is observed
 If the nasal iris , limbus and temporal iris are
illuminated , it indicates open angle

9
 If only temporal iris is illuminated , and the nasal iris not illuminated , i.e it indicates a shallow
anterior chamber. The non illuminated nasal iris is due to bowing forward of temporal iris . The not
illuminated nasal iris is called Eclipse sign or Crescent sign .
Gonioscopy
The principle of gonioscopy is to eliminate the total internal reflection. In the eye the light rays coming from
the Ac falls on the cornea at an angle greater than the critical angle (46 degrees) and is reflected back into
the angle of the anterior chamber of the eye. By keeping higher refractive index of Gonioscope (1.57) which
replaces corneal and air tear film interface the light rays enter into the gonio lens , refracted and the rays
falls on the gonio mirror. The mirror reflects the rays to the oculars of a slit lamp for viewing.
Basically gonioscope is a contact lens that replaces the cornea as a refracting medium by replacing cornea air
interface allowing the rays arising from the angle to come out of the angle.
There are indirect gonioscopes like Zeiss four mirror and Posner four mirror , and
Direct gonioscopes like Koeppe, Swan Jacob , Barkar. Figure14A - 11 Four mirror
Gonioscope
Structures visible through the Gonioscope (From Posterior to anterior)
 Root of Iris
 Attachment of iris to the ciliary body
 Ciliary band
 Scleral spur - Attachment of ciliary band to sclera
 Pigmented trabecular meshwork
 Non pigmented trabecular meshwork
 Schwalbe’s line -Termination of descemets membrane
 Behind the trabeculum is Schlemm canal.
Table 2
Interpretation of the gonioscopic findings
Shaffer interpretation Spaeth Spaeth interpretation Spaeth interpretation
Based on the visible structures interpretation Based on Insertion based on
Based on angular of the iris root On the configuration of the
width peripheral iris
All structures are visible (Wide open 35 to 45 degrees Insertion of the iris  Steep , anteriorly
angle) -Closure not possible (Wide open angle) root anterior to convex
Scleral spur is visible (open angle) - 10 to 20 degrees- Schwalbe’s line  Regular
Closure not possible narrow Insertion of iris root  Queer , anteriorly
Scleral spur is not visible but behind Schwalbe’s line concave
Schwalbe’s line ,trabecular meshwork is Insertion of iris root
visible - Narrow angle behind the scleral
Only Schwalbe’s line is visible (Closed) – spur
IV -Closure is possible Insertion of iris root
on the ciliary band
No structures visible – Closed angle

10
Other methods of assessing angle of AC – Non invasive higher resolution techniques.
Ultrasound biomicroscopy (UBM) – with 50MHz frequency sound waves are used for tissue penetration upto
4mm
ASOCT – Anterior segment OCT scan using 1310 nm light wavelength for higher resolution

Changes in the Retinal nerve fiber layer.

1.2 millions axons of ganglion cells constitutes of nerve fiber layer.
Retinal nerve fiber layer is studied with red free light or green light.
Ganglion cells and its axons is called nerve fiber layer of retina
Subtle retinal nerve fiber damage occurs before the detectable damage on the disc and visual field changes.

How to study retinal nerve fiber layer

• Direct ophthalmoscope with red free light
• OCT(Optical coherence tomograms)
Normal thickness of retinal nerve fiber layer is 100 to 200 microns

Changes in Glaucoma are

• Localized atrophy or, diffuse atrophy of retinal nerve fiber layer.

Examination of Optic Disc

 Direct ophthalmoscope and indirect ophthalmoscope
 Slit lamp Biomicroscopy with +90 D, +78 D, +60D, or with – 58.6D Hruby lens
Table 3
Normal optic disc Suspicious signs Definite signs
 Symmetry of both eyes  Asymmetry of cup  Pale optic dic
 Cup disc ratio is 0.3 : 1  Vertically enlarged oval  Notch in the neuroretinal
 Pink in color disc rim
 Neuroretinal rim is  Cup disc ratio is more  Enlargement of the cup
normal than 0.3  Deepening of the cup
 Cup is circular , no  Nasal shift of retinal  Apparent discontinuity of
notching vessels the vessels – Bayoneting
 Disc hemorrhages sign
 Notching of
neuroretinal rim in any
poles
 Nerve fiber layer wedge
shaped defect
 Glaucomatous optic
atrophy
 Peripapillary optic atrophy
Laminar dot sign

11
Other methods of computerized Optic disc study.
 Confocal scanning laser tomography (CSLO) – Heidelberg retinal tomography (HRT) uses 675 nm
diode laser as a light source. It is used to study optic nerve head morphology, and retinal nerve layer
thickness
 Spectral domain OCT
 Confocal scanning laser polarimetry (SLP) (Synonyms GD, PRO)– used to measure the retinal nerve
layer thickness using polarized diode laser 780nm .

Visual field examination and changes in glaucoma

Basics of visual field examination (Perimetry is explained in the visual field

Visual field defects in glaucoma Table 4

 Isopter contraction Figure14A- 12 Central 30 Figure14A- 13 Figure14A- 14
degrees visual field Isopter contraction Scotoma
 Baring of blind spot
 Paracentral scotoma
 Seidel’s scotoma
 Bjerrum/Arcuate scotoma
 Ring /Double arcuate scotoma
 Nasal step Figure14A- 15 Seidel's Figure14A- 16 Figure14A- 17
scotoma Bjerrum's scotoma Double arcuate
 Central and peripheral vision scotoma
 Tubular vision
 Temporal loss of vision(Total
blindness)

Diagnosis of glaucoma
The diagnosis of glaucoma is made after studing for a combination of clinical signs.
i.e. History, Tonometry- IOP.,Gonioscopy ,Nerve fiber defect ,Characteristic
changes in the optic nerve head and Abnormalities in the visual field.

----------------------------------------

12
Chapter 14. Clinical Examination of the Anterior Chamber (A.C)
Competency – OP 6.6
Identify and Demonstrate the clinical features and distinguish and diagnose common clinical conditions
affecting the anterior chamber.
Competency – OP 6.10
Counsel patients with the conditions of the iris and anterior chamber about their diagnosis , therapy and
prognosis in an emphatic manner in a simulated environment
-----------------------------------------------------------
The cavities of the eye ball are anterior aqueous cavity and Posterior Vitreous cavity
The anterior cavity is divided into anterior chamber and posterior chamber by the iris diaphragm and pupil .
The space in front of the iris is anterior chamber while the space behind the iris is posterior chamber.

Figure 1 Cavities of the eye ball Figure -14-1 Cavities of the eye ball
The posterior chamber is a trianglular space bounded anteriorly by
the posterior surface of the iris, pupillary margin and posteriorly by
the anterior surface of the crystalline lens, laterally it is bounded by
the part of the ciliary body while the apex is formed by the
iridoletecular apposition.
The angle of the anterior chamber examination requires a
Gonioscope and a Slit lamp (See Clinical examination of Glaucoma
written in this chapter )
Clinical points to be noted in the examination of
Figure14- 2Torch light Figure14- 3 Showing nasal
A.C exam for assessment of iris is not illuminated
 Depth of the anterior chamber (A.C) – Increased, anterior chamber

Decreased, Variable depth

 Abnormal contents in the A.C

Depth of the anterior chamber

168
• A beam of light is focused with a pen torch on the temporal limbus parallel to the iris and illumination
of the nasal limbus and iris is observed.
• If the nasal limbus and nasal iris are illuminated the chamber depth is normal or deep.
• If the nasal part of the iris near the pupil is not illuminated the anterior
chamber is shallow-This is called Eclipse sign or Crescent sign. Figure14- 4 Van Herick's sign

• Van Herick Method of assessing the depth of A.C –

 F.B  Vitreous

169
Abnormal contents in the A.C - Protein Particles, Hypopyon, cells, Hyphema, cysts, Larvae, F.Bs ( Metallic, or
wooden et)
Protein Particles
• Normally no proteins are present in the aqueous . Leak of protein particles from iris vessels into the
aqueous is pathological and is the earliest sign of uveal inflammation. The leak of proteins are due to
failure of blood aqueous barrier and the causes for proteins in the aqueous are irido cyclitis, pan
uveitis and trauma.
• The protein particle which is suspended as refractile bodies in the aqueous scatters light causing a flare
when a 0.2 mm light beam from slit lamp strikes it. This is what makes the slit lamp beam of light
visible as opalescent . This is called Aqueous flare due to Tyndall’s phenomena.
• Examination for protein particles is done by passing a 0.2mm beam of light of slit lamp (Smallest beam of
slit lamp ) oblique illumination into anterior chamber .Normally the aqueous is optically empty. If the
beam of light is seen as an opalescence, it indicates leak of protein particles
• The movement of the protein particles in the beam of light is called Brownian movement.

Pathogenesis of Hypopyon in corneal ulcer -

170
Types of Hypopyon Table 4
• Sterile Hypopyon Causes for Hypopyon
• Unsterile Hypopyon Causes of Unsterile Hypopyon Causes of Sterile Hypopyon
• Pseudo Hypopyon
 Fungal corneal ulcer.  Unperforated corneal ulcer
• Inverse Hypopyon
 Perforated corneal ulcer  Acute Uveitis
 Penetrating injuries  Toxic anterior segment
syndrome (TASS)
 Endophthalmitis
 Panophthalmitis
 Septicemia
Figure14- 5 Hypopyon Figure14- 6 Inverse Hypopyon Figure14- 7 Hyphaema

Pseudo Hypopyon
When Hypopyon is caused by non inflammatory exudates it is Called Pseudo Hypopyon.

Causes of Pseudo Hypopyon

171
Hyphaema : Blood in the A.C - Causes
 Blunt and penetrating injuries of the eye ball.
 Post operative Ocular surgeries
 Herpes zoster uveitis,
 Gonococcal iridocyclitis
 Blood dyscrasias
 Clotting disorders
Table 6
 Intraocular tumors
Format for the Examination of the Anterior Chamber (A.C)
 Rubeosis iridis
Examination of the Anterior Chamber (A.C) Right Eye Left Eye
Cysts
 Cysticercosis cysts Depth of the anterior chamber (A.C) –
 Hydatid cysts. Increased,
Larvae - Micro filarial Decreased,
F.Bs-- Metallic or wooden Variable depth
foreign bodies are commonly Abnormal contents in the A.C
seen. Protein Particles
OSCE Cells
 Assessment of the
Hypopyon –Sterile and Unsterile
anterior chamber with a
Hyphema
torch light.
Cysts
 Hypopyon Larvae
 Hyphema Ruptured Lens particles
 Aqueous flare Liquefied lens
Diagrams to learn A.C IOL
 Draw the diagram of the
Iris Clip IOLs
angle of anterior
Vitreous
chamber and diagram of
F.Bs
the drainage of aqueous .
Clinical skills
 Assessment of anterior chamber

OSCE and OSPE

 Hypopyon
 Hyphema
 Aqueous flare
-------------------------

172
Chapter 14-2 Clinical examination ( Investigations) of the eye for the diagnosis of
Glaucoma

General considerations

 Primary glaucoma is bilateral disease

 Causes irreversible blindness if not diagnosed and treated at the earliest.
 It is a hereditary disease

Clinical examination for Diagnosis of glaucoma

Age – POAG in more than 40 years

Sex-Females are more affected in PACG

Symptoms

 Gradual progressive painless dimness of vision present in Primary open angle glaucoma (POAG) and
chronic primary angle closure glaucoma . In PACS ( Primary angle closure suspect) , there may be
pain in the eye which is relieved on taking rest which becomes periodical over period of time ,
 Headache, .
Figure14A -1 Colored
 Colored halos around the bulb,
halos around the bulb
 Light minimum raised i.e Glaucoma patients require a maximum
illumination to appreciate an object ,
 Delayed dark adaptation,
 Change in color sense .
 Frequent change of presbyopic glasses

Risk factors for glaucoma

 Refractive errors – Hypermetropia in PACG and Myopia In POAG

 Diabetes
 Hypertension
 Bronchial asthma
 Association of vasomotor instability, emotional crisis , highly strung, Anxious in disposition , State of
fatigue

173
 Family history of glaucoma
Figure14 A -2 Van Herick's Figure14 A - 3 Iris Figure14-A 4 Torch light Figure14A -5 Rubeosis
sign atrophy assessment of depth of anterior iridis
chamber

Basic evaluation

Visual acuity for distance and near vision , examination of color sense by ishihara charts and
contrast sensitivity , light sense are also to be examined .

Slit examination

 CCC
 Corneal edema,
 VanHerick`s sign
 Gonioscopy (See below) Figure 14A - 6 Schiotz
 Rubeosis iridis, tonometer
 Iris atrophy,
 Pupil reaction – RAPD /TAPD
 Glaucom flecken
 Optic disc evaluation with +90 D lens (See below)

Clinical Methods of examination for the diagnosis of Glaucoma

 Tonometry – Intra ocular pressure (IOP)

 Measurement of Corneal thickness
 Assessment of depth of anterior chamber
 Gonioscopy – assessment of angle of anterior chamber
 Study of nerve fiber layer of retina with red free light of direct ophthalmoscope
 Study of optic disc changes with +90 D
 Study of visual field changes

174
Tonometry –

It is measurement of Intra ocular pressure (IOP).

Normal IOP is 11 to 21mm Hg (16 plus or minus 5 mm).

Normally the IOP is more in the morning between 8 to 12 noon and also in the evening .

The diurnal variations varies upto 5 mm Hg.

The bed side method of recording IOP is digital (the digits of hand )
Figure14A - 7 Digital

tonometry see examination of the eye ball tonometry

Measurement of Intra ocular pressure based on two principles –

 Indentation tonometry
 Applanation tonometry
Indentation tonometry –

The principle is that the fluid filled eye ball (sphere) is indented by known weight
plunger , the plunger will indent the Cornea of eyeball till the pressure of the plunger is equal to the pressure
inside the globe. .The depth of indentation is proportion to the pressure inside the eyeball

The instrument required for indentation tonometry is Schiotz tonometer

Practice of Schiotz tonometry :

The disadvantage of this instrument is the pressure reading

include ocular/sclera rigidity. Hence the border line pressure
changes is not reliable and not validated .

Applanation tonometry –
Applanation tonometry is based on Imbert Fick principle. i.e.

175
P= F/A i.e the force required to flatten the known surface of the cornea is equivalent to the IOP..
The instruments necessary for practice of applanation tonometry are Goldmann tonometer and slit lamp.

fluorescein , the biprism is illuminated with cobalt blue filter ,and gently the biprism is brought onto the
anaesthetized cornea. Slowly put a force to flatten the cornea and the end point of flattening is known by
touching of the internal margins of the two hemi circles . The IOP is calculated with dial reading.Advantage
of Goldmann tonometry is that ocular/sclera rigidity is not included in the IOP. Thus applanation tonometry
is the gold standard in the IOP measurement .

Measurement of Thickness of cornea. –

Assessment of angle of Anterior chamber

Assessment of angle of Anterior chamber is necessary to classify glaucoma into open angle closed angle .

 Van Herick’s Method

 Torch light examination to assess the depth of anterior chamber (AC)
 Gonioscopy
Van Herick’s Method –

It is a comparison between the peripheral anterior chamber depth(PACD) with corneal thickness (CT )

176
Torch light examination to assess the depth of anterior Figure14A - 10 Torch light assessment of depth
chamber (AC) of anterior chamber

Torch light is flashed on the temporal side of the eyeball

parallel to the iris and illumination of the nasal part of iris
and nasal limbus is observed

 If the nasal iris , limbus and temporal iris are

illuminated , it indicates open angle
 If only temporal iris is illuminated , and the nasal iris not illuminated , i.e it indicates a shallow
anterior chamber. The non illuminated nasal iris is due to bowing forward of temporal iris . The not
illuminated nasal iris is called Eclipse sign or Crescent sign .
Gonioscopy

The principle of gonioscopy is to eliminate the total internal reflection. In the eye the light rays coming from
the Ac falls on the cornea at an angle greater than the critical angle (46 degrees) and is reflected back into
the angle of the anterior chamber of the eye. By keeping higher refractive index of Gonioscope (1.57) which
replaces corneal and air tear film interface the light rays enter into the gonio lens , refracted and the rays
falls on the gonio mirror. The mirror reflects the rays to the oculars of a slit lamp for viewing.

Basically gonioscope is a contact lens that replaces the cornea as a refracting medium by replacing cornea air
interface allowing the rays arising from the angle to come out of the
angle. Figure14A - 11 Four mirror
Gonioscope
There are indirect gonioscopes like Zeiss four mirror and Posner four
mirror , and

Direct gonioscopes like Koeppe, Swan Jacob , Barkar.

Structures visible through the Gonioscope (From Posterior to anterior)

 Root of Iris
 Attachment of iris to the ciliary body
 Ciliary band
 Scleral spur - Attachment of ciliary band to sclera
 Pigmented trabecular meshwork
 Non pigmented trabecular meshwork
 Schwalbe’s line -Termination of descemets membrane
 Behind the trabeculum is Schlemm canal.

177
Table 2

Interpretation of the gonioscopic findings

Shaffer interpretation Spaeth Spaeth interpretation Spaeth interpretation

interpretation based on
Based on the visible structures Based on Insertion
Based on angular of the iris root On the configuration of the
width peripheral iris

All structures are visible (Wide open 35 to 45 degrees Insertion of the iris  Steep , anteriorly
angle) -Closure not possible (Wide open angle) root anterior to convex
Schwalbe’s line  Regular
Scleral spur is visible (open angle) - 10 to 20 degrees-
 Queer , anteriorly
Insertion of iris root
Closure not possible narrow concave
behind Schwalbe’s line

Scleral spur is not visible but

Insertion of iris root

Schwalbe’s line ,trabecular meshwork is behind the scleral

visible - Narrow angle spur

Only Schwalbe’s line is visible (Closed) – Insertion of iris root

IV -Closure is possible on the ciliary band

No structures visible – Closed angle

Other methods of assessing angle of AC – Non invasive higher resolution techniques.

Ultrasound biomicroscopy (UBM) – with 50MHz frequency sound waves are used for tissue penetration upto
4mm

ASOCT – Anterior segment OCT scan using 1310 nm light wavelength for higher resolution

Changes in the Retinal nerve fiber layer.

1.2 millions axons of ganglion cells constitutes of nerve fiber layer.

Retinal nerve fiber layer is studied with red free light or green light.

Ganglion cells and its axons is called nerve fiber layer of retina

Subtle retinal nerve fiber damage occurs before the detectable damage on the disc and visual field changes.

How to study retinal nerve fiber layer

178
• Direct ophthalmoscope with red free light
• OCT(Optical coherence tomograms)
Normal thickness of retinal nerve fiber layer is 100 to 200 microns

Changes in Glaucoma are

• Localized atrophy or, diffuse atrophy of retinal nerve fiber layer.

Examination of Optic Disc

 Direct ophthalmoscope and indirect ophthalmoscope

 Slit lamp Biomicroscopy with +90 D, +78 D, +60D, or with – 58.6D Hruby lens
Table 3
Normal optic disc Suspicious signs Definite signs
 Symmetry of both eyes  Asymmetry of cup  Pale optic dic
 Cup disc ratio is 0.3 : 1  Vertically enlarged oval  Notch in the neuroretinal
 Pink in color disc rim
 Neuroretinal rim is  Cup disc ratio is more  Enlargement of the cup
normal than 0.3  Deepening of the cup
 Cup is circular , no  Nasal shift of retinal  Apparent discontinuity of
notching vessels the vessels – Bayoneting
 Disc hemorrhages sign
 Notching of neuroretinal
rim in any poles
 Nerve fiber layer wedge
shaped defect
 Glaucomatous optic atrophy
 Peripapillary optic atrophy
Laminar dot sign
Other methods of computerized Optic disc study.

 Confocal scanning laser tomography (CSLO) – Heidelberg retinal tomography (HRT) uses 675 nm
diode laser as a light source. It is used to study optic nerve head morphology, and retinal nerve layer
thickness
 Spectral domain OCT
 Confocal scanning laser polarimetry (SLP) (Synonyms GD, PRO)– used to measure the retinal nerve
layer thickness using polarized diode laser 780nm .

Visual field examination and changes in glaucoma

179
Basics of visual field examination (Perimetry is explained in the visual field

Visual field defects in glaucoma Table 4

Figure14A- 12 Central 30 Figure14A- 13 Figure14A- 14
 Isopter contraction
degrees visual field Isopter contraction Scotoma
 Baring of blind spot
 Paracentral scotoma
 Seidel’s scotoma
 Bjerrum/Arcuate scotoma
 Ring /Double arcuate scotoma
 Nasal step
Figure14A- 15 Seidel's Figure14A- 16 Figure14A- 17
 Central and peripheral vision
scotoma Bjerrum's scotoma Double arcuate
 Tubular vision
scotoma
 Temporal loss of vision(Total
blindness)
Diagnosis of glaucoma

The diagnosis of glaucoma is made

after studing for a combination of
clinical signs.

i.e. History, Tonometry-

IOP.,Gonioscopy ,Nerve fiber defect ,Characteristic

changes in the optic nerve head and Abnormalities in the visual field.

----------------------------------------

180
Chapter 15. Clinical examination of the Iris

The uvea is the middle and vascular coat of the eye ball. It is divided into anterior Iris, middle ciliary body
and posterior choroid. The function is to supply nutrition to the eye ball while the pigments in it will
absorbs the U.V rays.

Clinical anatomy of the Iris:

 The extent of the iris is from the pupillary margin to anterior surface of the ciliary body
• The Iris is a Mobile Figure 15 - 1 Middle coat of the eye - Figure 15 - 2 Anterior surface of
Iris, Ciliary body, Choroid the iris
diaphragm in the eye
situated in coronal
position i.e. at right
angles to the sclera, 12
mm in diameter. It
separates the aqueous
cavity into anterior
chamber and posterior
chamber.
• In the centre there is a
round opening called
Pupil
• Because of the mobility, the iris regulates the diameter of the pupil there by regulates the light entry into
the eye.
• The Iris gets support from the zonules and the crystalline lens and absence of these structures causes
tremulousness or iridodonesis
• The thinnest part of the iris is the root of the iris, this is commonest site for traumatic Iridodialysis

Layers of the iris-

• Anterior limiting membrane I.e. the anterior surface of the iris
• Stroma of the Iris
• Anterior/outer epithelium layer
• The posterior surface of the iris -

Anterior limiting membrane i.e anterior surface of the iris

 Condensed part of stroma contains melanocytes
 The anterior surface of the iris consists of pupillary zone and ciliary zone. The two zones are separated
by a ridge called collarette. The collarette is 2 mm away from the pupillary margin.

1
 Ciliary zone - Radial in direction and contains chunks of depressions known as crypts. These crypts are
seen in the middle and at the root of the iris. Contraction lines concentric to the collarette are also
present.
 Pupillary zone - 1.6 mm in diameter, smooth and flat. Fringe of black pigment is present in the
pupillary margin. The fringe of black pigment is due to the slight extension of the posterior iris
pigment into the pupillary margin. The pupillary zone contains constrictor muscle fibers.
Stroma
 The Iris stroma contains melanocytes and Pigment clump cells,
 Vessels have non fenestrated endothelium and lacks an internal elastic lamina,
 At the periphery of the stroma of the ciliary zone there are dilator muscle fibers and around the pupil
is the constrictor muscles embedded in a fine fibril

Anterior/outer epithelium layer

 It is condensation of outer pigmented epithelium of ciliary body and retinal pigment epithelium
 Lacks melanocytes

The posterior/inner pigmented epithelium layer

 Continuation of the inner non pigmented epithelium of ciliary body and two layered pigment
epithelium, the margins of which are fringed at the pupillary margin.

Clinical examination of the Iris

Points to be noted in the Clinical examination of the iris
• Color of the iris -
• Edema of the iris
• Atrophy of the iris
• Nodules on the iris
• Abnormal blood vessels on the iris
• Holes in the iris
• Tremulousness of the iris
• Synechiae

Color of the iris

The colors of the iris depends on the amount of melanin pigment in the iris.
• Brown - thick pigment, commonly called `Black eyed`
• Grey –moderate pigment
• Blue - less pigment

2
Figure15 - 3 Brown Iris Figure15 - 4 Grey Iris Figure15 - 5 Blue Iris

• Heterochromia iridis - One sector of the iris of one eye has a color different from the other sector
it is called Heterochromia iridis. It may be congenital, atrophy after an attack of acute congestive
glaucoma.
• Heterochromia iridium - The color of one iris is different from the color of iris in the fellow eye .it
is called Heterochromia iridium. If it is hypochromic, the causes are Horner’s syndrome, Fuch’s
heterochromic Iridocyclitis, if it is hyperchromic the causes are melanomas and siderosis bulbi.

Figure 15 - 6 Heterochromia Iris Figure 15 - 7 Heterochromic Figure15 - 8 Iris mole (Freckles)

Iridium

• Pigmented spots – Freckles (Moles)

Moles or nevus are seen on the iris. They are darkly pigmented spots, Brown or black in color not
raised above the surface
• Brush field spots are seen in Down syndrome.
• Localized changes in the color of the iris with raised surface is due to tumors of the iris and the
ciliary body

Edema of the iris Figure15 - 9 Atrophy of the Iris

The iris looks muddy, the crypts and elevations are lost and the iris
surface is uniform, boggy and edematous in appearance. The pupil
becomes smaller in size and sluggish in reaction. And this is due to
exudation/edema into the stroma of the iris.
Causes
• Acute irido cyclitis
• Acute congestive Glaucoma

3
Atrophy of the iris
The iris becomes thin. The stroma of the iris is seen as white fibrils
and the pattern of the iris is ill defined due to atrophic patches.

Causes
• Essential iris atrophy
• Injury to the iris
• Chronic congestive glaucoma.
• Absolute glaucoma
• Chronic uveitis

Nodules on the iris

• Koeppe’s nodule – Flat nodules in the pupillary margin
• Busacca nodule –In the periphery at the base of the iris
• Lisch’nodule – Pedunculated nodules in neurofibromatosis.

Figure15 - 10 Koeppe's nodule Figure15- 11 Busacca nodule Figure15 - 12 Lisch’nodule

Abnormal blood vessels on the iris called as Rubeosis iridis.

This indicates hypoxia of the uveal or retinal tissue and is Figure15 - 13 Rubeosis iridis
seen in
 Chronic uveitis
 Diabetic retinopathy.

Holes in the iris

Congenital causes
• Normally there is one pupil in each eye. Rarely there may
be more than one pupil. This congenital anomaly is called Polycoria.
• Coloboma of the iris –It is typically seen at six o clock position.

4
Figure15 - 14 Figure15- 15 Coloboma of the Figure 15 - 16 D - shaped pupil
Polycoria. Iris

Acquired causes for the Holes in the iris

• Injuries – Iridodialysis, D - shaped pupil.
• Surgically if iris is removed it is called iridectomy and if a hole is made in the iris with lasers, it is called
iridotomy.

Types of Surgical iridectomy –

• Peripheral Buttonhole iridectomy done on the periphery of the iris for primary angle closure
glaucoma (PAC) to relieve the pupillary block
• Optical iridectomy done at inferio nasal quadrant of the Iris for central Leucoma cornea to see near
vision.
• Sector iridectomy done at 12 `o` clock position of the Iris for ICCE procedure (sometimes) to facilitate
easy delivery of cataract
• Peripheral Four dot iridectomy at 12,3,6,9 `0` clock positions for Keratoplasty
• Broad basal iridectomy done at the base of the Iris for Chronic congestive glaucoma to remove the
adhesions of posterior Synechiae.

Figure15 - 17 Figure 15 - – 18 Figure 15 - 19 Figure 15 - 20 Figure 15 - 21

Peripheral Peripheral buttonhole Optical iridectomy Sector /Key hole Peripheral Four
Buttonhole iridectomy iridectomy dot iridectomy
iridotomy

5
Tremulousness of the iris or iridodonesis
This occurs when the iris is not properly supported by the lens and zonules and iris is Shaky when the eye
is moved from side to side.
 Aphakia.
 Absorbed lens
 Dislocated lens
 Subluxated lens
 Absolute glaucoma due to degenerations of the zonules
 Blunt trauma injury to the zonules

Synechiae
The exudation produced by the inflammation of the uveal vascular tissue heals by fibrosis. This exudation
and fibrosis bind the iris to the adjacent tissues of the eye with a strong adhesions called Synechiae.
Types of Synechiae
 Posterior Synechiae - Attachment of the iris to the lens capsule.
 Total posterior Synechiae – Attachment of the total posterior surface of the iris to the anterior lens
capsule.
 Peripheral anterior Synechiae —Attachment of the peripheral anterior iris to the periphery of the
posterior surface of the cornea This is called pseudo angle of the anterior chamber.
 Ring Synechiae - Imprint of the pupil pigment on the anterior capsule of the crystalline lens.
 Seclusive pupil – Total attachment of the pupillary margin to the anterior capsule of the crystalline
lens.
 Occlusive pupil - Organized exudates in the pupillary area

Figure 15- 22 Figure 15 - 23 Figure15- 24 Figure 15 - 25

Posterior Synechiae Ring Synechiae Occlusive Pupil Seclusive pupil

Choroid and ciliary body examination requires Direct, and Indirect ophthalmoscope, Gonio scope. This
part of examination is not necessary for U. Gs

Diagrams to learn
 Diagram of gross anatomy of the iris and the cross section of the iris
 Diagrams of Various Synechiae

6
OSCE
All the diagrams in the chapter

Table 1
Format for the Examination of the Iris
Clinical exam RE LE

Color of the iris

Brown
Grey
Blue
Moles
Heterochromia iridis
Heterochromia iridum

Edema of the iris

Atrophy of the iris

Nodules on the iris

Koeppe’s nodule
Busacca nodule
Lisch’nodule
Abnormal blood vessels on the
iris -- Rubeosis iridis.

Holes in the iris

Tremulousness of the iris

Synechiae

-----------------------------------------------------------------

7
Chapter 15. Clinical examination of the Iris
(15.1 Clinical Anatomy of the Irs. 15.2 Clinical examination of the Iris )
15.1 Clinical Anatomy of the Irs.
The uvea is the middle and vascular coat of the eye ball. It is divided into anterior Iris, middle ciliary
body and posterior choroid. The function is to supply nutrition to the eye ball while the pigments in it
will absorbs the U.V rays.

Clinical anatomy of the Iris:

Layers of the iris-

• Anterior limiting membrane I.e. the anterior surface of the iris
• Stroma of the Iris
• Anterior/outer epithelium layer
• The posterior surface of the iris -

Anterior limiting membrane i.e anterior surface of the iris

181
 Ciliary zone - Radial in direction and contains chunks of depressions known as crypts. These crypts are
seen in the middle and at the root of the iris. Contraction lines concentric to the collarette are also
present.
 Pupillary zone - 1.6 mm in diameter, smooth and flat. Fringe of black pigment is present in the
pupillary margin. The fringe of black pigment is due to the slight extension of the posterior iris
pigment into the pupillary margin. The pupillary zone contains constrictor muscle fibers.
Stroma
 The Iris stroma contains melanocytes and Pigment clump cells,
 Vessels have non fenestrated endothelium and lacks an internal elastic lamina,
 At the periphery of the stroma of the ciliary zone there are dilator muscle fibers and around the pupil
is the constrictor muscles embedded in a fine fibril

Anterior/outer epithelium layer

 It is condensation of outer pigmented epithelium of ciliary body and retinal pigment epithelium
 Lacks melanocytes

The posterior/inner pigmented epithelium layer

 Continuation of the inner non pigmented epithelium of ciliary body and two layered pigment
epithelium, the margins of which are fringed at the pupillary margin.

182
15.2 Clinical examination of the Iris
Points to be noted in the Clinical examination of the iris
• Color of the iris -
• Edema of the iris
• Atrophy of the iris
• Nodules on the iris
• Abnormal blood vessels on the iris
• Holes in the iris
• Tremulousness of the iris
• Synechiae
Color of the iris
The colors of the iris depends on the amount of melanin pigment in the iris.
• Brown - thick pigment, commonly called `Black eyed`
• Grey –moderate pigment
• Blue - less pigment
Figure15 - 3 Brown Iris Figure15 - 4 Grey Iris Figure15 - 5 Blue Iris

Figure 15 - 6 Heterochromia Iris Figure 15 - 7 Heterochromic Figure15 - 8 Iris mole (Freckles)

Iridium

183
• Pigmented spots – Freckles (Moles)
Moles or nevus are seen on the iris. They are darkly pigmented spots, Brown or black in color not
raised above the surface
• Brush field spots are seen in Down syndrome.
• Localized changes in the color of the iris with raised surface is due to tumors of the iris and the
ciliary body

Edema of the iris Figure15 - 9 Atrophy of the Iris

Atrophy of the iris

The iris becomes thin. The stroma of the iris is seen as white fibrils
and the pattern of the iris is ill defined due to atrophic patches.

Causes
• Essential iris atrophy
• Injury to the iris
• Chronic congestive glaucoma.
• Absolute glaucoma
• Chronic uveitis

Nodules on the iris

• Koeppe’s nodule – Flat nodules in the pupillary margin
• Busacca nodule –In the periphery at the base of the iris
• Lisch’nodule – Pedunculated nodules in neurofibromatosis.

184
Figure15 - 10 Koeppe's nodule Figure15- 11 Busacca nodule Figure15 - 12 Lisch’nodule

Abnormal blood vessels on the iris called as Rubeosis iridis.

Figure15 - 13 Rubeosis iridis

185
This indicates hypoxia of the uveal or retinal tissue and is seen in
 Chronic uveitis
 Diabetic retinopathy.

Holes in the iris

Congenital causes
• Normally there is one pupil in each eye. Rarely there may be more than one pupil. This congenital
anomaly is called Polycoria.
• Coloboma of the iris –It is typically seen at six o clock position.

Figure15 - 14 Figure15- 15 Coloboma of the Iris Figure 15 - 16 D - shaped pupil

Polycoria.

Acquired causes for the Holes in the iris

• Injuries – Iridodialysis, D - shaped pupil.
• Surgically if iris is removed it is called iridectomy and if a hole is made in the iris with lasers, it is called
iridotomy.
Types of Surgical iridectomy –
• Peripheral Buttonhole iridectomy done on the periphery of the iris for primary angle closure
glaucoma (PAC) to relieve the pupillary block
• Optical iridectomy done at inferio nasal quadrant of the Iris for central Leucoma cornea to see near
vision.
• Sector iridectomy done at 12 `o` clock position of the Iris for ICCE procedure (sometimes) to facilitate
easy delivery of cataract
• Peripheral Four dot iridectomy at 12,3,6,9 `0` clock positions for Keratoplasty

Figure15 - 17 Figure 15 - – 18 Figure 15 - 19 Figure 15 - 20 Figure 15 - 21

Peripheral Peripheral buttonhole Optical iridectomy Sector /Key hole Peripheral Four
Buttonhole iridectomy iridectomy dot iridectomy
iridotomy

186
• Broad basal iridectomy done at the base of the Iris for Chronic congestive glaucoma to remove the
adhesions of posterior Synechiae.

Tremulousness of the iris or iridodonesis

This occurs when the iris is not properly supported by the lens and zonules and iris is Shaky when the eye
is moved from side to side.
 Aphakia.
 Absorbed lens
 Dislocated lens
 Subluxated lens
 Absolute glaucoma due to degenerations of the zonules
 Blunt trauma injury to the zonules

Figure 15- 22 Figure 15 - 23 Figure15- 24 Figure 15 - 25

Posterior Synechiae Ring Synechiae Occlusive Pupil Seclusive pupil

Choroid and ciliary body examination requires Direct, and Indirect ophthalmoscope, Gonio scope. This
part of examination is not necessary for U. Gs

Diagrams to learn
 Diagram of gross anatomy of the iris and the cross section of the iris

187
 Diagrams of Various Synechiae

OSCE
All the diagrams in the chapter

Table 1
Format for the Examination of the Iris
Clinical exam RE LE

Color of the iris

Brown
Grey
Blue
Moles
Heterochromia iridis
Heterochromia iridum

Edema of the iris

Atrophy of the iris

Nodules on the iris

Koeppe’s nodule
Busacca nodule
Lisch’nodule
Abnormal blood vessels on the
iris -- Rubeosis iridis.

Holes in the iris

Tremulousness of the iris

Synechiae

-----------------------------------------------------------------

188
Chapter 16. Clinical examination of the Pupil

Figure16- 2 Polycoria
Number of Pupil
Normally one pupil is seen in each eye.
But some times more than one pupil is seen, which is called Polycoria, a congenital
anomaly.

Position of the Pupil

Normally, the pupil is placed almost in the center of the iris slightly nasal and down.
Abnormal position of the pupil is seen
• Congenitally - Eccentric pupil (Corectopia).
 Post Trauma
 Iris prolapse,
Size of the Pupil (Diameter)
• The size of the normal pupil varies from 2.5 to 3mm depending upon the illumination.
• Both pupils are symmetrical in size and in reaction to light due to the joining of ipsilateral nasal fibers
with the contra lateral pretectal nucleus and from the pretectal nucleus some pupillary light reflex fibers
directly joins the ipsilateral Edinger Westphal nucleus and some fibers cross the midline and joins the
contra lateral Edinger Westphal nucleus.
• Constriction of the pupil is called Miosis. Miotic pupils are less than 2mm in diameter
• Dilatation of the pupil is called Mydriasis. Mydriatic pupils are greater than 7mm in diameter.

1
The actual size of the pupil can be estimated with a slit lamp.
The size of the Pupil depends on:
• Age: Smaller in infants and elderly
• Sleep: Smaller due to parasympathetic dominance
• Psychology of individual - smaller in placid people
• Refractive status of the eye: Hypermetropics will have a smaller pupil while myopics will have a bigger size
pupil
• People with Darker iris have smaller pupils
• Isocoria: Normally the two pupils are equal in size. A slight (one-tenth of a millimeter) anisocoria is present
in a significant percentage of normal pupil.
 Anisocoria: A difference of 0.3mm or more in pupillary diameter between both eyes . The most common
cause of anisocoria is central anisocoria (occurs in 20% of normal individuals) and is due to asymmetric
supranuclear inhibition of Edinger-Westphal nucleus.
• Anisocoria can be easily distinguished from other abnormal pupils by normal reaction to bright light, near
response and smaller degree of
inequality. Figure16- 3 Dilated pupil Figure16- 4 Constricted pupil

Causes for anisocoria -

• Drug induced Iridocyclitis,
• Trauma,
• Unilateral ophthalmoplegia,
• Horner’s syndrome.
• Argyll Robertson pupil,
• Adie’s pupil.
Table 1
Cause for Mydriasis Causes for Miosis
Young individuals, Dim light, apprehension Babies and Old people
Myopia – Pupil is dilated but retains motility Hypermetropia

Use of Mydriatic drugs --Parasympatholytic drugs like Use of Parasympathomimetic drugs like Pilocarpine
Atropine, Homatropine, Cyclopentolate. Use of sympatholytic drugs
Sympathomimetic drugs like –Adrenaline, Phenylephrine

Glaucoma- POAG, Chronic PNAG Acute congestive attack Acute iridocyclitis

of PNAG
Oculosympathetic irritation Oculosympathetic paralysis -
Horner’ syndrome
Afferent and efferent pupillary pathway defects.
Optic Atrophy due to various causes Diabetes mellitus
rd
3 cranial nerve palsy, Internal ophthalmoplegia. Organo phosphorus poisoning
Blunt Injuries-Traumatic Mydriasis Traumatic miosis
Cerebral Compression in head injury Pontine hemorrhage – Pin point pupil
Atropine poisoning Morphine poisoning

2
Shape of the Pupil
The normal Pupil is circular in shape. A Pupil which is not circular is called irregular pupil.
 Irregular pupil is seen in uveitis
 D- shaped pupil is seen in Iridodialysis
 Festooned pupil is due to segmental dilatation of iris due to the posterior synechiae
 Vertically oval pupil is seen in acute congestive glaucoma
 Pear shaped pupil is seen in Adherent leucoma cornea
 Key hole pupil is seen in sector iridectomy.
 Tadpole shaped pupils result from sector dilatation observed sometimes in Horner’s syndrome.
 Scallop shaped pupils are due to sector atrophy of the iris and are sometimes seen in amyloidosis and
neuropathy of short ciliary nerves.
 Hammock pupil or boat shaped pupil where the pupil is shifted upwards and the upper border of the pupil
is not visible and does not react to light, is seen in vitreous prolapse in ICCE.
 Tear drop pupil where narrow end is towards the limbus, is seen in vitreous prolapse in ICCE.
Figure16- 5 Irregular Figure 16-6 Figure16-7 Figure16-8 Figure16 -9
pupil D-Shaped pupil in Festooned pupil Vertically oval Pear shaped pupil
Iridodialysis pupil

Figure16-10 Key Figure16- 11 Figure16-12 Figure16-13Scallop Figure16-14

hole shaped pupils Tadpole shaped Hammock shaped pupils Tear drop pupil
pupil pupil

Margin of the Pupil –

Normally the margin of the pupil is regular.
• Irregular margin is seen in acute and chronic Uveitis,
• Rupture of the sphincter of the pupil is seen in blunt trauma

3
Color of the Pupil
• The normal color of the pupil is Black/ grayish black and is due to the color of the clear crystalline lens
and clear Vitreous. In S/L examination the color of crystalline lens appears translucent. Cortical and
Nuclear Cataracts are the commonest conditions in which the colors of the pupil are affected.
•
Table 2
Cortical cataract and Color of the Pupil Nuclear cataract and Color of the Pupil
Immature cataract -- Grayish white Grade – I Whitish yellow
Mature cataract Pearly white Grade - II Yellowish white
Hyper mature cataract sclerotic - yellow Grade - III Amber color
Hyper mature Morgagnian cataract - Milky white pupil Grade - IV Thin Brown
with brown nucleus floating at the bottom of the lens
Grade - V Thick Brown - Cataracta Brunescens
Grade - VI Black -Cataracta Nigra.

Figure16-15 Black Figure16-16 Figure16-17 Mature Figure16-18 Hyper Figure16-19 Hyper

Pupil Intumescent cataract - mature cataract mature cataract
cataract- Grayish Pearly white pupil sclerotic type Morgagnion cataract
white pupil

Figure16- 20 Brown Figure16-21 Black cataract Figure16-22 Red pupil Figure16- 23 Greenish
cataract pupil in Glaucoma

Other conditions in which pupil is in different colors.

Black pupil
• Young individual
• Aphakia
• Pseudophakia

4
• Cataracta Nigra.
• Yellowish: - Vitreous abscess (Endophthalmitis and Pan
Figure16-24 Cat eye reflex
ophthalmitis).
• Greenish: - Acute congestive glaucoma.
• Reddish: - Albinism.

Cat’s eye Pupil - Amaurotic cat’s eye reflex

(Whitish or purplish pink Pupil)
Differential Diagnosis of Cat’s eye Pupil
 Retinoblastoma (A malignant tumor of the retina in a child of two
years)
Figure16-25 Persistent Figure16-26 Figure16-27
 Persistent hyperplastic primary
Hyperplastic primary Myelinated optic disc Myelinated nerve
vitreous
vitreous fiber
• Congenital cataract
• Exudates in the pupil
• Cyclitic membrane
• Pseudo glioma
• Coat’s eye disease
• Retinal detachment
Figure16-28 Congenital Figure16- 29 Coat's Figure16-30
• Coloboma of Choroid
cataract eye disease Coloboma of the
• Myelinated optic disc choroid
• Myelinated nerve fiber layer of the
retina
• Drusen in the retina.
Puillary reflexes – see 16-1,16-2,16-3 in
the same chapter .
Format for Examination of the Pupil
Table 3
Examination of the Pupil Right Eye Left Eye
Number
Position
Size—Anisocoria. Mydriasis /
Miosis
Shape
Margin

Color

Pupillary light reaction

Direct / Indirect

5
Chapter 16. Clinical examination of the Pupil
(Chapter 16.1 Clinical examination of the pupil, Chapter 16.2 Oculosympathetic pathway and palsy, Chapter
16.3 Near reflex)

Chapter 16.1 Clinical examination of the pupil

The Pupil is an opening in the center of the iris. It connects the Figure16- 1 Pupil
posterior chamber to the anterior chamber through the irido
lenticular apposition. The Iris is sensitive to light and pupil
constricts and dilates with the illumination. This is the reason for
constriction of the pupil in bright light and dilatation in the dark.
The constriction and dilatation of the pupil regulate the passage of
light entering into the retina, and are also important in
accommodation and convergence.
Clinical points to be noted in the Examination of the Pupil:
• Number
• Position
• Size
• Shape
• Margin
• Color
• Pupil reaction to light –If the light is projected on the eye , the pupil reaction of that eye is called Direct
pupil reaction. The reaction of the fellow eye pupil is called consensual reaction otherwise called indirect
reaction.
• Pupillary reaction light – (16.1 Pupillary light reflex
Number of Pupil
Figure16- 2 Polycoria
Normally one pupil is seen in each eye.
But some times more than one pupil is seen, which is called Polycoria, a congenital
anomaly.
Position of the Pupil
Normally, the pupil is placed almost in the center of the iris slightly nasal and down.
Abnormal position of the pupil is seen
• Congenitally - Eccentric pupil (Corectopia).
 Post Trauma
 Iris prolapse,
Size of the Pupil (Diameter)
• The size of the normal pupil varies from 2.5 to 3mm depending upon the illumination.
• Both pupils are symmetrical in size and in reaction to light due to the joining of ipsilateral nasal fibers
with the contra lateral pretectal nucleus and from the pretectal nucleus some pupillary light reflex fibers

189
directly joins the ipsilateral Edinger Westphal nucleus and some fibers cross the midline and joins the
contra lateral Edinger Westphal nucleus.
• Constriction of the pupil is called Miosis. Miotic pupils are less than 2mm in diameter
• Dilatation of the pupil is called Mydriasis. Mydriatic pupils are greater than 7mm in diameter.
The actual size of the pupil can be estimated with a slit lamp.
The size of the Pupil depends on:
• Age: Smaller in infants and elderly
• Sleep: Smaller due to parasympathetic dominance
• Psychology of individual - smaller in placid people
• Refractive status of the eye: Hypermetropics will have a smaller pupil while myopics will have a bigger size
pupil
• People with Darker iris have smaller pupils
• Isocoria: Normally the two pupils are equal in size. A slight (one-tenth of a millimeter) anisocoria is present
in a significant percentage of normal pupil.
 Anisocoria: A difference of 0.3mm or more in pupillary diameter between both eyes . The most common
cause of anisocoria is central anisocoria (occurs in 20% of normal individuals) and is due to asymmetric
supranuclear inhibition of Edinger-Westphal nucleus.
• Anisocoria can be easily distinguished from other abnormal pupils by normal reaction to bright light, near
response and smaller degree of
inequality. Figure16- 3 Dilated pupil Figure16- 4 Constricted pupil

Causes for anisocoria -

Glaucoma- POAG, Chronic PNAG Acute congestive attack Acute iridocyclitis

190
Blunt Injuries-Traumatic Mydriasis Traumatic miosis
Cerebral Compression in head injury Pontine hemorrhage – Pin point pupil
Atropine poisoning Morphine poisoning

Shape of the Pupil

The normal Pupil is circular in shape. A Pupil which is not circular is called irregular pupil.
 Irregular pupil is seen in uveitis
 D- shaped pupil is seen in Iridodialysis
 Festooned pupil is due to segmental dilatation of iris due to the posterior synechiae
 Vertically oval pupil is seen in acute congestive glaucoma
 Pear shaped pupil is seen in Adherent leucoma cornea
 Key hole pupil is seen in sector iridectomy.
 Tadpole shaped pupils result from sector dilatation observed sometimes in Horner’s syndrome.
 Scallop shaped pupils are due to sector atrophy of the iris and are sometimes seen in amyloidosis and
neuropathy of short ciliary nerves.
 Hammock pupil or boat shaped pupil where the pupil is shifted upwards and the upper border of the pupil
is not visible and does not react to light, is seen in vitreous prolapse in ICCE.
 Tear drop pupil where narrow end is towards the limbus, is seen in vitreous prolapse in ICCE.
Figure16- 5 Irregular Figure 16-6 Figure16-7 Figure16-8 Figure16 -9
pupil D-Shaped pupil in Festooned pupil Vertically oval Pear shaped pupil
Iridodialysis pupil

Figure16-10 Key Figure16- 11 Figure16-12 Figure16-13Scallop Figure16-14

hole shaped pupils Tadpole shaped Hammock shaped pupils Tear drop pupil
pupil pupil

Margin of the Pupil –

Normally the margin of the pupil is regular.
• Irregular margin is seen in acute and chronic Uveitis,
• Rupture of the sphincter of the pupil is seen in blunt trauma

191
Color of the Pupil
• The normal color of the pupil is Black/ grayish black and is due to the color of the clear crystalline lens
and clear Vitreous. In S/L examination the color of crystalline lens appears translucent. Cortical and
Nuclear Cataracts are the commonest conditions in which the colors of the pupil are affected.
Table 2
Cortical cataract and Color of the Pupil Nuclear cataract and Color of the Pupil
Immature cataract -- Grayish white Grade – I Whitish yellow
Mature cataract Pearly white Grade - II Yellowish white
Hyper mature cataract sclerotic - yellow Grade - III Amber color
Hyper mature Morgagnian cataract - Milky white pupil Grade - IV Thin Brown
with brown nucleus floating at the bottom of the lens
Grade - V Thick Brown - Cataracta Brunescens
Grade - VI Black -Cataracta Nigra.

Figure16-15 Black Figure16-16 Figure16-17 Mature Figure16-18 Hyper Figure16-19 Hyper

Pupil Intumescent cataract - mature cataract mature cataract
cataract- Grayish Pearly white pupil sclerotic type Morgagnion cataract
white pupil

Figure16- 20 Brown Figure16-21 Black cataract Figure16-22 Red pupil Figure16- 23 Greenish
cataract pupil in Glaucoma

Other conditions in which pupil is in different colors.

Black pupil
• Young individual

192
• Aphakia
• Pseudophakia
• Cataracta Nigra.
• Yellowish: - Vitreous abscess (Endophthalmitis and Pan
Figure16-24 Cat eye reflex
ophthalmitis).
• Greenish: - Acute congestive glaucoma.
• Reddish: - Albinism.
Cat’s eye Pupil - Amaurotic cat’s eye reflex
(Whitish or purplish pink Pupil)
Differential Diagnosis of Cat’s eye Pupil
 Retinoblastoma (A malignant tumor of the retina in a child of two
years)
 Persistent hyperplastic primary
vitreous Figure16-25 Persistent Figure16-26 Figure16-27
• Congenital cataract Hyperplastic primary Myelinated optic disc Myelinated nerve
• Exudates in the pupil
• Cyclitic membrane vitreous fiber
• Pseudo glioma
• Coat’s eye disease
• Retinal detachment
• Coloboma of Choroid
• Myelinated optic disc
• Myelinated nerve fiber layer of the
retina
• Drusen in the retina.
Figure16-28 Congenital Figure16- 29 Coat's Figure16-30
cataract eye disease Coloboma of the
Pupil reaction to light – choroid
If the light is projected on the eye , the
pupil reaction of that eye is called Direct
pupil reaction. The reaction of the
fellow eye pupil is called consensual
reaction otherwise called indirect
reaction.

Pupillary reflexes – see 16-2,16-3,16-4

in the same chapter .

Table 3 Format for Examination of the Pupil

Examination of the Pupil Right Eye Left Eye
Number
Position
Size—Anisocoria. Mydriasis / Miosis
Shape
Margin
Color
Pupillary light reaction
Direct / Indirect

---------------------------------------------------------------------------------

193
16.1.Physiological reflexes in the eye

24. 1Physiology of the Pupil and Pupillaryreflexes

Competency Py.10.17
Physiology of pupil–
 Pupil is acircular opening in the Iris.
Figure1.2-1
 Normally Pupil is slightly decentered towards down and in,
from the center of the cornea. Eccentric pupil is called
corectopia.
 Normally one pupil is present in each iris ,more than one
pupil is called polycoria
 Normal size 2.5 to 4mm. Less than 2mm is miosis, more
than 7mm is called mydriasis. The difference in the pupil
diameter in the both eyes is called anisocoria.
 Th diameter of the pupil is controlled by constrictor and
dilator muscles of the iris. Constrictor muscle is supplied
by parasympathetic nerves and dilator is supplied by the
oculo sympathetic nerves.
 The color of the pupil is black to grayish black.
Normal Pupil reaction
When the light entering the eye is altered,pupil contracts, then
oscillates and again settles to contraction lesser than the first contraction.

Functions of the Iris

 The Pupil regulates the amount of light which enters into the eye after an axial refraction in the cornea
and prevents the entry of irregular refraction occurred at the periphery of the cornea and thus improves
the depth of focus.
 It allows the aqueous to flow from P.C to the A.C through the delicate irido lenticular opposition.

Pupillary reflexes
 Pupillary light reflexes
 Near reflex - Accommodation , Convergence , Constriction of the pupil
• Psycho sensory reflex – A dilatation of the pupil occurs on psychic and sensory stimuli
• Ciliospinal Reflex – Dilatation of the ipsilateral (Mydriasis), in response to pain on the neck, face, and
upper trunk.
Pupillary Light reflex Pathway.
Consists of afferent and efferent Pathway
Pupillary Light reflex afferentPathway-
 The pupillo motor fibers starts from the Retinal photo receptors, leaves the retina through the optic disc,
optic nerve and joins the chiasma. In the chiasma the nasal fibers of each eye cross in the midline and
joins the opposite optic tract and the temporal fibers of each eye will not cross and joins the ipsilateral
optic tract. Thus the eye optic tract contains ipsilateral temporal fibers and contralateral nasal fibers.
The pupillo motor fibers leave the optic tract and joins the pretectal nucleus in the midbrain.
 It is important to note that the afferent pathway fibers will not enter intothe lateralgeniculate body.
 The fibers at the pretectal nucleus are connected to the ipsilateral and contralateral Edinger Westphal
nucleus i.e. some fibers directly join the ipsilateral Edingerwestphal nucleus and some fibers cross the
midline to joins the contra lateral Edinger Westphal nucleus. These fibers are called internuncial fibers.
 The crossings of the internuncial fibers will explain the symmetrical contraction and symmetrical
diameter of the pupil.

Pupillary light reflexes Efferent Pathway-

 The efferent fibers. from the Edinger Westphal nucleus of the oculomotor nerve, leaves the superior
orbital fissure and enters the orbit and pass through the inferior branch of the oculomotortor nerve to
th einferior oblique muscle joins the ciliary ganglion. After making a synapse in the ciliary ganglion Post
ganglionic fibers. enters into the short ciliary nerves which enter the eye and supplies to the constrictor
muscles of the iris.

Examination of the Pupil reaction to light

Pupillary light reaction is best examined with S/L focal illumination bright light is focused on the pupil. Or
a small, bright, focused beam of light from a torch light is used with a binocular loupe is used to examine the
normal pupil reaction. The examination is done in a semi dark room. The patient should look at distant object
to avoid accommodation.

Light is focused on the pupil of one eye and reaction of the pupil is observed. Normally the pupil constricts.
This is called direct pupil reaction. Simultaneously observe the constriction of the fellow eye pupil without
shifting the light to the fellow eye. This is called consensual /indirect pupil reaction.

Explanation: When the light falls on the retina, the light energy is converted into neurological energy which
causes the constriction of the pupil called direct pupil reaction and this energy is equally shared to the fellow
eye and reaches the fellow eye through the crossing at internuncial fibers and intact efferent pathway
which causes consensual reaction of the pupil.
Abnormal pupillary light reactions are due to defects in the Afferent, Efferent pupillary pathway to the sphincter
pupillae and sympathetic nerve supply to the dilator papillae or the diseases of the iris and pupil.

Afferent pupillary pathway defects may be

 Relative (Partial) Afferent pupillary pathway defect (RAPD) also called Marcus Gunn Pupil
 Total Afferent pupillary pathway defect (TAPD) also called Amaurotic pupil
 Bitemporal hemianopic pupil
 Hemianopic pupil
 Argyll Robertson Pupil (APP)

Relative afferent pupillary defect (RAPD) (Marcus Gunn Pupil)

RAPD / Marcus gunn pupil: In RAPD, light stimulation of the diseased eye pupil, both direct and consensual
reaction is characterized by dilatation of the both pupils (i.e. Paradoxical reaction) and on light stimulation from
the normal eye pupil, both direct and consensual reaction is characterized by constriction of the both pupils
through the intact efferent in the diseased eye.

Explanation: The neurological energy which is created inthe diseasedeye is insufficient to constrict the pupil of the
diseased eye and thesame insufficientenergy in the diseased eye is also equally shared to the fellow eye Thus
the energy coming from the diseased eye to the fellow eye is also insufficient to constrict the pupil. Hence the two
eye pupils of both eyes will dialate.

And if one flashes a light in the normal eye , normal energy is created which is sufficient to constrict the pupil,
and the same energy is equally shared to the diseased eye through the crossings and through the intact
efferent pathway of the diseased eye , and thus both eyes pupils will constrict.

Finally RAPD is both pupils will dilate if one flashes a light in the diseased eye, and both pupils will constrict if one
flashes a light in the normal eye.

The RAPD/Marcus gunn pupil is examined by “Swinging flash light test”. This is done with a bright light of indirect
ophthalmoscope. The bright light is quickly and repeatedly shifted from the diseased eye to the normal eye and
normal eye to diseased eye which leads to fatigue of neural tissue earlier on the side of lesion. Thus both pupils
dilate. The disease eye pupil is more dilated than the normal eye , hence the name relative afferent pupil.

Causes for RAPD –

Partial diseases of the Retina, Retinitis, Neuro retinitis, POAG, Retinitis pigmentosa, Retinal detachment Etc.
• Optic disc diseases – Papillitis , Papilloedema, partial optic atrophy
• Diseases of the Optic Nerve - Optic neuritis, Acute retro bulbar neuritis
Total afferent pupillary defect (TAPD) / (Amaurotic pupil) –

 TAPD is characterized by the absence of direct pupil reaction in the diseased eye. E.g. if light is focused on
an eye with total optic atrophy i.e. total afferent pathway defect , no energy is created in the diseased
eye and thus no energy is available to share to the normal eye.Thus no consensual reaction in the
fellow eye.
 But on light stimulation of normal eye both Direct and consensual reaction is characterized by constriction
of both pupils. This is because the light energy created in the normal eye is equally shared to the
diseased eye through intact afferent pathway in normal eye and intact efferent pathway in the diseased
eye.
 TAPD is seen in – Complete lesions of the optic nerve and retina in the involved eye and eye is completely
blind i.e. No light perception and projection.
 Finally when affected eye is stimulated neither pupil reacts. Both pupils are unequal in size. When normal
eye is stimulated both pupils react normally.

Afferent pathway defect Bitemporal hemi anopic pupil, Hemianopic pupil, Argyll Robertson Pupil (APP) see
below Table
Efferent pupillary pathway Defect -
• In efferent pupillary pathway defect both Direct and Consensual pupil reactions are absent in the diseased
eye, while consensual reaction is normal in the fellow
Figure1.2-2
eye.

Explanation: This is because the pupil is dilated in the

diseased eye due to efferent pathway defect, and
the normal energy created in the fellow eye also
cannot reach the diseased eye dueto efferent pathway
defect in the diseased eye.

• If one flashes a light in the diseased eye normal energy

is created and this energy passes through the afferent
pathway of the diseased eye to the fellow eye through
the intact efferent pathway of a fellow eye and
consensual reaction will be present in the fellow eye.

• Finally In efferent pupillary pathway defect both Direct and Consensual pupil reactions are absent in the
diseased eye, while consensual reaction is present in the fellow eye.
How to differentiate pre ganglionic and post ganglionic paralysis of efferent pathway
• Pilocarpine –0.125% - Instillation of Pilocarpine –0.125% causes constriction of the pupil in post
ganglionic paralysis of the efferent pathway defect due to denervation hypersensitivity. , While the pupil
will not dilate in pre ganglionic paralysis of the efferent pathway defect

Causes for efferent pathwaydefect:

• Diseases involving third cranial nerve
• Diseases of the ciliary ganglion and post ganglionic fibers of the short ciliary nerves
• Diseases of the orbit
Pupillary Light reflexes : Afferent and efferent Pathway defects. ( Correlate Labelled Diagram with Numbers
of diagram 2.2)

Level of Pupillary light Name of Direct Pupil Consensual Direct Consensual Near
reflex Pathway. thePupil Reaction in the Pupil Pupil Pupil Reflex
Defect diseased eye reaction in Reaction in reaction in
(See Diagram 2.2 ) the fellow the fellow the
eye eye diseased
eye
1. Retina and optic RAPD (Relative Dilated pupil Dilated pupil Normal
afferent Pupil)
nerve
defect
(Partial diseases ) Normal
(Relative Normal
pupil
dilatation) pupil

1. Total disease of TAPD (Total Dilated pupil Normal pupil Normal Normal Normal
pupil
afferent Pupil) pupil
the retina and optic
defect
nerve

2. At Medial Bitemporal Bi temporal pupil will no reaction to light. Normal reaction of ----
Hemianopic the Nasal side of the pupil
Chiasmal lesions
paralysis of
the Pupil

3.Lateral Chiasmal BiNasalHemia Bi nasal pupil will no reaction to light. Normal reaction of the ------
nopic paralysis Temporal side of the pupil.
lesions
of the Pupil
4. Optic Tract AS the visual field defect is homonymous hemianopia (i.e.the ----
Wernicke nasal half of the one eye and temporal half of the other eye)
 Tuberculous
Hemianopic the corresponding half of the iris will have no direct and
meningitis
pupil consensual reaction, the non-corresponding iris will have a
 Syphilitic
direct and consensual reaction
meningitis

Bilateral Argyll Bilateral light reflex is absent Present

5. Bilateral inter
Robertson Bilateral accommodation is present i.eNear reflex present
nuncial fibers Pupil (APP) Both pupils will not constrict with pilocarpine
 Neuro Syphilis Both pupils will not dilate with mydriatics.

6. Unilateral Unilateral light reflex is absent

Argyll Unilateral accommodation is present i.e. Near reflex present
Unilateral inter nuncial
Robertson Unilateral pupil will not constrict with pilocarpine
fibers
Pupil (APP) Unilateral pupil will not dilate with mydriatics.

OccipitoTectal Tract Inverse Argyll Bilateral light reflex is present --

Diphtheria Robertson Bilateral near reflex is absent
Encephalitis Pupil (APP)

Efferent Pathway defects (See Below )

Affected eye dilated Fellow eye normal pupil Absent
7. Efferent Pathway pupil reaction
From EW
Oculomotor Nerve and
nucleus through
preganglionic fibers rd
3 cranial nerve
to ciliary
Both direct and Consensual pupi lreaction in the
ganglion
affected eye is absent. Hence Pupil is dilated
Consensual reaction in thefellow eye is normal pupil
reaction.

Adie Pupil or In the diseased eye both direct and consensual Present
8.and 9
Tonic Pupil reaction is absent. Bilaterally
Ciliary Ganglion Pupil constriction for Near reflex is present
Short ciliary nerves The iris shows slow vermiform movements in the near
 HZV reflex
ganglionitis Pupil will constrict with 0.125% pilocarpine due to
 Orbital trauma denervation hypersensitivity.
 Diabetes
Holmes adie pupil -
Tonic pupil + diminished
deep tendon reflexes.

-----------
---------------
Supra nuclear inhibition
Supra nuclear inhibition Parasympathetic Both direct and consensual reaction of the pupil are Absent
of the Edinger Westphal drug Mydriasis absent i.e. pupil is dilated.
nucleus Use of Atropine Consensual reaction of the fellow eye is normal.
and Pupil will not constrict with 1% pilocarpine thus
Homatropine differentiated from the tonic pupil

Affected eye pupil Fellow eye Normal

pupil Constricted
is Dilated

The pupil light reflex fibers follow the Visual pathway and associated with visual pathway defects.

_____________________________________________________________________________________
16.2 Oculo sympathetic Pathway and Palsy

Competency 31 .3 Describe the anatomical basis of Horner’s syndrome

Figure1.3-1 Figure1.3-2

Oculo sympathetic Pathway has three divisions

Central division, Preganglionic division, Postganglionic division
 Central division –
First order neuron - Hypothalamus to C8 to T1,2,3 of Ciliospinal center of Budge
 Preganglionic division –
Second order Neuron -Ciliospinal center of Budge to Superior cervical ganglion in the neck
 Postganglionic division- From Superior cervical ganglion in the neck to the Muller’s muscle , sweat glands
of face and forehead.

 Central division ( Hypothalamic – spinal Tract ) –

Starts from the hypothalamus,decussate in the mid brainand traverse the reticular substance of the midbrain and
passdownwards through the medulla oblongata, lateral column of the cord and joins contra lateral Ciliospinal
center of Budge.
The hypothalamic center has inhibitory pathway to the Edinger – Westphal group of nuclei of 3 cranial nerve.
rd

This center also has connections with cerebral cortex.

 Preganglionic sympathetic division –

The fibers pass through the ventral roots of C8, T1(mainly), T2, T3, via the white rami communicartes to the
cervical sympathetic chain in which the fibers traverse the inferior cervical ganglion and anterior loop of the Ansa
of vieussens and they run in the neck to terminateinthe superior cervical ganglion.

 Postganglionic sympathetic division –

Fromthe superior cervical ganglion the fibers enter the skull with the carotid plexus and then through the
cavernous plexus and cross over the Gasserian ganglion , along the first division of the ophthalmic division of the
trigeminal nerve and then nasociliary nerve and leave to join long ciliary nerves long ciliarynerves enter the
globe with the long ciliary arteries and pass through the suprachoroidal space and reach the iris and supplies the
Dilator muscle. Before entering the globe, some fibers may join the ciliary ganglion and may not make any synapse
inciliary ganglion.

rd
The muscles of the iris i.e. the constrictor muscle is supplied by the parasympathetic 3 cranial nerve and dilator
muscle is supplied by the sympathetic pathway. There is a delicate balance of tone between these two
innervations and however the constrictor muscle has superior tone.

Clinical signs of Paralysis of oculo sympathetic pathway causing Horner’s syndrome.

 Mild ptosis due to paralysis of the upper eye lid Muller muscle.
 Inverse ptosis i.e. elevation of the lower eye lid due to paralysis of the Lower eye lid Mullers muscle.
 Miosis isdue to paralysis of the dilator muscle and unopposed action of constrictor muscle of iris.
 Mild enophthalmos – Appears as if there is ptosis.it is pseudo ptosis.
 Anhidrosis of face and forehead. (Not seen in the post ganglionic lesions)
 Loss of Ciliospinal reflex

Clinical signs of Congenital Paralysis of oculosympathetic pathway

 Besides Signs of Horner’s syndrome there is associated heterochromia iridis i.e.involved iris is light
colored i.e. Hypochromic iris in one eye and normal iris in the other eye.
Clinical signs of over activity of oculo sympathetic pathway- Pourfour du Petit Syndrome. (PDP syndrome)
The clinical signs are oppositeof Horner’s syndrome
Mydriasis, Retraction of the lids, Apparentexophthalmos, Hydrosis of the face and fore head (sweating) and
conjunctival blanching.
Causes for over activity Causes for paralysis of Causes for paralysis of Causes for paralysis of
of oculosympathetic central division Preganglionic oculo Postganglionic division of oculo
pathway ( Hypothalamus – Spinal sympathetic pathway sympathetic pathway
Tract) of oculosympathetic
pathway
 Thyrotoxicosis,  Brain stem Tumors  Pancoast Tumor  Cluster Headache
 Brachial  Syringomyelia  Carotid and Aortic  Internal carotid artery
plexusanaesth  Syringobulbia aneurysm dissection
etic block  Diabetes  Neck lesions –  Otitis media
 Parotidectomy Deep  Cavernous sinus mass.
. lymphadenopathy
 Thyroid tumors

How to differentiate the paralysis of central, preganglionicfrom Postganglionic division of oculo sympathetic
pathway
Drugs Normal Pupil Paralysis of Central( Paralysis of Paralysis of Post ganglionic
Hypothalamus – Spinal Preganglionic oculo oculo sympathetic
Tract) sympathetic pathway pathway
4%Cocaine Both pupils will Horner’s pupil will NOT Horner’s pupil will Horner’s pupil will NOT
dilate dilate. NOT dilate. dilate

1% Hydroxy Both pupils will Both pupils will dilate Both pupils will dilate Horner’s pupil will NOT
Amphetamine dilate dilate, continues to
constrict

0.1%Adrenaline Both pupils will Horner’s pupil will NOT Horner’s pupil will Horner’s pupil Will dilate
dilate dilate NOT dilate

0.5% or 1% Unaffected Horner’s pupil will NOT Horner’s pupil will Horner’s pupil will dilate
Apraclonidine dilate NOT dilate
4% Cocaine:
 Rationale- cocaine blocks Noradrenaline uptake at postganglionic sympathetic nerve endings
Result – Normal pupil will dilate but Horner pupil will not because in Horner’s syndrome there is no Noradrenaline
being secreted.
Therefore, a post cocaine anisocoria of >0.8mm in a dimly lit room is significant.
• C ocaine continues constriction in Horner’s syndrome
Hydroxy amphetamine 1%:
• Rationale:Hydroxy amphetamine potentiates the release of Noradrenaline from post ganglionic nerve
endings
• Result: in the preganglionic lesion, both pupils will dilate.
• In postganglionic lesion, Horner’s pupil continues to constrict.

Adrenaline 0.1%: Differentiatespre and post ganglionic sympathetic paralysis in the eye --
• Rationale : the principle is based on denervation hypersensitivity to adrenergic neurotransmitters
• Result: in Preganglionic lesion, neither pupil will dilate because adrenaline is rapidly destroyed by MAO. In
postganglionic lesion, Horner’s pupil will dilate and ptosis will be relieved because adrenaline is not
broken down due to absence of MAO.

Apraclonidine 0.5% or 1%:

• Rationale – α1 receptors are unregulated in the denervated dilator pupillae
• Result - Horner pupil will dilate and the normal pupil is unaffected.

_______________________________________________________________________________________
16.2.Physiological reflexes in the eye

24. 1Physiology of the Pupil and Pupillary reflexes

Competency Py.10.17
Physiology of pupil–
 Pupil is acircular opening in the Iris.
Figure1.2-1
 Normally Pupil is slightly decentered towards down and in,
from the center of the cornea. Eccentric pupil is called
corectopia.
 Normally one pupil is present in each iris ,more than one
pupil is called poly coria
 Normal size 2.5 to 4mm. Less than 2mm is miosis, more
than 7mm is called mydriasis. The difference in the pupil
diameter in the both eyes is called anisocoria.
 Th diameter of the pupil is controlled by constrictor and
dilator muscles of the iris. Constrictor muscle is supplied
by parasympathetic nerves and dilator is supplied by the
oculo sympathetic nerves.
 The color of the pupil is black to grayish black.
Normal Pupil reaction
When the light entering the eye is altered, pupil contracts,
then oscillates and again settles to contraction lesser than the first contraction.

Functions of the Iris

194
Pupillary Light reflex Pathway.
Consists of afferent and efferent Pathway
Pupillary Light reflex afferent Pathway-
 The pupillo motor fibers starts from the Retinal photo receptors, leaves the retina through the optic disc,
optic nerve and joins the chiasma. In the chiasma the nasal fibers of each eye cross in the midline and
joins the opposite optic tract and the temporal fibers of each eye will not cross and joins the ipsilateral
optic tract. Thus the eye optic tract contains ipsilateral temporal fibers and contralateral nasal fibers.
The pupillo motor fibers leave the optic tract and joins the pretectal nucleus in the midbrain.
 It is important to note that the afferent pathway fibers will not enter intothe lateralgeniculate body.
 The fibers at the pretectal nucleus are connected to the ipsilateral and contralateral Edinger Westphal
nucleus i.e. some fibers directly join the ipsilateral Edingerwestphal nucleus and some fibers cross the
midline to joins the contra lateral Edinger Westphal nucleus. These fibers are called internuncial fibers.
 The crossings of the internuncial fibers will explain the symmetrical contraction and symmetrical
diameter of the pupil.

Pupillary light reflexes Efferent Pathway-

Examination of the Pupil reaction to light

195
Abnormal pupillary light reactions are due to defects in the Afferent, Efferent pupillary pathway to the sphincter
pupillae and sympathetic nerve supply to the dilator papillae or the diseases of the iris and pupil.

Afferent pupillary pathway defects may be

Relative afferent pupillary defect (RAPD) (Marcus Gunn Pupil)

Finally RAPD is both pupils will dilate if one flashes a light in the diseased eye, and both pupils will constrict if one
flashes a light in the normal eye.

Causes for RAPD –

196
Total afferent pupillary defect (TAPD) / (Amaurotic pupil) –

Explanation: This is because the pupil is dilated in the

diseased eye due to efferent pathway defect, and
the normal energy created in the fellow eye also
cannot reach the diseased eye dueto efferent pathway
defect in the diseased eye.

• If one flashes a light in the diseased eye normal energy

• Finally In efferent pupillary pathway defect both Direct and Consensual pupil reactions are absent in the
diseased eye, while consensual reaction is present in the fellow eye.

197
How to differentiate pre ganglionic and post ganglionic paralysis of efferent pathway
• Pilocarpine –0.125% - Instillation of Pilocarpine –0.125% causes constriction of the pupil in post
ganglionic paralysis of the efferent pathway defect due to denervation hypersensitivity. , While the pupil
will not dilate in pre ganglionic paralysis of the efferent pathway defect

Causes for efferent pathwaydefect:

1. Total disease of TAPD (Total Dilated pupil Normal pupil Normal Normal Normal
pupil
afferent Pupil) pupil
the retina and optic
defect
nerve

2. At Medial Bitemporal Bi temporal pupil will no reaction to light. Normal reaction of ----
Hemianopic the Nasal side of the pupil
Chiasmal lesions
paralysis of
the Pupil

3.Lateral Chiasmal BiNasalHemia Bi nasal pupil will no reaction to light. Normal reaction of the ------
nopic paralysis Temporal side of the pupil.
lesions
of the Pupil

198
4. Optic Tract AS the visual field defect is homonymous hemianopia (i.e.the ----
Wernicke nasal half of the one eye and temporal half of the other eye)
 Tuberculous
Hemianopic the corresponding half of the iris will have no direct and
meningitis
pupil consensual reaction, the non-corresponding iris will have a
 Syphilitic
direct and consensual reaction
meningitis

Bilateral Argyll Bilateral light reflex is absent Present

6. Unilateral Unilateral light reflex is absent

OccipitoTectal Tract Inverse Argyll Bilateral light reflex is present --

Diphtheria Robertson Bilateral near reflex is absent
Encephalitis Pupil (APP)

Efferent Pathway defects (See Below )

199
ganglionitis Pupil will constrict with 0.125% pilocarpine due to
 Orbital trauma denervation hypersensitivity.
 Diabetes
Holmes adie pupil -
Tonic pupil + diminished
deep tendon reflexes.

Affected eye pupil Fellow eye Normal

pupil Constricted
is Dilated

The pupil light reflex fibers follow the Visual pathway and associated with visual pathway defects.

_____________________________________________________________________________________

200
16.3 Near Reflex

Near Reflex Figure 1.4.1 Figure1.4.2

Near Reflex

Convergence reflex and

Accommodation reflex

Convergence reflex:
Initiated by medial rectus
which contracts on
convergence
. The afferent pathway for
convergence reflex isindicated
as running up throughthe third
cranial nerve to the
mesencephalic nucleus of the fifth nerve to the presumptive convergence center in the tectal or pretectal region.
From here the pathway is relayed to the EW nucleus and along the third nerve to the sphincter muscle of the iris
so that with the convergence, the pupil contracts commensurately.

(3 cranial nerve -- mesencephalic nucleus of the fifth nerve – to the convergence center in the tectal or pretectal
rd

region – relayed to the EW nucleus along the third cranial nerve to the sphincter muscles of the iris – pupil
constriction

Accommodation Reflex:
The accommodation reflex follows the visual fibers to the striate area of the calcarine cortex which is relayed to
the para striate area (19). From here efferent path travels to the occipitomesencephalic tract to the pontine center
forconvergence and then to the EW nucleus and along the third nerve to the muscle of ciliary body.

Accommodation reinforces the reflex by visual impulse relayed from the cortex to the EW nucleus. .

( Visual cortex -- to the striate area of the calcarine cortex -- para striate area (19) --- Efferent pathway travels to
--- mesencephalic tract --- Pontine center for convergence -- EW nucleus.- oculomotor nerve to the ciliary body
muscles )
Causes – Efferent pathway defects causes - Diseases of 3 cranial nerve.
rd
Sensory reflex / Cilio spinal reflex:
Initiated by the stimulation of any sensory nerve to create pain or emotional state or excitement. Both dilator and
constrictor center play part in the production of sensory reflex/ Cilio spinal reflex.
Sensory stimulation causes dilatation of the pupil due to stimulation of the cervical sympathetic and slowly
disappears due to inhibitory action by the constrictors.
Psychosensory reflex -
Dilatation of the pupil occurs on psychic and sensory stimuli.
Thus abnormal pupil reactions may be due to afferent pathway defect, efferent path way defect, sympathetic
pathway defect or due to the diseases of the iris.
---------------------------------------------------
16.2 Oculo sympathetic Pathway and Palsy

Competency 31 .3 Describe the anatomical basis of Horner’s syndrome

Figure1.3-1 Figure1.3-2

Oculo sympathetic Pathway has three divisions

 Central division ( Hypothalamic – spinal Tract ) –

201
Starts from the hypothalamus,decussate in the mid brainand traverse the reticular substance of the midbrain and
passdownwards through the medulla oblongata, lateral column of the cord and joins contra lateral Ciliospinal
center of Budge.
The hypothalamic center has inhibitory pathway to the Edinger – Westphal group of nuclei of 3 cranial nerve.
rd

This center also has connections with cerebral cortex.

 Preganglionic sympathetic division –

 Postganglionic sympathetic division –

Clinical signs of Paralysis of oculo sympathetic pathway causing Horner’s syndrome.

Clinical signs of Congenital Paralysis of oculosympathetic pathway

 Besides Signs of Horner’s syndrome there is associated heterochromia iridis i.e.involved iris is light
colored i.e. Hypochromic iris in one eye and normal iris in the other eye.

202
Clinical signs of over activity of oculo sympathetic pathway- Pourfour du Petit Syndrome. (PDP syndrome)
The clinical signs are oppositeof Horner’s syndrome
Mydriasis, Retraction of the lids, Apparentexophthalmos, Hydrosis of the face and fore head (sweating) and
conjunctival blanching.
Causes for over activity Causes for paralysis of Causes for paralysis of Causes for paralysis of
of oculosympathetic central division Preganglionic oculo Postganglionic division of oculo
pathway ( Hypothalamus – Spinal sympathetic pathway sympathetic pathway
Tract) of oculosympathetic
pathway
 Thyrotoxicosis,  Brain stem Tumors  Pancoast Tumor  Cluster Headache
 Brachial  Syringomyelia  Carotid and Aortic  Internal carotid artery
plexusanaesth  Syringobulbia aneurysm dissection
etic block  Diabetes  Neck lesions –  Otitis media
 Parotidectomy Deep  Cavernous sinus mass.
. lymphadenopathy
 Thyroid tumors

1% Hydroxy Both pupils will Both pupils will dilate Both pupils will dilate Horner’s pupil will NOT
Amphetamine dilate dilate, continues to
constrict

0.1%Adrenaline Both pupils will Horner’s pupil will NOT Horner’s pupil will Horner’s pupil Will dilate
dilate dilate NOT dilate

0.5% or 1% Unaffected Horner’s pupil will NOT Horner’s pupil will Horner’s pupil will dilate
Apraclonidine dilate NOT dilate

203
4% Cocaine:
 Rationale- cocaine blocks Noradrenaline uptake at postganglionic sympathetic nerve endings
Result – Normal pupil will dilate but Horner pupil will not because in Horner’s syndrome there is no Noradrenaline
being secreted.
Therefore, a post cocaine anisocoria of >0.8mm in a dimly lit room is significant.
• C ocaine continues constriction in Horner’s syndrome
Hydroxy amphetamine 1%:
• Rationale:Hydroxy amphetamine potentiates the release of Noradrenaline from post ganglionic nerve
endings
• Result: in the preganglionic lesion, both pupils will dilate.
• In postganglionic lesion, Horner’s pupil continues to constrict.

Apraclonidine 0.5% or 1%:

• Rationale – α1 receptors are unregulated in the denervated dilator pupillae
• Result - Horner pupil will dilate and the normal pupil is unaffected.

_______________________________________________________________________________________

204
16.3 Near Reflex

Near Reflex Figure 1.4.1 Figure1.4.2

Near Reflex

Convergence reflex and

Accommodation reflex

(3 cranial nerve -- mesencephalic nucleus of the fifth nerve – to the convergence center in the tectal or pretectal
rd

region – relayed to the EW nucleus along the third cranial nerve to the sphincter muscles of the iris – pupil
constriction

Accommodation reinforces the reflex by visual impulse relayed from the cortex to the EW nucleus. .

205
Sensory reflex / Cilio spinal reflex:
Initiated by the stimulation of any sensory nerve to create pain or emotional state or excitement. Both dilator and
constrictor center play part in the production of sensory reflex/ Cilio spinal reflex.
Sensory stimulation causes dilatation of the pupil due to stimulation of the cervical sympathetic and slowly
disappears due to inhibitory action by the constrictors.
Psychosensory reflex -
Dilatation of the pupil occurs on psychic and sensory stimuli.
Thus abnormal pupil reactions may be due to afferent pathway defect, efferent path way defect, sympathetic
pathway defect or due to the diseases of the iris.
---------------------------------------------------

206
Chapter 17. Clinical examination of the Crystalline lens

Clinical anatomy of the Crystalline lens

• The Crystalline lens is suspended in the anterior cavity of the eye ball by a suspensory ligament
called zonules of zinn
• Crystalline lens is located behind the iris and pupil, in a saucer shaped depression in the anterior
phase of vitreous called the patellar fossa, and a potential space between the attachment of the lens
and vitreous is called Berger space / Retrolental space
• The posterior surface of the lens is attached to the hyaloid phase of vitreous by a weigert ligament
in a circular area
• It is Biconvex in vivo and spherical in vitro

Figure 17-1 Crystalline lens Figure 17-2Optical section Figure 17-3Optical section of Figure17-4 Slit lamp
Crystalline lens crystalline lens appearance of
crystalline lens

The Crystalline lens is a specialized tissue in the body Figure 17-5 Adult Crystalline lens
because dimensions

• It is transparent
• It is Avascular tissue,
• It has No nerve supply.
• It has refractive power of +17 to 19 Diopters necessary
for refraction.
• The refractive index of cortex is 1.386 and nucleus is
1.406
• New lens fibers are laid through out life from womb to the grave

Anatomy of Lens Structure –

The substance of lens has two distinct divisions - Cortex and nucleus

1
 Cortex is the most peripheral part of the lens and are Youngest fibres.
 Nucleus is the central part of the lens

Layers of the crystalline lens

 Lens Capsule,
 Lens Epithelium
 Lens fibers
 Nucleus
 zonule of Zinn.

Lens Capsule
Lens capsule is transparent. homogenous, Elastic, Hyaline membrane made of type IV collagen with thickest
basement membrane. It is secreted by the lens epithelium , which has a thin membrane outer side – Zonular
lamella.
The lens has anterior lens capsule with Epithelium, Posterior lens capsule without epithelium. The junction
between anterior and posterior capsule is called equator .The anterior capsule is thicker than the posterior and
more thicker at pre equatorial area .

Lens Epithelium
The anterior capsule is lined by a single layer of cuboidal cells that form the anterior sub capsular epithelium.
There is no epithelium in the posterior capsule. The cells of epithelium are metabolically active contains Na, K,
ATPase and generate ATP to meet the energy demand of the lens. These cells show high mitotic activity and
form new cells which migrate towards equator..The lens epithelial cells continue to divide and develop into
new lens fiber.

Lens fibers
The lens fibers develops from the lens epithelial cells that continue to divide and get elongated and transform
into lens fibers. The fibers formed earlier lie in the deeper plane which surrounds the Embryonic nucleus, and
newer ones occupy the superficial plane forming cortex . The growth of lens fibers (secondary fibers)
continue through out life at a slower rate as age advances and is analogous to the growth of other epithelial
structures like skin , nails , hair.

Nucleus of Crystalline Lens

The fibrers of the central embryonic nucleus are developed by the primary lens fibers and meet around ‘Y’
shaped sutures surrounded by secondary lens fibrers. Out side this embryonic nucleus , successive nuclear
zones are laid down as development proceeds depending on the period of formation these zones named as
mentioned below.

2

st rd
Embryonic nucleus - lens fibers formed 1 to 3 month of gestation . These fibers are earliest lens
fibers
 Fetal nucleus – formed from 3 month to 8 month of gestation
rd th

 Infantile nucleus - formed from just before or immediately after birth till puberty
 Adult nucleus – formed after puberty, contains the youngest lens fibrers.

zonule of zinn.
Consists of bundle of fibers which pass from the surface of the ciliary body to the capsule where they join with
the zonular lamella.
The most posterior fibers arises from the ora serrata , and make contact with ciliary body and are inserted in
the capsule just anterior to the equator.
Second group arises from the ciliary processes and are inserted just posterior to the equator. Third group
arises from the summit of the ciliary processes and are inserted into the equator.

Crystalline Lens at advanced Age

As the age advances the central portion of the lens becomes compressed by the continuous growth of the lens
fibers surrounding it and this combined with a process of sclerosis makes the central portion of nucleus
denser than the peripheral portion i.e. the cortex.The cortex progressively diminishes in proportion to the
nucleus until the hardening process which takes place in old age involves the whole lens.

The function of the crystalline lens

Figure 17-6 Refraction of the eye Figure 17-7 Lens changes in accommodation

 Refraction- The light rays that fall on the cornea and crystalline lens are converged on the fovea
because of the converging power of the cornea and crystalline lens.
 Accommodation – during accommodation the contraction of the ciliary body causes relaxation of the
zonules of the lens which causes the increase of the anterior curvature of the lens there by increase
of anterio posterior diameter of the lens .This cause increasesed convergence power of the eye and
the light rays are converged on to the fovea .

3
Clinical examination of the Crystalline lens and confirmation of the cataract opacities requires the following
methods
 Diffuse illumination with torch light with Binocular Loupe
 Slit Lamp –Oblique illumination and retro illumination
 Direct Ophthalmoscope – For Distant Direct Ophthalmoscopy and Fundus Oculi
 Plain mirror examination – Commonly used plain mirror is Retinoscopy mirror

Clinical Points to be noted in the examination of the crystalline lens

 Present or absent
• Size
• Shape
• Position
• Opacities
• Colors of the cataract
• Phacodonesis
Whether Crystalline lens present or absent
The Presence of normal crystalline lens is called Phakia. The clear crystalline lens is identified in the optical
section of a slit lamp and appears as layers /zones i.e nucleus,
cortex, and capsule. Figure 17-8 Figure BBlack pupil
The Absence of normal crystalline lens in its anatomical position
is called Aphakia
The clinical findings of aphakia (Post surgical) are
 A linear scar at superior limbus between 10 to 1 `0`clock
position
 Deep anterior chamber
Figure17-9.Posterior Figure 17-10
 Tremulousness of the iris
chamber IOL Anterior chamber IOL
 Color of the pupil is Black
 Hypermetropic fundus – Small optic disc
 Retinoscopy reflex with plane mirror at 1 meter
distance - The reflex moves with the movement
of the mirror
 Limbal scar is absent in the congenital, or
Posterior dislocation of the crystalline lens
Causes of Aphakia
 Congenital
• Surgical removal of the lens by ICCE or ECCE technique.
• Post traumatic absorption of the lens
• Posterior Dislocated lens due to blunt trauma

4
Pseudophakia
Presence of artificial lens i.e. IOL in the eye is called Pseudophakia.It is implanted in the eye in ECCE cataract
surgery.

Clinical findings of Pseudophakia

 A scar at superior limbus between 10 to 1 `0` clock position or on the temporal limbus
 If the IOL is in the bag of the crystalline lens then the depth of the anterior chamber is deep
 Black pupil
 A Shining or shimmering reflex is present on flashing a light on the pupil.
 Retinoscopy reflex with plane mirror at 1 metre distance :
The Red reflex is the illuminated fundus oculi seen in the pupil. The movement of reflex depends on the
residual refractive error. If the reflex moves with the movement of the plane mirror the patient may be
emmetropic, hypermetropic or myopia of less than one diopter. If the reflex moves against the
movement of plane mirror then the patient is more than one diopter of myopia. If there is no
movement of red reflex then the patient is one diopter Myopic.
 S/L oblique illumination examination with dilated pupil : The optic and haptic of the IOL are seen while
the zones of crystalline lens are absent..
 Distant direct ophthalmoscopy : A red reflex seen at the pupil.
 Direct ophthalmoscopy : The details of fundus oculi are normal

Size / Dimensions of the lens

Clinically it is difficult to measure the normal dimensions of the lens unless it is brought out from the eye by
Enucleation, or ICCE procedures.
In the absence of accommodation the Normal diameter of the crystalline lens is 9 to 10 mm
The size / diameter of the crystalline lens
Increased in
In the process of accommodation (Physiological increase of anterio posterior diameter)
• Intumescent cataract
• Total nuclear sclerosis cataract
• Penetrating injury to the crystalline lens
Decreased in size in
• Spherophakia small and round lens , a congenital anomaly
Shape of the crystalline lens
• The shape of normal crystalline lens in vivo is Biconvex and in vitro is Spherical (Nonsymmetric ablate
spheroid)
In accommodation, contraction of the ciliary body causes relaxation of the zonules of the crystalline lens there
by increasing the antero posterior diameter and making the crystalline lens more spherical.

5
Abnormal shapes of the crystalline lens are
• Anterior lenticonus – Pathological increase of anterior curvature of the lens in Alport’s syndrome
• Posterior lenticonus – Pathological increase of posterior curvature of the lens, seen in Lowe syndrome
• Buphthalmos, Hypoglycaemia - Curvatures are decreased.
• Colobo Figure 17-11 Figure 17-12 Figure 17-13
ma in Subluxation crystalline Subluxated crystalline lens Anterior

the lens lens dislocation of the lens

–
Congen
ital
anomal
y

Position of the crystalline lens

Normally the crystalline lens is placed in the patellar fossa of the anterior vitreous behind the pupil
Abnormal Position of the Lens
 Subluxation –Partial displacement of the lens from its anatomical position is called Subluxation and the
lens equator is seen in the pupil .

Table 1
Sub luxated lens - Clinical finding Dislocated lens -Clinical finding
Irregular depth of anterior chamber Anterior chamber is deep,
The color of aphakic area of the pupil is black, The Color of the pupil is black due to clear vitreous.
color of the phakic pupil depends on the color of the
crystalline lens
Tremulousness of the iris is absent. Tremulousness of the iris is present.
Fundus oculi - The aphakic portion is Hypermetropic Fundus oculi is Hypermetropic i.e. small optic disc ,
i.e. small optic disc, while the phakic area of the
optic disc is normal
Retinoscopy reflex with plane mirror at a distance of Retinoscopy reflex with plane mirror at a distance of
1 meter : The red reflex moves with the movement 1 meter the red reflex moves with movement of the
of the plane mirror in Aphakic portion. And in the plane mirror.
phakic portion the movement of the reflex depends
on the refractive state of that area.

 Dislocation –Total displacement of lens from its anatomical position is called dislocation .The lens is not
seen in the pupil .
Table 2
Subluxated lens - Cause Dislocated lens - Cause
Blunt trauma Blunt trauma
Marfan’s –Up and out Degeneration of the zonules as in Glaucoma
Homocystinuria –Down and in
High Myopia.

6
Color of the senile cataract (color of the pupil)
Color of the crystalline lens gives various Colors to the Pupil
Described in the colors of the pupil and also in the diagnosis of senile cataract

Opacities of the crystalline lens

Opacity of the Crystalline lens or its capsule whether congenital or acquired is called Cataract
The senile cataract may be cortical cataract or nuclear cataract .
• Cataracts are classified as congenital, Acquired
• The acquired cataracts are -Senile cataract, Complicated cataract ,Traumatic cataract ,Metabolic
cataract ,Toxic cataract ,Radiation cataract , Electric Cataract, Atopic cataract -Cataracts associated
with bone diseases, Cataracts associated with syndromes.
The senile cataracts are cortical and nuclear which is a common cataracts and visually significant.
Clinical stages of senile cortical Cataract
Stages of cortical cataract senile cortical cataract
Stage -I Lamellar separation
Stage -II Incipient cataract –
Sub types - Cuneiform type, Cupuliform type
Stage -III Immature cataract
Complication- Intumescent type
Stage –IV Mature cataract
Stage – V Hypermature cataract
Subtype -Sclerotic and Morgagnian

Grades of senile nuclear cataract Color of the nuclear cataract by grade wise
Grade- 1 whitish yellow
Grade– 2 yellowish white color
Grade- 3 Amber color
Grade –4 Light brown
Grade –5 Thick brown color is called Cataracta Brunescens
Grade- 6 Black color is called Cataracta Nigra

Confirmation of the diagnosis of Cataract opacities are done by examination with the following clinical
methods
 Slit lamp oblique illumination and Retro illumination techniques,
 Distant direct ophthalmoscopy,
 Direct ophthalmoscopy fundus oculi examination and
 Plane mirror examination at 1 meter distance

7
Slit lamp examination
• Slit lamp Examination (S/L) - Two techniques of (S/L) i.e oblique illumination and retro illumination
technique are required for diagnosis of cataract
• Slit lamp Examination , oblique illumination technique: This technique is to make the optical section
of the crystalline lens. This technique shows position of the lens opacity in the layers of crystalline
lens and also can Stage the cortical cataract and Grade the nuclear cataract .
• Slit lamp Examination In retro illumination technique : In this technique a fine beam of slit lamp
light is placed behind the lens opacities and the color and shape and position of cataract is studied in
retro illuminated light. Early cortical opacities are seen as black . In early to moderate nuclear
cataract no opacity is seen,
 Distant Direct ophthalmoscopy
What is distant direct ophthalmoscopy - Ophthalmoscopy is performed with Direct ophthalmoscope at a
distance of 22 cms At a distance of 22 cms , focus the crystalline lens with the bright light of Direct
ophthalmoscope and observe the opacities of the crystalline lens in red fundus glow. In incipient cataract,
and early nuclear cataract the opacities are seen as black in the red fundus oculi . In total nuclear cataract
,mature cataract, hyper mature cataract no red reflex is seen .The red reflex is the illuminated fundus oculi by
the light of the direct ophthalmoscope seen at the pupil.

 Direct ophthalmoscopy fundus oculi examination

On Direct Ophthalmoscopy, visibility of the fundus oculi structures will contribute to the diagnosis of the
cataract . In stage I,II, III cortical cataract and grade I,II ,III Nuclear cataract the details of fundus oculi is seen
clearly , In immature cortical cataract and grade IV,V nuclear sclerosis , the details are hazily seen . In Mature
cataract , Hyper mature cataract and grade VI of nuclear cataract no details of the fundus oculi.

 Plane Mirror examination (Commonly used plane mirror is the Retinoscopy plain mirror)
Plane Mirror examination is done at 1 metre distance . A light is taken on to the plane mirror from a light
source and then reflect the light on to the pupil of the person. Immature cortical cataract and early
nuclear cataract is seen as black opacities in red fundus background and in total cataract ,no red reflex or faint
reflex is seen and also observation of the movement of the retinoscopy reflex will give the type of refractive
shift in cataract .The refractive shift is myopic in nuclear cataract and Hypermetropic in cortical cataract and
this type of refractive errors are called index Myopia in nuclear cataract and index Hypermetropia in cortical
cataract.
• In early cataracts it is difficult to confirm the cataract only with one method of clinical examination
and sometimes the diagnosis is missed.
• Eg. fine lenticular haze may be missed in S/L, but is best appreciated with Direct ophthalmoscopy and
plain mirror examination.

8
• Hence three clinical methods are necessary for confirmation of Diagnosis. particularly in early
cataracts
Comparative Clinical signs of various types of cataracts are discussed in chapters
20,21,22,23,24,25,26.

Phacodonesis
Tremulousness of the crystalline lens is called phacodonesis Clinical findings of Phacodonesis – Tremulousness
of iris and lens. It is due to weakness of Zonules of the crystalline lens.
Causes of Phacodonesis Figure 17-14
 Degeneration of the Zonules of crystalline lens as in Hyper mature
cataract.
 Blunt trauma on the eye ,
 Absolute Glaucoma.
OSCE
 Students must be able to identify the various colors of the cataractous lens
 Understanding of findings of cataract with S/L, Distant direct ophthalmoscopy , Direct ophthalmoscopy
and Plane mirror.

Diagram to be practiced
 Diagram of the optical section of the Crystalline lens and label the layers / zones .

Table 3
Format for Examination of the Crystalline lens
Examination of the Crystalline lens Right Eye Left Eye
Whether the Crystalline lens is
present or absent
Phakia.
Aphakia
Pseudophakia
Size of the lens
Shape of the lens
Position of the Lens
Subluxation
Dislocation
Opacities in the lens
Colors of the crystalline lens /
cataract
Phacodonesis

____________________________________________

9
Chapter 17. Clinical examination of the Crystalline lens
(17.1 Clinical anatomy of the Crystalline lens. 17.2 clinical points to be noted in the examination of
crystalline Lens)
17.1 Clinical anatomy of the Crystalline lens
• The Crystalline lens is suspended in the anterior cavity of the eye ball by a suspensory ligament
called zonules of zinn
• Crystalline lens is located behind the iris and pupil, in a saucer shaped depression in the anterior
phase of vitreous called the patellar fossa, and a potential space between the attachment of the lens
and vitreous is called Berger space / Retrolental space
• The posterior surface of the lens is attached to the hyaloid phase of vitreous by a weigert ligament
in a circular area
• It is Biconvex in vivo and spherical in vitro

Figure 17-1 Crystalline lens Figure 17-2Optical section Figure 17-3Optical section of Figure17-4 Slit lamp
Crystalline lens crystalline lens appearance of
crystalline lens

The Crystalline lens is a specialized tissue in the body Figure 17-5 Adult Crystalline lens
because dimensions

207
Anatomy of Lens Structure –
The substance of lens has two distinct divisions - Cortex and nucleus
 Cortex is the most peripheral part of the lens and are Youngest fibres.
 Nucleus is the central part of the lens

Layers of the crystalline lens

 Lens Capsule,
 Lens Epithelium
 Lens fibers
 Nucleus
 zonule of Zinn.

Nucleus of Crystalline Lens

208
zones are laid down as development proceeds depending on the period of formation these zones named as
mentioned below.

st rd
Embryonic nucleus - lens fibers formed 1 to 3 month of gestation . These fibers are earliest lens
fibers
 Fetal nucleus – formed from 3 month to 8 month of gestation
rd th

 Infantile nucleus - formed from just before or immediately after birth till puberty
 Adult nucleus – formed after puberty, contains the youngest lens fibrers.

Crystalline Lens at advanced Age

The function of the crystalline lens

Figure 17-6 Refraction of the eye Figure 17-7 Lens changes in accommodation

---------------------------------------------

209
17.2 Clinical Points to be noted in the examination of the crystalline lens

Clinical examination of the Crystalline lens and confirmation of the cataract opacities requires the following
methods

 Diffuse illumination with torch light with Binocular Loupe

 Slit Lamp –Oblique illumination and retro illumination
 Direct Ophthalmoscope – For Distant Direct Ophthalmoscopy and Fundus Oculi
 Plain mirror examination – Commonly used plain mirror is Retinoscopy mirror

Clinical Points to be noted in the examination of the crystalline lens

 Whether crystalline lens Present or absent
• Size
• Shape
• Position
• Opacities
• Colors of the cataract Figure 17-8 Figure BBlack pupil
• Phacodonesis
Whether Crystalline lens present or absent

The Presence of normal crystalline lens is called Phakia. The clear

crystalline lens is identified in the optical section of a slit lamp and
appears as layers /zones i.e nucleus, cortex, and capsule.

The Absence of normal crystalline lens in its anatomical

position is called Aphakia Figure17-9.Posterior Figure 17-10
chamber IOL Anterior chamber IOL

The clinical findings of aphakia (Post surgical) are

 A linear scar at superior limbus between 10 to 1
`0`clock position
 Deep anterior chamber
 Tremulousness of the iris
 Color of the pupil is Black
 Hypermetropic fundus – Small optic disc
 Retinoscopy reflex with plane mirror at 1 meter
distance - The reflex moves with the movement of

210
the mirror
 Limbal scar is absent in the congenital, or Posterior dislocation of the crystalline lens
Causes of Aphakia

 Congenital
• Surgical removal of the lens by ICCE or ECCE technique.
• Post traumatic absorption of the lens
• Posterior Dislocated lens due to blunt trauma
Pseudophakia

Presence of artificial lens i.e. IOL in the eye is called Pseudophakia.It is implanted in the eye in ECCE cataract
surgery.

Clinical findings of Pseudophakia

 A scar at superior limbus between 10 to 1 `0` clock position or on the temporal limbus
 If the IOL is in the bag of the crystalline lens then the depth of the anterior chamber is deep
 Black pupil
 A Shining or shimmering reflex is present on flashing a light on the pupil.
 Retinoscopy reflex with plane mirror at 1 metre distance :
The Red reflex is the illuminated fundus oculi seen in the pupil. The movement of reflex depends on the
residual refractive error. If the reflex moves with the movement of the plane mirror the patient may be
emmetropic, hypermetropic or myopia of less than one diopter. If the reflex moves against the movement of
plane mirror then the patient is more than one diopter of myopia. If there is no movement of red reflex
then the patient is one diopter Myopic.

 S/L oblique illumination examination with dilated pupil : The optic and haptic of the IOL are seen while the
zones of crystalline lens are absent..
 Distant direct ophthalmoscopy : A red reflex seen at the pupil.
 Direct ophthalmoscopy : The details of fundus oculi are normal

Size / Dimensions of the lens

Clinically it is difficult to measure the normal dimensions of the lens unless it is brought out from the eye by
Enucleation, or ICCE procedures.

In the absence of accommodation the Normal diameter of the crystalline lens is 9 to 10 mm

211
The size / diameter of the crystalline lens

Increased in
In the process of accommodation (Physiological increase of anterio posterior diameter)
• Intumescent cataract
• Total nuclear sclerosis cataract
• Penetrating injury to the crystalline lens
Decreased in size in

• Spherophakia small and round lens , a congenital anomaly

Shape of the crystalline lens

• The shape of normal crystalline lens in vivo is Biconvex and in vitro is Spherical (Nonsymmetric ablate
spheroid)
In accommodation, contraction of the ciliary body causes relaxation of the zonules of the crystalline lens there by
increasing the antero posterior diameter and making the crystalline lens more spherical.

Abnormal shapes of the crystalline lens are

• Anterior lenticonus – Pathological increase of anterior curvature of the lens in Alport’s syndrome
• Posterior lenticonus – Pathological increase of posterior curvature of the lens, seen in Lowe syndrome
• Buphthalmos, Hypoglycaemia - Curvatures are decreased.
• Coloboma in the lens – Congenital anomaly

Figure 17-11 Figure 17-12 Figure 17-13

Subluxation crystalline lens Subluxated crystalline lens Anterior dislocation of the lens

Position of the crystalline lens

Normally the crystalline lens is placed in the patellar fossa of the anterior vitreous behind the pupil
Abnormal Position of the Lens

212
 Subluxation –Partial displacement of the lens from its anatomical position is called Subluxation and the lens
equator is seen in the pupil .

Table 1

Sub luxated lens - Clinical finding Dislocated lens -Clinical finding

Irregular depth of anterior chamber Anterior chamber is deep,

The color of aphakic area of the pupil is black, The Color of the pupil is black due to clear vitreous.
color of the phakic pupil depends on the color of the
crystalline lens

Tremulousness of the iris is absent. Tremulousness of the iris is present.

Fundus oculi - The aphakic portion is Hypermetropic Fundus oculi is Hypermetropic i.e. small optic disc ,
i.e. small optic disc, while the phakic area of the
optic disc is normal

Retinoscopy reflex with plane mirror at a distance of Retinoscopy reflex with plane mirror at a distance of
1 meter : The red reflex moves with the movement 1 meter the red reflex moves with movement of the
of the plane mirror in Aphakic portion. And in the plane mirror.
phakic portion the movement of the reflex depends
on the refractive state of that area.

 Dislocation –Total displacement of lens from its anatomical position is called dislocation .The lens is not
seen in the pupil .
Table 2

Subluxated lens - Cause Dislocated lens - Cause

Blunt trauma Blunt trauma

Marfan’s –Up and out Degeneration of the zonules as in Glaucoma

Homocystinuria –Down and in

High Myopia.

Color of the senile cataract (color of the pupil)

Color of the crystalline lens gives various Colors to the Pupil
Described in the colors of the pupil and also in the diagnosis of senile cataract

213
Opacities of the crystalline lens
Opacity of the Crystalline lens or its capsule whether congenital or acquired is called Cataract
The senile cataract may be cortical cataract or nuclear cataract .

• Cataracts are classified as congenital, Acquired

• The acquired cataracts are -Senile cataract, Complicated cataract ,Traumatic cataract ,Metabolic cataract
,Toxic cataract ,Radiation cataract , Electric Cataract, Atopic cataract -Cataracts associated with bone
diseases, Cataracts associated with syndromes.
The senile cataracts are cortical and nuclear which is a common cataracts and visually significant.

Clinical stages of senile cortical Cataract

Stages of cortical cataract senile cortical cataract
Stage -I Lamellar separation
Stage -II Incipient cataract –
Sub types - Cuneiform type, Cupuliform type
Stage -III Immature cataract
Complication- Intumescent type
Stage –IV Mature cataract
Stage – V Hypermature cataract
Subtype -Sclerotic and Morgagnian

Grades of senile nuclear cataract Color of the nuclear cataract by grade wise

Grade- 1 whitish yellow

Grade– 2 yellowish white color

Grade- 3 Amber color

Grade –4 Light brown

Grade –5 Thick brown color is called Cataracta Brunescens

Grade- 6 Black color is called Cataracta Nigra

Confirmation of the diagnosis of Cataract opacities are done by examination with the following clinical methods

 Slit lamp oblique illumination and Retro illumination techniques,

214
 Distant direct ophthalmoscopy,
 Direct ophthalmoscopy fundus oculi examination and
 Plane mirror examination at 1 meter distance
Slit lamp examination

• Slit lamp Examination (S/L) - Two techniques of (S/L) i.e oblique illumination and retro illumination
technique are required for diagnosis of cataract
• Slit lamp Examination , oblique illumination technique: This technique is to make the optical section of
the crystalline lens. This technique shows position of the lens opacity in the layers of crystalline lens
and also can Stage the cortical cataract and Grade the nuclear cataract .
• Slit lamp Examination In retro illumination technique : In this technique a fine beam of slit lamp light is
placed behind the lens opacities and the color and shape and position of cataract is studied in retro
illuminated light. Early cortical opacities are seen as black . In early to moderate nuclear cataract no
opacity is seen,
 Distant Direct ophthalmoscopy
What is distant direct ophthalmoscopy - Ophthalmoscopy is performed with Direct ophthalmoscope at a
distance of 22 cms At a distance of 22 cms , focus the crystalline lens with the bright light of Direct
ophthalmoscope and observe the opacities of the crystalline lens in red fundus glow. In incipient cataract, and
early nuclear cataract the opacities are seen as black in the red fundus oculi . In total nuclear cataract ,mature
cataract, hyper mature cataract no red reflex is seen .The red reflex is the illuminated fundus oculi by the light of
the direct ophthalmoscope seen at the pupil.

 Direct ophthalmoscopy fundus oculi examination

On Direct Ophthalmoscopy, visibility of the fundus oculi structures will contribute to the diagnosis of the cataract
. In stage I,II, III cortical cataract and grade I,II ,III Nuclear cataract the details of fundus oculi is seen clearly , In
immature cortical cataract and grade IV,V nuclear sclerosis , the details are hazily seen . In Mature cataract ,
Hyper mature cataract and grade VI of nuclear cataract no details of the fundus oculi.

 Plane Mirror examination (Commonly used plane mirror is the Retinoscopy plain mirror)
Plane Mirror examination is done at 1 metre distance . A light is taken on to the plane mirror from a light source
and then reflect the light on to the pupil of the person. Immature cortical cataract and early nuclear cataract
is seen as black opacities in red fundus background and in total cataract ,no red reflex or faint reflex is seen and
also observation of the movement of the retinoscopy reflex will give the type of refractive shift in cataract .The
refractive shift is myopic in nuclear cataract and Hypermetropic in cortical cataract and this type of refractive
errors are called index Myopia in nuclear cataract and index Hypermetropia in cortical cataract.

215
• In early cataracts it is difficult to confirm the cataract only with one method of clinical examination and
sometimes the diagnosis is missed.
• Eg. fine lenticular haze may be missed in S/L, but is best appreciated with Direct ophthalmoscopy and
plain mirror examination.
• Hence three clinical methods are necessary for confirmation of Diagnosis. particularly in early cataracts
Comparative Clinical signs of various types of cataracts are discussed in chapters 20,21,22,23,24,25,26.

 Degeneration of the Zonules of crystalline lens as in Hyper mature

cataract.
 Blunt trauma on the eye ,
 Absolute Glaucoma.
OSCE
 Students must be able to identify the various colors of the cataractous lens
 Understanding of findings of cataract with S/L, Distant direct ophthalmoscopy , Direct ophthalmoscopy and
Plane mirror.
Diagram to be practiced
 Diagram of the optical section of the Crystalline lens and label the layers / zones .

216
Chapter 18. Clinical case discussion of Cataract.
Clinical evaluation and diagnosis of Senile cataract –
(Interpretations of History and clinical examination of the eye in cataract )
Introduction
Definition of cataract - Opacity of crystalline lens or its capsulewhether congenital, or acquired is
calledcataract.
Senile Cataract - The most common . Two Types - Cortical Cataract and Nuclear Cataract
Most patients are beyond their 50 s. The incidence goes up with aging. It is the common cause of ophthalmic
disease leading to blindness in India.

Bio data of the patient :

• Name, Age , Sex , Occupation , ID

Age of the patient -

Cataracts develops at various ages. It may be congenital, Senile.
Senile acquired cataracts are Two Types – They are cortical cataract and Nuclear cataract .
Cortical cataract starts at the age of 50yrs and above. Nuclear cataract Starts at the age of 40 yr i.e starts
much earlier than the cortical cataract

Sex –No sex predilection for cataract.

Occupation
• Agriculture workers are prone for early cataract due to exposure to UV light
• Workers in Iron foundries or glass industries are prone for cataract due to exposure to Infra red rays
radiation - (Glass blowers cataract )
• Industrial workers are prone for blunt trauma or penetrating trauma causing traumatic cataract.

Symptoms of cataract
 Diminution of vision- Gradual progressive painless diminution of vision
•Glare: scattered light rays
•Frequent change of glasses due to change in the refractive index in the cataract lens
• Uniocular Diplopia and Uniocular polyopia – Uniocular Diplopia is due to difference in refractive index
between the nucleus and cortex and the opacities come in the way of visual axis. And polyopia is due to
difference in the refractive index of the lens fibers which causes irregular refraction and polyopia is
commonly seen in incipient cataracts.
 Coloured halos - Due to hydration of the lens fibers and due to difference in the refractive index of the lens
fibers which causes irregular refraction resulting in Colored halos The colored halos produced by the
immature cataract ,PNAG, and corneal disease , can be differentiated by Fincham test
Finchamtest :Colored halos are demonstrated by keeping a fine film of lycopodium powder enclosed between
two transparent glass plates and kept in a trial frame . And a stenopeic slit is placed in front of the colored halo

217
and rotate it 360 degrees. . The colored rings of immature cataract will break into segments, where as the
colored rings of the cornea will be seen as continuous rings.
•Changes of vision in day and night
 White opacity in the pupillary area
•Decreased contrast sensitivity
•Altered color perception - Altered color perception and Poor discrimination of blue spectrum – these band
wave lengths being absorbed by the nuclear cataracts .
•Poor discrimination of blue spectrum.

H/O present illness – elaborate the symptom in H/o present illness

 Blurring of vision - The common symptom of cataract is Gradual progressive painless diminution of vision.
The most common cause of gradual ,progressive, painless, diminution of vision is cataract.
This symptom of Gradual progressive painless diminution of vision may be associated with glare, Pain,
Redness, colored halos, Watering of the eyes etc.
• Pain indicates cataract with secondary glaucoma
• Redness indicates Secondary Glaucoma or associated conjunctival inflammation
• Colored halos may be due to cataract or also due to PNAG
• Watering of the eye may be due to chronicDacryo cystitis.
• In early stages of cortical cataract , vision is good in day light or in bright light . It is because , in the day light
the pupil is constricted and peripheral cortical opacities are covered by the iris and the opacities will not
obstruct the light entry into the eye.
• In the early grades of nuclear cataract vision is good in night or in dim light . It is because , in the night the
pupils are semi dilated and the light enters into the eye from the peripheral clear cortical fibers of the lens
even though nuclear cataract opacity is in the center of crystalline lens .
Past History
 Diabetes- to be controlled before surgery otherwise causes postoperative panophthalmitis, delayed
wound healing , papilloedema , CRVO . .Cortical Cataracts gets early maturation in those with Type –
II Diabetes. Any treatment taken for retinopathy should be noted for visual prognosis
 Hypertension - to be controlled before surgery otherwise it may cause peroperative expulsive
haemorrhage.
 Retention of Urine ,Chronic Constipation – strain to the eye on valsalva. is transmitted to the eye may
cause p.o complications like iris prolapse. May cause Post operative iris prolapse due to strain
 Cardiac disease and COPD – post operative use of B- Blockers may precipitate asthmatic attacks in
asthma patients and sino atrial conduction defects may get precipitated in cardiac patients
 Any Septic foci – Chronic Dacryocystitis, Chronic meibomianinitis, any other local and systemic foci to
be treated before surgery otherwise causes postoperative panophthalmitis.
 .Drugs use like clopidogrel , Aspirin – to be stopped before surgery to reduce peroperative bleeding
 H/o corticosteroids use to rule out toxic cataract .

218
 Use of High powered glasses-- to know the refractive state of the eye and may be associated with
ocular degenerations as in myopia, or amblyopia in hyperopia. , and to plan to prevent operative
complications.
 Chronic systemic infections like HIV, Hansen’s diseases, Koch’s – to be controlled before surgery as
these cause delayed hypersensitive uveitis.
 Thyroid – Associated with dry eye and post operative cataract surgery may precipitate dry eye.
 Joint pains /associated juvenile Rheumatoid arthritis / Arthralgia – may cause post operative uveal
inflammation
Family history – Any member of the family suffered with cataract such as zonular cataract , a congenital
cataracts are transmitted to next generations.

Personal History –
• Smoking, Alcohol are the risk factors for cataract and also causes chronic optic neuropathy.

General examination :
• General physical examination from hair to toe to find any lesions, for ocular posture, abnormal head posture
vitamin deficiencies etc

Vital data to be recorded.

• Pulse rate – most important as bradycardia reveal heart block
• B.P ,
• Temperature,
• Respiratory rate .

Visual Acuity Examination

 In cupuliform cataract/posterior sub capsular cataract and nuclear cataract the visual acuity is
disproportionate to the size of opacity of the lens.
• Range of Visual Acuity in immature cataract is 6/9 to 6/60 to CF 3meters
• Range of Visual Acuity in Mature cataract is CF 3 meters to Pl+ PR +
• Range of Visual Acuity in Hyper Mature cataract and Morgagnian cataract is Pl+ PR only

Examination of the lids - For infections - to be treated before surgery

▪ Chronic Blepharitis.
▪ Chronic Meibomitis
▪ Hordeolum Externum
▪Hordeolum internum
▪ Chalazion

219
Examination of the Lacrimal sac -
• Exclude chronic Dacryocystitis, by regurgitation test or Syringing .
• In cases of Cataract with chronic Dacryocystitis, first treat chronic Dacryocystitis as it is a source of focal
infection and during the cataract surgery the infection enters into the cavities of the eye ball leading to
endophthalmitis or Panophthalmitis.

Eye ball examination –

• Hirschberg’s corneal reflection test Cover test , cover and uncover test and ocular movementsare done to
know the Phorias or tropias which may cause reduced vision due to amblyopia and poor visual outcome
after surgery

Examination of the Conjunctiva –

• For any type of conjunctivitis .
• And senile cataract some times associated with pterygium , conjunctival congestion for conjunctivitis .
Circum ciliary congestion for phacomorphic glaucoma and phacolytic glaucoma , . The pterygium can be
operated along with cataract surgery . The visual out come is reduced in post cataract with pterygium surgery
as there is existing astigmatic errors and corneal opacities due to pterygium.

Examination of the Cornea -. S/L examination for corneal infections. Opacities like nebula , macula, leucoma ,
transparency, K.Ps for previous iridocyclitis, endothelial cell count- minimum 2500 per square mm to be
present.

Examination of Anterior chamber-

Assessment of Depth of A.C with Pen Torch light -Flash a light on the temporal side of the eye and observe the
illumination of the nasal iris and limbus. If the nasal iris and limbus is illuminated the chamber is normal or
deep if not shallow.
• Shallow anterior chamber – Indicates Intumescent cataract , phacomorphic glaucoma
• Normal A.C depth – Mature cataract
• Deep A.C. – Hyper mature cataract , with Morgagnian cataract
• Any signs of intraocular inflammation by aqueous flare, liquefied lens matter or A.C IOL (Pseudophakia)

Examination of the iris –

• Pattern of the iris – iris atrophy indicates blunt trauma, glaucoma . previous uveitis
• Synechiae indicates for signs of previous iritis or iridocyclitis , suggestive of complicated cataract.

Examination of Pupil and pupil Reaction –

• Brisk pupil reaction indicates the anatomical structures of afferent and efferent pathway to the pupil are
working normally.

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• Pupil reaction assess the post operative prognosis of the cataract surgery . Preoperative brisk reaction
indicates good prognosis because retina and optic nerve are good in function . Sluggish pupil reaction
indicates RAPD and suggest guarded prognosis as the retina and optic nerve are diseased.

Color of the Pupil

• The color of the pupil is due to the color of the crystalline lens and vitreous
• The normal color of the pupil is black and this color will change in the cataract

Colors of the pupil in cataract -- Type of colors in various stages of cataract

 Greyish White - Immature cataract
 Pearly White - Mature Cataract
 Hyper mature cataract sclerotic - yellow
 Milky White with brown colored nucleus in the lens - Morgagniancataract .
 Whitish yellow – Grade I nuclear cataract
 Yellowish white - Grade II nuclear cataract
 Amber color - Grade III nuclear cataract
 Thin Brown color - Grade IV Cataracta Brunescent
 Thick Brown - Grade V Cataracta Brunescent
 Black color - Grade VICataractaNigra

The grading of the lens opacities is done by LOCS III system , developed by Chylack et al based on comparing
cataract opacities of the patient with a set of standard cataract opalescence and colored photographs.

Clinical Examination of opacities in the crystalline lens and Confirmation of diagnosis of cataract opacities
Clinical examination of crystalline lens and Cataracts requires three important methods of examination which
confirms the diagnosis of cataract .
•Examination with a Slit lamp - with oblique illumination and Retro illumination techniques
• Distant direct ophthalmoscopy
•Direct ophthalmoscopy
• Plane mirror examination at 1 meter distance confirms the diagnosis of cataract,

Slit lamp Examination –

In oblique illumination technique - Keep the slit lamp light source and oculars at 40 to 60 degrees .
• In oblique illumination technique the optical section of the crystalline lens is made and located/identified
in which zone of the lens the opacity is situated and also the stage of the cortical cataract and grade of the
nuclear cataract is noted.
• In retro illumination – keep the light source of the slit lamp behind the lesion (opacity) and keep the light
source and oculars at 2 degrees angulations and observe the shape and color of the crystalline lens .

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•In retro illumination technique the immature cortical cataract is seen as black opacities in red fundus
background
•In retro illumination technique in early nuclear cataract , no opacity is seen , but only red fundus glow seen.

Direct Ophthalmoscopy procedures

• Distant Direct Ophthalmoscopy
• Direct Ophthalmoscope fundus oculi examination
Distant Direct Ophthalmoscopy - is done at 22 cms distance and crystalline lens is focused with direct
ophthalmoscope . In incipient , immature cataract and in early nuclear cataract the opacities are seen as
black opacities in red fundus background.
Direct Ophthalmoscopy fundus oculi - Direct ophthalmoscopy fundus oculi examination , the visibility of
fundus structures will contribute to the diagnosis of the cataract. In immature cortical cataract and grade I,II,III
the details of the fundus is seen hazily and in mature and hyper mature and grade IV,V nuclear cataract, no
fundus view because the opacity will mask the view of the fundus.

Plane Mirror examination for cataract opacities is done at 1 meter distance

Reflect the light from plane mirror on to the dilated pupil and observe the opacities
•In Incipient, immature cortical cataract opacity and early nuclear cataract , the opacities are seen as black
opacities in red fundus background and in total cataract ,no red reflex or faint reflex is seen.
• Observation of the movement of the retinoscopy reflex with plane mirror will give the type of cataract and
refractive state of cataract .
• The refractive shift In nuclear cataract is myopic side and this type of refractive errors is called index Myopia
• The refractive shift in cortical cataract is Hypermetropic side and this type of refractiveerrors is called index
Hypermetropia

In early stages of cataracts

 In early stages of cataracts it is difficult to confirm the cataract only with one method of clinical
examination and sometimes the diagnosis is missed.
 Hence the combination of three clinical methods are necessary for confirmation of Diagnosis. particularly
in early cataracts

Examination of Iris shadow – Flash a light tangentially on the

temporal side of the pupil margin and observe the image/shadow
of the pupil margin in the immature cataractous lens. . Iris shadow is
seen in the clear lens fibers of immature cataractous lens The image
is formed on the temporal side of the lens .
• Iris shadow is present in immature cortical cataract or early nuclear cataract.
 Absence of iris shadow indicates Mature, Hyper mature ,Morgagnian cataract.

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Purkinje’s images
First Purkinje’s image is formed by anterior curvature of the cornea as it acts as a convex mirror, Second
Purkinje’s image is formed by posterior curvature of the cornea as it acts as a convex mirror , Third Purkinje’s
image is formed by anterior curvature of the crystalline lens as it acts as a convex mirror, Fourth Purkinje’s
image is formed by posterior curvature of the crystalline lens as it acts as a concave mirror.
and third and fourth are relevant for cataract examination

Convex mirrors produces vertical, virtual and erect Images. And the concave mirror produce real, small,
inverted image. Hence the Purkinje’s images 1,2,3 are vertical and 4 is inverted

Third and fourth Purkinje’s images are relevant for cataract examination and First and second Purkinje’s
images are not relevant for cataract examination.

Even though these images are theoretically explained, but difficult to see except Purkinje’s image 1. The
corneal light reflex is Purkinje’s images 1
.
Visual field Examination by confrontation test
Peripheral visual Field -Peripheral visual Field is masked in Immature cataract due to peripheral cataract
opacity , how ever sensitivity of the retina is normal .
In Mature, Hyper mature and Morgagnion cataract – Peripheral and central visual field are totally masked
however sensitivity of the retina is normal .

In nuclear cataract – as the opacity is in the center and periphery is clear peripheral fields are normal In
grade I,II, III nuclear cataract , and IV,V grades the Peripheral visual and central visual Field are totally masked
, however sensitivity of the retina is normal.

Digital Tonometry – Bed side Tonometry , (Tactile Tonometry)

• Gross IOP changes in the eye ball can be tested with digital Tonometry .
• Ideal pressure for intra ocular surgeries is 12mm of Hg.• If the cataract surgery is done with high IOP then
Posterior Capsule rupture and expulsive hemorrhage are the Complications.
Systemic examination
A brief systemic examination for respiratory, cardiac , abdomen should be done to rule out any pathology and
appropriate referrals are done.

How to write a Diagnosis of cataract

Acquired / Senile/ Cortical /cataract with stage of cortical cataract . Eg : Acquired Senile Mature cataract.
• Acquired Senile Nuclear Cataract - Grade of the nuclear cataract .Eg : Acquired Senile nuclear cataract Grade
–II .

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Write salient findings for the diagnosis -After writing a Diagnosis it is ideal to write a brief note of relevant
salient clinical features (both positive and Negative) pertaining to the case which make such a diagnosis.

Confirmation of diagnosis of cataract opacities

 Slit lamp examination – oblique and retroillumination
 Direct ophthalmoscopy – Distant direct ophthalmoscopy and direct ophthalmoscopy fundus oculi
examination
 Plain mirror examination at 1 meter distance

Write relevant investigations

Local investigations
 Macular Function test
 Ascan Biometry to calculate IOL power.
 Regurgitation test or syringing test to rule out chronic dacryocystitis ,
 Tonometry for intraocular pressure .

Systemic investigations –
 Blood examination for RBS ,Fasting, postprandial blood sugar if necessary,
 HbsAg ,
 HIV.
 ECG for cardiac status.

Macular Function test

 Pupil reaction and Perception of light  Potential Acuity meter - Refer text book -
 Two pin point discrimination  Entoptic visualization - Refer text book -
 Maddox rod – High power cylindrical lenses arranged  Haidinger brushes - Refer text book - Refer

224
parallel to one another and if view the object through the
Maddox rod the object seen perpendicular to the position
of the lens.
 Vernier acuity – Refer text book  ERG ,EOG ,VEP -Refer text book
 Laser interferometry - Refer text book  Photo stress test - Refer text book

 Simplest macular function test which can be done clinically with a torch light is PL and PR, brisk Pupil
reaction (Except in cortical blindness) and Two point discrimination

A Scan Biometry
A scan Biometry – To calculate IOL power, Keratometer and ‘Ascan ’ (Amplitude scan) is required.
The refractive status of the eye depends on the corneal curvature i.e Dioptric power of the cornea and axial
length of the eye . These measurements varies from person to person.

Keratometer Keratometer Mires

Measurement of IOL Power.
Keratometry - first step is to do keratometry
keratometer measures the corneal curvature in two
meridians and curvature equivalent dioptric power
.For calculation of IOL power the soft ware of
biometry requires curvature equivalent dioptric
power of the cornea .
‘A’ scan - Second step is to measure the axial length of
the eye ball by ‘A’ scan
‘A’ stands for amplitude scan . 8MHz frequency sound
waves are sent to the eye and echoes that returns to the
transducer will be converted into amplitudes. It measures
the axial length of the eye ball .

The curvature equivalent dioptric power of the cornea and

the axial length of the eye ball is incorporated into theSRK
formula in soft ware , then IOL power will be displayed on
the screen of computer.

SRK formula - (Sanders, Retzlaff, Kraff ) for IOL power calculation= P = A – 2.5L X 0.9 K
 P = Power of the IOL
• A = Constant of the IOL . A Constant –Indicates Per operative Position of the IOL in cataract Surgery
• L = Axial Length of the eye ball
• K = Dioptric power of the Cornea.

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• .A Constant – 118 indicates Capsular Bag IOL
• 116 Indicates ciliary Sulcus IOL
• 114 Indicates A.C IOL
• 119 Scleral Fixation IOL

What is the capsular Bag of crystalline Lens

 Peripheral rim of crystalline lens, Equator of crystalline lens, and Posterior capsule is called bag of
crystalline lens
What is the ciliary Sulcus anatomy of the eye
 Anatomy of the cilary sulcus is posteriorly peripheral rim of the anterior surface of the anterior capsule,
 Laterally anterior surface of the ciliary body
 Superiorly posterior surface of the iris.
Systemic investigations – Blood examination for
 RBS ,Fasting, postprandial blood sugar if necessary,
 HbsAg ,
 HIV. And
 ECG for cardiac status.
Plan of treatment –Extra capsular cataract extraction ( ECCE ) by small incision or phacoemulsification
technique and posterior chamber intraocular lens implantation (PCIOL) under peribulbar anesthetic block.

Differential Diagnosis for cataract –

All the causes of gradual progressive painless diminution of vision are the differential Diagnosis of cataract.

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Chapter 19 . Salient clinical findings documentation for the diagnosis of Cataract
and for discussion.

What are the salient points to be noted for making a diagnosis of cataract
 Age
 Symptom
 Visual acuity
 Depth of anterior chamber
 Color of the pupil/ color of the crystalline lens
 Pupil reaction to light
 Description of the opacity of the crystalline lens
 Iris shadow
 Confrontation test
Confirmation of diagnosis of cataract opacities
 Slit lamp examination – oblique and retro illumination
 Direct ophthalmoscopy – Distant direct ophthalmoscopy and direct ophthalmoscopy fundus oculi
examination
 Plain mirror examination at 1 meter distance
Importantsystemic investigations
 Diabetes
 Hypertension
 HIV
 Hbs Ag
 ECG
Local investigation
 Regurgitation test
 Digital tonometry/applanation tonometry
 Ascan biometry for IOL power calculation
Surgery –
 ECCE with Posterior chamber IOL implantation under peribulbar block
Important complications
 Early Acute complications – endophthalmitis and Pan ophthalmitis
 Delayed complications – Cystoid macular edema
 Late complications – Posterior capsular opacification
------------

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Chapter 20. Diagnosis of acquired cataracts

Aetiological classification of acquired cataracts

• Age related Cataract or Senile Cataract
• Complicated cataract
• Traumatic cataract
• Metabolic cataract
• Toxic cataract
• Radiation cataract ,
• Electric Cataract
• Atopic cataract
• Cataracts associated with bone diseases
Craniofacial dysostosis
Osteogenesis imperfecta
Chondrodystrophia calcifican congentia
 Cataracts associated with syndromes.
Diagnosis of various types of acquired cataract.
(The diagnosis of senile cataract , Complicated cataract , Diabetic cataract and toxic cataract is written in this
topic ) For other types of cataracts please refer text books)
Age related Cataract or Senile Cataract
• The most common type .It is the common cause in ophthalmic diseases leading to blindness
Senile cataract - Two Types
• Cortical type
• Nuclear Cataract/Sclerotic cataract
Differences between Cortical cataract and Nuclear cataract
Table 1
Differences between Cortical cataract and Nuclear cataract
Cortical cataract Nuclear cataract
Starts at the age of 50yrs and above Starts at the age of 40 yrs i.e Starts much earlier than the cortical
cataract
In early stages Day vision is good In early stages Night vision is good
Color of the pupil is Greyish white, pearly, Milky Color of the pupil is Whitish yellow , yellowish white , Amber ,
white based on the stage Brown, Black (Cataracta Nigra, Brunescent ) white based on the
stage
Refractive shift is Index Hypermetropia Refractive shift is Index myopia
Stages of maturation are present No stages of maturation

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Stages and Grades of senile cataracts
Table 2 Stages of Cortical cataract and Grades of Senile Nuclear cataract
Stages of Senile Cortical cataract Grades of Senile Nuclear cataract

 Lamellar separation  Grade – 1 – Whitish yellow.

 Incipient cataract  Grade – 2 – Yellowish white.
 Immature cataract  Grade – 3 – Amber colour
 Mature cataract  Grade – 4 – Brown.
 Hyper mature cataract  Grade - 5– Black.
Morgagnian cataract
Sclerotic Type

Table 3 . 1.Diagnosis of Lamellar cataract

Diagnosis of Lamellar cataract
Slit lamp retro Confirmation of the diagnosis

 Age of the patient is 50 illumination showing  Diagnosis is made by slit lamp examination only

years and above Fluid vacuoles  In S/L examination by oblique illumination and

 Glare is an important retro illumination technique, the lamellae of

symptom crystalline lens are separated and fluid vacuoles

 Gradual progressive painless are seen in between the lens fibers .

diminution of vision may be  Distant Direct ophthalmoscopy there may be fine

present lenticular haze

 Visual acuity is 6/9 to 6/18.  Direct ophthalmoscopy the details of fundus oculi

 Depth of anterior chamber is normal is seen clearly

 Pupil reaction is normal  Plane Mirror examination at one meter distance

 Colour of the pupil otherwise the colour of the crystalline lens very fine lenticular haze may be seen.

is slightly grey due to scattering of light and reflection of light.

 Digital tonometry is normal.
 Confrontation test - Peripheral and central field is normal.

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Diagnosis of incipient cataract
Cuneiform cataract

Table 4
Diagnosis of Cuneiform cataract
 Age of the patient is 50 years and above
 Gradual progressive painless loss of vision
 Monocular diplopia or polyopia
 Day vision is good in bright light
 Visual acuity ranges from 6/9 to 6/18
 Depth of A.C normal
 Pupil reaction normal
 Colour of the pupil otherwise the colour of the crystalline
lens is slightly greyish white
 Peripheral visual field is slightly masked with normal
central visual field.
 Digital tonometry is normal
Conformation of the diagnosis --
 In S/L oblique illumination technique the cataract
opacities are seen at the periphery and equator of the
crystalline lens commonly at inferior nasal quadrant.
 In S/L examination by retro illumination technique black
wedge shaped cataract opacities with base of the wedge
towards the equator in red fundus glow are seen
 Distant direct ophthalmoscopy at 22 cms black wedge
shaped cataract opacities in red fundus glow are seen
 Direct ophthalmoscopy fundus Oculi – Details of the
fundus oculi are seen clearly.
 In Plane mirror examination at one meter distance black
Wedge shaped peripheral cataract opacities are seen in
red fundus background.

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Diagnosis of immature cataract
Table 5
Diagnosis of immature cataract Diagnosis of intumescent Cataract
 Age of the patient 50 years and above What is intumescentCataract
 Gradual progressive painless diminution of vision Some of the immature cataracts may imbibe aqueous due

 Visual acuity ranges from 6/9 to 6/60 or CF 3meters to loss of semi permeability of the anterior capsule and the

 Depth of the anterior chamber is normal lens swells due to progressive hydration and becomes

 Pupil reaction is normal intumescent cataract .

 Colour of the pupil otherwise the colour of the

crystalline lens is Greyish white How to diagnose intumescent cataract.

 Iris shadow present  All the findings of immature cataract except one clinical

 Visual field examination by confrontation method - finding i.e anterior chamber depth is shallow as the iris

Peripheral field is masked and central field is normal diaphragm is pushed forward by the swollen lens

 Digital tonometry is normal  visual acuity is HM to PL + and PR

Confirmation of the diagnosis The intumescent cataract may lead to Phacomorphic

 In S/L oblique illumination technique - cortical fibrers glaucoma at any time

are opaque
 In S/L Retro illumination technique - Black cataract
opacities in red fundus glow are seen
 Distant Direct ophthalmoscopy at a distance of 22 cms
- Black opacities in red fundus glow are seen
 The Fundus oculi details are seen hazily
 In Plain mirror examination at one metre distance -
Black opacities are seen in red fundus glow

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Table 6 Diagnosis of Phacomorphic Glaucoma
What is Phacomorphic Glaucoma
 In the stage of immature cataract some times the lens suddenly swells and the iris diaphragm is
pushed forwards causing mechanical block of the angle of the anterior chamber , thereby raised IOP.
 All Clinical signs and symptoms of intumescent cataract
 Sudden history of severe pain in the eye ,
 CCC,
 Corneal edema
 Raised IOP

Diagnosis of Mature cataract

Table 7. Diagnosis of Mature cataract
 Total or near total cataract Confirmationof the diagnosis
 Age of the patient is fifty years and above  In S/L oblique illumination technique - Total or nearly
 Gradual progressive painless diminution of vision total opacities of crystalline lens is seen

 Visual acuity counting Fingers 3 meters to PL+ and PR  In S/L Retroillumination no red reflex
 Depth of the anterior chamber is Normal  Distant Direct ophthalmoscopy - No red reflex
 Pupil is briskly reacting  Direct ophthalmoscopy fundus oculi - Details of the
 Colour of the pupil otherwise the colour of the fundus oculi are absent

crystalline lens is Pearly white  In Plane mirror examination at a distance of one meter -
 Iris shadow is absent A faint red reflex or no red reflex is seen at pupillary

 Peripheral and central Visual field nearly or totally area.

masked

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Diagnosis of Hyper mature cataract (HMSC) - Two types
Hyper matureSclerotic cataract and Hyper mature -Morgagnian cataract
Table 8
Hyper mature cataract and Hypermature sclerotic cataract HypermatureMorgagniancat
aract

Diagnosis of Hyper mature cataract Diagnosis of Hyper matureSclerotic Diagnosis of Hyper mature -
 Age of the patient is fifty years and above cataract(shrunken Cataract) Morgagnian cataract
 Gradual progressive painless Diminution of The cortex is disintegrated and  All the signs of
vision transformed into a pultaceous mass . Hypermature cataract
 Visual acuity is PL+ and PR only The cortex is inspissated and shrunken  Additional clinical signs are
 Anterior Chamber depth is deep and decrease in the anterio posterior - the colour of the pupil is
 Pupil is briskly reacting diameter of the crystalline lens milky white.

 Colour of the pupil or otherwise the colour of  All the signs of Hypermature cataract  The cortex is liquefied
 The color of the pupil sometimes yellow
the crystalline lens is milky white with slight  Nucleus is seen in liquefied
yellowish tinge in colour
cortex limited above by the
 Iris shadow is absent .  The anterior capsule is thickened , edge of the nucleus seen as
 Digital tonometry is normal wrinkled
as a semicircular line, alters
 The central and peripheral field is totally  There are deposits of calcium and its position with the
masked cholesterol on the anterior position of the head.
 Purkinje’s images I,2,3 are present and 4 is capsule

absent  The liquefied cortex is absorbed and

 In Plane mirror
Confirmation of the diagnosis only brown nucleus is seen
examination at distance of
 S/L oblique illumination technique - Total  Due to shrinkage of lens there may
one meter - No red reflex
opacities of crystalline lens. be iridodonesis and phacodonesis
is seen in the pupillary
 Distant Direct ophthalmoscopy - No red due to weakness of zonules of
area
reflex is seen at the pupillary area crystalline lens , there is subluxation
 Direct ophthalmoscopy fundus oculi - of the lens – most common
Details of fundus oculi are not seen complication of (HMSC)

Diagnosis of Phacolytic Glaucoma -- What is Phacolytic Glaucoma

In Hyper mature , Morgagnian , sclerotic cataract the liquefied lens matter leaks through the anterior capsule of the lens into the
anterior chamber causing iridocyclitis and also trabeculitis and the inflammatory material blocks the trabecular meshwork
increasing the IOP. All Clinical signs and symptoms of Hyper mature Morgagnian and sclerotic cataract with Sudden history of
severe Pain in the eye , CCC, Corneal edema , Raised IOP.

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Table 9
Absolute Glaucoma
In the untreated phacomorphic or phacolytic glaucoma the eye goes into a stage of absolute Glaucoma. A painful
blind eyewith no Pl and PR. ,Increased IOP, Corneal edema, dilated fixed Pupil , suggestive of TAPD (Optic atrophy)

Diagnosis of Cupuliform cataract.

Table 10 Diagnosis of Cupuliform cataract.
Diagnosis of Cupuliform cataract. / Posterior sub capsular cataract –
Dysplasia of cataract fibers at the equator , migrates towards the posterior capsule,
enlargement of dysplasia cells called bladder cells or wedl cells
Opacities are seen in the posterior cortex and in front of the posterior capsule
Opacities are plaque like , granular
Seen at the nodal point , gradually progresses towards the equator of crystalline lens
Grey in appearance
 Age of the patient is 50 years or much less i.e as against the age of cortical cataract
 Gradual progressive painless diminution of vision
 Diminution of vision more for near than distance
 Vision improves in dim illumination and poor in day light /bright light as in the case of
nuclear sclerosis
 Visual acuity affected early as it is in the pathway of visual axis at nodal point
 The reduced visual acuity is disproportionate to the size and position of the opacity.
 Visual acuity ranges from 6/60 to CF 3 meter.
 Slowly undergoes maturation
 Depth of A.C is normal
 Pupil is briskly reacting
 The colour of the pupil otherwise the colour of the crystalline lens is greyish white
 Central visual field is more masked than the peripheral field
 Digital tonometry is normal
Confirmation of the diagnosis
 In S/L examination in oblique illumination technique Posterior cortical opacities or
posterior subcapsular cataract opacities are seen
 In S/L retroillumination technique – Black Posterior sub capsular cataract opacities in
red fundus glow are seen
 In Distant Direct ophthalmoscopy black central lenticular opacity in red fundus glow is
seen
 In Direct ophthalmoscopy details of the fundus oculi is seen clearly
 In Plane mirror examination at one meter distance a central lenticular opacity is seen..

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Diagnosis of Senile Nuclear cataract or Sclerotic cataract
Table 11 Diagnosis of Senile Nuclear cataractor Sclerotic cataract

 Starts at the of age of 40 years i.e. earlier than cortical Confirmation of Senile Nuclear cataract.
cataract  In S/L – Examination with oblique illumination
 Gradual progressive painless diminution of vision more technique – colour of the lens is whitish yellow in grade -I,
for distance than near and near vision improves which yellowish white in grade II , amber color in grade –III ,
causes the removal of presbyopic lenses (Second sight) brown in grade IV , black in grade – V .
 Diminution of vision is more in daylight as pupil constricts  Cortex is clear in the early stage and total nuclear
and the light is not allowed to enter the eye opacities are seen in the late stage.
 In early stages the vision is good in the dim illumination  In S/L– Examination with retroillumination technique in
/at night , when the pupil is dilated in the dim early stages the opacified nucleus is not seen and only a red
illumination the light enters into the eye away from the reflex is seen but in late stages the opacity is seen as black
central nuclear sclerosis opacities in red reflex
 Early disability of vision as the nuclear sclerosis opacity is  Distant direct ophthalmoscopy– in the early cases central
present in the centre of crystalline lens and the opacities dark nucleus is seen against red background, however in
are in the line of visual axis and Visual acuity is 6/18 to PL advanced cases there is no red reflex.
+ and PR depending on the grade of the opacity.  Direct ophthalmoscopy fundus oculi – Details of fundus oculi
 Change in the refractive index of the nucleus causes is seen hazily in grade I,II,III,IV and not seen in grade V
index myopia and IV.
 Anterior chamber depth is normal  Plane mirror examination at one metre distance same as
 Pupil reaction is normal Distant direct ophthalmoscopy
 Colour of the Pupil or otherwise the colour of the nucleus
depends on the grade of the nuclear cataract , i.e whitish
yellow in grade -I, yellowish white in grade II , amber color
in grade –III , brown in grade IV , black . in grade – V .
 The colors of the nucleus are due to Pigmentary
deposits of oxidative biproduct of tryptophan, protamine ,
cysteine ,and urochrome, lipofuscin, melanin produced
from aminoacidsaltered by the sunlight
 Iris shadow is present in early stages and is absent in the
late stages of nuclear cataract
 .Digital tonometry is normal.
 In the early grades of nuclear sclerosis , Central Visual
fields is masked than the peripheral field , however in the
late grades both central and peripheral field is masked .

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Diagnosis of Aphakia

Table 12 Diagnosis of Aphakia

A Aphakia : Absence of crystalline lens in its  Fundus oculi examination shows the finding of
anatomical position is called Aphakia. Hypermetropic fundus i.e small optic disc,
Diagnosis of Aphakia
 Plane mirror examination – The pupil (shadow)
 H/O Gradual progressive painless loss of
vision for which History of cataract surgery is reflex moves with the movement of the plane

present mirror., Astigmatism is present

Refractive correction of aphakia
 Unaided VA is 1/60 in uncomplicated
Spectacle -(An emmetropic eye which is made
aphakia.
aphakia commonly will have a spectacle power of
 Near vision is absent due to loss of
+9D or +10 D .
accommodation
 Contact lens
 Limbal scar- usually at superior limbus at 11
 Secondary IOLs implantation- either by A.C IOL,
to 1 clock position or some times at temporal
Iris fixed IOL, or scleral fixated IOL:
limbus.
 Refractive surgeries: keratophakia,
 Deep anterior chamber
keratomileusis, epikeratophakia
 Unaided Visual
acuity 1 metre
 Iridodonesis
 Jet Black pupil

Confirmation
In S/ L oblique illumination technique of
examination shows the absence of crystalline
lens i.e no zones of crystalline lens.

Table 13 Disadvantage of Aphakic glasses

Requires spectacle correction with Aphakic Jumping of the image at the bifocal junction.
glasses.
Aphakic glasses are thick and heavy glasses. Peripheral Distortions of the object
Near vision correction is required Reduced peripheral visual field
Image is magnified 20 times. Thus Eyes Roving ring scotoma (“Jack-in –the –box phenomenon )
appear very big – Bulls eye appearance due i.e One object appear in one gaze . If the gaze is changed
magnification by the lens . Cosmetically object disappears and another object comes into view.
not acceptable
Erythropsia – Objects appear red Vitreous touch syndrome i.eIntractable Corneal oedema,
Secondary glaucoma.
Blue vision – seen in aphakia as blue vision Retinal detachment
is filtered by yellowish cataract lens

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Diagnosis of Pseudophakia

Table 14 Diagnosis of Pseudophakia

What is Pseudophakia Comparison of Crystalline lens and IOL in S/L oblique
Presence of artificial intraocular lens in the pupillary area illumination technique.
of the eye is called Pseudophakia.
In S/L oblique illumination technique in a dilated pupil,
IOL is implanted to correct Aphakia.
 Normally the Optical section shows various zones of
Diagnosis of Pseudophakia the crystalline lens but in pseudophakic eye the
various zones of the crystalline lens are absent and
 Gradual progressive painless diminution of vision for
Optics and Haptics of IOL are only seen..
which there is History of cataract surgery and IOL
Confirmation
implantation is present.
 Limbal scar at superior limbus or Temporal limbus  In S/L – Optics and Haptics are seenin a dilated pupil
 Uncomplicated IOL surgery will have a normal visual  Direct ophthalmoscopy - Fundus details are seen
acuity .  In Plane mirror retinoscopy - ,red reflex is seen in the
 Postoperative Visual acuity may be Emmetropia or pupil and the movement of reflex depends on the post
residual ametropia operative refractive status of the eye
 Depth of the anterior chamber depends on intra  Central and peripheral field is normal
operative position of IOL .If the IOL is sulcus fixated Anterior chamber IOL
the chamber is shallow .If the IOL is fixed in capsular
Bag the chamber is deep
 Shining or shimmering reflex in the pupil on the IOL
 Colour of the pupil is Black

Anterior chamber IOL

Posterior chamber IOL

Names given to various types of cataract

Table 15
Sun flower cataract- copper metabolism derangement Oil drop cataract – Galactosemia
Snow flake cataract – Type I diabetes Honey comb appearance – After cataract
Rosette cataract – Blunt Trauma on crystalline lens
Delayed Rosette cataract – Micro perforation on crystalline lens capsule

238
Secondary cataract/After cataract or Posterior capsular opacification (PCO)

Table 16
Secondary cataract or Posterior capsular opacification (PCO)
 Opacity of the posterior capsule Types of PCO How to treat PCO
after extra capsular cataract  Membranous Cataract If the PCO is amicable to the Nd.YAG
extraction  Elschnig’s pearls Laser it is opened with Nd.YAG lasers
 It is the most common sequel /  Soemmering rings
(1054 nanometers)
complication of IOL cataract surgery Slit lamp oblique illumination examination
What is the action of Nd.YAG laser – The
.Up to 30%-50% of all adult patients  The membranous PCO appearance as
light is converted into photo disruptive
develop a PCO after IOL cataract Honey comb
mechanical energy.
surgery  Elschnig’s pearls PCO – The injured
 It is a significant problem in almost If the PCO is thick and not amicable to
anterior capsular epithelium balloons
all pediatric patients unless the and forms as PCO which is called the Nd.YAG Laser then a second surgical
posterior capsule and anterior Elschnig’s pearls. procedure is done called
vitreous are removed at the time of  Soemmering rings type of PCO - The membranectomy. With a vitrectomy
surgery. injured anterior capsular epithelium probe, enter into vitreous cavity through
Clinical findings of Secondary Cataract: lays new distorted lens fibers which a parsplana area and the central PCO is
 H/o Gradual progressive loss of get opacified .
cut .
vision after IOL surgery.

1Membranous type Soemmering rings Elschnig’sPearals

Other etiological cataract –

• Complicated cataract,
• Diabetic cataract ,
• Traumatic cataract,
• Toxic cataract (See below )
• The diagnosis of Radiation cataract , Electric Cataract,Atopic cataract , Cataracts associated with bone
diseasesi.eCraniofacial dysostosis, Osteogenesis imperfecta, Chondrodystrophia ,
calcificanscongentia,
Cataracts associated with syndromes , please refer the text book .

239
Cataracts other than senile cataracts

Complicated cataract

Table 17 Complicated cataract

Definition --Cataract due to Clinical findings of complicated Distant direct ophthalmoscopy –

diseases of the eye. cataract
 in the early stages Black opacities seen in
Ocular causes for complicated  Disease of the eye must be the red back ground and in the late
cataract present eg. stages nearly total opacities and no red
 Iridocyclitis/uveitis reflex at the pupil.
 Degenerative myopia  Retinitis pigmentosa  In early stages Fundus oculi details are
 Corneal ulcer  Chronic retinal detachment visible but in near total or total opacities
 Acute. Congestive glaucoma - Slit lamp findings. no fundus details
Glaukoma flecken Plain mirror exam – same as direct
 Presentation of cataract when  Anterior and Posterior Sub ophthalmoscopy
the age of the patient is capsular opacities depending
between 20 to 40years on the severity of inflammation
 Bread crumb appearance
 Poly chromatic appearance.

Diabetic cataract

Table 18

Type 1 cataract Type 2 cataract

Type -I Diabetes causes Snow flake cataract Type 2 Diabetes Cataract start early,

 Type I diabetes cataract otherwise called Real diabetic  Fast progression and maturation occurs
cataract . in senile cortical cataract
 Teenagers are affected,
 Bilateral,
 Rapidly progressive leading to total cataract,
 Combined with refractive changes according to blood
sugar

240
Traumatic cataract

Table 19

Traumatic cataract -- Blunt injury Traumatic cataract - Penetrating injury

 Blunt trauma causes Rosette Causes for cataract –

cataract
 Due to rupture of the capsule , aqueous enter into the lens and
causes cataract.
 Even if the perforation is small and very fine some times it
cause a delayed Rosette cataract

Toxic cataract

Table 20

Toxic cataract – Drug Induced Cataract Clinical description of Corticosteroid induced

cataract

 Corticosteroids  Posterior Sub capsular cataract in

 Miotics Prolonged use of corticosteroids such as
 Chlorpromazine Prednisolone as in Bronchial Asthmaand
 Busulphan(myleran) Kidney Transplant, collagen diseases Etc

 Amiodarone
 Trinitrotoluene cataract
 Metal - Gold

------------------------------------------------------------

241

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