Preface

Agam is a group of budding medicos, who are currently doing their under graduation in
various Medical Colleges across Tamil Nadu and Pondicherry. The group was initiated on 18th
November 2017, in the vision of uniting medicos for various social and professional causes.

We feel delighted to present you Agam Ophthalmology notes prepared by Agam Divide and
Rule 2020 Team to guide our fellow medicos to prepare for university examinations.

This is a reference work of 2017 batch medical students from various colleges. The team
took effort to refer many books and make them into simple notes. We are not the authors of the
following work. The images used in the documents are not copyrighted by us and is obtained from
various sources.

Dear readers, we request you to use this material as a reference note, or revision note, or
recall notes. Please do not learn the topics for the 1st time from this material, as this contain just the
required points, for revision.
Acknowledgement

On behalf of the team, Agam would like to thank all the doctors who taught us Ophthalmology.
Agam would like to whole heartedly appreciate and thank everyone who contributed towards the
making of this material. A special thanks to Barath Raj R, who took the responsibility of leading the
team. The following are the name list of the team who worked together, to bring out the material in
good form.

 Anchitha
 Kareeshmaa H C  Gowsigan
 M.Jayashree  Abidivya
 Mruddula V  Nahveena
 Praveena  Saahini
 Indhumathi  Arun vidhyasagar
 Yogesh  Shobana
 Kavya kala  Manasa
 Ramya  Anupama Bhaskaran
 Aparna  D.Vijay
 Adithya  S.Aakash
 Yogesh  K.Karthik Raja
 Syed  Sneha
 Ragha Dharshini  Kamakshi
 Bhavik Shah  Maya sundar
 Pranesh  Arun
 Shane  Bhavik shah
 Juwain  Annapoorna
 Menaka
 Aravind Krishna
 Sudharshan
 Aparna
 Mrudhulagi
 Heera
 Anusha
 Shrilekha
 Harini
 Vignesh
 Sneha jenifer
 Ramprasad
 Shanmathi
 Puvashree
 Volume 2

 Diseases of Vitreous
 Diseases of Retina
 Neuro Ophthalmology
 Ocular motility and Strabismus
 Diseases of Eyelids
 Diseases of Lacrimal Apparatus
 Diseases of Orbit
 Ocular Injury
 VITREOUS

What You Will Learn Here?

• Anatomy of Vitreous
• Vitreous Haemorrhage
• Vitreous Detachment
• Vitreous Opacities
• Vitreous Surgeries

Anatomy of the Vitreous

Vitreous humour:

➢ Inert, transparent, jelly like structure that fills the posterior four fifth(80%) of the cavity of eye ball
➢ 4ml in volume and 4g in weight
➢ It is a fluid-like substance composed of more than 99% water.
➢ The remaining part is formed of collagen and hyaluronic acid (rigidity and viscosity).
➢ Bounded :
• anteriorly: by the lens, iris and ciliary body
• Posteriorly: by the retina and optic disc.
Vitreous body:
➢ Somewhat spherical posteriorly
➢ Cup shaped depression (patellar fossa) anteriorly
➢ The outer portion of the vitreous body is called the cortex (denser), and its surface is called the hyaloid
membrane.
➢ Cloquet’s canal runs antero-posteriorly in the center of the vitreous (site of the embryonic hyaloid artery)
➢ The strongest attachment of the vitreous is to the retina and pars plana in the area of the vitreous base.

Functions of the vitreous:

❖ Stabilizes the volume of the globe.
❖ Being a hydrophilic gel, serves optical functions
❖ Pathway for nutrients to reach the lens and retina
❖ Acts as a cushion for the retina.
 ❖ One of the optical media of the eye.

Embryology:
➢ Vitreous body (secondary vitreous) is secreted by neuroectoderm of optic cup
➢ Secondary vitreous is mesenchymal in origin
➢ Tertiary vitreous is developed from neuroectoderm in the ciliary region

Liquefaction (synchysis).

➢ Most common degenerative change in vitreous

➢ This results in the formation of fluid lacunae inside the vitreous gel.
➢ These may rupture through the cortical vitreous and cause separation of the cortical vitreous from the
inner retinal surface (posterior vitreous detachment).

Causes of liquefaction include:

➢ Age related liquefaction

➢ Degeneration
➢ Post inflammatory
➢ Trauma to vitreous
➢ Thermal effects(Diathermy, photocoagulation and cryocoagulation)
➢ Radiation effects

The patient may complain of

❖ Flashes of light (photopsia)

❖ Vitreous floaters.
❖ black dots, rings or other shapes moving in his/her field of vision (Musca volitantes).

On slit lamp biomicroscopy, synchysis is characterized by absence of normal fine fibrillar structure and visible pockets
of liquefaction associated with appearance of coarse aggregate material which moves freely in free vitreous

Vitreous Hemorrhage

Causes:
 1. Proliferative retinopathies, as diabetic retinopathy.

2. Retinal breaks.

3. Central retinal vein occlusion.

4. Trauma.

5. Blood diseases as anemia, leukemia and purpura.

6. Intraocular tumors.

VITREOUS DETACHMENT

Vitreous detachment occurs in three forms:

❖ posterior
❖ basal
❖ anterior

Posterior Vitreous Detachment

❖ occurs posterior to the vitreous base

❖ senile phenomenon

Symptoms:

❖ sudden onset of photopsiae(due to vitreoretinal adhesions and are provoked by ocular movement)
❖ floaters.
❖ ring-like opacity, Weiss ring or Fuchs ring(detached attachment of the vitreous to the edges of the optic
nerve head).

Anterior and Basal Vitreous Detachments

❖ These occur secondary to trauma and are often accompanied by vitreous haemorrhage

Complications of PVD:
❖ Retinal breaks
❖ Vitreous hemorrhage
❖ Retinal hemorrhage
❖ Cystoid maculopathy
❖ Retinal detachment

Management OF PVD:
❖ Uncomplicated PVD – no treatment
❖ Retinal tear complicating PVD – Photocoagulation
❖ Vitreous hemorrhage complicating PVD – conservative treatment, treatment of cause and Vitrectomy
❖ Retinal detachment complicating PVD – urgent treatment

VITREOUS OPACITIES:
 ➢ Vitreous is a transparent structure, any relatively non transparent structure present in it will form an opacity
and cause floaters
➢ Vitreous opacities cast a shadow on the retina and appear as black spots moving in and out of the visual
field, especially when reading.
➢ They are commonly mistaken for small flying insects, and are termed muscae volitantes or floaters.
➢ Most floaters are merely compressed cells or strands of the vitreous gel which have clumped together so
that they are less transparent than the rest of the vitreous.

They may be due to the following conditions:

1. Developmental opacities which are located in the canal of Cloquet and are remnants of the hyaloid system
2. Persistent Hyperplastic Primary Vitreous (PHPV)
3. Inflammatory Vitreous opacities:
▪ Anterior uveitis
▪ Posterior uveitis
▪ Pars plantis
▪ Pan uveitis
▪ endophthalmitis
4. Degenerative changes:
❖ Asteroid hyalosis:
• Characterized by the unilateral appearance of spherical or disc-shaped white bodies in the vitreous cavity.
• These are calcium-containing lipid complexes attached to the collagen fibrils and suspended throughout
the vitreous.
• They may be commonly seen in diabetes.
• It is unilateral in the majority of cases and affects both sexes, is asymptomatic but may make examination of
the fundus difficult with the ophthalmoscope.
• Treatment is rarely required unless vision is affected, in which situation a vitrectomy may be considered.

❖ Synchysis scintillans(Cholesterolosis bulbi):

• This degenerative condition leads to deposition of cholesterol crystals in the vitreous.
• These are also found in the anterior chamber and subretinal space.
• It affects damaged eyes which have been subjected to trauma or inflammatory disease in the past.
• The crystals are multicoloured, glittering particles which settle in the lower part of the vitreous cavity due
to gravity but can be thrown up by eye movements to form a shower of iridescence.
• The vitreous in such cases is liquefied and no treatment is indicated.

❖ Amyloid degeneration:
• Amorphous amyloid material is deposited in vitreousas a part of generalized amyloidosis
• The clinical features consist of diplopia, diminution of vision, external ophthalmoplegia, vitreous opacities,
retinal haemorrhages and exudates.
• Both eyes are involved and the vitreous becomes opaque.
• The earliest lesion originates in the wall of a retinal vessel which has a cloudy margin and this slowly
invades the vitreous body from behind forwards.
• Diagnosis is confirmed by biopsy of the conjunctiva, rectum, skin or sternal marrow.
• The vitreous opacities themselves are linear with footplate attachments to the retina and posterior surface
of the lens and this is a helpful diagnostic feature.
• Vitreous amyloidosis may be treated surgically by pars plana but the prognosis must always be guarded.
5. Red cell opacities
6. Tumor cell opacities

VITREOUS SURGERY

An abnormality leading to opacification of the vitreous body or the development of vitreoretinal scar tissue may
require vitreous surgery.

Common indications for vitreous surgery include :

• vitreous haemorrhage
• complications from diabetic retinopathy such as tractional retinal detachment
• complicated retinal detachment
• preretinal membrane fibrosis
• injury with or without an intraocular foreign body, macular hole, endophthalmitis and complications of
prior intraocular surgery.

The aims of vitreous surgery are:

• To remove any vitreous abnormalities, e.g. haemorrhage, traction bands
• To restore retinal anatomy by removal of epiretinal membranes or drainage of subretinal fluid
• To treat abnormal retinal vessels or breaks by endophotocoagulation or cryotherapy
• To provide tamponade to maintain chorioretinal apposition, internally by silicon oil and gases, or externally by
an encirclage or plomb (buckle)
• To obtain tissue for biopsy.

Procedure:

➢ A vitrectomy is performed through a surgical microscope allowing coaxial illumination and fine movements by
X–Y coupling.
➢ Special planoconcave lenses are placed on the cornea to provide a clear image of the posterior third of the
eye.
➢ Microscope attachments allow re-inversion of the image seen.
➢ All these provide the surgeon with a magnified, binocular view of the retina and vitreous.
➢ Three sclerotomies of 20, 23 or 25 gauge size are made at the pars plana, 3–3.5 mm away from the limbus.
➢ In one an infusion line is inserted for balanced salt solution.
➢ In the second, a fibreoptic light source provides endoillumination and through the third, a vitrectomy
instrument for suction and cutting of the vitreous (Figs 21.4 and 21.5) is passed into the vitreous cavity.
➢ Any abnormalities in the vitreous can be cleared bimanually under direct vision using the vitrectomy
instrument and the endoilluminator as support when needed.
➢ It is necessary to completely clear all the central vitreous and also the region of the vitreous base to prevent
later fibrovascular proliferation.
➢ Once the visibility of the retina is restored, the cause for the vitreous disturbance is treated.
➢ Endophotocoagulation with a fibre optic probe delivering diode laser may be required to seal a retinal break
or treat areas of retinal neovascularization.
➢ Endodiathermy can be utilized to coagulate bleeding vessels.
➢ Vitrectomy is seldom carried out as an isolated procedure, but is often associated with surgery for
vitreoretinal proliferation, complicated retinal detachments or foreign bodies in the eye.
➢ In the presence of vitreoretinal proliferation it is important to relieve all traction on the retina.
➢ Vitreous bands can be cut using the vitrectomy instrument or special miniature vitreoretinal scissors.
➢ Epiretinal membranes are removed by gentle peeling with a vitreoretinal pick and forceps, or by cutting them
with vitreoretinal scissors, to allow the retina to fall back into place.
➢ Small foreign bodies are dissected of their fibrous capsule with a vitreoretinal pick or forceps and then
removed by intravitreal foreign body forceps.
➢ An intravitreal magnet is occasionally employed.
➢ Maintenance of chorioretinal apposition to allow chorioretinal adhesions to occur and to prevent recurrence
of fibrovascular proliferation in the vitreous necessitates an internal tamponade with gases or liquids.

➢ Visual prognosis after vitreous surgery is often guarded and depends upon the basic disease process and the
degree of damage to the retinal receptors.
➢ Meticulous surgery has greatly increased the chances of anatomical success.
➢ Open sky vitrectomy leads to instability of the entire vitreous and anterior segment while making the patient
aphakic. It is indicated only when the cornea is not transparent.
 DISEASES OF RETINA

What we will learn here?

• Anatomy of Retina
• Hypertensive retinopathy
• Retinal Artery Occlusion
• Retinal Venous Occlusion
• Retinopathy of Blood disorders
• Retinopathy of prematurity
• Retinal dystrophy and degeneration
• Macular degeneration
• Macular disorders
• Retinal Detachment

Retina is innermost layer of the eyeball Highly developed tissue of the eye ball

It consist of light sensitive cells rods and cones

Its extends from the optic disc to ora serrata

It consists of two regions posterior pole and peripheral retina by the retinal equator

RETINAL EQUATOR which lie in line with the exit of four vena verticosa
Posterior pole consists of two regions MACULALEUTEA and OPTIC DISC

Optic disc is pink coloured area lies 3.4mm to nasal fovea

All the layers of retina terminate at optic disc except the nerve fibres which passes through lamina cribrosa

to run into optic nerve

Thus the area reffered to as optic nerve head

Due to the absence of photoreceptor cells it produces absolute scotoma in the visual field called 2frica22ival2 blind spot
Macula lutea is the yellow spot

Fovea centralis is the central depressed part of the macula

It has lowest threshold for light and high visual activity It has highest number of cones

Pheriperal retina is the area bounded posteriorly by the retinal equator anteriorly by the ora serrata. Ora serrata is the peripheral margin where
retina ends

MICROSCOPY OF RETINA

It consist of ten layers

Fuctinally it has two components Pigment epithelium Neurosensory retina

Functinally retina is divided into nasal retina and temporal retina

BLOOD SUPPLY OF RETINA

outer four layer is supplied by choroidal vascular system supplied by anterior and posterior cilliay arteries

Inner six layer is supplied by central retinal artery branch of opthalamic artery

Central retinal vein which drains directly into the cavernous sinus
CONGENITAL AND DEVELOPMENTAL DISORDERS OF RETINA

Congenital disorders classified into ANOMALIES OF OPTIC DISC

Crescents Site inverses

Congenital pigmentation Coloboma

Drusen and hypoplasia of optic disc

ANOMALIES OF VASCULAR ELEMENTS:

Persistent hyaloid artery

Congenital tortuosity of retinal vessels

ANOMALIES OF NERVE FIBRES:

Medullated nerve fibres

ANOMALIES OF RETINA PROPER:

Albinism

Congenital retinal blindness Oguchis disease Congenital retinal cyst

Congenital retinal detachment Coloboma of the fundus

ANOMALIES OF MACULA:

Hypoplasia, aplasia, coloboma

HYPERTENSIVE RETINOPATHY

Occurs at BP over 140/90Hg

Pathogenesis

1.vasoconstriction

2.arteriosclerosis

3.increased vascular permeability

It may occur under four circumstances

1.Simple hypertension without sclerosis

Young patients

Retinal signs-constriction of arterioles ,flame shaped hemorrhages, cotton wool spots

2.Hypertension with involuntary sclerosis

Vasoconstriction , thickening of vessel wall, deposition of hard exudates, hemorrhages without

edema

Nipping and perpendicular placement of veins at arteriovenous crossing: Gunn sign

3.Arteriolar sclerosis

In young patients arterioles respond to HT by proliferative and fibrous changes

In kidneys- chronic glomerulonephritis

Retinal signs-multiple hemorrhages edema cotton patches hard exudates

4.Malignant hypertension

Accelerated progression of hypertensive stage in young arterioles undefended by sclerosis

Associated with renal insufficiency

Retina – oedema , marked disc oedema, multiple cotton patches hard exudates
Prognosis -grave

Classification

Grade 1 – barely detectable arterial narrowing or sclerosis

Grade 2-moderate to marked narrowing of arterioles exaggeration of light reflex ,changes in AV

crossings

Grade 3 – grade 2+ retinal hemorrhage

Grade 4 - grade3+ pappiloedema

Management –blood pressure control

Pregnancy induced

Occurs in late pregnancy (6th -9th month)

Retinal changes :

Narrowing of nasal branches of arterioles

Spasm of vessels causes hypoxia characterized by ‘cotton wool spots’ and ‘superfcial hemorrhages’

Retinal edema and exudation

Profuse exudation may cause retinal detachment

Management : preorganic stage –maintenance of pregnancy in close observation

Inflammatory disease of retina:

Retinitis:

Nonspecific retinitis:

Caused by pyogenic organisms.

Acute purulent retinitis:

Occurs as Metastatic infections in patients with pyemia.

As endophthalmitis and panophthalmitis

Subacute retinitis of Roth:

Occurs in patients with subacute bacterial endocarditis (SABE)

Characterized by

Multiple superficial hemorrhages in posterior part of fundus. With white spot at the centre
(rothspots).

Blurring of vision due to involvement of macular region.

Specific retinitis:

Bacterial infections – tuberculosis ,syphilis,leprosy,actinomycosis.

Cytomegalo virus retinitis – cytomegalo virus.

Progressive outer retinal necrosis (PORN) – varicella zoster virus.

Acute retinal necrosis (ARN) – herpes simplex ll in patients under the age of 15 years and herpes
simplex l in older individuals . ( More chances in AIDS patients).

RETINAL VASCULITIS

Inflammation of the retinal vessels’ wall - Primary (Eales’ disease) or Secondary to uveitis.

EALES’ DISEASE : ( Periphlebitis retinae)

Idiopathic inflammation of the peripheral retinal veins

Classical triad – Young males ( more common in India), spontaneous vitreous hemmorhage
,recurrences are common.

Etiology – Unknown but seen commonly in TB patients (considering to be a hypersensitivity to

tubercular proteins)

Clinical features:

Sudden painless loss of vision ( due to vitreous hemmorhage)

Sudden appearance of floaters( black spots in front of eye)

Bilateral but assymetrical

Systemic neurological features and mild uveitis present

Clinical course :

1.Stage of active inflammation – peripheral veins are congested ,perivascular exudates and
sheathing present along the surface,sheets of hemorrhages near veins

2.Stage of vascular occlusion- obliterated vessels and areas ofcapillary non- perfusion in the
periphery is seen on fundus flourescin angiography.

3.Stage of retinal neovascularisation- Abnormal fragile vessels at the junction of perfused and non-
perfused retina.(Bleeding from these vessels causes hemorrhage)

4.Stage of sequelae – Development of complications( proliferative vitreoetinopathy,fractional

retinal detachment,rubeosis iridis,neovascular glaucoma.

{Occlusion – hypoxia – VEGF stimulus-Neovascularisation}

Treatment :
 1.Oral, corticosteroids + Antitubercular therapy

2.Laser photocoagulation to reduce the neovascular stimulus.

3.Vitreoretinal surgery for nonresolving hemorrhage

4.Intravitreal VEGF inhibitors.

RETINAL ARTERY OCCLUSIONS

ETIOLOGY : Common in old age males >40 years and patients with HT,DM and cardiovascular
diseases.

EMBOLI (from carotid artery and cardiac valves) –

- Most common cause

- Most common site – Narrowest site of CRA where it pierces the dural sheath of optic
nerve,posterior to lamina cribrosa.

- Types : # Hollenhorst plaque – Cholesterol EMBOLI at retinal vessel bifurcation ( refractive

,orange and from atheroma in carotid artery)

# Calcium emboli – close to optic disc(white and from valves)

# Platelet fibrin emboli – full white and arises from atheroma in carotid artery)

2.ATHEROSCLEROSIS RELATED THROMBOSIS

3.RETINAL ARTERITIS ( Giant cell arteritis) and periarteritis (associated with polyarteritis nodosa,SLE,
Wegener’s granulomatosis , scleroderma)

4.ANGIOSPASM (associated with amaurosis)

5.RAISED IOP

6.THROMBOPHILIC DISORDERS

7.SUSAC SYNDROME – CRAO (+) Sensorineural hearing loss (+) encephalopathy.

8.HYPERCOAGULATION DISORDERS ( oral contraceptives,polycythemia,antiphospholipid

syndrome)

Rare causes – retinal migraine, sickling hemoglobinopathies.

CLINICAL FEATURES: Clinically RAO presents as Central retinal artery occlusion(CRAO -60%) OR
Branch artery occlusion(BRAO-35%) OR Cilioretinal artery occlusion(5%)

CRAO – occurs due to obstruction at the level of lamina cribrosa

 1.Unilateral sudden painless loss of vision ( painful in GCA)

2.HISTORY of Amaurosis fugax in the past

3.Visual acuity reduced ( except with those having patent cilioretinal artery supplying
macula )

4.Direct puppilary reflex -absent ,RAPD positive

5.On fundus examination,

- Marked narrowing of retinal arteries and mild narrowing of retinal veins.

- Milky white retina due to ischemic retinal edema ( except with those with
patent cilioretinal artery)

- Cherry Red Spot – seen in the centre of macula due to vascular choroid shining
through the thin retina in the foveal region,in contrast to the surrounding pale retina.

DD for Cherry red spot in macula

Cherry Trees Never Grow Tall in SAND ,Mud and Grime

1.C RAO 2.Trauma(Blunt) 3.Neimann- Pick disease 4.GM1 gangliosides 5.Tach-Sach’s disease
6.Sandhoff’s disease 7.Metachromatic leukodystrophy, Multiple sulfatase deficiency 8.Gaucher’s
disease( only type2).

- Cattle tracking/Box caring fundus – segmentation of blood column of veins and

arteries.

- Atrophic changes in the form of attenuated thread like arteries and consecutive
optic atrophy in chronic cases.

- Fundus flourescin angiography shows delay arterial filling(early filling in case of

patients with those with patent cilioretinal artery)

BRAO – Sudden and profound painless sectoral visual field loss(goes unnoticed when central
vision is spared)

1.Occurs following lodgement of embolus at a birfurcation

2.Cloudy white edematous retina with narrowed arterioles

MANAGEMENT:

1.Adoption of supine posture.( To improve ocular perfusion)

2.Lowering of IOP :

- Ocular massage (to improve perfusion and dislodging the embolus or thrombus)

-Anterior chamber paracentesis

-Intravenous azetazolamide,mannitol,topical apraclonidine

3.Vasodilation – sublingual isosorbide dinitrate and inhalation of carbogen(95% oxygen and

5%carbondioxide)- 9frica99 angiospasm.
 4. Fibrinolytic therapy

5.Intravenous steroids are indicated in patients with GCA

6.Laser photodisruption of the embolus

7.Work-up for associated systemic conditions.

Complication – Neovascular glaucoma.

RETINAL VENOUS OCCLUSION

Etiology and risk factors:

• Older age
• Hypertension
• Diabetes mellitus
• Hyperviscosity – polycythemia,Hyperlipidemia,leukemia, multiple
myeloma,macroglobulinemia
• Periphlebitis retinae – associated with sarcoidosis,syphilis,SLE.
• Raised. Intra ocular pressure

Local causes -Orbital cellulitis,orbital tumors,facial erysipelas,Cavernous sinus thrombosis.

Use of contraceptives in young females.

Classification:

1.Central retional vein occlusion – non ischemic and ischemic

2.Branch retinal vein occlusion.

CENTRAL RETINAL VEIN OCCLUSION:

Pathology:

Venous occlusion due to systemic or local factors causes stasis of bloodflow (nonischemic type)
Hypoxia of the involved retina Damage of capillary endothelial cell and leakage from neovascularized
vessel. (Ischemic type)

NOTE:

Occlusion usually occurs posterior to lamina cribrosa due to sharing of common adventitia by retinal
artery and vein.

15% of nonischemic type leads to ischemic occlusion in 4 months

Clinical features :

Non ischemic CRVO Ischemic CRVO

Most common (75%cases) Less common
 Sudden,painless, loss of vision(partial) Sudden,painless,complete loss of vision

RAPD – Absent or mild Marked

Mild hemorrhage in the periphery Severe hemorrhages involving periphery and posterior
pole – giving rise to Tomato ketchup
/Tomatosplash/Blood and thunder 11frica1111iv.

Cotton wool spots and tortuosity of vessels Extensive cotton wool spots and tortuosity of vessels

Loss of vision due to macular edema. Lossbof vision due to macular ischemia.

Doesnot occur Neovascularization at iris (NVI) occurs after 100 days

and causes glaucoma secondary to CRVO known as 100
day glaucoma

In FFA<10 disc area of nonperfusion. In FFA>10 disc area of nonperfusion

ERG- Normal ERG – amplitude of b wave <60%

Treatment – Treatment –
Laser photocoagulation notdone. Intravitreal PRP/ scatter photocoagulation done only on
triamcinolone 2 injections (1mg). 11frica1111iv of NVI/NVD.
0.7 mg dexamethasone intravitreal implant. Prophylactic PRP not done.
Intravitreal anti VGEF drugs –
ranibizumab,aflibercept

Branch retinal vein occlusion:

More common than central retinal vein occlusion

Occurs as Hemispheric occlusion – at the main branch of the disc

Quadrantic Occlusion – at the level of AV crossing

Small branch occlusion – either macular or peripheral occlusion.

Clinical features:

Retinal edema and hemorrhage

Loss of vision is due to macular edema

Neovascularization occurs.

Treatment:
 It may benefit from laser photocoagulation contrary to nonischemic type of venous occlusion.

Nasal cycle and nasal resistance. Mechanism of sinonasal allergy and mucociliary clearance
mechanism.

NASAL CYCLE:

Nasal mucosa undergoes rhythmic cyclical congestion and decongestion- controls the airflow
through nasal chambers.

When one nasal chamber is working, the total nasal respiration equal to that of both nasal chambers
is carried out by it.

Variation- every 2-4 hours in an individual

Congestion and decongestion of the nasal venous cavernous tissue is under the control of the ANS

Factors influencing nasal cycle:

Physiological factors:

• Age
• Sleep
• Posture
• Exercise

Pathological factors:

1.Acute upper respiratory tract infection (URTI)

2.Allergic rhinitis

3.Nasal septal deviation

NC and drugs:

1.Nasal decongestants were shown to influence the NC.

2. The administration of nasal topical vasoconstrictor on the congested side is able to cause a
prompt cycle reversal.

3.While it has been demonstrated that decongestants have little action on the patent side, they
cause a significant increase in airflow on the naturally congested side with the least sympathetic
nervous activity.

NASAL RESISTANCE:

Nasal vestibule is the first component of nasal resistance.

The nasal vestibule is composed of compliant walls that are liable to collapse from the negative
pressures generated during inspiration.

The vestibule is termed as the external nasal valve.

It contributes to 1/3rd of the nasal resistance

The remaining 2/3rd is contributed by the nasal septum.

Inferior and middle turbinates contain erectile tissues, the anterior end of it has a major influence on
the nasal resistance and functions as the internal nasal valve.

Factors influencing nasal resistance:

• Age
• Nasal cycle
• Exercise
• Respiration
• Nasal reflexes
• Skin and temperature
• Emotional and psychological response

MECHANISM OF MUCOCILIARY CLEARANCE:

Nasal mucosa-rich in – goblet cells, secretory glands ( both serous and mucous)

Their secretion forms a continuous sheet called mucous blanket ( spread over the normal mucosa)

Mucous blanket consists of:

Superficial mucus layer+ deep serous layer, floating on top of the cilia which are constantly beating
to carry it like a “conveyer belt” into the nasopharynx.

It moves at a speed of 5-10 mm/min

Complete sheet of mucus is cleared into pharynx every 10-20 min.

Inspired bacteria, viruses and dust particles →entrapped on the viscous mucous blanket→ carried to
nasopharynx→ swallowed.

Presence of turbinates- doubles the surface area yo perform this function.

About 600-700 ml of nasal secretion is produced in 24 hours.

Cilia beat 10-20 times per sec in room temperature.

Two strokes:

Rapid “effective stroke”- extended cilia reach the mucus layer

Slow “recovery stroke”- cilia bend and travel slowly in the reverse direction in the thin serous layer,
thus moving the cilia in one direction.
Factors affecting the movements of cilia:

Drying

Drugs (adrenaline)

Excessive heat or cold

Smoking

Infections and noxious fumes like sulfur dioxide and carbon dioxide.

Disorders of cilia:

Immotile cilia syndrome:

Cilia are defective and cannot beat effectively→stagnation of mucus in the nose, sinuses and
bronchi→chronic rhinosinusitis and bronchiectasis.

MECHANISM OF SINONASAL ALLERGY:

Aetiology:

Inhalent allergens (pollens,dust)

Genetic predisposition

Pathogenesis:

Inhaled allergens→ produce specific IgE antibody→ antibody becomes fixed to the blood basophils
or tissue mast cells by its Fc end.

Subsequent exposure→ antigen combines with IgE antibody in the Fab end→ degranulation of mast
cells→ release of several chemical mediators.

Mediators -responsible for the symptomatology of allergic disease.

They cause vasodilation, mucosal edema, infiltration with eosinophils, excessive secretion from nasal
glands or smooth muscle contraction.

“Priming effect”- mucosa earlier sensitized to an allergen will react to smaller doses of subsequent
specific allergen.

Allergic response occurs in two phases:

Acute or early phase- occurs 5-30 min after exposure to specific allergen.

Characterised by-sneezing, rhinorrhea nasal blockage and bronchospasm due to histamine.

Late or delayed phase: Occurs 2-8 hours after exposure to allergen without additional exposure.

It is due to the infiltration of inflammatory cells- eosinophils, neutrophils, basophil, monocytes and
CD4+ T cells at the site of antigen deposition.

Characterised by- Swelling, congestion and thick secretion.

In the event of repeated or continuous exposure to allergen, acute phase symptomatology overlaps
the chronic phase.

Complications:

• Recurrent sinusitis
• Formation of nasal polyp (2% of cases)
• Serous otitis media
• Orthodontic problems
• Bronchial asthma

Treatment:

Avoidance of allergen

Treatment with drugs ( anti-histamines, sympathomimetic drugs ,corticosteroids, sodium

cromoglycate, anticholinergics, leukotriene receptor agonists, Anti-IgE)

Immunotherapy.

Retinopathy of Blood disorder

Sickle cell retinopathy

Retinal changes in patient suffering from sickle cell hemoglobinopathies

When deoxygenated it becomes insoluble and distorts the normally discoid RBCs into characteristic
sickle shape. It obstructs the capillaries supplying retina and causes infraction especially in the
periphery of retina.

Pathogenesis:

Glutamic acid is replaced with valine in 6th position

This causes changes in the RBC Morphology and

Thus sickle cells are formed.

The Damaged RBC gets slowed down in the movement across the miocrovessels

High expression of adhesins by sickle cells causes increased stickiness to the endothelium
Aggregation of sickle cells in the vessel leading to blockage of vessel

Thus there occurs a lysis of RBC which causes release of free Hb.

Causes inactivation of NO

Narrows the blood vessels.

Microvascular Stasis

Clinical Manifestation:

• Retinopathy
• Angioid Streaks
• Glaucoma
• Pappilary edema
• Cataract
• Circumscribed dilation and constriction of conjunctival cappilaries.

Fundus:

Proliferative changes B. Non proliferative changes.

Proliferative changes:

Stage 1:

Peripheral artery occlusion and ischemia

Stage 2:

Peripheral arterio venous anomalies of dilated pre existing capillary channels.

Stage 3:

Sprouting of new vessels from pre existing anamolies

SEA-FANS Configuration

They involute spontaneously as a result of auto infraction.

They appear as greyish fibrovascular lesions.

Stage 4:
Neovascular tufts continues to proliferate and bleed into the vitreous.

Stage 5:

Extensive fibrovascular proliferation and retinal detachment.

Non Proliferative Retinopathy:

Asymptomatic lesions:

Venous tortuosity

Salmon patches

Black sunburst spots

Macular depression

Peripheral retinal holes

Symptomatic lesions:

Macular arteriolar occlusion

Acute central retinal artery occlusion

Choroidal vascular occlusion (Particularly in children).

Treatment:

Pan Retina photocoagulation: Regresses neovascularization.

Pars Mena vitrectomy.

Vitrearetinal surgery.

Anaemic Retinopathy:

Retinal changes are liable to occur when Hb levels falls by 50% and consequently present when it is
below 35% (5gm%)

Retinopathy increases as severity of anemia increases.

Pathogenesis:

Anemia

Retinal Hypoxia

Vascular dilation

Infraction of nerve fiber layer

Increased transmural pressure

Hypoproteinemia
Retinal Edema and Hemorrhage

Characteristic Features:

Fundus Background – Pale.

Retinal Arterioles – Pale.

Retinal Veins – Tortuous and dilated.

Retinal Hemorrhage – Superficial flame shaped and preretinal (Suhyloid) may be seen in the
posterior half of the fundus.

Roth Spot: Hemorrage with white Centre and platelet fibrin emboli.

Cotton wool spots: Seen in the patient with co-existing thrombocytopenia + Aplastic anemia.

Retinal Edema – Microtrauma of vessel wall secondary to increased transmural pressure.

Hard exudate – Seen due to resolved retinal edema when these are severe and located at the
macula – “Macular Star” is seen.

Optic nerve Changes – Edema or in later stages of optic neuropathy, Optic disc pallor is seen.
 Retinal Changes
seen in special
situations like

IDA Vit B12 Deficiency Sickle cell Anemia

Central Retinal Conjunctival

Optic Neuropathy
vein occlusion sickling sign

Retinal artery
Disc Pallor Choroidal infract
occlusion

atropy and
Disc Edema
neovascularisation

Anterior ischemic
optic neuropathy
 Retinal Changes seen
in special situations
like

Myeloproliferative
Thalasemia Malaria
Disorders

Retinal Pigment
Roth Spots Anemia
Epithelial Changes

leukemia infilterates
Increased ICP
in Retina

Choroidal infilteration
with 20 degree Retinal changes - Disc
serous retinal Edema
detachment.

Vascular sheathing

Symptoms:

Most cases are asymptomatic

At Macula – Hemorrhages, Edema ana Hard Exudates – patient can complain of loss of vision.

Investigation and Treatments:

Ocular investigations are indicated only if treatment is planned.

Fibro angiography demonstrates delay in arteriovenous transit time which indicates venous
occlusion

Optical Coherence tomography (OCT) is used to demonstrate vascular occlusion and macular edema.

Blood Investigations :

PBS examination

Complete blood count.

Bone Marrow Biopsy indicated in some cases.

Treatment:

Vascular occlusion and macular edema must be treated first

Laser hyaloidectomy is indicated in case of subhyoidal hemorrhage.

RETINOPATHY OF PREMATURITY

Bilateral proliferative retinopathy

occurs in premature infants with

low birth weight

exposed to high concentration of O2

Earlier it was known as retrolental fibroplasia

ETIOPATHOGENESIS:

➢ Primary Factors:
➢ Low gestation age, especially less than 32 weeks
➢ Low birth weight (less than 1500g, especially less than1250g)
➢ Supplemental O2 therapy
➢ Other risk factors:
➢ Vitamin E deficiency
➢ Respiratory distress syndrome
➢ Asphyxia
➢ Shock
➢ Acidosis

PATHOGENESIS

Normal development of retina

VEGF
 Retinal vessels

Reach 1 month after delivery

8thMonth Reach

Nasal periphery Temporal Periphery

Premature birth

VEGF Downregulated

Vessel Migration halted

Increased metabolic demands

with growing age

Activation of (excess production)

O2 regulated VEGF’s Non O 2 regulated

insulin like growth factors (IGF-1)

Neovascularization

Retinopathy of prematurity (ROP)

CLINICAL FEATURES:

Can be divided into

Active ROP Cicatricial ROP

International classification of ROP:

Staging of ROP:

Stage 1

Demarcation line formation at the edge of vessels dividing the vascular from avascular retina

Stage 2

Line structure of stage 1 acquire a volume to form a ridge with height & width

Stage 3

Ridge with extra retinal fibrovascular proliferation into the vitreous.

Stage 4

Stage 4 a) – Subtotal retinal detachment not involving macula.

Stage 4 b) – Subtotal retinal detachment involving macula.

Stage 5

Total retinal detachment

(b)Zones of ROP:

Divided into 2 zones

Centre of the retinal map is the optic disc

ZONE 1

Any ROP in the zone –

Very severe – Because of a large peripheral area of avascular retina

ZONE 2

Area between ZONE 1 & the boundary contributes ZONE 2

ZONE 3

Temporal are of retina left beyond the radius of ZONE 2 is ZONE 3

Extent of involvement

It is denoted by the clock hours of retinal involvement in particular zone.

CLINICALLY IMPORTANT TERMS

1)PLUS DISEASE- Dilatation and tortuosity of posterior pole vessels in at least 2 quadrants at the
posterior pole with any stage of ROP

2)PRE PLUS DISEASE- Normal < Venous dilation< <Defined plus disease.

3) Aggressive posterior ROP

Also called Rush disease

Require immediate treatment

ROP – location Zone I

Posterior ZONE 2

Flat proliferation with vascular loops and haemorrhages

4)Threshold disease

Stage 3 + ROP

Plus disease located -> Zone 1 or 2

Involves 5 continuous or 8 discontinuous clock hours

Requires Laser therapy in less than 42 hours

Pre-threshold disease

(has two types)

Type I or high-risk pre-threshold disease desire (requires photocoagulation)

Type 2 or low risk pre-threshold disease (which requires weekly follow up)
Differential diagnosis:

Familial exudative vitreoretinopathy (FEVR)

Incontinentia pigmenti in girls

Persistent fetal vasculature

Advanced retrolental fibroplasia

Management

1)Prophylaxis:

Premature new borns should not be placed in incubator with an O2 concentration of more than 30%.

Infections and attacks of apnoea must be avoided.

Early diagnosis and treatment to prevent blindness in high risk cases.

SCREENING PROTOCOL

All premature babies < 34 weeks of gestational age & those weighing 1750g or less must be
screened.

1st EXAMINATION

Indirect ophthalmoscopy:

Infants < 28 weeks of gestation < 1200gm : at 2-3 weeks of age

Infants born between 28-34 weeks of gestation / 1175gm: at 3-4 weeks of age

Infants between 34-36/7 weeks of gestation or between 1750-2000 gm should be screened

only if exposed to high rank factors.(prolonged O2 therapy, mechanical ventilation)

Further line of action – depends on the status of retina

Subsequent Follow Up Examinations

Spontaneous regression of disease occurs in about 80% of the cases

Patients should be examined till regression occurs

TREATMENT PROTOCOL

Laser is preferred over Cryotherapy

Laser treatment:
Photocoagulation using diode laser lesions with laser indirect ophthalmoscope

carried out in patients with high risk pre threshold, threshold & aggressive posterior ROP

Post-laser treatment & follow-up

Antibiotic & steroid eye drops prescribed for a week.

Treatment- Surgery
Surgical Management of Stage 4 ROP

ROP

Stage 4a Stage 4b

Lens sparing vitrectomy

Focal Generalized Generalized

traction traction traction

No RD No RD with RD

Followup Followup/ Buckling/Lens

Buckling sparing

Vitrectomy

Leukemic Retinopathy
Ocular involvement – more common with acute leukemia

Leukemia

Acute Chronic

• Myeloid • Myeloid
• Lymphoid • Lymphoid

Clinical Manifestation

Primary Secondary
(Direct Infiltration of neoplastic Cells) (Indirect involvement from non-viable or dysplastic cells or
chemotherapy)
Manifestation Include

Retinal involvement
Non Retinal involvement

Background is pale and orangish • Iris Infiltration

• Ocular Haemorrhages
Retinal veins – Tortuous and Dilated Sub Conjunctival
Retinal Arterioles – Pale and Narrow Haemorrhage and hyphaema
(bleeding of anterior
Perivascular Leukemic Infiltrates- chamber)
Grayish white lines along the course of veins, Roth’s Spots • Pseudohypopyon
Collection of White cells in
Subhyaloid Hemorrhages (Large pre-retinal Hemorrhage) the anterior chamber.
 Investigations

Complete blood count with platelets/differential (Significantly high or low WBC should be
considered)
Peripheral Blood Smear > 20% blast cells (Acute Leukemia).

Treatment – The key is to treat the malignancy

Induction Phase – Reduce the tumor burden by clearing the leukemic cells in the bone marrow using
chemotherapeutics.
Consolidation Phase – Eliminate all the Leukemic cells that remain viable.
Maintenance Phase – Chemotherapeutics and steroids are given to prevent relapse.

Opportunistic infection and side effects due to chemotherapy

Bacterial Virus Fungus Parasite

• Pseudomonas • HSV • Candida • Toxoplasma

(starts as • VZV • Aspergillus gondii (ocular
blephro • CMV (Cause • Focal, Toxoplasmosis
conjunctivitis necrotizing white, deep )
and spread to retinitis and lesions in
cause orbital retinal the vitreous
cellulitis detachment.

Ocular adverse effects of chemotherapeutic drugs:

Busulfan – Posterior subcapsular cataract.

Vincristine – Optic atrophy, corneal hyposthesia, transient cortical blindness, nystagmus.
Dexamethasone – Increased intra ocular pressure, sub capsular posterior cataract.
Fludarabine – Visual disturbances (15% of patients)
Cytarabine – Corneal toxicity and Hemorrhagic cystitis
Anthracyclines – Discoloration of tears and conjunctivitis.
Imitanib – Peri- orbital edema, blurred vision, conjunctival hemorrhage.

Hematopoitic stem cell transplantation

 Graft v/s Host disease

Kerato- Conjunctivitis, Corneal ulceration, Ischemic retinopathy

PRIMARY RETINAL TELANGIECTASIA

Idiopathic congenital or acquired retinal vascular malformation
Characterized by:
Dilation of capillary bed
Segmental dilation of neighbouring venules and arterioles

1o retinal telangiectasia includes

Idiopathic juxtafoveolar retinal telangiectasia
Also known as idiopathic macular telangiectasia
Mild decrease in visual acuity due to exudation from the juxtafoveal telangiectatic retinal capillaries.

Types
Type 1: - Unilateral disease characterized by parafoveal dilation of capillaries. Microaneurysms,
leakages and lipid deposition.
Type 2: - (Most Common form)
Bilateral juxtafoveal telangiectasia
Minimal exudates
Type 3: - (Extremely Rare)
Occlusive telangiectasia

Pathogenesis
Abnormalities in parafoveal muller cells
Muller cells – Important for the health of retinal capillary endothelium and surrounding retina.
Muller cell dysfunction – endothelial degeneration – Retinal capillary proliferation and telangiectasia

Clinical Presentation
Parafoveal graying of retina
Superficial crystalline deposits
Subfoveal cystoid cavities
Parafoveal cystoid cavities
Right angle vessels
Reduced visual acuity
Hyperplasia of retinal pigment epithelium

Investigations
Fluorescein angiography
Highlights parafoveal telangiectasia vessels
Demonstrate early hyperfluorescence with leakage
Optical coherence Tomography
Subfoveal cystoid space (without cystoid macular edema)
Advanced stages:
Photoreceptor dysfunction and outer retinal atrophy
Fundus autofluorescence
Pathognemonic of Type-II
Loss of Physiologic hypoauto fluorescence i.e., increased autofluorescence in the fovea.

Differential Diagnosis

Diabetic macular Pseudophakic Macular hole Retinal vein

edema macular edema occlusion

Treatment
Chemotherapeutic drug like (bevacizumab, ranibizumab)
Oral carbonic anhydrase inhibition
Focal grid laser, photodynamic therapy, intravitreal triamcinolone
Parafoveal telangiectasia.
If only the capillaries of fovea are involved, then it’s called Parafoveal telangiectasia.
Characterized by:
Microaneurysmal saccular dilation
Capillary non-perfusion of parafoveal capillaries
Parafoveal telangiectasia can be considered as having 2 basic forms:
Coat’s disease – A developmental or congenital vascular anomaly which may be the largest part of a
spectrum
Presumably an acquired form found in middle aged or older patients.

COAT’s DISEASE
Also known as exudative retinopathy of coats
Severe form of retinal telangiectasia (Idiopathic congenital retinal vascular malformation)
Characteristic Features:
Affects one of the eyes of boys in the 1 st decade of life
Early Stages – Large areas of intra and sub retinal yellowish exudates and hemorrhages associated
with “OVERLYING DILATED AND TORTUOUS RETINAL BLOOD VESSELS” and a number of
small aneurysms near the posterior pole and around the disc.
It might present with VISUAL LOSS, STRABISMUS or LEUCOCORIA (whitish pupillary reflex)
and thus it should be differentiated from retinoblastoma tones.

Progression
Produce exudative retinal detachment and a retrolental mass
Late stages – Complicated cataract, uveitis and secondary glaucoma and end in phthisis bulbi
(shrunken, nonfunctional eye)
Stages
Stage 1
Retinal telangiectasia only (dilation of capillaries in the retina)
Stage 2
Telangiectasia and exudation (escape of fluids and material from blood vessels into surrounding
tissues)
Extrafoveal exudation
Foveal exudation (exudation of fovea)
Stage 3 – Exudative Retinal Detachment
Subtotal Foveal and Subtotal Extrafoveal (partial detachment)
Total retinal detachment.
Stage 4
Total retinal detachment and glaucoma
Stage 5 – Advanced end stage disease
Blind, non-painful eye with total retinal detachment with cataract and phthisis bulbi
Investigation
Fundus Fluorescein Angiography – Highlights abnormal vessels, leakage and areas of capillary
drop out.
Treatment
Laser photocoagulation- Uses laser to shrink or destroy blood vessels
Cryotherapy – A procedure that uses extreme cold to destroy abnormal blood vessels
Anti-vascular endothelial growth factor (Anti-VEGF) injection
In more advanced stages,
Retinal detachment –Vitrectomy
Scleral buckling to correct the detached retina and external drainage of fluids.

LEBER’S MILIARY ANEURYSMS

Less severe form of Coat’s disease presenting in adults.
Characterized by:
Decreased vision.
Local area of fusiform and vascular aneurysmal dilation of venules and arterioles associated with
local exudation.
Investigation
Fundus Fluorescein Angiography (FFA)
Leakage as well as capillary drop out.
Late hypofluorescence.
Treatment
Direct photocoagulation of abnormal vessels.
 OCULAR ISCHAEMIC SYNDROME
Rare condition
Results due to chronic ocular hypoperfusion secondary to > 90% stenosis of carotid artery
Carotid Stenosis
Atherosclerotic occlusive carotid artery disease
Associated with – ulceration at the bifurcation of common carotid artery
Risk Factors:
Male (2:1)
Old age (60-90)
Smoking
Hypertension
Diabetes Mellitus
Hyperlipidaemia
Manifestations
Amaurosis fugax (transient retinal ischaemic attack)
Retinal artery occlusion (due to embolus)
Transient cerebral ischemic attack
stroke
Clinical features: (Symptoms)
Usually unilateral (80%)
Ocular discomfort
Pain around the orbit
Transient blackout (amaurosis fugax)
Delayed dark adaptation
Loss of vision, precipitated by exposure to bright light (bright light amaurosis)

SIGNS:
Cornea: Edema & striae
Anterior chamber: Reveal faint aqueous flare, with few cells (ischaemic pseudoritis)
Pupil: mid dilated and poorly reacting
Iris:
rubosis iridis (66%cases), atrophic patches
Iris neovascularization (90% of cases)
(Poor prognosis)
POSTERIOR SEGMENT: (fundus examination)
Venous dilation with or without tortuosity, peripheral retinal hemorrhages and micro aneurysms.
Easily induced retinal artery pulsations with gentle digital pressure
Retinal neovascularization (in 37% of cases)
Macular edema
COMPLICATIONS:
Anterior ischemic optic neuropathy in association with OIS- Due to inadequate perfusion pressure
within the deep capillaries of the optic nerve head.
Cataract – advanced cases.
Neovascular glaucoma – (as a sequelae to anterior segment neovascularization)
DIFFERENTIAL DIAGNOSIS:
Non- ischaemic Central retinal vein Occlusion (CRVO)
Diabetic retinopathy
Hypertensive retinopathy
Aortic arch disease
Atherosclerosis
Syphilis

INVESTIGATIONS:
Doppler ultrasound
Magnetic resonance angiography
Fluorescein fundus angiography
Delayed and patchy choroidal filling
Increased retinal arteriovenous circulation times
Leakage from retinal (new) vessels
Macular edema.
TREATMENT MANAGEMENT:
Treatment of neovascular glaucoma
Pan-retinal photo-coagulation
Glaucoma drainage device (i.e) artificial filteration shunt may control IOP.
Treatment of proliferative retinopathy by pan-retinal photocoagulation.
Treatment of pseudoiritis:
Topical steroid eye drops.
Treatment of carotid stenosis:
Anti-platelet therapy, oral anti- coagulants
Surgical – carotid endarterectomy

Retinal dystrophies and Degeneration

INTRODUCTION
Retina is the innermost nervous layer of the eye ball.

It extends from optic disc to ora serrata with surface area of 266 sq.metre.

Gross division:

1. Posterior pole - optic disc -beginning of optic nerve- devoid of rods and cones
(physiological blind spot)

- Macula lutea (yellow spot)- it has highest visual acuity. Fovea centralis is
central depressed part of macula with highest visual acuity as it contains only cones.

2. Peripheral retina –anterior to the retinal equator limited by ora serrata

Separated by retinal equator (imaginary line in line with exit of four vena
verticose).

Layers of Retina:

➢ Layers of rods and cones

➢ External limiting membrane
➢ Outer nuclear layer
➢ Outer plexiform layer
➢ Inner nuclear layer
➢ Inner plexiform layer
➢ Ganglion cell layer
➢ Nerve fibre layer
➢ Internal limiting membrane

Blood supply of retina:

Outer four layers are avascular and get their nutrition from choroidal vascular system formed by
anterior and posterior ciliary arteries.

Inner six layers are supplied by the central retinal artery, branch of ophthalmic artery

RETINAL DYSTROPHIES:
Hereditary dystrophies commonly affect the outer retina (RPE and photoreceptor)

Classsification:

General photoreceptor dystrophies:

They involve the entire retina (periphery more than the macula)

Typical retinis pigmentosa and its variants

Progressive cone dystrophy

Leber congenital amaurosis

Congenital stationary night blindness

Congenital monochromatism

Macular dystrophies:

Juvenile best macular dystrophy

Stargardt’s disease

Vitelliform dystrophy

RETINITIS PIGMENTOSA:

This is a slow, degenerative disease of retina.

Affecting both eyes

Beginning in childhood resulting in blindness in middle or advanced age.

The degeneration primarily affects rods and cones, rods first and cones later.

Commences in equator of eye then spreading gradually anteriorly and posteriorly.

Inheritance: Sporadic disorder include mutation of rhodopsin(40%)

Inherited disorder: AR-most common-intermediate severity

AD-next common-least severe

X linked –least common-most severe

Prevelance: Occurs 1 in 5000 of population, common in males (3:2).

Pathogenesis: Death of rod photoreceptor(apoptosis),later the cones die
Clinical features:

Visual symptoms(Due to loss of rods)

Night blindness
Dark adaptation: Light threshold of peripheral retina is increased
Tubular vision: Loss of peripheral vision with preservation of central vision.
Loss of central vision after many years.

Fundus change

Retinal pigmentary change : Small, jet-black spots resembling bone corpuscles with spidery outline
(the pigment of RPE migrates into retinal layer-epithelium becomes decolorized –choroidal vessels
are seen ,fundus appears tessellated)
Retinal arterioles become thread like
Thinning and atrophy of RPE at peripheral retina.
Optic disc: Has a pale, wax like yellowish appearance – ‘consecutive optic atrophy’
Progressive posterior cortical cataract is formed.

Visual field change

Annular or Ring shaped scotoma: Degenerated equatorial zone of retina.

Electrophysiological changes

Subnormal Electroretinogram(ERG) and Electrooculogram(EOG).

Assosiations:

Occular: Myopia
Primary open angle glaucoma
Microphthalmus
Posterior subcapsular cataract

General:
Laurence-Moon-Biedl-Bartum syndrome – retinitis pigmentosa , obesity, hypogonadism, mental
defect, polydactyl
Usher’s syndrome – retinitis pigmentosa, cardiac conduction defects and abetalipoproteinemia .
Refsum’s syndrome – retinitis pigmentosa , cerebellar ataxia and peripheral neuropathy

Atypical retinitis pigmentosa

Retinitis pigmentosa sine pigmento: Al symptoms are same , no pigmentary change in retina.
Retinitis punctate albicans: Numerous white dots scattered over the fundus.
Cone –rod dystrophy:
Cones are degenerated first
Symptoms:
Loss of central vision
Colour vision is defective

Defective vision in bright light

Sectorial retinitis pigmentosa: Segment of retina is affected.

Pericentric retinitis pigmentosa: Area around macula is affected

TREATMENT

Measures to stop progression-------vasodilators, placental extracts, light exclusion therapy, ultrasonic

therapy, acupuncture therapy

Correction of refractive error ------Glasses

Systemic acetazolamide ------- associated cystoid macular oedema

Low vision aids--------magnifying glasses, night vision device

Rehabilitation

Prophylaxis:------Generic counselling-no consaguinous marriage

-affected not to produce children

RETINAL DEGENERATION:
These acquired disorders of retina characterized by degenerative changes

Classification:

Peripheral retinal degeneration

Vitreoretinal degeneration

Macular degeneration

Peripheral retinal degeneration:

Occurs at the periphery in front of the equator.

1. Lattice degeneration:

-Characters:

White arborizing lines arranged in lattice pattern in upper peripheral fundus

Retinal thinning

Abnormal pigmentation

Typical lesion –spindle shaped

Mainly involves superior temporal region of fundus

Snail tract degeneration:

Variant of lattice-white lines replaced by snow flake areas-retina-white frost like appearance.
Acquired(senile) retinoschisis:

Splitting of retina at the level of outer plexiform layer

Common in hypermetropes

Occurs bilaterally

Involves lower temporal quadrant

Thin , transparent, immobile elevation of inner layers of retina

White without pressure:

Pale, discrete areas of retinal periphery due to vitreous traction

White with pressure:

Greyish translucent appearance of retina seen on scleral indendation

6.Focal pigment clumps:

Small, irregular pigmentation seen in equatorial region associated with vitreous detachment or
retinal tear.

7.Diffuse chorioretinal degeneration:

Common in myopic eyes

Choroid depigmented

Retina thin

Prone to tears

8.Peripheral cystoid retinal degeneration:

Common in old people

May predispose to retinal detachment in very old people.

 Vitreoretinal degenerations:

Wagner’s syndrome

AD

Vitreous is liquefied with condensed membranes

Retina-narrow sheathed vessels,pigmented spots in periphery

Choroid -atrophied

Cataract-late complication

Stickler syndrome:

AD

Vitreous liquefied –optically empty vitreous cavity

Progressive myopia

Radial lattice like degeneration

Bilateral retinal detachment

Ectopia lentis

Pre senile cataract

Orofacial abnormalities – flattened nasal bridge , maxillary hypoplasia, cleft palate , high arched
palate…
Arthropathy

Deafness

Mitral valve prolapse

3.Favre –goldmann syndrome:

AR

Vitreous shows syneresis

Retinoschisis

Pigmentary chnges present

ERG is subnormal

MACULAR DEGENERATION

Age related macular degeneration :

Leading cause of blindness in people over 65 years of age in developed countries.

Bilateral

Risk factors: hereditary factors , age , nutrition , sunlight , hyperopia , blue eyes, nuclear cataract

Two types:

Dry or atrophic

Wet or exudative

Dry or atrophic:

Thinning of macular tissue

Amorphous deposits and pigmentation in macula(drusens-yellowish white deposits)

Symptoms: Gradual diminution of vision, difficulty in reading due to central shadowing

Stages: Early stage: macular drusens (<20),focal hyper pigmentation ,

RPE atrophy

Intermediate stage: RPE atrophy with >20medium drusens

and one large drusen

Advanced stage: large atrophic areas with visible choroidal

Vessels and disappearance of drusen

Wet or exuadative type:

New leaky vessels forma choroidal neovascular membrane(CNV)

(sub-RPE --- greenish grey and subretinal---halo or pigment plaque)

Symptom: Sudden painless loss of vision

Typical lesion: drusen with RPE detachment , hemorrhagic pigment epithelium detachment ,
disciform subretinal scarring .

Diagnosis:

1.Typical signs

2. Fundus fluorescein angiography and indocyanine green angiography----CNV

3. Optical coherence tomography–reveals subretinal fluid CNV,hemorrhages,intraretinal thickening

Treatment:

1.Atrophic ARMD

Vitamin C , A and E supplements , zinc oxide , cupric oxide and other antioxidants

Smoking cessation

Amsler grid

Correction of refraction

Low vision aid

2.Exudative ARMD

Intravitreal anti-VEGF therapy-Bevacizumab,Ranibizumab,..

Photodynamic therapy

Transpupillary thermotherapy

Photocoagulation

Surgical treatment
2.MYOPIC MACULAR DEGENERATION:
Chorioretinal atrophic patches at macula with heaping up of pigment around them.

Foster-Fuchs’ spot seen at macula(dark red patch due to subretinal CNV)

3.MACULAR HOLES:

CAUSES: Senile, traumatic,tractional forces associated with early PVD.

Symptoms: decreased vision, metamorphopsia,central scotoma.

Investigation: OCT, fundus fluorescein angiography.

Stages: Stage 1 : absent foveal reflex and yellow spot

Stage 2: small,l full thickness hole in centre or margin of ring

Stage 3: full thickness reddish spot surrounded by grey halo

Stage 4:Full thickness hole with Srf cuff and complete PVD.

Treatment: Stage 2 -4 : pars plana vitrectomy with posterior hyaloid removal ,ILM peeling and gas or
silicon tamponade with strict post-operative face down position for 7-14 days.

MACULAR DISORDERS
HEREDITARY MACULAR DYSTROPHIES

SOLAR RETINOPATHY

CENTRAL SEROUS CHORIORETINOPATHY

CYSTOID MACULAR OEDEMA

MACULA
Macula is an oval shaped pigmented area near the centre of retina of human eye. (5.5mm in
diameter)

It is responsible for central, high resolution, colour vision.

It is subdivided into umbo, foveola, foveal avascular zone, fovea, parafovea, and perifovea areas.
Macular disorders are classified into

Congenital anomalies

Hereditary dystrophies

Acquired maculopathies

HEREDITARY MACULAR DYSTROPHIES

They can be classified according to anatomical level of retinal involvement as

 Hereditary macular disorders

INNER RETINA PHOTORECEPTORS

RETINAL PIGMENT EPITHELIUM
• X LINKED • CONE-ROD
JUVENILE DYSTROPHY • BEST’S DISEASE
RETINOSCHISIS • STARGARDT’S DISEASE
• FUNDUS
FLAVIMACULATUS

X LINKED JUVENILE RETINOSCHISIS

Juvenile retinoschisis is characterized by bilateral maculopathy, with associated peripheral

retinoschisis in 50%.

The basic defect is mediated via the Muller cells, leading to splitting of the retinal nerve fibre layer
from the rest of the sensory retina. [Muller cells are located in the inner nuclear layer of retina and
maintains structural and functional stability of retinal cells.]

Implicated gene is RS1

Affects mainly young males

Signs:

Gradual progressive loss of vision during first or second decade of life

Symptoms:

The most common appearance is foveal schisis, appearing as spoke-like striae radiating from the
foveola.
Peripheral retinoschisis in 50% cases

Presence of vitreous veils in extreme cases- floating of retinal blood vessels

Investigations:

Fundus Fluorescein Angiography (FFA) – Normal posterior pole

Electroretinogram (ERG) – negative

Electrooculogram (EOG) – normal

Treatment:

Topical carbonic anhydrase inhibitors

Gene therapy

CONE ROD DYSTROPHY

(also known as cone dominant dystrophy)

Mostly sporadic but may e autosomal dominant, autosomal recessive or X linked.

Symptoms:

Reduced central vision which is more marked in bright light (Hemeralopia).

On fundus examination, fundus may be normal or in some cases, bilateral Bull’s eye pattern of
macular depigmentation maybe seen.

Investigations:

FFA – patchy areas of hypo and hyper fluorescence.

Bull’s eye pattern- zone of hypo fluorescence over a central non fluorescent part.

ERG- marked loss of cones and moderate loss of rods

 BEST’S DISEASE

(also known as Best vitelliform macular dystrophy)

Autosomal dominant. It is due to allelic variation in the BEST1 gene.

Clinical picture of Best’s diseases is divided into:

Pre- vitelliform stage – normal fundus, abnormal EOG

Vitelliform stage- egg yolk lesion at macula

Pseudohypopyon stage- partially absorbed egg yolk lesion

Vitelli eruptive stage- scrambled egg appearance of macula

Stage of scarring – hypertrophic or atrophic vascularised scar at macula

Investigations:

Normal ERG, abnormal EOG

Fundus auto fluorescence – intense hyper auto fluorescence of the yellowish lesions and hypo auto
fluorescence in the atrophied areas.

STARGARDT’S DISEASE AND FUNDUS FLAVIMACULATUS

Stargardt disease (juvenile macular dystrophy) and fundus flavimaculatus (FFM) are regarded as
variants of the same disease, and together constitute the most common macular dystrophy.

Stargardt disease is a recessive, progressive tapetoretinal dystrophy of the central retina and
develops between the ages of 8 and 14 years.

Increased vitamin A intake is associated with the progression of the disease.

The condition is characterized by the accumulation of lipofuscin within the RPE.

Symptoms:
Gradual impairment of central vision.

On fundus examination, Stargardt’s disease show beaten bronze or snail slime reflex in macular area
and fundus flavimaculatus shows yellowish white retinal flecks of variable size and shape distributed
over whole of posterior pole

snail slime lesion

Investigations:

ERG is usually normal for Stargardt’s disease but there will be changes in full field ERG for fundus
flavimaculatus.

SOLAR RETINOPATHY

(also known as photo retinitis, eclipse retinopathy, blue light retinal injury)

Causes of solar retinopathy:

Religious sun gazing, solar eclipse observing, telescopic solar viewing, sun bathing and sun watching
in psychiatric disorders.

Welding arc exposure

Lightening retinopathy

Retinal phototoxicity from ophthalmic instruments like operating microscope

Pathogenesis:

Photochemical reaction following exposure of retina to shorter wavelength in the visible spectrum.

Symptoms:

Persistence of negative after image of the sun

Decreased vision
Signs:

Small yellow spot with grey margin may be noted in the foveolar and para foveolar region

Typical lesion: central burnt-out hole in the pigment epithelium surrounded by aggregation of
mottled pigment

Through ophthalmoscope: bean-or kidney shaped pigmented spot with yellowish white centre in the
foveal region, macular holes in worse cases.

CENTRAL SEROUS CHORIORETINOPATHY

(also known as central serous choroidopathy, central serous retinopathy)

Central serous choroidopathy is a focal disease of the retinal pigment epithelium and
choriocapillaris.

Risk factors:

Males of 20-50 years are more at risk

Type A personality

Steroid intake

Emotional stress

SLE

Pregnancy

Cushing’s disease

Pathogenesis: Choroidal vascular hyperpermeability theory

Sympathetic drive,
sympathomimetics,
corticosteroids

Alter choroidal vascular

permeability
Affects auto regulation
 Increases tissue
hydrostatic pressure

Pigment epithelial defect

Breach in outer blood

retinal barrier

Leakage of fluid

Development of localised
serous detachment of
neurosensory retina
Symptoms:

Unilateral blurring, metamorphopsia, micropsia and mild dyschromatopsia

Signs:

Fundus examination shows:

Mild elevation of macular area, demarcated by a circular ring-reflex

Small, yellow grey elevations

Absence of foveal reflex

Subretinal deposits

Clinical Course

Acute classic CSCR (central serous chorioretinopathy): short clinical course with spontaneous
resolution within 3-6 months

Chronic CSCR: diffuse retinal pigment epitheliopathy

Bullous CSCR: rare, large and more numerous areas of serous detachments

Investigations:
in-point defect in Bruch’s membrane results in a smokestack or inkblot appearance in the late

phases.

FFA: Ink blot pattern: small hyperfluorescent spot which gradually increases in size

FFA: Smoke stack pattern: small hyperfluorescent spot which ascends vertically like a smoke-stack
and gradually spreads laterally to take a mushroom or umbrella configuration

Indocyanine angiography: multiple areas of hyper fluorescence (hyperpermeability of choroid)

Treatment:

Corticosteroid treatment should be discontinued if possible

Laser photocoagulation in chronic and recurrent cases

Photodynamic therapy (PDT)

Anti- VEGF

CYSTOID MACULAR OEDEMA

Accumulation of fluid in the outer plexiform and inner nuclear layers of the retina with the
formation of tiny cyst-like cavities.

Etiology:

Complication of ocular treatment (e.g.: ocular surgery)

Retinal vascular disorders (e.g.: diabetic retinopathy)

Intraocular inflammations (e.g.: pars planitis)

Retinal dystrophies (e.g.: retinitis pigmentosa)

Vitreomacular traction

Systemic disease

Fundus tumours (e.g.: retinal capillary haemangioma)

Drug-induced (e.g.: topical prostaglandin derivatives)

Pathogenesis:

Breakdown of inner
blood retinal barrier

Leakage of fluid
 Accumulation in
outer plexiform and
inner nuclear layer
of retina and
formation of cyst-
like changes

Symptoms:

Blurring, distortion and micropsia

Signs:

Loss of the foveal depression, thickening of the retina and multiple cystoid areas in the sensory
retina

Investigations:

Ophthalmoscopy reveals a typical Honey-comb appearance

Fundus fluorescein angiography: flower petal appearance

Treatment:

Treatment of the causative factor

Topical anti prostaglandin drops

Topical and systemic steroids

Systemic carbonic anhydrase inhibitors (CAIs) e.g., oral acetazolamide

Age Related Macular Degeneration (ARMD)

aka Senile macular degeneration

Bilateral disease affecting people above 50yrs of age

Most common cause of Irreversible visual loss in developed countries

Risk Factors:-

Age – Major risk factor

Race – More common in white individuals than other races

Heredity –

Risk of ARMD is 3x higher if a first degree relative has the disease

Variation in Complement factor H gene and ARMS2 gene increase risk

Smoking – Doubles the risk

Hypertension and CVS risk factors aggravate ARMD

Dietary factors – High fat intake and obesity promotes ARMD

Aspirin – Increases risk of neovascular ARMD

Other-

Cataract surgeries

Blue iris

High sunlight exposure

Female gender

Classification:-

Conventional classification

Clinical classification

Conventional classification:

1.Non exudative (or) Atrophic ARMD

aka Dry (or) Geographic ARMD

90% of cases

Symptoms – Gradual loss of vision, Distorted vision and Difficulty in reading

Lesions are described in 3 stages:

1.Early stage, characterized by:

# Small or medium sized Drunsens(They are well defined, yellowish white, slightly elevated spots)

#Focal pigmentation

#Pale area of Retinal Pigment Atrophy(RPE)

2.Intermediate stage, shows:

#Sharply circumscribed areas of RPE atrophy

#Loss of Choriocapillaries with large/medium drunsen

3.Advanced stage, with:

#Enlargement of atrophic areas

#Choroidal vessels become visible

 #Pre-existing Drunsen disappear

2.Exudative ARMD

aka Wet (or) Neovascular ARMD

10% of cases

Major symptom is Rapidly progressing loss of vision

Chronological appearance of lesions :

Drunsen with Retinal Pigment Epithelial Detachment(PED)

Choroidal neovascularization

Haemorrhagic PES

Haemorrhagic detachment of neurosensory retina

Disciform sub-retinal scarring

Clinical classification:
Diagnosis:-

Above signs are detected using Slit Lamp Biomicroscopy

Fundus Fluorescence Angiography helps to detect Choroidal Neovascularization (CNC).

It’s of 2 types-

1.Classical CNV – Seen as lacy hyperfluorescence

2.Occult CNV – Seen as stippled hyperfluorescencec Optic Coherence Tomography(OCT) reveals

Subretinal fluid, Intraretinal thickening, CNV and haemorrhage in exudative ARMD

Treatment:-

1.Treatment for Non exudative ARMD:

Dietary supplements and antioxidants

Smoking cessation

Amsler grid is used to detect new or progressive metamorphosis

Refraction with increased near add is useful in early cases

Low vision aid is useful in advanced cases

2.Treatment for Exudative ARMD:

Intravitreal anti-VEGF therapy – First choice treatment. Improves vision in 30%-40% of cases

Photodynamic Therapy (PDT) – Treatment of choice after anti VEGF injections

Transpupillary thermotherapy(TTT)

Double frequency YAG 532nm photocoagulation

Surgical treatment

Macular Hole

It refers to a partial or full thickness hole in the Neurosensory Retina

Causes:-

1.Idiopathic(83%) -More common in females than males(3:1 ratio)

2.Traumatic(5%)

3.Other causes – Cystoid Macular oedema, Vitreomacular traction, Post surgical

Pathogenesis:-

Caused by Tractional forces associated with early PVD(Post Vitreous Detachment)

Clinical Features:--
1.Decreased vision

2.Metamorphopsia (or) distortion of vision

3.Central scotoma

Signs:-

1.Amsler Grid testing – shows central scotoma

2.Watze Allen test – shows a line appearing broken which indicates macular hole

3.Fundus Examination – basis for Gass classification of Macular hole

Gass classification of Macular hole:

Stage 1 (or) Impending hole

Absence of foveal reflex

Yellow spot/ring in foveal region

OCT reveals pseudocyst

Stage 2

Small full thickness hole seen centrally or eccentric

Less than 400 mm(micrometer)

Stage 3

Full thickness hole seen as round reddish spot

Grey halo surrounds it

No PVD

OCT shows macular hole greater than 400mm

Stage 4

Full thickness hole with SRF(Subretinal fluid) cuff

Complete PVD

OCT confirms large thick holes with PVD from disc and macula
Differential Diagnosis of fundus appearance:-

Macular pucker with pseudohole

Solar retinopathy

Intraretinal cyst

Vitreomacular traction syndrome

Investigation:-

1.Fundus fluorescein angiography

2.OCT

Treatment:-

Stage 1 : Treatment not recommended. Close follow up and observation only required

Stage 2-4 : Treatment with

Pars plana vitrectomy with post hyaloid removal

Internal Limiting Membrane peeling

Gas or silicon oil tamponade with strict post-op

Prognosis:-

80%-90% show anatomical closure

Visual improvement reported in 70% of recent onset hole

Complications of surgery:-

Occurrence or progression of Cataract (common complication)

Other complications-Retinal breaks, detachment, phototoxicity, endophthalmitis.

RETINAL DETACHMENT:

Retinal detachment (RD) refers to separation of neurosensory retina from the retinal pigment
epithelium (RPE).

CLASSIFICATION:

1. Rhegmatogenous or primary retinal detachment,

2. Tractional retinal detachment, and

3. Exudative retinal detachment.

RHEGMATOGENOUS OR PRIMARY RETINAL DETACHMENT

PREDISPOSING FACTORS:

Age-Most common 40-60 years

Sex-Male: Female: 3:2

Myopia-40% cases

Aphakia or pseudophakia (previous cataract surgery)

• Retinal degenerations such as:

- Lattice degeneration (most common)

-Snail track degeneration

-White-with-pressure and white-without pressure lesions

-Diffuse chorioretinal degeneration

-Acquired (senile) retinoschisis.

6. Trauma

7. Senile posterior vitreous detachment (PVD).

8.Retinoschisis. This is a condition where there is splitting of the neurosensory retina and
vitreous degeneration. It is of two types: -

-Typical Retinoschisis: Split at the level of Outer Plexiform Layer

- Reticular Retinoschisis: Split at the level of Nerve Fibre Layer.

PATHOGENESIS:

CLINICAL FEATURES:

PRODROMAL SYMPTOMS
Photopsia (flashes of light) due to vitreoretinal traction

Dark spots (floaters) in front of the eyes (muscae volitantes).

SYMPTOMS OF DETACHED RETINA

Localized relative loss in the field of vision of detachment retina, which is described by the patient as
a black curtain or veil in front of the eye.

Loss of vision in detachment involving macula area.

SIGNS

Hypotony: The liquefied vitreous in the subretinal space is absorbed through the RPE leading to
hypotony.

Shafer’s sign: Pigments in anterior vitreous (tobacco dusting) is a feature of fresh RD.

Detached retina gives grey reflex, is raised, thrown into folds which oscillate with the movements of
the eye.

Retinal breaks holes (round, horse-shoe-shape or slit like) look reddish and are most frequently
Round in the periphery (commonest in the upper temporal quadrant).

Thinning of detached retina, secondary intraretinal cysts, subretinal demarcation lines are signs of
old RD

COMPLICATIONS

Proliferative vitreoretinopathy

Complicated cataract

Uveitis

Phthisis bulbi

TREATMENT

Prophylactic laser barrage:

It is done in Symptomatic break (associated with photopsia and floaters), Horse shoe tear, Superior,
especially superotemporal tears, Aphakia, One eyed patient

Surgery for retinal detachment

Scleral buckling: In this procedure, the sclera is indented by attaching an explant known as a buckle.
This pushes the RPE inwards towards the neurosensory retina. Subretinal fluid is drained and the
break is closed by laser or cryotherapy

Pneumatic retinopexy: In this procedure, the neurosensory retina is pushed towards the RPE by
injecting an expansile gas in the vitreous cavity. The break is then sealed with laser. Th commonly
used are Sulphur Hexafluoride and Perfluoropropane (C3F8)

Pars plana vitrectomy

TRACTIONAL RETINAL DETACHMENT:

PATHOPHYSIOLOGY

Fibrovascular membranes in the vitreous due to long standing vitreous hemorrhage exert traction on
the retina. This pulls the retina forward leading to retinal detachment.

CAUSES

Proliferative diabetic retinopathy(PDR)

Central retinal vein occlusion

Eales’ disease

Retinopathy of prematurity (ROP).

SIGNS

Detached retina is concave in configuration with highest elevation at the site of the tractional band.
No breaks are seen

Minimal mobility

TREATMENT

Pars plana vitrectomy and endophotocoagulation.

EXUDATIVE RETINAL DETACHMENT

PATHOPHYSIOLOGY

Exudative fluid, mainly from choroid, collects in the sub retinal space leading to retinal detachment.

CAUSES

Inflammatory conditions like choroiditis, choroidal vasculitis, posterior scleritis

Choroidal tumor like melanoma, hemangioma, metastasis

Toxemia pregnancy

Malignant hypertension

Coat’s disease,

Symptoms

Floaters due to vitritis but no photopsia

Visual field defect

Loss of vision due to involvement of macula

SIGNS

Detached retina has a convex configuration. Surface is smooth. No break Is seen.

Shifting fluid is seen

TREATMENT
Systemic steroid

Treatment of the cause,

1. Classification:

A. Primary tumours

1. Neuroblastic tumours. : These arise from sensory retina (retinoblastoma and astrocytoma) and

Pigment epithelium (benign epithelioma and melanotic malignant tumours).

2. Mesodermal angiomata :e.g., cavernous haemangioma.

3. Phakomatoses:

Angiomatosis retinae (von Hippel-Lindau disease),

tuberous sclerosis (Bourneville’s disease),

neuro- fibromatosis (von Recklinghausen’s disease and

Encephalo-trigeminal angiomatosis (Sturge-Weber syndrome).

B. Secondary tumours

1. Direct extension: e.g., from malignant melanoma of the choroid.

2. Metastatic carcinomas from the gastrointestinal tract, genitourinary tract, lungs, and pancreas.

3. Metastatic sarcomas.

4. Metastatic malignant melanoma from the skin.

B.RETINOBLASTOMA

Most common ocular tumour of childhood

INCIDENCE

rare, occurring in up to 1:18000 live births

most common primary intraocular malignancy of childhood

GENETICS

Mutations in retinoblastoma gene, which is RB 13q14

Deletion or inactivation of this gene by Hudson’s two hit hypothesis

May arise as hereditary or non hereditary forms

Hereditary or familial case

Mutation will occur in all germ cells

Accounts for 40% of all cases

Mostly bilateral

Mostly multifocal

Some have trilateral retinoblastoma

Non hereditary or sporadic cases

Mutation takes place in somatic cells

Accounts for60% of all cases

Unilateral and bifocal

Tumour is not transmissible

3. PATHOLOGY:

a. ORIGIN:

Malignant proliferation of immature retinal cells (retinoblasts)

HISTOPATHOLOGY:

Flexner -Wintersteiner rosettes

Homer Wright Rosettes

Pseudo rosettes

Fleurttees formation

Areas of necrosis and calcification

CLINICAL PICTURE:

4 STAGES

QUIESCENT STAGE

GLAUCOMATOUS STAGE

STAGE OF EXTRAOCULAR EXTENSION

STAGE OF DISTANT METASTASIS

A.QUIESCENT STAGE (6months to 1 yr.)

Leukocoria or yellowish white papillary reflex(amaurotic cats eye appearance)

Squint

Nystagmus

Defective vision
Ophthalmoscopic features like endophytic and exophytjc retinoblastoma

B.GLAUCOMATOUS STAGE (if left untreated)

Severe pain, redness, watering

Enlarged eyeball

Conjunctiva is congested

Cornea becomes hazy

IOP raised

C.STAGE OF INTRAOCULAR EXTENSION

Progressive enlargement followed by the burst through acler

Rapid fungation

Marked proptosis

D.STAGE OF DISTANT METASTASIS

Lymphatic spread

Direct extension

Metastasis by blood stream

5.DIFFERENTIAL DIAGNOSIS :

D/D of leukocoria

Retinoblastoma

Congenital cataract

Persistenthyperplastic primary vitreous (PHPV)

Coats disease

Toxacariasis

ROP

Endophthalmitis

Coloboma

Endophytic retinoblastoma

Exophytic retinoblastoma

6.DIAGNOSIS
EXAMINATION UNDER ANAESTHESIA:Fundus examination,measurement of IOP,corneal diameter

PLAIN X RAYS OF THE ORBIT: Calcification present

LACTIC DEHYDROGENASE :level is raised in aqueous humour

ULTRASONOGRAPHY AND CT SCANNING

7.TREATMENT

1.FOCAL

Cryotherapy

Laser photocoagulation

Transpupillary thermotherapy

SYSTEMIC

Chemotherapy

ENUCLEATION

RETINAL VASCULAR TUMOURS:

Capillary haemangioma

Von Hippel–Lindau disease

Cavernous haemangioma

Racemose haemangioma

Vaso proliferative tumour

CAPILLARY HAEMANGIOMA:

Early tumour-small red oval or round lesions

well-established tumour – round orange-red mass

juxta papillary site is common

TREATMENT:

Observation

Laser photocoagulation

Cryotherapy

Brachytherapy
Vitreoretinal surgery

VON HIPPEL LINDAU DISEASE:

Mutation in the VHL tumour suppressor gene

CLINICAL FEATURES:

CNS haemangioma

Phaeochromocytoma.

Renal carcinoma

Polycythaemia

Cysts of testes , kidney, ovaries, lungs,liver and pancreas

CAVERNOUS HAEMANGIOMA

Rare unilateral congenital hamartoma.

SIGNS

Clusters of saccular aneurysms resembling a ‘bunch of grapes’

‘menisci’

Haemorrhage and epiretinal membrane formation

TREATMENT :

Vitrectomy

CONGENITAL RETINAL ARTERIOVENUS COMMUNICATION (racemose haemangioma)

Vasoproliferative tumour

rare gliovascular lesion

can be primary (80%) or secondary

TREATMENT

Cryotherapy or brachytherapy

PRIMARY INTRAOCULAR LYMPHOMA

The main classification and ocular manifestations

Hodgkin disease.

Non-Hodgkin lymphoma can manifest with conjunctival involvement, orbital involvement, Mikulicz
syndrome and uveal infiltration.

CNS B-cell lymphoma may be associated with intermediate uveitis and sub-RPE infiltrates.

Primary vitreoretinal lymphoma (PVRL)

Primary uveal lymphoma

TREATMENT

Radiotherapy

Intravitreal methotrexate

Systemic chemotherapy

TUMOURS OF THE RETINAL PIGMENT EPITHELIUM

Congenital hypertrophy of the RPE

Congenital hypertrophy of the retinal pigment epithelium (CHRPE) used to encompass three entities
with distinct features and implications:

Solitary CHRPE, grouped CHRPE, Atypical CHRPE.

PHACOMATOSES

Phacomatoses or neurocutaneous syndromes refer to a group of familial conditions (having

autosomal AB dominant transmission) which are characterized by development of neoplasms in eye,
skin and central nervous system. Phacomatoses includes the following conditions:

1. Angiomatosis retinae (Von Hippel Lindau’s syndrome). This is a rare condition affecting males
more often than females, in the third and fourth decade of life. Angiomatosis involves retina, brain,
spinal cord, kidneys and adrenals. Clinical course of angiomatosis retinae comprises vascular
dilatation, tortuosity and formation of aneurysms which vary from small and 72frica7272 to balloon-
like angiomas

2. Tuberous sclerosis (Bourneville disease). It is characterized by a classic diagnostic triad of

adenoma sebaceum, mental retardation and epilepsy associated with hamartomas of the brain,
retina and viscera. The name tuberous sclerosis is derived from the potato-like appearance of the
tumors in the cerebrum and other organs.

3. Neurofibromatosis (von Recklinghausen’s disease). It is characterized by multiple tumours in the

skin, nervous system and other organs. Cutaneous manifestations are very characteristic and vary
from I-au-lait spots to neurofib romata. Ocular manifestations include neurofibromas of the lids and
orbit, glioma of optic nerve and congenital glaucoma.
 4. Encephalofacial angiomatosis (Sturge-Weber syndrome). It is 73frica7373ival73 by angiomatosis
in the form of port-wine stain (naevus flammeus), involving one side of the face which may be
associated with choroidal haemangioma, leptomeningeal angioma and congenital glaucoma on the
affected side.

ENUCLEATION

Enucleation refers to excision of the eyeball. It can be performed under local anaesthesia in
adults and under general anaesthesia in children. Indications

1. Absolute indications are retinoblastoma and malignant melanoma.

2. Relative indications are painful blind eye, nonresponsive to conservative measure mutilating
ocular injuries

3. Indication for eye donation from cadaver is presently the most common indication
 NEURO – OPHTHALMOLOGY

What will we learn here???

▪ Anatomy of visual pathway

▪ Physiology of vision
▪ Lesions of visual pathway
Optic nerve lesions
Chiasmal lesions
Retrochiasmal lesions
▪ Pupillary reflexes and their abnormalities
Light reflex
Near reflex
Abnormalities of pupillary reactions
Anisocoria
▪ Diseases of optic nerve
Optic neuritis
Leber’s hereditary optic neuropathy
Autosomal heredity optic atrophy
Toxic optic neuropathy
Anterior ischemic optic neuropathy
Traumatic optic neuropathy
Papilloedema
Optic atrophy
▪ Symptomatic disturbance of vision
Night blindness
Day blindness
Color blindness
Amaurosis
Amblyopia
Cortical blindness
Malingering
Disorders of higher visual functions
▪ Ocular manifestation of diseases of CNS
 ANATOMY OF VISUAL PATHWAY

The visual pathway starts from retina and ends in visual cortex

lateral
optic optic optic visual
retina optic tracts geniculate
nerves chiasma radiations cortex
bodies

Blood supply: (important)

• Surface layer of optic disc – capillaries from retinal arterioles

• Prelaminar region – centripetal branch of peripapillary choroid
• Lamina cribrosa – posterior ciliary arteries branches and arterial circle of Zinn
• Retrolaminar part – centrifugal branches of central retinal artery and centripetal
branches from pial plexus

PHYSIOLOGY OF VISION

Feature Somatic sensation Visual sensation

Sensory end organ Nerve endings in the skin
Neurons of 1st order Lie in posterior root
ganglion
Neurons of 2nd order Lies in nucleus gracilis or
cuneatus
Neurons of 3rd order Lies in thalamus
Rods and cones
Lies in bipolar cell layer of
the retina
Lies in ganglion cells of the
retina
Lies in geniculate body
 LESIONS OF THE VISUAL PATHWAY

lesions of visual
pathway

retrochiasmal
optic nerve lesions chiasmal lesions
lesions

OPTIC NERVE LESIONS

Lesions in distal part of optic nerve Lesions in proximal part of optic

nerve
Salient • Ipsilateral complete blindness • Ipsilateral blindness
features • Abolition of the direct light reflex • Contralateral hemianopia
and consensual of contralateral • Abolition of the direct light reflex
side and consensual of contralateral
• Accommodation reflex is present side
• Accommodation reflex is present
Common • Optic atrophy
causes • Trauma
• Indirect optic neuropathy
• Ischemic optic neuropathy
• Acute optic neuritis

CHIASMAL LESIONS
Causes:

• Intrinsic
→ Glioma and multiple sclerosis
• Extrinsic
→ Pituitary adenoma, craniopharyngiomas and meningioma
• Other causes
→ Metabolic, toxic, traumatic and inflammatory conditions
 Chiasmal syndrome

Chiasmal Features Causes

syndrome
Anterior • Junctional scotoma – a combination • Lesions affecting the ipsilateral
of central scotoma in one eye and optic nerve fibres and contralateral
temporal hemianopia defect in inferonasal fibres located in
another eye Willebrand knee
Middle • Bitemporal hemianopia and • Lesions involving the decussating
• Bitemporal hemianopic paralysis of fibres in the body of chiasma
pupillary reflex
Posterior • Paracentral bitemporal field defects • Lesions affecting caudal fibres in
• Contralateral homonymous chiasma
hemianopia
Lateral • Binasal hemianopia • Distension of 3rd ventricle
• Binasal hemianopic paralysis of • Atheroma of posterior
pupillary reflexes communicating arteries or carotids

RETROCHIASMAL LESIONS

Retrochiasmal
lesions

lesions of lateral
lesions of optic lesions of optic lesions of visual
geniculate
tract radiations cortex
nucleus

Lesions of optic tract

→ Causes
▪ Intrinsic lesions – demyelinating diseases and infarctions
▪ Extrinsic lesions – compressive lesions
▪ Other causes – syphilitic or tubercular meningitis

→ Characteristic features
▪ Incongruous homonymous hemianopia
▪ Wernicke’s reaction
▪ Descending type of partial optic atrophy
▪ Ipsilateral third nerve palsy and ipsilateral hemiplegia
Lesions of lateral geniculate nucleus
→ Characteristic features
▪ Homonymous hemianopia
▪ Descending type of partial optic atrophy

Lesions of optic radiations

→ Common lesions – vascular occlusions, tumours, trauma, temporal lobectomy for
seizures
→ Characteristic features

Depending on the site it could be

▪ Superior quadrantic hemianopia
▪ Inferior quadrantic hemianopia
▪ Complete homonymous hemianopia

Lesions of visual cortex

→ Characteristic features

Visual field defects

▪ Congruous homonymous hemianopia
▪ Congruous homonymous macular defects
▪ Bilateral homonymous hemianopia with macular sparing
▪ Bilateral homonymous macular defects
Other defects
▪ Cortical blindness
▪ Dyschromatopsia
▪ Visual hallucinations
▪ Palinopsia
▪ Visual anaesthesia
▪ Polyopsia
PUPILLARY REFLEXES AND THEIR ABNORMALITIES

LIGHT REFLEX
NEAR REFLEX
 ABNORMALITIES OF PUPILLARY REACTIONS
• Amaurotic light reflex – absence of direct light reflex on affected side and consensual
reflex on the normal side
• Efferent pathway defect – absence of both direct and consensual light reflex on the
affected side only
• Wernicke’s hemianopic pupil – lesion in optic tract. ipsilateral direct and
contralateral consensual reflex is absent
• Marcus Gunn pupil – due to relative afferent pathway defect.
• Argyll Robertson pupil – both pupils are small and irregular. light reflex absent. near
reflex present.
• Adies tonic pupil – light reflex absent. near reflex is slow and tonic

ANISOCORIA
Definition
Difference between the size of two pupils is known as anisocoria
Causes

• physiological
o minimal
• pathological
o due to abnormal miosis and mydriasis of one pupil

Evaluation

• pupil size
• pupillary light reflex
• pharmacological tests
 DISEASES OF OPTIC NERVE

diseases of
optic nerve

congenital inflammatory vascular

trauma degeneration tumours
anomalies conditions distrubances

OPTIC NEURITIS
Introduction:
An inflammation of the optic nerve is known as optic neuritis.

Etiology:

• Idiopathic
• Hereditary optic neuritis
• Demyelinating disorders
• Parainfectious optic neuritis
• Infectious optic neuritis
• Autoimmune disorders
• Toxic optic neuritis

Clinical profile:
Anatomical types

anatomic
classification

retrobulbar
papillitis neuroretinitis
neuritis
 ▪ Typical neuritis – optic neuritis associated with demyelinating disorders as in multiple
sclerosis
▪ Atypical neuritis – optic neuritis associated with causes other than demyelinating
disorders

Clinical features
Symptoms Signs
• Vision loss – monocular, sudden, • ↓ visual acuity
progressive and profound loss • ↓ colour vision
• ↓ dark adaptation • Marcus Gunn pupil
• Visual obscuration in bright light • Central or centrocaecal scotoma
• Impaired colour vision • ↓ contrast sensitivity
• Uhthoff’s symptom
• Pulfrich’s phenomenon

Differential diagnosis
▪ Papillitis
▪ Acute retrobulbar neuritis

Investigations
▪ Multifocal VEP
▪ MRI scan of brain and orbit

Treatment
▪ Treat the underlying cause
▪ Corticosteroid therapy
o Oral prednisolone therapy
o Methylprednisolone i.v.
▪ Interferon therapy
 LEBER’S HEREDITARY OPTIC NEUROPATHY

Introduction
▪ It is characterised by sequential subacute
optic neuropathy in males aged 11 – 30
years.

Etiology
▪ Point mutation in mitochondrial DNA – MT-
ND4 GENE.
▪ Transmitted by carrier females.

Clinical features
▪ Early cases – asymptomatic
▪ ↓ bilateral visual acuity
▪ Centrocaecal scotoma among others

Investigations
▪ Oct optic disc – peripapillary retinal thinning
▪ Fluorescein angiography
▪ Genetic testing

Treatment
▪ No known effective treatment
▪ Avoid smoking and alcohol
▪ Avoid dietary deficiency – vitamin B12
▪ Low vision aids
 AUTOSOMAL HEREDITY OPTIC ATROPHY

autosomal

recessive dominant

Autosomal recessive optic atrophy (infantile)

▪ Severe visual loss at birth or within 2 years of life
▪ Commonly associated with nystagmus

Autosomal dominant optic atrophy (juvenile)

▪ Associated with mutation of opa1 gene on chromosome 3
▪ Characteristic feature
o Onset – insidious
o Slowly progressive
o ↓ colour vision
o Temporal pallor of optic disc
o Centrocaecal scotoma in visual field

Wolfram’s syndrome – gene defect localised in chromosome 4

Consists of
▪ Diabetes mellitus
▪ Optic atrophy
▪ Deafness
 TOXIC OPTIC NEUROPATHY

Also known as nutritional optic neuropathy and toxic amblyopia

types

tobacco ethyl alcohol methyl alcohol quinine ethambutol

amblyopia amblyopia amblyopia amblyopia amblyopia

Tobacco – alcohol / nutritional amblyopia

Predisposing factors
▪ Pipe smokers
▪ Heavy drinkers
▪ Diet deficiency in proteins and vitamin b complex

Pathogenesis
Excessive tobacco smoking
↓ ↓ cyanide detoxification due to
↑ cyanide in blood ← alcoholic’s dietary deficiency of
↓ sulfur rich proteins
Degeneration of ganglion cells
particularly of the macular region
↓
Degeneration of Toxic
Papillo- macular bundle → Amblyopia
in the nerve
 Clinical features Treatment Prognosis

▪ Bilateral ▪ Complete cessation of tobacco and alcohol Good

centrocaecal consumption
scotoma ▪ Hydroxocobalamin
▪ Thiamine
▪ Peripapillary ▪ Folate
haemorrhage ▪ Care of general health and nutrition

Ethyl alcohol amblyopia

▪ Usually occurs in tobacco amblyopia
▪ Can occur in non-smokers, heavy drinkers suffering from chronic gastritis.
▪ Clinical features and treatment are similar to tobacco amblyopia
▪ Prognosis not good

Methyl alcohol amblyopia (methanol poisoning)

Etiology
▪ Intake of wood alcohol
Pathogenesis
▪ Methyl alcohol oxidised into formic acid and formaldehyde in tissues. They cause
edema followed degeneration of ganglion cells of retina resulting in complete
blindness.

Clinical features
General symptoms Ocular features
Headache Complete blindness
Nausea Mild disc edema
Vomiting Markedly narrowed blood vessels
Dizziness Bilateral primary optic atrophy
Delirium

Treatment
▪ Gastric lavage
▪ Administration of alkali
▪ Ethyl alcohol
▪ Eliminative treatment

Prognosis is poor
 ANTERIOR ISCHAEMIC OPTIC NEUROPATHY

Introduction
▪ It refers to ischemic damage to the optic nerve head from occlusion of the short
posterior ciliary arteries.

Types
▪ Arteritic anterior ischemic optic neuropathy (AAION)
▪ Non arteritic anterior ischemic optic neuropathy (NAAION)

AAION NAAION
Etiology ▪ Inflammatory and thrombic ▪ Unknown
occlusion of short posterior
ciliary arteries caused giant
cell arteritis
Clinical ▪ Headache ▪ Headache
features ▪ Tenderness ▪ Scalp tenderness
▪ Jaw claudication ▪ Jaw claudication
▪ Transient ischemic attacks ▪ Amaurosis fugax
▪ Central retinal artery ▪ Visual loss
occlusion ▪ Optic disc edema
▪ Diplopia
Investigations ▪ Fundus fluorescein ▪ ESR
angiography ▪ C reactive proteins
▪ Visual fields ▪ FFA
▪ ESR & c – reactive protein
levels
▪ Temporal artery biopsy
Treatment ▪ Corticosteroid therapy ▪ Addressing systemic
risk factors
▪ Aspirin
 TRAUMATIC OPTIC NEUROPATHY
Types
▪ direct
▪ indirect

Direct Indirect
Less common More common
Due to Direct anatomical disruption of optic Due to Shearing or avulsion of nutrient
nerve in cranio-orbital trauma vessels or by pressure transmitted along
bone to the optic canal

Characteristic features
▪ loss of vision
▪ pupil dilation
▪ loss of ipsilateral direct reflex and contralateral consensual light reflex
▪ Marcus Gunn pupil
▪ diminished light brightness sensitivity
▪ diminished contrast sensitivity
▪ central or centrocaecal scotoma

Investigations
▪ CT
▪ MRI

Treatment
▪ methylprednisolone i.v. in high doses
▪ surgical decompression of optic canal
 PAPILLOEDEMA

Papilloedema is referred to as disc swelling associated with bilateral asymmetrical

increased intracranial pressure

Etiopathogenesis
▪ Congenital conditions
▪ Intracranial space occupying lesions
▪ Intracranial infections and hemorrhages
▪ Obstruction of CSF absorption
▪ Tumours of spinal cord
▪ Idiopathic intracranial hypertension
▪ Systemic conditions
▪ Diffuse cerebral edema

Unilateral papilloedema is seen in Foster Kennedy Syndrome and Pseudo Foster Kennedy
Syndrome

Pathogenesis
Hayreh’s theory is the most accepted theory

alteration in pressure results in stasis of axoplasm

gradient across the lamina in prelaminar region of resulting in papilloedema
cribrosa optical disc

Clinical features
General features
▪ Headache
▪ Nausea
▪ Projectile vomiting
▪ Diplopia
Ocular features
Early Established Chronic Atrophic
Symptoms Absent Transient visual - -
obscuration
Visual Normal Normal ↓ Severely impaired
acquity
Ophthalmic ▪ Obscuration of ▪ Disc edema ▪ Dome of ▪ Greyish white
features disc margins ▪ Obliterated champagne discoloration
▪ Blurring of physiological cork and pallor of
peripapillary cup of optic appearance disc
nerve fiber disc ▪ Central cup ▪ ↓ prominence
layer ▪ Multiple obliterated of the disc
▪ Absence of cotton wool ▪ Presence of ▪ Narrowed
spontaneous spots and corpora retinal
venous superficial amylacea arterioles
pulsation in the hemorrhages ▪ Congested
disc ▪ Tortuous and veins
▪ Mild hyperemia engorged ▪ White
of disc veins sheathing
▪ Splinter ▪ Paton’s lines around blood
hemorrhages vessels
present
Pupillary Normal Normal Normal Impaired light
reactions reflex
Visual Normal Enlargement of Blind spot Concentric
fields blind spot enlarge and contraction of
visual field peripheral field
constrict

Treatment

▪ It’s a neurological emergency

▪ Requires immediate hospitalization
▪ If causative agent isn’t identified, cerebral decompression is done

Prognosis is bad
 OPTIC ATROPHY

▪ It refers to the degeneration of optic nerve which occurs as an end result of any
pathologic process that damages axons in the anterior visual system

ophthalmic
classification

primary consecutive glaucomatous post neuritic vascular

pathological features
Following 3 situations can occur
▪ Degeneration of nerve fibres associated with excessive gliosis
▪ Degeneration and gliosis may be orderly
▪ Degeneration of nerve fibres with negligible gliosis

Etiology
Type Etiology
Primary ▪ Multiple sclerosis
▪ Idiopathic retrobulbar neuritis
▪ Leber’s optic atrophy
▪ Intracranial tumours
▪ Trauma or avulsion
▪ Toxic amblyopia
▪ Tabes dorsalis
Consecutive Secondary to
o Diffuse chorioretinitis
o Retinitis pigmentosa
o Pathological myopia
o Occlusion of central retinal artery
Post neuritic ▪ As a sequela to long standing papilloedema or papillitis
Glaucomatous ▪ Long standing raised ICT
Vascular ▪ Giant cell arteritis
▪ Severe hemorrhage
▪ Severe anemia
▪ Quinine poisoning
Clinical features
▪ Loss of vision
▪ Semi-dilated pupil
▪ Sluggish or absent direct light reflex
▪ Presence of Marcus Gunn pupil

Differential diagnosis
FEATURE PRIMARY SECONDARY CONSECUTIVE
APPEARANCE Chalky white Dirty grey white Waxy pallor
MARGINS Well defined Ill defined Well defined
LAMINA CRIBROSA Well seen Obscured Well seen
VESSELS Normal Peripapillary Allenuation
sheathing
SURROUNDING Healthy Hyaline bodies / Pathology seen
RETINA drusen

Treatment
▪ Treat the underlying cause
▪ Once there is complete atrophy, vision cannot be recovered

SYMPTOMATIC DISTRUBANCES OF THE VISION

NIGHT BLINDNESS

Another name: nyctalopia

Etiology:
▪ Rod dysfunction – vitamin a deficiency, retinitis pigmentosa, congenital high myopia,
oguchi’s disease
▪ Advanced POAG
▪ Media opacities – paracentral lenticular and corneal opacities
 DAY BLINDNESS
Another name: hemeralopia
Causes
▪ Congenital deficiency of cones
▪ Central lenticular opacities
▪ Central corneal opacities

COLOR BLINDNESS
• Normal color vision- trichromate (see 3 primary colors i.e. Red, blue and green)
• Absence of one or more primary colors is defective or absent

dyschromatopsia
congenital
color blindness achromatopsia
acquired

Congenital color blindness – males > females

Dyschromatopsia [color confusion due to deficient to perceive colors]

Anomalous The mechanism to
trichromacy appreciate all the three
colors is present but is
defective in one or two of
them
Protanomalous – defective red color
appreciation
Deuteranomalous – defective green
color appreciation

Tritanomalous – defective blue color

Dichromacy The ability to perceive one
of the 3 primary colours is
absent
Such individuals are known
as dichromates
Blue cone Complete absence of red
monochromatism and green cone function
appreciation
Protanopia – complete red colour
defect
Deuteranopia – complete green color
defect
Tritanopia – complete blue color defect
Achromatopsia
• rod monochromatism
• extremely rare
• autosomal recessive
• Male=female

Characteristics:
▪ Total color blindness
▪ Day blindness (6/60 visual acuity)
▪ Nystagmus
▪ Fundus is usually normal

Acquired color blindness

▪ Following macular and optic nerve damage
▪ Associated with central scotoma and decreased visual acuity
▪ Blue yellow impairment: retinal lesion by CSR, macular edema, shallow retinal
detachment
▪ Red green deficiency: optic nerve lesions such as optic neuritis, Leber’s optic
atrophy, compression of optic nerve
▪ Acquired blue color defect: in old age due to increased sclerosis of lens;
physical absorption of blue rays by increased amber coloured pigments

Tests for color vision:

• Pseudo chromatic charts: most commonly used test using ishihara’s plates; quick
method to screen red color defect
• Hardy rand rittler plates: more sensitive than ishihara’s plates
• Edridge green lantern test: name various colors shown to him by lantern
• Farnsworth munsell 100 hue test: most sensitive test both congenital and acquired
High score= poor vision
• Farnsworth d 15 hues
• City university color vision test
• Nagel’s anomaloscope
• Holmgren’s wools test
currently, there is no treatment for color blindness
 AMAUROSIS

Complete loss of sight in one or both in absence of ophthalmoscopic or other marked

examination

Amaurosis fugax:
Sudden temporary painless monocular loss of vision due to transient failure of retinal
circulation.

Causes:
▪ Carotid transient ischemic attacks
▪ Embolization of retinal circulation
▪ Papilloedema
▪ Giant cell arteritis
▪ Raynaud’s disease
▪ Migraine
▪ Hypertensive
▪ Venous stasis retinopathy

Clinical characteristics:
▪ Typical present as curtain that descends from above or ascends from below to
occupy upper or lower half of visual fields
▪ Lasts for 2 to 5 mins
▪ Resolves in reverse pattern of progression
▪ Shortly after the attack, fundus may normal or show signs of retinal ischemia as
edema, hemorrhage or emboli

Uraemic amaurosis:
▪ Sudden, bilateral complete loss of sight due to toxic materials upon cells of visual
centre in patients with acute nephritis, eclampsia of pregnancy, renal failure.
▪ Presentation: loss with dilated pupil responses to light, fundus normal except
hypertensive retinopathy
▪ Vision returns in 12 to 48 hrs
 AMBLYOPIA
▪ Partial loss of sight in one or both eyes in absence of ophthalmoscopic or other
marked signs
▪ May be congenital or acquired (functional or organic)
▪ Functional amblyopia: from psychical suppression of retinal image, it may be
anisometric/strabismic/stimulus deprivation

CORTICAL BLINDNESS
▪ Bilateral occipital lobe lesion

Causes:
▪ Bilateral occipital infarction by vascular causes
▪ Head injury involving bilateral occipital lobes
▪ Tumors among others

Clinical features:
▪ Bilateral loss of vision
▪ Normal pupillary light reflexes
▪ Visual imagination
▪ Anton syndrome: denial of blindness by the patient who obviously cannot see
▪ Riddoch phenomenon: able to perceive kinetic but not static targets.

Management: thorough neurological and cardiovascular examination to find cause

Treatment: based on the cause

MALINGERING
▪ Person poses to be blind but he is not
▪ He does to gain advantage. He does not show any objective sign. Usually one eye is
said to be blind

Differential diagnosis: to rule out condition with normal anterior segment and fundus.
▪ Amblyopia
▪ Cortical blindness
▪ Retro bulbar neuritis
▪ Cone rod dystrophy
▪ Chiasmal tumors
 Tests for malingering:
▪ Convex lens test:
Place low convex/concave lens (0.25) before blind eye and high power(10d) in
front of normal eye if the patient reads distant words, malingering is proved

▪ Prism base down test:

Place the prism base in normal eye, if the patient says seeing two lights
confirms malingering.

▪ Prism base out test:

Ask to see light source, place the prism of 10d is placed before blind eye. If
patient eye moves inwards proves malingering.

▪ Snellen’s colored types test:

It has letters printed on red and green. Ask the patient to see through red glass
if he reads all letters it confirms malingering because normally red letters only
can be read through red glass.

Hysterical blindness
o It is a form of psychoneurosis, commonly seen in attention seeking females

Characteristic features
o Sudden bilateral loss of vision
o Lacrimation
o Blepharospasm
o Visual fields are concentrically contracted
o Treatment
o Psychological support and reassurance
o Placebo tablets
 DISORDERS OF HIGHER VISUAL FUNCTIONS

Visual agnosia
▪ Definition
It refers to a rare disorder in which ability to recognise the objects by sight is
impaired while the ability to recognise by touch, smell or sound is intact

▪ Types
Prosopagnosia – can’t identify familiar faces
Object agnosia – can’t identify familiar objects

▪ Site of lesion – bilateral inferior occipitotemporal junction

▪ Associated features
Bilateral homonymous hemianopia
Dyschromatopsia

Visual hallucinations
▪ Definition

It refers to conditions in which patient alleges of seeing something not evident

to others in the same environment

▪ Types
o Elementary – colours, flashes, etc
o Complex – includes objects, peoples or animals

▪ Causes
o Occipital and temporal lobe lesions
o Drug induced
o Charles bonnet syndrome
o migraine
o Psychiatric disorders
Alexia and agraphia
▪ Alexia – inability to read
▪ Agraphia – inability to write

Causes
▪ Alexa associated with agraphia – lesions of angulate gyrus of the dominant
hemisphere
▪ Alexa without agraphia – lesions that destroy the visual pathway in left occipital
lobe and associated fibres from right occipital lobe

Visual illusions
▪ E.g.: palinopsia, optic anaesthesia, etc can also occur.
▪ It mostly occurs in lesions in occipital, occipitoparietal or occipitotemporal regions

OCULAR MANIFESTATIONS OF DISEASES OF CNS

Intracranial infections
o Meningitis
o Encephalitis
o Brain abscess
o Neurosyphilis

Intracranial aneurysms
▪ they produce complications by following mechanisms
o Pressure effects
o Aneurysm of circle of Willis
o Posterior communicating artery aneurysm
o Vertebrobasilar artery aneurysms
o Production of arteriolar venous fistula
o Subarachnoid hemorrhage
o Intracranial hemorrhage

▪ They include primary and secondary tumors

 ▪ Clinical features

General effects of False localising signs Focal signs of intracranial mass

↑ ICP lesions
▪ Headache ▪ Diplopia ▪ Prefrontal tumors – Foster
▪ Vomiting ▪ Sluggish pupillary Kennedy syndrome
▪ Papilloedema reflexes ▪ Chiasmal tumours – chiasmal
▪ Giddiness ▪ Unilateral mydriasis syndrome
▪ Hypertension ▪ Bitemporal hemianopia ▪ Cerebellar tumours – corneal
▪ Homonymous anaesthesia
hemianopia

Demyelinating diseases
Ocular manifestations
▪ Multiple sclerosis – unilateral optic neuritis, internuclear ophthalmoplegia and
vestibular or cerebellar nystagmus
▪ Devic’s disease – bilateral optic neuritis
▪ Schilders disease – optic neuritis, cortical blindness, ophthalmoplegia and nystagmus

Ocular signs in head injury

Concussion injuries to brain
▪ Hutchinson’s pupil – initially ipsilateral miosis, later dilatation with no light reflex –
indicates immediate cerebral compression
▪ papilloedema – if it appears with 48 hours, it indicates extra or intracerebral
hemorrhage. If it appears after a week it is due to cerebral edema

Fractures of base of skull

▪ Cranial nerve palsies
▪ Optic nerve injury
▪ Subconjunctival hemorrhage
▪ Ipsilateral dilated pupil
 OCULAR MOTILITY & STRABISMUS

OCULAR MANIFESTATION

Binocular Single Vision

Definition :

It is the co-ordinated use of both eyes so as to produce a single mental impression

i.e in normal individual the image is formed on fovea of both eyes, but the individual
perceives a single image.

Development of BSV:

• It is a conditioned reflex
• acquired after 6 months
• normal retinal correspondence is prerequisite for BSV

Important milestones:

Motor mechanism Straight eyes – starting from neonatal period

precise coordination for all directions of gaze
Sensory mechanism Reasonably clear vision in both eyes for similar
images in both retina
Mental process Ability of visual cortex to produce BSV

Grades of BSV:

There are 3 grades

Grade 1: Simultaneous Perception - Power to see 2 dissimilar objects
simultaneously

Grade 2:Fusion - It consist of power to superimpose two incomplete but

similar images to form one complete image

Grade3:Stereopsis - Ability to perceive the third dimensions i.e depth

perception. Tested with stereopsis slides in synoptophore

Anomalies of Binocular Single Vision

1. SUPPRESSION

2. AMBLYOPIA

3. ABNORMAL RETINAL CORRESPONDENCE

4. CONFUSION
 5. DIPLOPIA

SUPRESSION

• temporary active cortical inhibition of image formed on retina of squinting eye

• occurs only during both eyes open

• when normal eye is( fixating eye) is covered the squinting eye is fixed (suppression
disappears)

• test to detect suppression

1. worth’s 4 dot test

2. 4 dioptre base out prism test

3. red glass test

4. synoptophore test

AMBLYOPIA

Partial reversible loss of vision in one or both eyes, for which no cause can be found by
physical exam. i.e Absence of any organic disease to ocular media, retina, visual pathway

Pathogenesis:

• amblyogenic factors @ critical period of visual development Birth – 6to 7

years

• At this stage (a) visual pathway develops

(b) brain learns to interpret signals from eyes

• If the child cannot use one or both eyes for any reason the vision is not
developed

• this condition is termed amblyopia

AMBLYOGENIC FACTORS:

1. Visual deprivation eg; anisometropia

2. Light deprivation eg; congenital cataract

3. Abnormal binocular interaction eg; strabismus

TYPES OF AMBLYOPIA
1. STRABISMIC AMBLYOPIA

. due to uniocular suppression with unilateral constant squint who fixate with normal eye

. Squint is most common amblyopia

2. STIMULUS DEPRIVATION AMBLYOPIA

. also amblyopia ex anospia

. one eye is totally excluded from seeing early in life in congenital or traumatic 3frica33,
complete ptosis, Dense central corneal opacity

3. ANISOMETROPIC AMBLYOPIA

. occurs in the eye having higher degree of refractive error than the other

. most common in anisohypermetropic children

. 1-2D hypermetropic anisometropia cause amblyopia but 3D myopic anisometropia does not

4. ISOAMETROPIC AMBLYOPIA

bilateral amblyopia in children with bilateral uncorrected hidh refractive error

5. MERIDIONAL AMBLYOPIA

occurs in uncorrected astigmatic refractive error

Selective amblyopia for specific for specific visual meridian

CLINICAL CHARACTERISTICS

1. Visual acuity:

- decreases

- recognition acuity affected more than resolution

6. Effect of neutral density filtor:

visual acuity is

- amblyopia is improved

-decreases in organic lesion

7. Crowding phenomenon :

visually acuity is less when tested with multiple letter charts- snellen’s charts.

8. Fixation pattern :

central/ eccentric

Degree of amblyopia in eccentric fixation is proportional to the distance of the eccentric point
from the fovea

9. Colour vision :
 usually normal but affected in deep amblyopia

TREAMENT

must be started as early as possible (<3 yrs)

10. Occlusion therapy

. occlusion of normal eye forcing the use of amblyopia eye is the main treatment

. Before starting ensure,

- opacity in the media (if any should be removed, eg:cataract)

- refractive errors corrected completely

. Simplified schedule for occlusion therapy upto 2 years ->2:1 (2 days normal eye 1 day
amblyopic eye)

3rd year->3:1(3 days normal eye 1 day amblyopic eye)

4th year->4:1

5th year ->5:1

6th year ->6:1

Duration of occlusion should be until the visual acuity develops fully, or there is no further
improvement of vision after 3 months of occlusion.

11. Penalization

blurring of vision of normal eye 2methods

- use of atropine-> atropine penalization

- use of over plus lens->optical penalization

12. Pleoptic exercise

re-establish foveal fixation

13. Pharmacological manipulation

use of levodopa/carbidopa as adjunct

Perceptual learning

adjunct to occlusion therapy

14. Computerised vision therapy

.useful for treatment of amblyopia with 4frica44ival4 result

. works on the concept of operant conditioning i.e psychological treatment

ABNORMAL RETINAL CORRESPONDENCE

 In a state of normal binocular single vision, there exists a precise physiological relationship b/w
the corresponding points of the two retinae. This the fovea of corresponding points and have the
same visual direction. This is normal retinal correspondence

Definition:

In squint , there occurs an active cortical adjustment in the directional values of the two retinae.
Hence, fovea of normal eye& extra foveal point on the retina of the squinting eye acquire a common
visual direction.

This is abnormal retinal correspondence(ARC)

Test to detect ARC;

1. Worth’s four dot test

2. litmus stereo test

3. Bagolini striated glasss test

4. Synoptophore test

DIPLOPIA:

refers to formation of images on the dissimilar points of the two retinae. There are 2

-UNIOCULAR

-BINOCULAR

BINOCULAR VISION:

occurs on formation of image of dissimilar points of the 2 retinae

causes;

1. paralysis of extraocular muscles

2. displacement of one eyeball

3. mechanical restrictions of ocular movement like pterygium, symblepharon, thyroid

ophthalmopathy

4. deviation of ray of light in one eye

5. anisometropia ->disparity of image size b/w 2 eyes as in high anisometropia

TYPES ;

1. Uncrossed

2. Crossed

Uncrossed:- (harmonious)

-false image is on the same side as deviation

-occurs in convergent squint as in lateral rectus paralysis

Crossed:- (unharmonious)

-false image is seen on the opposite side

- occurs in divergent squint as in the medial rectus paralysis

UNIOCULAR VISION:

an object appears double from the affected eye even when the normal eye is closed

causes:

1. Subluxated clear lens

2. subluxated intreocular lens

3. double pupil due to congenital anomaly/pheriperal iridectomy/iridodialysis

4. Incipient 6frica66-> polyopia

5. Keratoconus -> diplopia due to changed refractive power of cornea in different parts

Treatment of diplopia;

1. Treat the causative disease

2. Temporary relief by occluding the ajjected eye

STRABISMUS

Contents:

• Definition
• Heterophoria
• Concomitant strabismus

DEFINITION

• A misalignment of the visual axes of the two eyes is called squint or strabismus
• The visual axis passes from the fovea, through the nodal point of the eye, to the
point of fixation.

Pseudo strabismus:

• The visual axis passes from the fovea, through the nodal point of the eye, to the point of
fixation
PSEUDOESOTROPIA PSEUDOEXOTROPIA

• Apparent convergent squint • Apparent divergent squint

• Prominent epicanthal folds • Hypertelorism (wide separation of 2
eyes)
• Negative angle kappa • Positive angle kappa

• Angle kappa is the angle, usually about 5°, subtended by the visual and anatomical axes.
 • The angle is positive(normal) when the fovea is temporal to the centre of the posterior
pole resulting in a nasal displacement of the corneal reflex, and negative when the converse
applies.

CLASSIFICATION OF STRABISMUS

STRABISMUS

MANIFEST
SQUINT
LATENT SQUINT
(heterotropia)
(heterophoria)

CONCOMITANT INCOMITANT
SQUINT SQUINT
 HETEROPHORIA

• Heterophoria implies a tendency of the eyes to deviate when fusion [correct blending of
images of both eyes] is blocked (latent squint).
• Orthophoria implies perfect ocular alignment in the absence of any stimulus for fusion;
this is uncommon.
Types of heterophoria:
ESOPHORIA (latent convergent EXOPHORIA (latent divergent HYPER CYCLOPHORIA
squint) squint) PHORIA (Latent torsional deviation)

Tendency of eye ball to deviate Tendency of eye ball to deviate Tendency of eye ball Tendency of eye ball to rotate
inward outward to deviate upward around anteroposterior axis
[downwards:
hypophoria]
Types: Types: Types:
• Convergence excess • Convergence weakness • Incyclophoria: When 12’o
type (esophoria more type (exophoria more clock meridian of cornea
for near fixation than for near fixation) rotates nasally
distant) • Divergence excess type • Excyclophoria: When 12’o
• Divergence weakness (more for distant clock meridian of cornea
type (more for distant fixation) rotates temporally)
fixation) • Nonspecific type
• Nonspecific type
Aetiology:
1.Anatomical factors:
• Orbital symmetry
• Abnormal interpupillary distance (wide: exophoria, small: exophoria)
• Faulty insertion of extraocular muscles
• A mild degree of extraocular muscle weakness
• Abnormal innervation
• Anatomical variation in the position of the macula

2.Physiological factors:

• Age: esophoria more common in younger age, exophoria more common in

elders
• Role of accommodation: increased accommodation: esophoria, decreased:
exophoria
• Role of convergence: increased convergence: esophoria, decreased
convergence: exophoria
• Dissociation factor: e.g.: prolonged constant use of one eye results in
exophoria

Symptoms:
 • Compensated heterophoria: Compensation of heterophoria depends upon the reserve
neuro-muscular power to overcome the muscular imbalance and individual’s desire for
maintenance of binocular vision
• Decompensated heterophoria: they are grouped as:
Symptoms of muscular fatigue Symptoms of failure to Symptoms of defective
maintain binocular singular postural sensations
vision
• Headache and eye • Blurring • Problems in
ache • Intermittent diplopia judging distances
• Difficulty in changing • Intermittent squint and positions of
the focus moving objects
• Photophobia

Examination:

1.Testing for vision and refractive error

2.Cover- uncover test:

• Cover one eye with an 9frica9 and the other is made to fix on an object
• Deviation of eye undercover is observed

3.Measurement of heterophoria:

• Prism cover test:

1.Prisms of increasing strength with apex towards the deviation are
placed in front of one eye and the patient is asked to fixate an object
with the other.
2.The cover-uncover test is performed till there is no recovery
movement of the eye under cover.
3.This will tell the amount of deviation in prism dioptres. Both
heterophoria as well as heterotropia can be measured by this test.
• Maddox- rod test: Maddox rod consists of a series of fused cylindrical
red glass rods that convert the appearance of a white spot of light in the
centre of the Maddox tangent scale into a red streak. When the
glass rods are held horizontally, the streak will be vertical and vice
versa.
• Maddox wing test: Maddox wing is an instrument by which the amount
of phoria for near (at a distance of 33 cm) can be measured.
Right eye sees a vertical white arrow and a horizontal red arrow and the
left eye sees a vertical and a horizontal line of numbers.
The number seen by the patient on horizontal line with white arrow
gives amount of horizontal phoria and that on vertical line with red
arrow gives vertical phoria
The cyclophoria is measured by asking the patient to align the red arrow
with the horizontal line of numbers.
4.Measurement of convergence and accommodation

• Measurement of near point of convergence measurement ( NPC- the

nearest point on which the eyes can maintain binocular fixation) using
RAF rule A target is slowly moved along the rule towards the patient’s
eyes until one eye loses fixation and drifts laterally
 • Measurement of near point of accommodation (NPA- the nearest point
on which the eyes can maintain clear focus using RAF rule
15. Measurement of fusional reserve:
• Fusional reserve is the maximum amount the eyes can converge or diverge
• Vertical fusional reserve: 1.5°-2.5°
• Horizontal negative fusional reserve (abduction range): 3°-5°
• Horizontal positive fusional reserve (adduction range): 20°-40°

Treatment

• Correction of refractive error

• Orthoptic treatments (non- computerised exercises using synoptophore, prisms etc or
computerised exercises)
• Prescription of prism in glasses
• Surgical treatment

CONCOMITANT STRABISMUS

• It is a type of manifest squint in which the amount of deviation in the squinting eye remains
constant (unaltered) in all the directions of gaze; and there is no associated limitation of
ocular movements.

Aetiology:

The obstacles in the development of binocular vision and coordination of ocular movements are:

Sensory obstacles Motor obstacles Central obstacles

• Refractive errors
• Anisometropia
• Prolonged use of
14frica1414ival14
spectacles
• Corneal opacities
• Lenticular opacities
• Diseases of macula
• Optic atrophy
• Abnormal shape and size
of orbit
• Abnormalities of
extraocular muscles
• Abnormalities of
accommodation,
convergence and their
ratio
• Deficient
development of fusion
faculty
• Abnormalities of
cortical control of
ocular movements

General features of concomitant strabismus

• Ocular deviation
• Ocular movements are not limited
• Refractive error (may or may not be present)
• Suppression and amblyopia (decreased eyesight due to abnormal visual development)
• A-V patterns in horizontal strabismus

Types of concomitant squint

• Convergent squint (esotropia)

• Divergent squint (exotropia)
• Vertical squint (hypertropia)
CONVERGENT SQUINT

• Concomitant convergent squint or esotropia denotes inward deviation of one eye.

• It is more common than divergent type
• The deviation is not always purely horizontal; in many cases the eye deviates upwards as
well as inwards.

Clinico-etiological types:
1. Infantile esotropia
2. Accommodative esotropia (refractive, non-refractive and mixed)
3. Acquired non accommodative esotropia
4. Sensory esotropia
5. Consecutive esotropia

1. Infantile esotropia:

• Age of onset: 2-4 months

• Angle of deviation >35 degrees
• Fixation in most infants is alternating in the primary position
• There is cross fixating in side gaze, so that the child uses the left eye in right gaze and the
right eye on left gaze
 • Amblyopia develops in 25-40 % cases
• Surgery is the treatment of choice

2. Accommodative esotropia

Refractive accommodative esotropia Non-refractive Mixed esotropia

accommodative
esotropia

AC/A (accommodative AC/A ratio: large High AC/A ratio with

convergence/accommodation ratio: hypermetropia
normal with high hypermetropia
For near and distance Greater for near
Fully correctable by use of spectacles It is fully corrected by Esotropia for
bifocal glasses adding distance is corrected
+3 DS for near vision. by correction of
 hypermetropia; and
the residual
esotropia for near is
corrected by an
addition of +3 DS
lens.

3. Acquired non accommodative esotropias

It includes:

• Essential acquired or late onset esotropia

• Acute concomitant esotropia
• Cyclic esotropia
• Nystagmus blockage syndrome
• Esotropia in myopia and microtropia

Essential acquired or late onset esotropia is of 3 types:

Basic type Convergence excess type Divergence insufficiency type

Deviation is equal at distance Deviation is large for near and Greater deviation for distance
and near small for distance than near

4. Sensory esotropia
• Sensory or secondary esotropia is caused by a unilateral reduction in visual
acuity that interferes with or abolishes fusion; causes can include cataract,
optic atrophy or hypoplasia, macular scarring or retinoblastoma.
5. Consecutive esotropia
• Consecutive esotropia follows surgical overcorrection of an exodeviation

DIVERGENT SQUINT

• Concomitant divergent squint (exotropia) is characterised by outward deviation

of one eye while the other eye fixates

Clinico- etiological types:

• Congenital exotropia
 • Primary exotropia (intermittent and constant)
• Sensory exotropia
• Consecutive exotropia

1. Congenital exotropia
• Presentation is often at birth.
• Signs – Normal refraction
-Large and constant angle.
• Neurological anomalies are frequently present, in contrast
with infantile esotropia.
• Treatment is mainly surgical and consists of lateral rectus
recession and medial rectus resection.
2. Primary exotropia
• Intermittent exotropia: most common type. Age of onset 2-5 years
Deviation is present at times and remains latent at others
• If untreated, intermittent exotropia may decompensate into constant exotropia

Types:

• Convergence insufficiency type (exotropia greater for near than distance)

• Divergence excess (exotropia greater for distance than near)
• Basic non-specific type (exotropia equal for near and distance).

3. Sensory exotropia
• Secondary (sensory) exotropia is the result of monocular or binocular visual
impairment by acquired lesions, such as cataract or other media opacity.
4. Consecutive exotropia
• Consecutive exotropia develops spontaneously in an amblyopic eye, or more
frequently following surgical correction of an esodeviation.
EVALUATION OF A CASE OF CONCOMITANT STRABISMUS

• History:

• Examination:
• Inspection
• Ocular movements
• Pupillary reactions
• Media and fundus examination
• Testing of vision and refractive error
• Cover tests
▪ Direct cover test: the patient is asked to fixate on a point light.
Then, the normal looking eye is covered while observing the
movement of the uncovered eye. In the presence of squint the
uncovered eye will move in opposite direction to take fixation,
while in apparent squint there will be no movement.
 ▪ Cover- uncover test (mentioned in examination for heterophoria)
▪ Alternate cover test: It reveals whether the squint is unilateral or
alternate and also differentiates concomitant squint from
paralytic squint (where secondary deviation is greater than
primary).
• Estimation of angle of deviation can be done by
▪ Hirschberg corneal reflex test:
the patient is asked to fixate at point light held at a
distance of 33 cm and the deviation of the corneal light
reflex from the centre of pupil is noted in the squinting
eye. Roughly, the angle of squint is 15o and 45o when the
corneal light reflex falls on the border of pupil and limbus,
respectively
▪ The prism and cover test (refer examination of
heterophoria)
▪ Modified Krimsky corneal reflex test:

It involves placement of prisms in

front of the fixating eye until the
corneal light reflections are
symmetrical. This test reduces the
problem of parallax and is
 more commonly used than the
prism reflection test.

▪ Measurement of deviation with

synoptophore:

All types of heterophorias and heterotropias

(both objective and subjective angle of squint)
can be measured accurately with it.
• Tests for grade of binocular vision and sensory function:
o Worth’s four dot test: patient wears goggles with red lens in front
of the right and green lens in front of the left eye and views a box
with four lights – one red, two green and one white
Results are:
Normal binocular vision: All 4 lights in the absence of
a manifest squint

Abnormal retinal All 4 lights even in the

correspondence: presence of a manifest
squint

Left suppression: 2 red lights

Right suppression: 3 green lights

 Alternating suppression: 3 green lights and 2 red lights
alternatively

Diplopia: 2 red lights and 3 green lights

o Tests for fixation: It can be tested with the help of a visuoscope

or fixation star of the ophthalmoscope. Patient is asked to cover
one eye and fix the star with the other eye. Fixation may be
centric (normal on the fovea) or eccentric (which may be
unsteady, parafoveal, macular, paramacular, or peripheral

o After- image test: In this test the right fovea is stimulated with a
vertical and left with a horizontal bright light and the patient is
asked to draw the position of after-images. Results are:
Normal retinal correspondence Draws cross

Esotropic patient with abnormal retinal Draws vertical image to the left
correspondence: of horizontal

Exotropic patient with abnormal retinal Draws vertical image to the right
correspondence: of horizontal

o Sensory function tests with synoptophore: Synoptophore (major

amblyoscope) consists of two tubes, having a right-angled bend,
 mounted on a base. Each tube contains a light source for
illumination of slides and a slide carrier at the outer end, a
reflecting mirror at the right-angled bend and an eyepiece of +6.5
D at the inner end. Uses are:
1. Estimation of grade of binocular vision
2. Detection of normal/ abnormal retinal correspondence

o Neutral density filter test: visual acuity is measured without and

with neutral density filter placed in front of the eye. In cases with
functional amblyopia visual acuity slightly improves while in
organic amblyopia it is markedly reduced when seen through the
filter.

TREATMENT OF STRABISMUS:

1. Spectacles with full correction of refractive error

2. Occlusion therapy. It is indicated in the presence of amblyopia. After correcting the refractive
error, the normal eye is occluded and the patient is advised to use the squinting eye.
3. Preoperative orthoptic exercises.
4. Squint surgery:
• In operating for squint with a general or local anaesthetic it is important
to remember that the position of the eyes varies in different stages of
anaesthesia so that it gives no indication of the final position after the
anaesthetic has worn off.

5. Postoperative orthoptic exercises.

REFERENCES:

1. A K KHURANA Comprehensive ophthalmology

2. Kanski’s Clinical Ophthalmology
 3. Parsons’ Diseases of the Eye
4. Oxford handbook ophthalmology

CONCOMITANT SQUINT

Concomitant Strabismus

It is a type of heterotropia (manifest squint) in which the amount of deviation varies in different
directions of gaze. It includes following conditions:
1. Paralytic squint.
2. ‘A’ and ‘V’ pattern heterotropias.
3. Restrictive squint.

Paralytic strabismus

It refers to ocular deviation resulting from complete or incomplete paralysis of one or more
extraocular muscles.
Etiology
1. Neurogenic lesions.
2. Myogenic lesions.
3. Neuromuscular junction lesions.

Neurogenic lesions
1. Neurogenic lesions may occur at the level of nerve nucleus, nerve root, or any part of the in its
course.
2. Nuclear ophthalmoplegia refers to paralysis of extraocular muscles due to lesions of 3rd cranial
nerve. They are more often bilateral.
Causes of neurogenic lesions:
16. Congenital.
Hypoplasia or absence of nucleus is a known cause of third and sixth cranial nerve palsies. Birth
injuries may mimic congenital lesions.
17. Inflammatory lesions.
These may be in the form of encephalitis, meningitis, neurosyphilis or peripheral neuritis
(commonly viral). Nerve trunks may also be involved in the infectious lesions of cavernous sinus and
orbit.
18. Neoplastic lesions.
These include brain tumours involving nuclei, nerve roots or intracranial part of the nerves; and
intraorbital tumours involving peripheral parts of the nerves.
4. Vascular lesions.
(a) These are known in patients with hypertension, diabetes mellitus and atherosclerosis. These
may be in the form of haemorrhages, thrombosis, embolism, aneurysms or vascular occlusions.
Cerebrovascular accidents are more common in elderly people.
(b) Ophthalmoplegic migraine or episodic ophthalmoplegia is a well-known vascular condition
characterized by recurrent attacks of headache associated with paralysis of 3rd (most common), 4th or
6th cranial nerve.
I The condition is often unilateral, persists for days or weeks and even tends to become
permanent, in some cases.
5. Traumatic lesions.
These include head injury and direct or indirect trauma to the nerve trunks. Head injury is common
cause of 6th nerve palsy.

19. Toxic lesions.

 These include carbon monoxide poisoning, effects of diphtheria toxins (rarely), alcoholic and lead
neuropathy.
20. Demyelinating lesions.
Ocular palsy may occur in multiple sclerosis and diffuse sclerosis.
II. Myogenic lesions
21. Congenital lesions.
These include absence, hypoplasia, malinsertion, weakness and musculofacial anomalies.
22. Traumatic lesions.
These may be in the form of laceration, disinsertion, hemorrhage into the muscle substance or
sheath and incarceration of muscles in blow out fractures of the orbital walls (floor or medial wall).

Eye injury

23. Inflammatory lesions.

Myositis is usually viral in origin and may occur in influenza, measles and other viral fevers.
24. Myopathies.
These include thyroid myopathy, carcinomatous myopathy and that associated with certain drugs.
Chronic progressive ophthalmoplegia (CPO) is a bilateral myopathy of extraocular muscles; which may
be sporadic or inherited as an autosomal dominant disorder.
It is the most common (75% cases) type of mitochondrial myopathy. It is characterized by:
25. Bilateral ptosis with slowly progressive ophthalmoplegia
is typical presentation.
(2). Diplopia is usually not a complaint since all eye movements are reduced equally.
 (3).Other associated symptoms of CPO include exercise intolerance, hearing loss, ataxia, sensory
axonal neuropathy, parkinsonism, and clinical depression.
III. Neuromuscular junction lesion
It includes myasthenia gravis. The disease is characterized primarily by fatigue of muscle groups,
usually starting with the small extraocular muscles, before involving other large muscles.

Clinical features
Symptoms
26. Diplopia.
It is the main symptom of paralytic squint. It is more marked in the field of action of paralyzed
muscle. It may be crossed (in divergent squint) or uncrossed (in convergent squint). It may be
horizontal, vertical or oblique depending on the muscle paralyzed.
Diplopia occurs due to formation of image on dissimilar points of the two retinae. The false image
(seen by the squinting eye)
is less distinct than the true image (seen by the other eye).

27. Confusion.
It occurs due to formation of image of two different objects on the corresponding points of two
retinae.
28. Nausea and vertigo.
These result from diplopia and confusion and may cause vomiting also.
29. Ocular deviation is typically a sudden onset.

Signs
30. Primary deviation.
It is deviation of the affected eye and is away from the action of paralysed muscle, e.g., if lateral
rectus is paralysed the eye is converged. Angle of deviation varies in different directions of
gaze (incomitant).
2. Secondary deviation.
(1) It is deviation of the normal eye seen under cover, when the patient is made to fix with the
squinting eye. It is greater than the primary deviation.
(2) This is due to the fact that the strong impulse of innervation required to enable the eye with
paralysed muscle to fix is also transmitted to the yoke muscle of the sound eye resulting in a greater
amount of deviation. This is based on Hering’s law
of equal innervation of yoke muscles.
31. Restriction of ocular movement
It occurs in the direction of the action of paralysed muscles.
4. Compensatory head posture.
(1) It is adopted to avoid diplopia and confusion. Head is turned towards the direction of action
of the paralysed muscle, e.g., if the
right lateral rectus is paralysed, patient will keep the head turned towards right.
(2) Ocular torticollis refers to tilting of head and chin depression occurring to compensate for the
vertical diplopia. It needs to be
differentiated from the true torticollis occurring due to undue contracture of sternocleidomastoid
muscle.
32. False projection or orientation.
It is due to increased innervational impulse conveyed to the paralysed muscle. It can be
demonstrated by asking the patient
to close the sound eye and then to fix an object placed on the side of paralysed muscle.Patient will
locate it further away in the same direction.

Varieties of Ocular Paralysis

33. If one muscle alone is affected it is generally the lateral rectus or the superior oblique, since each
of these is supplied by an
independent nerve.
 (2) Affection of several muscles simultaneously extrinsic and intrinsic muscles of one or both eyes
may be paralysed called total ophthalmoplegia.
(3) If only the extrinsic muscles are affected the condition is called external ophthalmoplegia;if
only the intrinsic muscles (sphincter pupillae and ciliary muscle) are affected it is termed as internal
ophthalmoplegia.

Pathological sequelae of an extraocular muscle palsy

In all cases of extraocular muscle palsy, certainsequelae take place after some time. These occur
more in paralysis due to lesions of the nerves than the lesions of muscles. These include:
1. Overaction of the contralateral synergistic muscle.
2. Contracture of the direct antagonist muscle.
3. Secondary inhibitional palsy of the contralateral antagonist muscles.

Pathological sequelae of the right lateral rectus muscle paralysis

Clinical varieties of ocular palsies

34. Isolated muscle paralysis.

Lateral rectus and superior oblique are the most common muscles to be paralysed singly, as they
have separate nerve supply. Isolated paralysis of the remaining four muscles is less common, except
in congenital lesions.
35. Paralysis of the third cranial nerve.
It is of common occurrence. It may be congenital or acquired.
Clinical features of third nerve palsy include:
(1) Ptosis due to paralysis of the LPS muscle.
(2) Deviation. Eyeball is turned down, out and slightly intorted due to actions of the lateral rectus
and
superior oblique muscles. Ocular movements are restricted in all the directions except outward.
 (3) Pupil is fixed and dilated due to paralysis of the sphincter pupillae muscle.
(4) Accommodation is completely lost due to paralysis of the ciliary muscle.
(5) Crossed diplopia is elicited on raising the eyelid.
(6) Head posture may be changed if pupillary area remains uncovered.
3. Double elevator palsy
It is also known as monocular elevationan and is a deficiency is a congenital condition caused by
third nerve nuclear lesion. It is characterised by paresis of the superior rectus and the inferior oblique
muscle of the involved eye.
36. Total ophthalmoplegia.
In this condition, all extraocular muscles including LPS and intraocular muscles, viz., sphincter
pupillae, and ciliary muscle
are paralysed. It results from combined paralysis of third, fourth and sixth cranial nerves. It is a
common feature of orbital apex syndrome and cavernous sinus thrombosis.
37. External ophthalmoplegia.
In this condition, all extraocular muscles are paralysed, sparing the intraocular muscles. It results
from lesions at the level of motor nuclei sparing the Edinger-Westphal nucleus.
38. Internuclear ophthalmoplegia.
In this condition, there is lesion of the medial longitudinal
Fasciculus (MLF). It is the pathway by which various ocular motor
nuclei are linked.
Internuclear ophthalmoplegia is characterised by:
Defective action of medial rectus on the side of lesion, horizontal nystagmus of the opposite
convergence is normal, as the pathway of convergence runs directly into the midbrain without
involving the MLF.
 A patient with third cranial nerve paralysis showing:
A, ptosis; B, divergent squint

Examination of case of paralytic squint

History Taking and Preliminary Clinical Examination

Visual acuity examination
Following common devices should be used to assess the vision:
1. Snellen’s visual acuity chart (can be used with patients of all ages, who are literate)
2. Illiterate E chart (used with illiterate patients)
3. Catford Drum – Based on Osscillatory movements
4. Teller’s acuity cards – for children from 6 months to 2 years
5. Cardiff vision chart – Based on vanishing optotypes (for children from 2-3 years)
6. Sheridan Gardiner cards (useful in case of children above 3 years)
7. Angular visual acuity cards can be used to avoid crowding phenomenon
8. Near vision should be assessed by near vision charts for each eye separately.

Tests for paralytic squint

1.Diplopia charting.
 (1) It is indicated in patients complaining of confusion or double vision. In it patient is asked to wear
red and green diplopia
charting glasses. Red glass being in front of the right eye and green in front of the left.
(2) Then in a semi-dark room, he is shown a fine linear light from a distance of 4 ft. and asked to
comment on the images in primary position and in other positions of gaze.
(3) Patient tells about the position and the separation of the two images in different fields.

Diplopia charting in a patient with right lateral rectus palsy

2. Tests to Help Identify the Affected Muscle
I. Park 3-step test
Step 1: Identify the hypertropic eye in the primary (straight ahead) position. This implies that either
one of the two depressors of the hypertropic eye or one of the two elevators of the hypotropic eye is
weak.
Step 2: Ask the patient to look horizontally right and then left and see in which position the deviation
is more. Considering that the deviation increases in the direction of action of the paralysed muscle,
identify which two of the four muscles are likely to be affected. Step 3: Tilt the patient’s head towards
each shoulder and see in which direction the vertical squint increases. Remembering that on tilting
the head towards one shoulder the eye on the same side intorts and the other eye extorts, the
ipsilateral synergist of the paralysed muscle will try to intort or extort the globe as the case may be,
and since the muscle also has a vertical action, that vertical effect will be more prominent in the
paralysed eye.
39. Bielschowsky head tilt test
It is based on the same principle as the third step of the Park 3-step test and is useful for diagnosing
superior rectus palsy. In a case of right superior oblique palsy, for example, the right hypertropia will
become more prominent when the head is tilted to the right shoulder and will disappear when the
head is tilted to the left shoulder.
40. Hess chart
Hess screen/Lees screen test tells about the paralysed muscles and the pathological sequelae of
the paralysis, viz., overaction, contracture and secondary inhibitional palsy.
Procedure
(1) It consists of a tangent screen marked in red lines on a black cloth with red spots at the
intersection of the l5° and 30° lines with themselves and with the horizontal and vertical lines
(2) Over it three green threads are suspended in such a way that they can be moved over the screen
in any direction by a pointer.
(3) The patient, wearing red-and-green glasses, is asked to place the junction of the three threads
over the red spots in turn.
(4) Through the red glass he can only see the red markers and through the green, thegreen threads,
so that he indicates the point at which one eye islooking when the other fixes a spot.
(5) The position on which the indicator appears to coincide with the spot gives a permanent record
of the primary and secondary deviation.
Inference
The smaller chart belongs to the eye with paretic muscle and the larger to the eye with overacting
muscle.

Hess chart of a recent right lateral rectus paralysis

41. Field of binocular fixation.

It should be tested in patients with paralytic squint where applicable, i.e., if patient has some field
of single vision. This test is
performed on the perimeter using a central chin rest.
42. Forced duction test (FDT).
 It is performed to differentiate between the incomitant squint due to paralysis of extraocular
muscle and that due to mechanical restriction of the ocular movements.
Inference
FDT is positive (resistance encountered during passive rotation) in cases of incomitant squint due
to mechanical restriction and negative in cases of extraocular muscle palsy.
Management
1. Treatment of the cause: An exhaustive investigative work-up should be done to find out the cause
and, if possible, treat it.
2. Conservative measures: These include: wait and watch for self-improvement to occur for a period
of 6 months, vitamin B-complex as neurotonic; and systemic steroids for non-specific inflammations.
3. Treatment of annoying diplopia:It includes use of 38frica38 on the affected eye, with intermittent
use of both eyes with changed headposture to avoid suppression amblyopia.
4. Chemodenervation of the contralateral muscle with botulinum toxin may be useful during the
recovery period.
A’ and ‘V’ Pattern Heterotropia
The terms ‘A’ or ‘V’ pattern squint are 38frica3838 when the amount of deviation in squinting eye
varies by more than 10° and 15°, respectively, between upward and downward gaze.
The ‘A’ and ‘V’ phenomena should be assessed by the cover test in 25° upward and downward
gaze. This test should be carried out for near and distance fixation.

‘A’ Esotropia
In the absence of vertical muscle anomaly, resection of the lateral recti with displacement of the
insertions downwards should be effective in patients with a greater deviation for distance than for
near.
In those with ‘A’ esotropia associated with convergence excess, recession of the medial recti with
shifting of the insertions upwards is effective. Large degrees of esotropia in small children, with gross
overaction of the superior obliques, may respond to bilateral weakening of the muscle.
 ‘A’ esotropia

‘A’ Exotropia
Smaller degrees may be helped by resection of the medial recti with elevation of the insertions
but the results are disappointing. Large degrees in small children with overaction of the superior
obliques respond to bilateral weakening of this muscle.

‘A’ exotropia

Causes
1. Primary superior oblique overaction is usually associated with exodeviation in the primary
position of gaze.
2. Inferior oblique underaction/palsy with subsequent superior
oblique overaction.
43. Inferior rectus underaction.
Treatment
Patients with oblique dysfunction are treated by superior oblique posterior tenotomy. Treatment
of cases without oblique muscle
dysfunction is as follows:
1. ‘A’ pattern esotropia is treated by bilateral medial rectus recessions and upward transposition
of the tendons.
2. ‘A’ pattern exotropia is treated by bilateral lateral rectus recessions and downward
transposition of the tendons.

‘V’ Esotropia
In the absence of vertical muscle anomaly, recession of the medial recti with displacement of the
insertions downwards is effective. If overaction of the inferior obliques is present, this responds to
bilateral anteroposition of this muscle with recession of the medial rectus muscles. If the overaction
is gross, the anteroposition should be combined with recession of the inferior oblique.

V pattern Esotropia

‘V’ Exotropia
In the absence of marked vertical muscle anomaly, recessions of the lateral recti with
displacement of the insertions upwards is effective.
If overaction of the inferior obliques is present, bilateral anteroposition of the muscle is effective,
with or without recession of the muscle, depending on the degree of overaction. Recession of the
lateral recti may be performed at the same time.
 V pattern Exotropia

Causes of ‘v’ pattern heterotropia

1.Inferior oblique overaction associated with fourth nerve palsy.

2. Superior oblique underaction with subsequent inferior oblique overaction, seen in infantile
esotropia as well as other childhood esotropias. The eyes are often straight in upgaze with a marked
esodeviation in downgaze.

3.Superior rectus underaction.

4. Brown syndrome.
5.Craniofacial anomalies featuring shallow orbits and down-slanting palpebral fissures.
Treatment
Treatment is by inferior oblique weakening or superior oblique strengthening when oblique
dysfunction is present. Without
oblique muscle dysfunction treatment is as follows:
44. ‘V’ pattern esotropia can be treated by bilateral medial rectus recessions and downward
transposition of the tendons.

2.‘V’ pattern exotropia can be treated by bilateral lateral rectus recessions and upward
transposition of the tendons.

Strabismus Surgery
The most common aims of surgery on the extraocular muscles are to correct misalignment to
improve appearance.
Surgical techniques
1. Muscle weakening procedures include recession, marginal myotomy and myectomy.
2. Muscle strengthening procedures are resection, tucking and advancement.
3. Procedures that change direction of muscle action.These include:
(a) Vertical transposition of horizontal recti to correct ‘A’ and ‘V’ patterns,
(b) Posterior fixation suture (Faden operation) to correct dissociated vertical deviation, and
ITransplantation of muscles .
Weakening procedures
Recession
Recession slackens a muscle by moving it away from its insertion.It can be performed on any muscle
except the superior oblique.
Steps of recession :
1. Muscle is exposed by reflecting a flap of overlying conjunctiva and Tenon’s capsule.
2. Two vicryl sutures are passed through the outer quarters of the muscle tendon near the insertion.
3. The muscle tendon is disinserted from the sclera with the help of tenotomy scissors.
4. The amount of recession is measured with the callipers and marked on the sclera.
5. The muscle tendon is sutured with the sclera at the marked site posterior to original insertion.
6. Conjunctival flap is sutured back.

Technique of recession

Disinsertion
 1. Disinsertion (or myectomy) involves detaching a muscle from its insertion without reattachment.
2. It is most commonly used to weaken an overacting inferior oblique muscle, when the technique
is the same as for a recession except that the muscle is not sutured.
3.Very occasionally, disinsertion is performed on a severely contracted rectus muscle.

Strengthening procedures
Resection shortens a muscle to enhance its effective pull. It is suitable only for a rectus muscle and
involves the
following steps:
. 1. Muscle is exposed as for recession and the amount to be resected is measured with callipers
and marked.
2. Two absorbable sutures are passed through the outer quarters of the muscles at the marked
site.
3. The muscle tendon is disinserted from the sclera and the portion of the muscle anterior to
sutures is excised.
4. The muscle stump is sutured with the sclera at the original insertion site.
5. Conjunctival flap is sutured back.

Technique of resection

Posterior fixation suture

 The principle of this (Faden) procedure is to suture the muscle belly to the sclera posteriorly so as
to decrease the pull of the muscle in its field of action without affecting the eye in the primary
position. The Faden procedure may be used on the medial rectus
to reduce convergence in a convergence excess esotropia and on the superior rectus to treat DVD.
When treating DVD, the superior
rectus muscle may also be recessed. The belly of the muscle is then anchored to the sclera with a
non-absorbable suture about
12 mm behind its insertion.

Transposition
Transposition refers to the relocation of one or more extraocular muscles to substitute for the
action of an absent or severely
deficient muscle. The most common indication is severe lateral rectus weakness due to acquired
sixth cranial nerve palsy other applications include CCDD (e.g. Duane syndrome), alphabet patterns
and monocular elevation deficit.

Transposition of the superior and inferior rectus muscles in lateral rectus palsy

Adjustable sutures
Indications
 The results of strabismus surgery can be improved by the use of adjustable suture techniques on
the rectus muscles. These are particularly indicated when a precise outcome is essential and when
the results with more conventional procedures are likely to be
unpredictable; for example, acquired vertical deviations associated with thyroid myopathy or
following a blow-out fracture of the
floor of the orbit.
Other indications include sixth nerve palsy, adult exotropia and re-operations in which scarring of
surrounding tissues may make the final outcome unpredictable. The main contraindication is
inability to tolerate postoperative suture
adjustment (e.g. young children).

Postoperative adjustment
This is performed under topical anaesthesia, usually a few hours after surgery when the patient is
fully awake.
1.The accuracy of alignment is assessed.
2. If ocular alignment is satisfactory the muscle suture is tied off and its long ends cut short.
3.If more recession is required, the bow is pulled anteriorly along the muscle suture, thereby
providing additional slack to the recessed muscle and enabling it to move posteriorly

45. If less recession is required, the muscle suture is pulled anteriorly and the knot tightened against
the muscle stump
46. Once alignment is satisfactory, the main knot is secured, the sliding loop removed and the
conjunctiva closed.

Nystagmus

• Definition –
o It is the term applied to the rapid oscillatory movements of the eyes, independent of
normal eye movements.
o Oscillations are involuntary
o Lateral (Usually)/ Vertical/ Rotatory/ Mixed
o Almost always bilateral

• Classification
 Based on Aetiology
Physiological Pathological
1. End gaze Congenital Acquired
2. Optokinetic a)Infantile manifest a)Secondary to visual loss
3. Vestibulo-ocular reflexes b)Infantile latent b)Toxic and Metabolic
c) Infantile manifest- c)Neurological disorders
latent
d)Nystagmus blockage
syndrome

Physiological Nystagmus –

• Optokinetic Nystagmus –
o Jerky nystagmus
o Induced by moving repetitive visual patterns across the visual field.
o Slow phase – direction of moving pattern
Fast phase – opposite direction
o Rail road nystagmus
o Clinical Application – Testing visual acuity in infants or young children and for
detecting malingering.

• End-Gaze Nystagmus –
o Fine jerk horizontal nystagmus
o Seen in extreme gaze positions

• Vestibulo-ocular Nystagmus –
o Jerk Nystagmus
o Involves semicircular canals
o Can be produced physiologically by- rotation in specially designed chair or syringing
the ears
o Conjugate movement to opposite side induced by syringing one ear with cold water
o COWS {Cold – OPPOSITE; Warm – SAME} – one ear
o CUWD {Cold – UP; Warm – DOWN} – both ears
o Vestibular nystagmus + Interstitial keratitis = Cogan Syndrome
Pathological Nystagmus –

1) Early onset Nystagmus

✓ Infantile nystagmus syndrome
✓ Fusion mal-development nystagmus syndrome
✓ Spasmas nutans syndrome

• Infantile nystagmus syndrome –

o Idiopathic/ Associated with sensory deprivation due to albinism, aniridia, Leber’s
congenital amaurosis, Macular disease etc.
o Jerky type and horizontal, absent during sleep
o Persists throughout life
o Visual prognosis dependent on integrity of sensory system
o Progression : Pendular-> Jerk
o Family history : Often positive

• Latent Manifest Nystagmus –

o Fusion mal-development nystagmus syndrome
o Bilateral jerky, horizontal nystagmus
o Elicited by covering one eye – fast component towards the uncovered eye
o No nystagmus when both eyes are open but appears when one eye is covered
{LATENT}
o Visual acuity – normal when both eyes are open; rapidly decreases when one eye is
covered
o Associated with Strabismus
o Intensity decreases with age

• Spasmus Nutans Syndrome

o Occurs in the first year of life
o Associated with nodding movements of the head – anteroposterior/ Lateral/
Rotatory
o Fine and rapid nystagmus; more marked in one eye
o Disappears over time on its own

2) Acquired Nystagmus
✓ Late onset or acquired nystagmus
✓ Usually characterized by Oscillopsia and other neurological abnormalities
✓ [Oscillopsia – is the perception of the environment appearing to oscillate horizontally,
vertically or torsionally]

• Nystagmus due to disorders of visual fixation

o Visual loss nystagmus
✓ Diseases of the retina
✓ Diseases of the Optic nerve
 ✓ Diseases affecting the optic chiasma
✓ Diseases affecting the post chiasmal visual system

• Vestibular Nystagmus

❖ Peripheral Vestibular Nystagmus

o Conjugate horizontal jerk nystagmus with fast phase away from the side of the
lesion
o Improves with fixation
o Worsens with gaze towards fast phase
o Associated with destructive lesions of the vestibular system, labyrinthitis, vestibular
neuritis
❖ Central Vestibular Nystagmus

I. Up beat Nystagmus
o Fast phase in upward direction
o Cause: Phenytoin sodium intoxication/ vermis of cerebellum – lesions

II. Down beat Nystagmus

o Jerky nystagmus, with fast phase downwards
o Cause: Lesion at the cervicomedullary junction at the foramen magnum
o Arnold Chiari Malformation

III. See-Saw Nystagmus

o One eye rising and intorting while the other eye falls and extorts
o Cause: Chiasmal lesion (bitemporal hemianopia)

IV. Periodic alternating Nystagmus

o Jerky nystagmus with rhythmic changes in amplitude and direction (60-
90 seconds)
o Congenital or acquired
o Cause: Demyelinating disease of the brainstem/ blindness/ lesions at
cervicomedullary junction

• Nystagmus due to disorders of gaze holding

❖ Gaze evoked nystagmus
o Slow, conjugate horizontal jerk nystagmus in the direction of gaze
o Occurs in smaller angles than physiological end-gaze nystagmus
o Cause: Neurological lesions of brain stem and posterior fossa/ Drug
intoxication- alcohol, barbiturates

❖ Dissociated or conjugated nystagmus

o Ataxic Nystagmus
o Nystagmus of abducted eye
o Unilateral or asymmetric
 o Cause: Internuclear ophthalmoplegia

❖ Convergence retracted syndrome

o Jerk nystagmus with bilateral fast component to the medial side
o Associated with retraction of the globe in convergence
o Cause: Pineal gland tumors, stroke, trauma, MS
o Parinaud Syndrome or Sylvian aqueduct syndrome
➢ Features –
Retraction nystagmus
Vertical Nystagmus
Difficult voluntary vertical gaze
Defective convergence
Adduction movements with attempted vertical gaze
Pupillary abnormalities
Pathological lid retraction

❖ Brun’s Nystagmus
o Low frequency, large amplitude nystagmus when the patient looks towards the
side of the lesion – GAZE EVOKED
o High frequency, small amplitude nystagmus when the patient looks towards
the side opposite to the lesion – VESTIBULAR IMBALANCE
o Cause: Tumors in cerebro-pontine angle

❖ Centripetal and rebound nystagmus

o Patient – gaze-evoked nystagmus -> attempts to look eccentrically for a
sustained period of time -> Nystagmus-↓amplitude -> May Reverse direction ->
CENTRIPETAL NYSTAGMUS
o Eyes returned to centre -> Short lived nystagmus with slow drifts in the
direction of the prior eccentric gaze occurs -> REBOUND NYSTAGMUS
o Centripetal and Rebound nystagmus – attempt by brainstem and cerebellar
mechanisms to correct the drift of gaze evoked by nystagmus.
o Causes: Cerebellar diseases, Lateral Medullary infarction, Tumors confined to
flocculus.

• Acquired pendular Nystagmus –

o Usually disconjugate with horizontal, vertical and torsional components
o May be associated with involuntary, repetitive movements of palate, pharynx and
face – oculopalatal myoclonus

• Differential diagnosis –
o Ocular bobbing –
✓ Neoplasms involving pontine brainstem – poor prognosis
✓ Loss of caloric response
o Flutter-like oscillations
 ✓ Interruptions of cerebellar connections into the brainstem
✓ Overshooting/ Undershooting the target
o Opsoclonus
✓ Wild, chaotic movements
✓ Frequent myoclonic movement of face, arms and legs
✓ Follows an episode benign encephalitis
✓ Good prognosis
• Treatment –
o Proper history must be taken and the exact cause must be identified before
prescribing suitable treatment
o Optical aids such as spectacles, prisms and contact lenses
o Medications for specific conditions
o Biofeedback – Training mechanisms to reduce nystagmus

Surgery – correct nystagmus and head posture.

 DISORDERS OF EYELIDS

What will we learn here???

Applied anatomy

Congenital anomalies of eyelid

Edema of eyelids
Inflammatory edema
Solid edema
Passive edema

Inflammatory disorders of eyelids

Blepharitis
External hordeolum
Chalazia
Internal hordeolum
Molluscum contagiosum

Eyelash disorders
Trichiasis
Distichiasis
Madarosis
Trichomegaly
Poliosis

Anomalies in the position of lid margin

Entropion
Ectropion
Symblepharon
Ankyloblepharon
Blepharophimosis
Lagophthalmos
Blepharospasm
Ptosis
Lid retraction

Tumours
Benign
Pre malignant
Malignant
 APPLIED ANATOMY

GROSS ANATOMY

Introduction
o Mobile tissue curtains placed in front of eyeballs
o Protect eyes from injuries and excessive light
o Spread tear film over cornea and conjunctiva
o Drainage of tears by lacrimal pump system

Parts
Divided by horizontal sulcus
• Orbital part
• Tarsal part

Position: when eye is open

• Upper lid – covers 1/6th of cornea
• Lower lid – just touches the limbus

Canthi:
• The region where the two eyelids meet – medial and lateral angles

Palpebral aperture:
• Elliptical space between the upper and lower lid (10-11mm vertically in the centre;
28-30mm horizontally)

Lid margin:
• 2mm broad – divided by punctum – medial lacrimal portion (rounded and devoid of
lashes) and lateral ciliary portion (rounded anterior border sharp posterior border
and an intermarginal strip between the two borders)
 STRUCTURE
⑦ layers

1) Skin – elastic and thinnest in

the body

2) Subcutaneous areolar
tissue – loose connective tissue
containing no fat; readily distended
by edema or blood

3) Layers of striated muscle –

orbicularis muscle [Orbital part
(encircles orbital margin), Preseptal
part, Pretarsal part (Horner’s
muscle), Levator palpebrae
superioris muscle

4) Submuscular areolar tissue

– layer of loose connective tissue-
nerves and vessels lie in this layer;
anesthetic injections given in this
plane

5) Fibrous tissue – Central Tarsal plate, Peripheral Septum orbitale – Framework of

eyelid

6) Layer of non-striated muscle - Palpebral muscle of Muller – supplied by

sympathetic fibres and paralysis leads to Horner’s Syndrome

7) Conjunctiva – Palpebral conjunctiva lines the eyelids

 GLANDS OF EYELIDS
o Meibomian glands
✓ Tarsal glands
✓ Upper lid – 30 to 40; Lower lid – 20 to 30
✓ Modified sebaceous glands
✓ Oily layer of tear film
o Glands of Zeis
✓ Sebaceous glands
✓ Open into follicles of eyelashes
o Glands of Moll
✓ Modified sweat glands situated near hair follicle
✓ Open into ducts of Zeis glands
o Accessory lacrimal glands of Wolfring

BLOOD SUPPLY
o Arteries – Marginal arterial arcades; another- Superior arterial arcade in the
upper eyelid alone
o Veins – Two plexuses – Post-tarsal -> Ophthalmic veins; Pre-tarsal ->
Subcutaneous veins
o Lymphatics – Pre-tarsal and Post-tarsal - Lateral half -> Preauricular lymph
nodes; Medial half -> Submandibular lymph nodes

NERVE SUPPLY
o Motor nerve – facial nerve (orbicularis muscle); Oculomotor (LPS Muscle);
Sympathetic fibres (Muller’s muscle)
o Sensory nerve – Branches of trigeminal – lacrimal, supraorbital, supratrochlear
for upper eyelid; Infraorbital and Infratrochlear branch for lower eye lid.
 CONGENITAL ANOMALIES OF EYELIDS

CONGENITAL PTOSIS:
• Congenital weakness of Levator palpebral superiors
• Abnormal drooping of eyelids

CONGENITAL COLOMBOMA:
• Full thickness triangular gap in tissue of lids
• Usually occurs near nasal side & involves upper lid

EPICANTHUS:
• Semicircular fold of skin covers medial canthus

DISTICHIASIS:
• Extra row of cilia occupies the position of meibomian glands which open into their
follicles as ordinary sebaceous gland

CRYPTOPHTHALMOS:
• Lids fail to develop and skin passes continuously from the eyebrow

MICROBLEPHARON:
1. Eyelids are small
2. Associated with microphthalmos or Anophthalmus
• May be very small or absent as like ablepharon

EPIBLEPHARON:
• Horizontal fold of tissue rises above lower eyelid margin.
• Usually disappears with growth of face

EURYBLEPHARON:
• Unilateral or bilateral horizontal widening of palpebral fissure
• Associated with lateral canthal malposition & lateral ectropion.

CONGENITAL ANKYLOBLEPHARON:
• also known as ankyloblepharon filiforme adnatum (AFA)
• single or multiple strands of connective tissue join the upper and lower lid margins
except in medial and lateral canthi
 OEDEMA OF EYELIDS

INFLAMMATORY OEDEMA
Inflammation of lid Inflammation of eyeball Inflammation of orbit
• Dermatitis • Acute iridocyclitis • Orbital cellulitis
• Stye • Endophthalmitis • Orbital abscess
• Insect bites • Panophthalmitis • Pseudotumor
• Cellulitis
• Lid abscess

Inflammation of Inflammation of conjunctiva Inflammation of lacrimal

paranasal sinus • Such as acute, Purulent, sac
• Maxillary sinus Pseudomembranous • Acute dacryocystitis
conjunctiva • Lacrimal abscess

Inflammation of lacrimal
gland
• Acute dacryoadenitis

SOLID OEDEMA OF THE EYELIDS

• Chronic irritation of lids, follows recurrent attack of erysipelas.
• Hard in consistency & is inflammatory

PASSIVE OEDEMA Of THE EYELIDS

Local:
o Cavernous sinus thrombosis
o Head injury
o Angioneurotic oedema
General:
o Congestive heart failure
o Renal failure
o Hypoproteinemia
o Severe anaemia
 INFLAMMATORY DISORDERS OF EYELIDS

inflammatory
disorders

external internal molluscum

blepharitis chalazion
hordeolum hordeolum contagiosum

BLEPHARITIS
Clinical types:
• Bacterial blepharitis
• Seborrheic / squamous blepharitis
• Mixed staphylococcal with seborrheic blepharitis
• Posterior blepharitis/ meibomitis
• Parasitic blepharitis

Bacterial blepharitis
• also known as Chronic anterior / staphylococcal / ulcerative blepharitis
• Chronic infection of anterior part of lid margin
• Occurs usually in childhood and continues throughout life

Etiology:
• Mostly coagulase +ve staphylococci
• Rarely streptococci, Moraxella, etc.

Clinical features:
Symptoms: Signs:
• Chronic irritation • Yellow crust at root cilia
• Itching • Small ulcers that bleed on crust removal
• Mild lacrimation • Red, thick margins with dilated blood vessels
• gluing of cilia • associated with Mild papillary conjunctivitis and
• Mild photophobia conjunctival hyperthermia
Complications & sequelae:
• Lash abnormalities
• Madarosis
• Trichiasis
• Poliosis
o Tylosis
o Eversion of punctum
o Eczema of skin and ectropion
o Recurrent styles
• Marginal keratitis
• Tear film instability
• Secondary inflammatory changes & mechanical changes in conjunctiva or cornea

Treatment:
• Lid hygiene – warm compresses, crust removal, avoid rubbing of eyes
• Antibiotics – ointment or drops – erythromycin or doxycycline in unresponsive
patients
• Topical steroids - Fluorometholone
• Ocular lubricants – artificial tear drops

Seborrheic/ squamous blepharitis:

• Also called primary anterior blepharitis

Etiology
• Associated with seborrhea of scalp
• Zeis gland secretes excessive neutral lipid which are split by cornybacterium acne
into free fatty acid

Clinical features
Symptoms: Signs:
• Whitish scales in lid margin • Accumulation of white dandruff like
• Mild discomfort scales
• Irritation • Lash fall out easily
• Occasional Watering • Lid margin is thickened
• H/O falling eyelashes • Signs of bacterial blepharitis
Complications:
• Similar to bacterial blepharitis

Treatment:
• Balanced diet
• Associated seborrhea should be treated
• Lukewarm solution of 3% sodium bicarbonate used to remove scales
• Antibiotics – similar to bacterial blepharitis

Meibomitis (posterior blepharitis)

• Meibomitis – inflammation of meibomian glands

Chronic meibomitis:
• Chronic dysfunction of meibomitis gland. those especially with seborrhea dermatitis

Pathogenesis:
• Bacterial lipase plays main role

Clinical features:
• Chronic irritation
• Itching
• Burning
• Grittiness
• Mild lacrimation

Signs:
• White frothy secretion – meibomian seborrhea
• Thick secretion released from openings of meibomian gland – toothpaste appearance
• Vertical yellowish streaks through conjunctiva
• Hyperemia and telangiectasia
• Oily & foamy tear film

Acute meibomitis:
• Due to staphylococcal infection
• Painful swelling around the gland
• Pressure on it releases serosanguinous discharge
Treatment of meibomitis:
• Lid hygiene – warm compresses
• Topical antibiotics
• Systemic tetracyclines – doxycycline drug of choice. erythromycin can be used if
doxycycline is contradicted
• Ocular lubricants – artificial tear drops
• Topical steroids – fluorometholone

Parasitic blepharitis (lash infection)

Etiology:
Includes
• Phthiriasis palpebrarum - infestation by phthirus pubis (crab louse) occurs in adults.
It is also acquired as sexually transmitted disease.
• Pediculosis – infestation by pediculus humanus corporis or capitis (head louse)
• demodex blepharitis

Clinical features:
Ingestion of lash with lice causes chronic blepharitis or chronic follicular conjunctivitis

Symptoms:
Chronic irritation, itching, burning and mild lacrimation
Signs:
• Lid margins are red and inflamed
• Life anchoring lashes may be seen on slit lamp examination
• Conjunctival congestion and follicles are seen.
• Nits (eggs) are seen as opalescent pearls

Treatment:
• Mechanical removal of lices and nits
• Application of antibiotic ointment and yellow mercuric oxide 1%
• Delousing of the patient, family members and accessories.
 EXTERNAL HORDEOLUM (STYE)
Acute suppurative infection of lash follicle and its associated Zeis or moll gland

Etiology:
Predisposing factor
• Age – more common in children and young adults
• Habitual rubbing of eyes
• Metabolic factors – excessive intake of carbohydrates and alcohol

Causative organism - staphylococcus aureus

Clinical features
Symptoms:
• Acute pain with a swelling
• mild watering
• photophobia

Signs:
• Stage of cellulitis – localized, red, firm, tender swelling associated with marked
edema
• Stage of abscess formation – visible pus point on lid margin in relation to affected
cilia

Treatment:
• Hot compress 2-3 times a day
• Evacuation of pus
• Surgical incision
• Antibiotic eyedrops
• Systemic anti-inflammatory analgesics and systemic antibiotics
 CHALAZION
• also known as Tarsal or meibomian cyst.
• Chronic non- suppurative lipogranulous inflammation of meibomian glands

Etiology:
Predisposing factors – similar to hordeolum externum

Pathogenesis

non infective lipo

mild grade proliferation of infiltration and retention of enlargement of acts as irritant
granulomatous
infection epithelium blockage of ducts secretion gland and causes
inflammation

Clinical features
Symptoms: Signs: Clinical course and complications:
➢ Painless swelling • Nodule is slightly • Complete spontaneous resolution
in eyelid noted • Slightly increase in size
➢ Mild heaviness • Projection of main bulk • Fungating mass of granulation
of the lid of the swelling tissue may be formed
➢ Blurred vision • Marginal chalazion • Secondary infection may occur
➢ Watering of eyes present as reddish grey • calcification
(epiphora) nodule. • Malignant change into meibomian
adenocarcinoma

Treatment:
➢ Conservative treatment – hot fomentation, topical antibiotic eye drops and oral anti-
inflammatory drugs
➢ Intralesional infection of long acting steroids - triamcinolone
➢ Incision and curettage
Surface anesthesia given. incision is made, contents are curetted out. Carbolic acid
cautery with methylated spirits for neutralization. Patching of eye is done and post-
operative treatment to decrease the discomfort.
➢ Diathermy
➢ Oral tetracyclines – as prophylaxis in recurrent chalazia
 INTERNAL HORDEOLUM
Suppurative infection of meibomian gland associated with blockage of duct.

Etiology:
Predisposing factors:
Similar to external HORDEOLUM
Causative organism:
• Occur as primary staphylococcal infection.
• Secondary infection in chalazion

Clinical features:
Symptoms:
• Acute pain
• Swelling
• Watering
• Photophobia

Signs:
• Localized, firm, red, tenderness and oedema of eyelids.
• Internum and externum can be differentiated by the point of maximum tenderness
and swelling away from Lid margin and pus usually points on the tarsal conjunctiva
and not on root of cilia

Treatment:
• Similar to externum.
• Pus formation alone can be drained by vertical incision from tarsal conjunctiva
 MOLLUSCUM CONTAGIOSUM
Etiology:
• Viral infections affecting children
• Usually caused by large pox virus.

Clinical features:
Typical lesion is
▪ Multiple
▪ Pale
▪ Waxy
▪ Umbilicated swelling around the skin of lid margin.

Complications:
▪ Chronic follicular conjunctivitis
▪ Superficial keratitis

Treatment:
Skin lesion can be incised and interior cauterized with tincture of iodine or pure carbolic
acid.
 DISORDERS OF EYELASHES

TRICHIASIS

• It refers to inward misdirection of cilia with normal position of the lid margin (which rub
against the eyeball)

Pseudotrichiasis:
The inward turning of lashes along lid margin (sun in entropion) is called pseudo trichiasis

Etiology:
• Cicatrizing trachoma
• Ulcerative blepharitis
• Healed membranous conjunctivitis
• Hordeolum externum
• Mechanical injuries
• Burns
• Operative scar on the lid margin

Clinical features:
Symptoms: Signs:
• Foreign body sensation • Misdirected cilia one or more touching the cornea
• Photophobia • Reflex blepharospasm and photophobia occur
• Irritation when cornea is abraded
• Pain • Conjunctiva may be congested
• Lacrimation • Signs of causative disease: trachoma, blepharitis
may be present

Complications:
• Recurrent corneal abrasions
• Superficial corneal opacities
• Corneal vascularization
• Non healing corneal ulcer
Treatment:
Epilation:
• Mechanical removal with forceps
• It is temporary measures as recurrence occurs within 3-4 weeks
Electrolysis:
• Method of destroying the lash follicle by electric current
Procedure:
→ Infiltration anesthesia is given to the lid
→ A current of 2ma is passed for 10 secs through a fine needle inserted into the
lash root
→ The loosened cilia with destroyed follicles are then removed with epilation
forceps
Cryoepilation:
• It is also an effective method
• after infiltration anaesthesia, cryoprobe (-200 C) is applied for 20 to 25 seconds to
external lid margin by double freeze thaw technique
• disadvantage – depigmentation of skin
Surgical correction:
When many cilia are misdirected operative treatment similar to cicatricial entropion should
be employed.

DISTICHIASIS
Congenital distichiasis:
• Rare anomaly in which an extra row of cilia occupies the position of meibomian
glands which open into their follicles as ordinary sebaceous glands.
• These cilia are usually directed backwards and if rubs the cornea, it should be
electroepilated or cryoepilated.
Acquired distichiasis:
• Metaplastic lashes
• Occurs due to metaplasia and differentiation
• The meibomian glands are transformed into hair follicles
 • The most important cause is late stage of cicatrizing conjunctivitis associated with
chemical injury, stevens Johnson syndrome, ocular cicatricial pemphigoid.

MADAROSIS
• Partial or complete loss of eyelashes
Causes
Local causes: Systemic causes:
1. Chronic blepharitis 1. Alopecia
2. Cicatrizing conjunctivitis 2. Psoriasis
3. Complication of cryotherapy 3. Hypothyroidism
4. Radiotherapy or surgery 4. Leprosy

TRICHOMEGALY
→ excessive growth of eyelashes
→ causes: congenital, familial, topical prostaglandin analogues, phenytoin, malnutrition,
hypothyroidism, porphyria, AIDS

POLIOSIS
→ greying of eyelashes and eyebrows

Causes
Ocular Systemic

Chronic anterior blepharitis Waardenburg syndrome

Sympathetic ophthalmitis Vitiligo
Idiopathic uveitis Marfan syndrome, etc.
 ANOMALIES IN THE POSITION OF LID MARGIN

ENTROPION

Definition
→ Inward rolling and rotation of the lid margin toward globe.

Etiological types:

types

congenital cicatricial senile mechanical

congenital entropion
▪ rare condition – since birth
▪ more common – upper eyelid
▪ lower eyelid congenital entropion
→ caused by improper development of the lower lid retractors.
▪ upper eyelid congenital entropion
→ usually secondary to mechanical effects of microphthalmos.

Cicatricial entropion
• common
• involves upper eyelid
• caused by cicatricial contraction of palpebral conjunctiva with or without associated
distortion of tarsal plate.
• common causes are:
1. trachoma
2. membranous conjunctivitis
3. chemical burns
4. pemphigus
5. stevens-Johnson syndrome

Senile entropion
 • Affects only the lower lid in elder people.

Etiological factors:
• horizontal laxity – due to weakening of orbicularis muscle
• vertical lid instability – due to weakening of dehiscence of capsulopalpebral fascia
• overriding of pretarsal orbicularis
• laxity of orbital septum

Mechanical entropion
• occurs due to lack of support provided by globe to the lids.
• occurs in patients with:
1. phthisis bulbi
2. enophthalmos
3. after enucleation / evisceration operation

Clinical features:
Symptoms: occurs due to rubbing of cilia over cornea and conjunctiva similar to trichiasis
• Foreign body sensation
• Irritation
• Lacrimation
• Photophobia

Signs:
Inturning of lid margins are found
▪ Depending upon degree of inturning it can be divided into three grades.
• Grade i entropion – posterior lid in rolled
• Grade ii entropion – inturning upto inter marginal strip
• Grade iii entropion – whole lid inturned

Signs of causative disease:

• scarring of palpebral conjunctiva in cicatricial entropion
• horizontal lid laxity in involutional entropion

Signs of complication:
• recurrent corneal abrasions
 • superficial corneal opacities
• corneal vascularization
• corneal ulceration

TREATMENT:
Congenital entropion.
• resolve with time without need of any intervention
• or may require excision of a strip of skin and muscle with plastic reconstruction of lid
crease (HOTZ PROCEDURE)

Cicatricial entropion:
• alteration of direction of lashes or
• transplanting lashes or
• straightening the distorted tarsus

SURGICAL PROCEDURES:
1. anterior lamellar resection
2. tarsal wedge resection
3. transposition of tarsoconjunctival wedge
4. posterior lamellar graft
Anterior lamellar resection:
• simplest operation
• to correct mild degree of entropion
• procedure: an elliptical strip of skin and orbicularis muscle is resected 3mm
away from the lid margin.
Tarsal wedge resection:
• It corrects moderate degree of entropion associated with strophic tarsus.
• PROCEDURE:
o In addition to elliptical resection of skin and muscle, a wedge of tarsal
plate is also removed

Transposition of tarsoconjunctival wedge:

Also known as Modified ketssey’s operation
• This is indicated to treat mild to moderate amount of cicatricial entropion.
 • It basically involves tarsal fracture and eversion of distal tarsus.
• A horizontal incision is made along the whole length of sulcus subtarsalis
involving conjunctiva a tarsal plate
• the lower end is undermined up to lid margin.
• Mattress sutures are then passed from upper cut end of the tarsal plate to
emerge on the skin 1mm above lid margin
• When sutures are tied entropion is corrected by transposition of
tarsoconjunctival wedge.
Posterior lamellar graft
INDICATIONS: severe entropion with upper eyelid retraction
Procedure:
• The deficient or keratinized conjunctiva and the scarred and contracted
tarsus are replaced by composite posterior lamellar graft.
• Tarsus may be replaced by preserved sclera or ear cartilage or hard palate
along with conjunctival or mucous membrane graft.

Senile entropion:
1. Transverse everting suture
2. Weis operation
3. Plication of lower lid retraction
4. Quickest procedure
Transverse everting suture:
• Temporary cure (upto 18 months)
• Indicated in very old patients
• Transverse suture – applied through full thickness of lids
• To prevent over riding of preseptal muscles
• Everting sutures tighten the lower lid retractors, similar to transverse
sutures except these passes at lower part of inferior fornix and emerge out
from skin near lash line.
Weis operation:
▪ Transverse lid split and everting sutures
▪ Indicated for long term cure in patients with little horizontal laxity.

Procedure:
• Incision (involving skin orbicularis & tarsal plate along whole length of
eyelid
 • Mattress sutures are then passed through the lower cut end of the tarsus
to emerge on skin 1mm below lid margin and are firmly tied
• The entropion is corrected by prevention of overriding of preseptal
muscle by horizontal scar tissue barrier
• Transferring of pull of eyelid retractors to upper border of tarsus by
everting sutures

Plication of lower lid retractors (jones operation)

• It is performed in severe cases or when recurrence occurs when
recurrence occurs after the above described operations.
Procedure:
• The lower lid retractors are exposed via horizontal skin incision at lower
border of tarsal plate shortened and sutures are used to create a barrier
to prevent overriding of the preseptal muscles.
Quickest procedure:
• Indication – horizontal lid laxity
Procedure:
• Transverse lid split to create barrier for overriding of preseptal
muscle, everting sutures to transfer pull of lower lid retractor to upper
border of tarsus and horizontal lid shortening to correct the laxity.
• Quickest procedure: horizontal lid shortening + Weis procedure

Lateral tarsal strip (LTS)

▪ Lateral canthal tightening is done by excising of lateral tarsal strip
▪ Useful in marked lid laxity of lateral tarsal strip
 ECTROPION
Out rolling or outward turning of lid margin is called ectropion.

Etiology types

types

congenital involutional cicatricial paralytic mechanical

Congenital ectropion:
• Very rare, may be seen in down’s syndrome & blepharophimosis syndrome.
• It may occur in both upper and lower lids and is due to congenital shortage of skin

Involutional entropion:
• Involves lower lids
• Commonest
• Occurs due to age related changes
1. Horizontal laxity of eyelid
2. Medial canthal tendon laxity
3. Lateral canthal tendon laxity
4. Disinsertion of lower lid retractors.

Cicatricial ectropion:
• It occurs due to scarring of skin scarring of skin and can involves both the lids
• Common causes of skin scarring
1. Thermal burns
2. Chemical burns
3. Lacerating injuries
4. Skin ulcers

Paralytic ectropion
• Due to paralysis of seventh nerve
• Occurs in lower lids
• Common causes of facial nerve palsy are
 1. Bell’s palsy
2. Head injury
3. Infection
4. Infections of the middle ear
5. Operation of the middle ear
6. Operations on parotid gland

Mechanical ectropion
• Occurs in condition where either lower lid is pulled down (as in tumors)
• Pushed out and down (as in proptosis and marked chemosis of conjunctiva)

Clinical features:
Symptoms:
• epiphora – main symptom
• Irritation
• Discomfort
• Mild photophobia
Signs:
• Lid margin is out rolled
→ Grade I – only punctum is everted
→ Grade II – lid margin is everted and palpebral conjunctiva is visible
→ Grade III – the fornix is also visible
• Signs of etiological condition
Skin scars in cicatricial ectropion
Seventh nerve palsy in paralytic ectropion
• Involvement ectropion
Signs:
1. Horizontal lid laxity – by positive snap test
2. Medial canthal tendon laxity – severe – inferior punctum moves till pupil
3. Lateral canthal tendon laxity – rounded appearance of lateral canthus 72mm.

Complications:
• Dryness and thickening of conjunctiva and corneal ulceration
• Eczema and dermatitis of lower lid
Treatment
Congenital ectropion:
• Mild – no treatment
• Moderate & severe – cicatricial ectropion with horizontal lid tightening full thickness
skin graft to vertically lengthen anterior lamella.
Involutional ectropion:
• Medial conjunctivoplasty:
o Used in mild case involving punctum area.
o Consists of excising spindle shaped piece of conjunctiva and subconjunctiva
tissue from below the punctal area.
• Horizontal lid shortening:
o Performed by full thickness pentagonal excision in patients with moderate
degree of ectropion.
• Byron smith’s modified kuhnt-szymanowski operation.
o Severe degree of ectropion, More marked in lateral lid
o base up pentagonal full excision of lateral third of eyelid + combined triangular
excision of skin from area just Lateral canthus to elevate the lid.
• Lateral tarsal strip technique.
For generalized ectropion with horizontal lid laxity

Paralytic ectropion:
Resolves spontaneously within 6 months when its due to bell’s palsy.
Temporary measures: Permanent measures
1. Topical lubricants 1. Horizontal lid tightening
2. Taping temporal side of eyelid 2. Palpebral sling operation
3. Suture tarsorrhaphy

Cicatricial ectropion:
Depending on degree
➢ V-y operation – mild ectropion
V shaped incision is given skin is sutured in Y shaped pattern.
➢ Z-Plasty (Elschnig’s operation) - mild to moderate ectropion
➢ Excision od scar tissue and full thickness skin grafting – in severe ectropion
Mechanical ectropion:
It is corrected by treating underlying mechanical force causing ectropion.
 SYMBLEPHARON
• Adhesion between palpebral and bulbar conjunctiva thus resulting in adhesion of
globe to eyelid
Etiology – results from healing of the kissing raw surfaces upon palpebral and bulbar
conjunctiva
▪ Common causes
• Thermal heat
• Chemical injury
• Membranous conjunctivitis
• Injuries and conjunctival ulceration
• Ocular pemphigus
• Stevens Johnson syndrome

Clinical features - Restricted ocular movements, Diplopia, Lagophthalmos, cosmetic

disfigurement

Types: -
• Anterior symblepharon- Adhesion only in anterior part
• Posterior symblepharon- Adhesion present upto the fornices
• Total symblepharon- Adhesion involving whole of the eyelid. Completely adherent

Complications: - Dryness, thickening, keratinistation of conjunctiva, corneal ulceration.

Treatment:
• Prophylaxis to prevent adhesion during the stage of raw surfaces - Glass rod is kept in
the fornix to prevent adhesion. Done several times a day. Therapeutic soft contact
lens.
• Curative – symblepharectomy –
• mobilizing the surrounding conjunctiva
• Conjunctival/buccal mucosa graft
• Amniotic membrane transplantation (AMT).
 ANKYLOBLEPHARON
• Adhesion between margins of upper and lower eyelid.
Etiology
• Congenital
• Acquired – chemical burns, thermal burns, ulcers, trauma.

Types - Complete/ Incomplete

Associated with symblepharon
Treatment:
• Separate the adhesions by excision - it should be kept apart during the healing
process.
• if adhesion extend to angles - Epithelial graft to prevent recurrences

BLEPHAROPHIMOSIS
• Decreased extent of palpebral fissure
• Eyelid appears contracted at outer canthus
Etiology:

❖ Congenital – Blepharophimosis syndrome – Congenital ptosis+

Blepharophimosis + Telecanthus + Epicanthus inversus
❖ Acquired – Epicanthus lateralis (due to formation of vertical skin fold at lateral
canthus following eczematous contraction)

Treatment:

❖ mild cases- No treatment

❖ severe cases- Canthoplasty operation.

LAGOPHTHALMOS
- Inability to close eyelids voluntarily
Etiology – Orbicularis oculi paralysis, Symblepharon, Severe ectropion, Proptosis, Coma.
- Physiological lagophthalmos – some people sleep with their eye open – nocturnal
lagophthalmos
C/F: - Incomplete closure of palpebral aperture leads to
 1. Corneal and conjunctival xerosis
2. Exposure keratitis

Treatment - Aim to prevent exposure keratitis and treat cause of lagophthalmos

1. Frequent instillation of Artificial tear drops + Antibiotic eye drops (during
sleep)
2. Soft-bandage contact lens
3. Measure to treat the cause of lagophthalmos
4. Tarsorrhaphy - Operation in which adhesions are created between the
eyelids to close the palpebral aperture.

Temporary tarsorrhaphy Permanent tarsorrhaphy

Indications
• Recovering VII cranial nerve palsy
• to assist healing of indolent corneal ulcer
• to assist healing of skin grafts in correct position.
Steps
▪ Incision of about 5mm marked on corresponding
parts of upper and lower lid margins which are
3mm from midline on either side.
▪ 2mm deep incision is made on the marked grey
line.
▪ marginal epithelium is excised.
▪ care is taken not to damage the ciliary line
anteriorly and sharp lid border posteriorly.
▪ the raw surfaces are Sutured with double armed
6-0 silk sutures passed through rubber bolster.
Indications
• VII nerve palsy (non-recovering)
• Neuroparalytic keratitis with
severe corneal sensation loss.
Steps
▪ Performed at the lateral canthus
to create permanent adhesions.
▪ The eyelids are overlapped after
excising a triangular flap of skin
and orbicularis from lower lid
and corresponding triangular
tarsoconjunctival flap from
upper lid
 BLEPHAROSPASM
• Involuntary, sustained, forceful closure of eyelid.

Etiology
1. Essential or spontaneous blepharospasm – Rare idiopathic, age 45-60
2. Reflex blepharospasm - Reflex sensory stimulation through branches of V
cranial nerve due to conditions such as
▪ Phlyctenular keratitis
▪ Interstitial keratitis
▪ Corneal foreign body
▪ Corneal ulcer and iridocyclitis
▪ Hysterical patients
▪ Dazzling light causing excessive stimulation of retina

C/F – Persistent epiphora, edema of eyelid, spastic entropion (elderly) and ectropion
(children and young adults), Blepharophimosis.
Treatment
1. Essential blepharospasm – Botox (subcutaneously – relieves spasm), Facial denervation
in severe cases
2. Reflex blepharospasm – Treat causative disease and associated complications.

LID RETRACTION
normal: the upper eyelid covers 1/6th of the cornea (about 2mm)
lid retraction: when the lid margin is either at or above the level of superior limbus

Causes:
• Congenital: Down’s syndrome, Duane’s retraction syndrome
• Thyroid eye disease
• Mechanical causes: Surgical overcorrection of ptosis, Scarring of upper eyelid skin
• Neurogenic causes: Facial palsy, third nerve misdirection, Marcus Gunn-jaw winking
syndrome
• Systemic causes: Uraemia
 PTOSIS

Definition: abnormal drooping of upper eyelid is called ptosis

▪ Normally upper lid covers 2mm of cornea, when its more than 2mm it is referred to
as ptosis

Clinic-etiological types

▪ Congenital
▪ Acquired

Congenital ptosis

Etiology – maldevelopment of the levator palpebrae superioris muscle

Characteristic features Associated features

Drooping of one or both upper Simple congenital ptosis

lids Congenital ptosis with associated weakness of superior
Lid crease rectus muscle
Lid lag on downward gaze Blepharophimosis syndrome
Functioning of LPS muscle may Congenital synkinetic ptosis – Marcus Gunn jaw
vary winking ptosis

Acquired ptosis

Depending on the cause it can be

▪ Neurogenic
▪ Myogenic
▪ Aponeurotic
▪ Mechanical

Neurogenic ptosis Acquired myogenic Aponeurotic ptosis Mechanical ptosis

ptosis
Caused by Occurs due to LPS Develops due to Due to excessive
innervational muscle disorders defect of levator weight in upper lid
defects aponeurosis when
 Myasthenia gravis the muscle function Lid tumors
3rd nerve palsy Dystrophia myotonica is normal Multiple chalazia
Horner’s syndrome Ocular myopathy lid edema
Ophthalmoplegic Thyrotoxicosis Senile ptosis Cicatricial ptosis
migraine Post op ptosis
Multiple sclerosis Trauma

Clinical evaluation

1. History
2. Examination
a. Exclude pseudoptosis
b. observe following points
i. Unilateral or bilateral ptosis
ii. Function of orbicularis oculi muscle
iii. Eyelid crease +/-
iv. Jaw- winking phenomenon +/-
v. Any associated weakness of extraocular muscle
vi. Bell’s phenomenon
c. Measurement of degree of ptosis
i. Mild – 2mm
ii. Moderate – 3mm
iii. Severe – 4mm
d. Margin reflex distance
e. Assessment of levator function
i. Normal – 15mm
ii. Good >= 8mm
iii. Fair – 5 – 7 mm
iv. Poor < = 4mm
f. Special investigations
i. Tensilon test
ii. Phenylephrine test
iii. Neurological investigations
g. Photographic record
Treatment

Congenital

- Almost always need surgical correction

1. Tarso conjunctivo mullerectomy
2. Levator resection
a. Done in moderate and severe cases

Moderate ptosis
i. Good function = 16 – 17 mm
ii. Fair function = 18 – 22 mm
iii. Poor function = 23 – 24 mm

Severe ptosis = 23 – 24 mm

b. Techniques
i. Conjunctival approach
ii. Skin approach

3. Frontalis sling operation

Acquired

• Treat the underlying cause

• Conservative treatment
• Surgical procedures
• Horner’s syndrome – fasanella servat operation
• Neurogenic ptosis in 3rd nerve palsy – frontalis sling operation
 TUMOURS OF EYELID

CLASSIFICATION

tumors of eyelid

benign pre malignant malignant

BENIGN TUMOURS PREMALIGNANT MALIGNANT TUMOURS

TUMOURS

• PAPILLOMAS • KERATOSIS • BASAL CELL CARCINOMA

• XANTHELASMA • XERODERMA • SQUAMOUS CELL
• HEMANGIOMA PIGMENTOSA CARCINOMA
• NEUROFIBROMA • SEBACEOUS GLAND
• KERATOCANTHOMAS CARCINOMA
• NAEVI • MALIGNANT MELANOMA

BENIGN TUMOUR
1. PAPILLOMAS:
• Most common tumour
• Occurs in surface epithelium
• In 2 forms
- Squamous papilloma
- Basal cell papilloma

Squamous papilloma Basal cell papilloma

• Derived from squamous cells
• Seen mostly in adults
• Pedunculated lesion or raspberry like
growth
TREATMENT: Simple excision.
• Derived from basal cell
• Middle age / older age
• Slightly pigmented
2. XANTHELASMA:
• Creamy yellow plaque like lesion.
• Occurs on skin of upper and lower lids near the inner canthus.
• Common in middle age women
• associated with diabetics and those with high cholesterol level.
TREATMENT:
• Excision may be advised for cosmetic reasons.
• high rate of recurrence

3. HAEMANGIOMA:

• Common tumour
• In 3 forms.
- Capillary haemangioma
- Naevus flammeus
- Cavernous haemangioma

Capillary hemangioma Naevus flammeus Cavernous

hemangioma
• most common variety • Part of Sturge weber • Developmental
• occurs at birth syndrome. venous anomaly.
• Superficial, bright red in colour – • Dilated vascular • occurs in 1st decade
strawberry naevus channels present. of life
• Endothelial cells. they do not grow or • Endothelium lined
regress like capillary vascular channels.
TREATMENT: haemangioma
TREATMENT:
OBSERVATION: Left untouched until similar to capillary
7 years haemangiomas.

MEDICAL TREATMENT:
-Intralesional steroid
-High dose oral steroid
therapy
-oral prednisolone

SUPERFICIAL RADIOTHERAPY
- Given for large tumours

SURGERY: Rarely necessary

4. NEUROFIBROMA:
• Lids and orbit are commonly affected.
EYELID NEUROFIBROMA:
- Solitary neurofibroma
- Diffuse neurofibroma – “bag of worms” feel

5. KERATOCANTHOMA:
• Non pigmented protrusions.
• TREATMENT - Complete Excision and biopsy.

6. NAEVI:
Naevi are cutaneous lesions that arise from the arrested epidermal melanocytes.

PIGMENTED NAEVI

Acquired
Congenital
Junctional Intradermal Compound

• Small and uniform • Location: • Location: • Slightly

in colour. epidermis dermis elevated
• Split naevus • Brown in • Elevated
appearance lesions

PREMALIGNANT TUMOUR

SOLAR KERATOSIS XERODERMA PIGMENTOSA

- Common lesion of sun exposed skin
- Uncommon of eyelids. - Autosomal recessive disease
- Progressive cutaneous
CLINICAL FEATURES:
pigmentation
-Flat, scaly lesion
- Bird like facies
-Hyperkeratosis
- Predisposition to develop lid
tumours
HISTOLOGY:
- Characterized by parakeratosis
- Cellular atypia
MALIGNANT TUMOUR

malignant

basal cell squamous cell sebaceous gland malignant

carcinoma carcinoma carcinoma melanoma

BASAL CELL CARCINOMA

▪ Commonest malignant tumour seen in elder people
▪ involves most commonly lower lid
▪ Predisposing factors: sun exposure, old age, xeroderma pigmentosa, basal cell
naevus syndrome
▪ Clinical features: 4 forms
o Non ulcerated nodular form
o sclerosing type
o Pigmented basal cell
o Noduloulcerative basal cell (Rodent ulcer)
▪ Histology: commonest pattern: solid basal cell carcinoma with palisading appearance
▪ Treatment:
• Surgery: Moh’s microsurgical technique
• Radiotherapy and cryotherapy

SQUAMOUS CELL CARCINOMA

▪ Second commonest malignant tumour
▪ In elderly patient
▪ Pre-existing lesion such as Bowen’s disease, actinic keratosis.
▪ Risk factors: sun exposure, radiation, injury, fair skin.
▪ Clinical features:
o Ulcerated SCC – scaly, erythemous plaque like growth with elevated and
depressed margins
o Nodular SCC – rare presentation, polypoid verrucous lesion
o Cutaneous horns – with underlying invasive SCC
▪ Metastasis: metastasized in preauricular and sub mandibular lymph nodes.
▪ Histology: whorled arrangement forming epithelial pearls containing laminated
keratin material in the centre
▪ Treatment: similar to basal cell carcinoma.
SEBACEOUS GLAND CARCINOMA:
▪ Rare tumour arising from the meibomian glands
▪ Clinical features:
o Initially as a nodule.
o Rarely a diffuse tumour along the lid margin.
▪ Treatment:
o Surgical excision with reconstruction of lid margin.
o Recurrences are common

MALIGNANT MELANOMA:
▪ Rare tumour of the lid arises from the melanocytes in the skin.
▪ Clinical features: Present in 3 forms
o Lentigo maligna type:
▪ Flat, pigmented, well defined lesion, later on becomes elevated and
invades the dermis
o Superficial spreading type:
▪ mildly elevated, Pigmented lesion with irregular margins.
o Nodular type:
▪ rapidly growing lesion which ulcerates and bleeds frequently.

▪ Metastasis: Tumour spreads locally as well as to distant sites by lymphatics and

bloodstream.
▪ Treatment: It is a radio-resistant tumour. Therefore, Surgical excision and
Reconstruction of the lid.
 LACRIMAL APPARATUS

What will we learn here???

• Anatomy of lacrimal apparatus

Lacrimal gland
Lacrimal apparatus
• Tear film
• Dry eye disease
• Watering eye
• Dacryocystitis
Congenital
Adult
▪ Chronic
▪ Acute
• Dacryocystectomy
Conventional external approach DCR
Endonasal (surgical or laser) DCR
Endocanalicular laser DCR
• Swellings of lacrimal gland
Dacryoadenitis
▪ Acute
▪ Chronic
Mikulicz’s syndrome
Dacryops
Tumours of lacrimal gland
 ANATOMY OF LACRIMAL APPARATUS

Lacrimal apparatus = lacrimal glands + lacrimal passages

Lacrimal gland

ORBITAL PART
MAIN LACRIMAL
GLAND
PALPEBRAL PART
LACRIMAL
GLAND GLAND OF
ACCESSORY KRAUSSE
LACRIMAL
GLAND GLAND OF
WOLFRING

All lacrimal glands are structurally similar to salivary gland

Blood supply
• Lacrimal artery branch of ophthalmic artery

Nerve supply
• Sensory – lacrimal nerve, branch of ophthalmic division of trigeminal nerve
• Sympathetic – carotid plexus of cervical sympathetic chain
• Secretomotor fibres:

superior
greater pterygo
salivary zygomatic lacrimal lacrimal
petrosal palatine
nucleus in nerve nerve gland
nerve ganglion
pons
 Lacrimal passages:

LACRIMAL GLAND

DUCTS OF LACRIMAL
GLAND

LACRIMAL PUNCTA

LACRIMAL CANALICULI

LACRIMAL SAC

NASO LACRIMAL DUCT

INFERIOR MEATUS OF
THE NOSE

Lacrimal puncta: each punctum is situated in lacrimal papilla, tears drain in puncta
Lacrimal canaliculi: there are two canaliculi – superior and inferior, they together form a
common canaliculus which drain in lacrimal sac. Reflux of tears is prevented by valve of
Rosenmuller.
Lacrimal sac: the lacrimal which lies in lacrimal fossa has 3 parts – fundus, body and neck.
The neck is continuous with nasolacrimal duct
Nasolacrimal duct: located in bony canal formed by maxilla and the inferior turbinate. It
drains into the inferior meatus in nose. In the lower end of the duct, there is a valve – valve
of Hasner. This valve prevents reflux from nose
 TEAR FILM

TEAR FILM LAYERS

MUCOUS LIPID LAYER :
LAYER : AQUEOUS prevents the
LAYER : overflow of tears,
mucin secreted by retards their
conjunctival consists of tears evaporation, and
goblet cell and secreted by main lubricates the
gland of manz and accessory eyelids as they
cornea becomes lacrimal glands slide over the
hydrophilic surface of globe

Functions of tear film:

1. Keeps the cornea and conjunctiva moist
2. Provides oxygen to corneal epithelium
3. Washes away debris and noxious irritants
4. Presence of anti-bacterial substance that prevents infection
5. Facilitates movements of lids over globe

Tears are continuously secreted by

→ Main lacrimal glands (reflex secretion)
→ Accessory lacrimal glands (basal secretion)

Tears are drained by an active lacrimal pump mechanism

When eyelids close tears are drained by
→ Contraction of pretarsal orbicularis
oculi
→ Contraction of preseptal fibres of
orbicularis
When eyelids open tears are drained by
→ Relaxation of pretarsal orbicularis
oculi
→ Relaxation of preseptal fibres of
orbicularis
 DRY EYE DISEASE

Definition:
Dry eye is a multifactorial disease of ocular surface characterised by loss of
homeostasis pf the tear film and accompanied by ocular symptoms in which tear film
instability and hyperosmolarity, ocular surface inflammation and damage and
neurosensory abnormalities play etiological roles

Etiological classification:

lacrimal deficiency

sjogren' syndrome
aqueous deficiency dry lacrimal gland
eye obstruction
non - sjogren's
dry eye

keratoconjunctivitis sicca
hypersecretory state
disease related to
meibomian gland
others
evaporative
disorders of lid aperture
dry eye

disorders related to
ocular surface

Clinical features
Symptoms
• Irritation
• Foreign body sensation
• Feeling of dryness
• Itching
• Non-specific ocular discomfort
• Chronically sore eyes
 Signs

Tear film signs Conjunctival signs Corneal signs Signs of

causative disease
→ Stingy mucous → Lustreless → Punctate epithelial Such as
and particulate erosions, Filaments
matter → Mildly congested and Mucous → Posterior
presence plaques blepharitis

→ Marginal tear → Conjunctival → Cornea may lose → Conjunctival

strip xerosis lustre scarring diseases
reduced/absent
→ Keratinization → Vital stains, → Lagophthalmos
→ Froth in tears fluorescein, Rose maybe depicted
→ Rose Bengal / Lisamin
Bengal/Lisamin green staining (+ve)
green staining
(+ve)

Complications:

• Threatening vision loss

• Epithelial breakdown
• Corneal ulceration
• Melting
• Perforation
Tear film tests

tear film tests

tear film break rose bengal

schirmer - I test
up test staining

Tear film break up test (BUT)

→ It is the interval between a complete blink and appearance of first randomly
distributed dry spot of the cornea
→ It serves as an indicator of adequacy of mucin component of tears
→ Procedure: a drop of fluorescein is instilled. The cornea is then examined using a
cobalt blue light in slit lamp
→ Normal value: 15 – 35 seconds

Value <10 means unstable tear film

Schirmer I test
→ It measures total tear secretions

>15 mm Normal
5 – 10 mm Mild keratoconjunctivitis sicca
<5 mm Severe keratoconjunctivitis sicca

Rose Bengal staining

→ Very useful in detecting even mild cases of KCS

A Severe
B Moderate
C Mild or early cases
Grading
LEVEL - 1 - mild dry eye
LEVEL - 2 - moderate dry eye
LEVEL - 3 - severe dry eye
LEVEL - 4 - very severe dry eye

Treatment

• Supplementation of tear substitutes:

▪ Artificial tear drops – cellulose derivatives / polyvinyl alcohol
• Anti-inflammatory agents:
▪ Fluorometholone
▪ Topical cyclosporine
▪ Chloroquine eye drops
▪ Omega fatty acid supplements
• Mucolytics:
▪ 5% acetyl cysteine – QID
• Secretagogues:
▪ Pilocarpine and cevimeline
• Preservation of existing tears by reducing tears and decreasing drainage
• Treatment of causative disease of dry eye
• Additional measures
▪ Serum eye drops
▪ Contact lenses
▪ Submandibular gland transplantation
 WATERING EYE

→ Overflow of tears from the conjunctival sac.

Etiology

watering eye

hyperlacrimation epiphora

physiological mechanical
primary
cause obstruction

lacrimal sac nasolacrimal

reflex punctal causes canaliculi causes
causes duct causes

eversion of lower
central
punctum

punctal
obstruction

Clinical evaluation

→ Ocular examination with diffuse illumination using magnification.

▪ Done to rule out reflex hypersecretion, punctual causes of epiphora and
any swelling in the sac area

→ Regurgitation test
▪ A pressure with index finger is applied over the lacrimal sac.
▪ Reflex mucopurulent discharge indicates NLD blockage with chronic
dacryocystitis.

→ Fluorescein dye disappearance test

▪ A 2 ml of fluorescein dye is instilled in conjunctival sac.
▪ If it disappears in 2 minutes, it is normal.
▪ If it presents, it indicates partial blockage of NLD or atonia of lacrimal sac.
 → Lacrimal syringing test
▪ Normal saline is pushed into lacrimal sac from lower punctum with syringe
and cannula.
▪ In partial obstruction saline passes with considerable pressure on the
syringe. In complete obstruction it reflexes back through the same punctum
indicating common canaliculi obstruction and through the lower punctum
indicates lower sac or NLD obstruction.

→ Jones dye tests

▪ In the suspect of partial lacrimal sac block.

Jones test 1
➢ 2% fluorescein dye are instilled in the conjunctival sac and a cotton
bud dipped in 1% xylocaine is placed in the inferior meatus at the
opening of nasolacrimal duct.
➢ A dye-stained cotton bud indicates adequate drainage through the
lacrimal passages and the cause of watering is primary
hypersecretion.
➢ Unstained cotton bud indicates partial obstruction or failure of
lacrimal pump.
Jones test 2
➢ The cotton bud is again placed in the inferior meatus and lacrimal
syringing is performed.
➢ Positive: Partial obstruction
➢ Negative: lacrimal pump failure.

→ Dacryocystography
▪ In patients with mechanical obstruction.
▪ To perform it a radiopaque material such as lipiodol, pantopaque, dianosil
or condray-280 is pushed in the sac with the help of a lacrimal cannula and
X-rays are taken after 5 minutes and 30 minutes to visualize the entire
passage.

→ Radionucleate dacryocystography
▪ A non-invasive technique to assess the functional efficiency of lacrimal
drainage apparatus.
 DACRYOCYSTITIS

• Inflammation of lacrimal sac is referred to as dacryocystitis

• Two forms:
→ Congenital dacryocystitis
→ Adult dacryocystitis
▪ Chronic form
▪ Acute form

Congenital dacryocystitis
Also known as Dacryocystitis neonatorum or infantile dacryocystitis.

• Definition:
It is the chronic inflammation of the lacrimal sac occurring in newborn infants

• Etiology:
Follows stasis of secretions in the lacrimal sac due to Congenital blockage in
the nasolacrimal duct (NLD)
Causes of stasis:
➢ Membranous occlusion at lower end, near the valve of Hasner –
commonest cause
➢ Presence of epithelial debris and membranous occlusion at its upper end
near lacrimal sac, complete non-canalisation and rarely bony occlusion.
➢ Bacteria commonly associated- Staphylococcus, Streptococcus and
Pneumococcus species.

• Clinical features:
➢ Epiphora after 7 days
➢ mucopurulent discharge from eyes.
➢ Regurgitation test +ve.
➢ Swelling on the sac area.

• Differential diagnosis
➢ Ophthalmia neonatorum
➢ Congenital glaucoma.
 • Complications:
➢ Recurrent conjunctivitis
➢ Acute or chronic dacryocystitis
➢ Lacrimal abscess and fistulae formation

• Treatment:
➢ Massage over the lacrimal sac area (4 times a day) and topical antibiotics
for 6 to 9 months.
➢ Lacrimal syringing (irrigation) with normal saline and antibiotic solution.
(Started at the age of 3 months-once a week or once in 2 weeks)
➢ If not cured after 6 months – Probing of NLD with Bowman’s probe. (careful
probing should be done so that canaliculi are not damaged) In case of
failure, repeated after 3-4 weeks.
➢ Balloon catheter dilatation-Done when repeated probing is failed and
where obstruction is due to scarring or constriction.
➢ Intubation with silicone tube in NLD for six months if 4.and 5. Are a failure.
➢ If all the above are a failure, Dacryocystorhinostomy (DCR) can be done
after 4 yrs.

Adult dacryocystitis:

i. Chronic dacryocystitis
• More common
• Etiology:

factors responsible for

predisposing factors source of infection causative orgaism
statis of tears
• 40 - 60 years • anatomical factors like • infections from • Staphylococci
• female narrow bony canal conjunctiva, • Pneumococci
preponderance • foriegn bodies paranasal sinuses, • Streptococci
• heredity • excessive lacrimation etc.
• Pseudomonas
• poor personal • mild inflammation of pyocyanea
hygiene lacrimal sac
• poor socio • obstruction of lower
economic status end of nasolacrimal
duct
 • Clinical features:

Stages Clinical features

Stage of chronic ▪ Watering eye and mild redness.

catarrhal ▪ On syringing, clear fluid or few fibrinous mucous flakes
dacryocystitis regurgitate.
▪ Upon dacryocystography, block in NLD, a normal sized
lacrimal sac with healthy mucosa is revealed.
Stage of lacrimal ▪ Constant epiphora, associated swelling below inner
mucocele canthus.
▪ Regurgitation – Milk or gelatinous mucoid fluid from lower
punctum.
▪ Dacryocystography- distended sac with blockage in NLD.
▪ ENCYSTED MUCOCELE – Both canaliculi are blocked – large
fluctuations swelling with -ve regurgitation test.
Stage of chronic ▪ Epiphora, recurrent conjunctivitis and swelling in the inner
suppurative canthus and mild erythema of the skin.
dacryocystitis ▪ Regurgitation- purulent discharge in the lower punctum.
▪ Openings of canaliculi are blocked – ENCYSTED PYOCOELE.
Stage of chronic ▪ Persistent epiphora and discharge.
fibrotic sac ▪ Dacryocystography- small sac with irregular mucosal folds.

• Complications:
➢ Chronic intractable conjunctivitis
➢ Acute or chronic dacryocystitis
➢ Entropion of lower lid
➢ Maceration
➢ Eczema of lower lid skin
➢ Corneal ulceration
➢ Endophthalmitis when intraocular surgery is done in the presence of
dacryocystitis.

• Treatment:
➢ Conservative treatment – probing and lacrimal syringing
➢ Balloon catheter dilatation
 ➢ Dacryocystorhinostomy (DCR)
➢ Dacryocystectomy (DCT)
➢ Conjunctivodacryocystorhinostomy (CDCR)

ii) Acute dacryocystitis:

Acute suppurative inflammation of the lacrimal sac, characterised by presence
of painful swelling in the region of sac.

• Etiology:
➢ Acute exacerbation of chronic dacryocystitis.
➢ Acute peridacryocystitis
➢ Causative organisms- S. hemolyticus, Pneumococcus, Staph sp.

• Clinical features and treatment:

Stages Clinical features Treatment

Stage of ▪ Painful swelling ▪ Antibiotics – both systemic and

cellulitis ▪ Epiphora topical
▪ Malaise ▪ Systemic anti-inflammatory
▪ Redness and edema analgesics
▪ Hot fomentation

Stage of ▪ Occlusion of canaliculi ▪ 1st stage treatment (+)

lacrimal ▪ Pericystic swelling ▪ Pus drainage
abscess ▪ Later DCR / DCT

Stage of ▪ External fistula formed if ▪ Systemic antibiotics

fistula lacrimal abscess is ▪ Fistulectomy with DCT / DCR
formation unattended
▪ Rarely internal fistula

• Complications:
➢ Acute conjunctivitis
➢ Corneal abrasion
➢ Lid abscess
➢ Osteomyelitis of lacrimal bone
➢ Orbital cellulitis
➢ Cavernous sinus thrombosis
➢ Generalised septicaemia
 SURGICAL TREATMENT OF DACROCYSTORHINOSTOMY

3 types:
• Conventional external approach, DCR and
• Endonasal (surgical or laser) DCR
• Endocanalicular laser DCR.

Conventional external approach DCR

1. Anaesthesia. General anaesthesia is preferred

2. Skin incision. Either a curved incision along the anterior lacrimal crest or a straight
incision 8 mm medial to the medial canthus is made.
3. Exposure of medial palpebral ligament (MPL) and anterior lacrimal crest. MPL is
exposed by blunt dissection and cut with scissors to expose the anterior lacrimal crest.
4. Dissection of lacrimal sac. Periosteum is separated from the anterior lacrimal crest and
along with the lacrimal sac is reflected laterally with blunt dissection exposing the lacrimal
fossa.
5. Exposure of nasal mucosa. A 15 mm × 10 mm bony osteum is made by removing the
anterior lacrimal crest and the bones forming lacrimal fossa, exposing the thick pinkish
white nasal mucosa.
6. Preparation of flaps of sac. A probe is introduced into the sac through lower canaliculus
and the sac is incised vertically. To prepare anterior and posterior flaps, this incision is
converted into H shape.
7. Fashioning of nasal mucosal flaps is also done by vertical incision converted into H
shape.
8. Suturing of flaps. Posterior flap of the nasal mucosa is sutured with posterior flap of the
sac using 6–0 vicryl or chromic cat gut sutures. It is followed by suturing of the anterior
flaps.
9. Closure. MPL is sutured to periosteum, orbicularis muscle is sutured with 6–0 vicryl and
skin is closed with 6–0 silk sutures.

anaesthesia and skin incision

med palpebral ligament and anterior

lacrimal crest exposure

dissection of lacrimal sac

exposure of nasal mucosa

preparation of flaps of sac

fashioning and suturing of nasal flaps

closure

In simple words: post flap of sac and post flap of nasal mucosa are sutured together and
anterior flap of sac and mucosa are sutured together, so that tears from the eye drains
directly into the nasal mucosa
CAUSES OF FAILURE COMPLICATIONS
• Inadequate size and position of • Cutaneous scarring
ostium • Haemorrhage
• Unrecognized common canalicular • Cellulitis
obstruction • CSF rhinorrhoea
• Scarring
• Sump syndrome

Endoscopic DCR

1. Preparation and anaesthesia. Conjunctival sac is anaesthetised with topically

instilled 2% lignocaine. Then 3 ml of lignocaine 2% with 1 in 2 lac adrenalines is
injected into the medial parts of upper and lower eyelids and via subcaruncular
injection to the lacrimal fossa region.

2. Identification of sac area A 20-gauge light pipe is inserted via the upper canaliculi
into the sac. With the help of endoscope, the sac area which is trans illuminated by
the light pipe is identified and a further injection of lignocaine with adrenaline is
made below the nasal mucosa in this area.
 3. Creation of opening in the nasal mucosa, bones forming the lacrimal fossa and
posteromedial wall of sac can be accomplished by two techniques:
i. By cutting the tissues with appropriate instruments or
ii. By ablating with Holmium YAG laser (endoscopic
laser-assisted DCR).
Note. The size of opening is about 12 mm × 10 mm

4. Stenting of rhinostomy opening. The outflow system is then stinted using fine
silicone tubes passed via the superior and inferior canaliculi into the rhinostomy
and secured with a process of knotting. Nasal packing and dressing is done.

5. Postoperative care and removal of silastic lacrimal stents. After 24 hours of

operation nasal packs are removed and patient is advised to use decongestant,
antibiotic and steroid nasal drops for 3–4 weeks. The silastic lacrimal stents are
removed 8–12 weeks after surgery
CAUSES OF FAILURE COMPLICATIONS CONTRAINDICATIONS

• Inadequate bony • Orbital emphysema • Lacrimal sac tumours

opening • Trauma to canaliculi • Dacryoliths
• Anastomotic block by tubes • Large abscess of sac
• Iatrogenic • Infection
obstructions • Haemorrhage

ENDONASAL DCR EXTERNAL DCR

Advantages Disadvantages
No external scar Cutaneous scar
Relatively blood less surgery More blood loss
Less chance of injury to ethmoidal vessels Greater chance of damaging the
and cribriform plate surrounding structures
Less time consuming (15-30 mins) Time consuming (45-60 mins)
Time consuming (45-60 mins) Significant postoperative morbidity

Advantages Disadvantages
Less success rate (70-90%) More success rate (95%)
Requires more skilled ophthalmologists Easily performed
Expensive equipment Cheap
Requires reasonable access to middle Does not require familiarity with
meatus and familiarity with endoscopic endoscopic anatomy
anatomy

Endocanalicular laser DCR

→ A quick procedure carried under local anaesthesia

→ Useful in elderly
→ Success rate is 70%

laser probe passed an opening is created by

through a canaliculus ablation of structures

In Dacryocystectomy, the 1st four steps are similar to external DCR, after that we have
→ Removal of lacrimal sac
→ Curettage of bony NLD
→ Closure
 SWELLINGS OF LACRIMAL GLAND

1. DACRYOADENITIS
Inflammation of lacrimal gland

ACUTE
ETIOLOGY Primary infection or secondary
to some local or systemic causes → In association with chronic
CLINICAL Painful swelling
FEATURES Red and swollen lid
Proptosis
Fistula as a complication
TREATMENT Systemic antibiotics
Analgesics
Anti-inflammatory drugs
CHRONIC
→ As sequel to acute form
inflammation of conjunctiva
→ Due to systemic diseases
Painless swelling
Proptosis, Diplopia
A firm lobulated mobile mass is
present
Treat the cause

2. MIKULICZ’S SYNDROME

→ Bilateral symmetrical enlargement of lacrimal and salivary glands.

→ Associated with systemic diseases

3. DACRYOPS

→ Cystic swelling
→ Caused due to blockage of lacrimal glands causing retention of lacrimal secretion

4. TUMOURS OF LACRIMAL GLAND

tumours

epithelial non epithelial

benign malignant lymphoproliferative

pleomorphic lacrimal gland inflammatory

adenoma carcinoma conditions
Pleomorphic adenoma

→ Benign mixed tumour

→ It is a slowly progressive painless swelling of upper outer quadrant of orbit
→ Treatment consists of surgical removal with capsule

Lacrimal gland carcinoma

→ Occurs in 4th – 5th decade of life

→ They present as painful mass in supratemporal quadrant of orbit
→ On CT, there is an infiltrative tumor moulding the globe
→ Treatment includes complete macroscopic excision and high dose radiotherapy to
orbit
 ORBIT
What you learn here?

• Anatomy of Orbit
• Development anomalies of orbit
• Orbital mucormycosis
• Orbital infections
• Orbital cellulitis
• Cavernous sinus thrombosis
• Non infective orbital inflammation
• Orbital tumours

Anatomy of Orbit
Each orbit is a bony cavity containing an eye ball and extraocular appendages and muscles.
Bony orbit
• Quadrilateral pyramid shape
• Roof frontal and sphenoid
• Medial maxilla, lacrimal, ethmoid and sphenoid
• Lateral zygomatic, greater wing of sphenoid
• Base/inferior “roof of maxillary sinus” i.e Maxilla, Zygomatic, Palatine
Strongest wall lateral
Easily fractured floor and medial
Fracture of floor of orbit leads to maxillary sinusitis

• Apex of the bony orbit contains three openings.

a. Superior orbital fissure
i. Superior and inferior branch of oculomotor nerve (CN 3)
ii. Troclear nerve (CN 4)
iii. Ophthalmic branch of Trigeminal nerve (CN 5-1)
iv. Abducens nerve (CN 6)
v. Superior ophthalmic vein
b. Inferior orbital fissure
i. Inferior ophthalmic vein
ii. Maxillary branch of trigeminal nerve (CN 5-2)
c. Optic foramen
i. Optic nerve (CN 2)
 ii. Superior ophthalmic vein
Extraocular muscles

Extraocular appendages
1. Eyelids
2. Conjunctiva
3. Lacrimal apparatus
4. Orbital fat
 DEVELOPMENTAL ANOMALIES OF ORBIT

The orbit and its contents may be affected by a number of developmental abnormalities involving the
bones of the skull or face.
They are commonly hereditary (auto somal dominant)

The common abnormalities are :

1. Cranio-synostosis
● Due to premature closure of one or more cranial sutures.
● This closure causes a complete arrest of bone growth perpendicular to the closed suture, and
the compensatory growth of the cranium in other diameters, which causes the typical shape of
the skull.
Types :
1. Scaphocephaly (boat-shaped skull): Premature closure of sagittal suture.
2. Oxycephaly (tower-shaped skull): Premature closure of coronal suture
3. Trigonocephaly egg-shaped skull) : premature closure of frontal suture
4. Brachy-cephaly (clover-leaf skull) : Premature closure of all sutures.
The clinical features are :
1. Bilateral proptosis due to shallow orbit.
2. Esotropia or exotropia.
3. Papilloedema, due to increased CSF pressure
4. Optic atrophy primarily due to traction on the optic nerve, or secondary to papilloedema.
Treatment :
Craniotomy or orbital decompression to reduce CSF pressure and papilloedema.
2. Craniofacial dysostosis (Crouzon)
Brachycephaly is combined with hypoplasia of the maxilla
• Ophthalmic features:
● Widely separated eyeballs hypertelorism)
● Shallow orbits with proptosis.
● Corneal problems due to exposure.
● Divergent squint
● Optic atrophy.
• Non-ophthalmic features :
● High-arched palate.
● Irregular dentition
● Hooked (parrot-beak) nose.
● Mental retardation.
3. Mandibulo-facial dysostosis (Treacher Collins)
Hypoplasia of the zygoma and mandible
• Ophthalmic features
● Indistinct inferior orbital margin.
● Coloboma (notching) of the lower lid
● Anti-mongoloid slanting,
• Non-ophthalmic features :
● Bird-like face.
● Macrostomia with high-arched palate.
● External ear deformity.
4. Median facial cleft syndrome
● Hypertelorism with telecanthus
● Cleft nose, lip and palate.
● V-shaped frontal hairline (widows peak.
● Divergent squint.
5. Oxycephaly syndactyly (Apert)
● Tower skull with flat occiput.
● Mental retardation,
● Ventricular septal defect
● High-arched palate.
● Hypertelorism, shallow orbits and proptosis.
● Antimongoloid slanting with ptosis and exotropia.
● Syndactyly of the fingers and toes.
6. Hypertelorism
● Increased separation of eyes
● Widely separated orbits, and broad nasal bridge.
● The interpupillary distance (IPD) may be 85 mm or more.
● Divergent squint, telecanthus and mongoloid slanting.
● There may be optic atrophy due to associated narrowing of the optic canals.
● Hypertelorism also occurs in – median facial-cleft syndrome, Apert’s syndrome, Crouzon’s
syndrome etc.

ORBITAL MUCORMYCOSIS

● Other name: Phacomycosis

● Fungal infection ( mostly Mucor and Rhizopus)
● Begins in sinuses , erodes to orbital cavity.
● Can invade vessels and cause ischemic necrosis

Clinical features:
1. Pain
2. Proptosis
3. Necrotic areas with black eschar
Complications:
1. Meningitis
2. Brain abscess
3. Death
Diagnosis:
 1. Clinical
2. Biopsy ( finding nonseptate broad branching
hyphae) Treatment:
1. Correction of underlying disease (eg: diabetic ketoacidosis)
2. Surgical excision
3. IV Amphotericin B
4. Adjunctive hyperbaric oxygen
5. Exenteration

Orbital infection

ORBITAL INFECTIONS AND INFLAMMATIONS

CLASSIFICATION :

A.ORBITAL INFECTIONS:

• Acute orbital infections and related infections :

1. Preseptal cellulitis
2. Orbital cellulitis and intra orbital abcess
3. Orbital thrombophlebitis
4. Orbital osteo periostitis
5. Tenositis
6. Cavernous sinus thrombosis

B.CHRONIC ORBITAL INFECTION :

• Tberculosis
• Syphilis
• Actenomyosis
• Mycotic infections eg. Mucormycosis
• Parasitic infections

C.NON-INFECTIOUS ORBITAL INFLAMMATIONS:

• Isolated orbital inflammation

1. Idiopathic orbital inflammatory disease
2. Idiopathic sclerosis inflammation or orbit
3. Mysositis
• Systemic inflammation
1. Thyroid eye disease
2. Wogners granulomatosis
3. Sarcoidosis

A.ORBITAL INFECTION :

• Preseptal cellultis
Preseptal (or post septal) cellulitis refers to infection of the subcutaneous tissues anterior to
the orbital disease but is included here under because the facial veins are valves and
preseptal cellulitis .
ETIOLOGY :

• Causative organism : one usually staphylococcus aureus (or) streptococcus pyogenes and
occasionally haemophilly synthesis .

MODES OF INFECTION :

1. Enogenous infection may result following skin laceration insert and eyelid penetration .
2. Endotropin from local infections such as from an weak bordelum (or) areolar dacrocytosis .
3. Endogenous infection may occur by haematogenous spread drown remote infection or the
middle our (or) upper respiratory tract .

CLINICAL FEATURES :

Preseptal cellulitis presits as inflammatory ostoma of the eyelids and periorbital star with no
movement of the orbit .

CHARACTERISTIC FEATURES :

• Painful ocular periorbital swelling

• Erythema and hyporaemic or the lids
• Proptosis is absent
• occular movements are normal
• conjunctiva is usually not congested and unusual society is normal .

TREATEMENT :

• Systemic antibiotic , form the maintenance or treatment

• Mild to molecular cases may be treated by oral co-amoiodrone 500/125 mg tds (or)
fluconaccilin 500 mg for about 10 days.

Severe cases need hospitalization for infrastructure ceffticome 1-2 g/day in distilled doses .

2.systemic analgesic and anti-inflammatory dress help in radius pain and swelling .

3.warm compress , 2-3 times a day , hours a 500 this effect

4.surgical operation and debidecent is requires on the preforms or thickest mass (or) citra the
foreign bodies is suspected .

ORBITAL CELLULITIS

ORBITAL CELLULITIS :

• Acute inflammation of soft tissue of orbit behind the orbital septum .

• May or may not progress to a subperiostal abscess or orbital abcess .

CAUSATIVE AGENTS:

• Staph. Aureus , S.pyogenes

• Strep. Pneumonia , haemophillus influenza

MODE OF INFECTION :
 • Exogenous – trachoma
• Contiguous – from adjacent structre
• Endogenous – blood spread

CLINICAL FEATURES :

SYMPTOMS :

• Swelling and severe pass increased by occular movement .

• Fever , prostration and defective vision .

SIGNS:

• Lid edema
• Chemosis of conjunctiva
• Axial proptosis
• Restriction of ocular movement
• Fundus : congestion of veins and disc edema

COMPLICATIONS :

Occular complications :

• Exposure keratitis , occlusion of central retinal artery or vein .

• Endophthal mitis , optic neuropathy .

Intra cranial complications :

• Meningitis , brain stem absecess

• Cavernous sinus thrombosis

Sub periostal abscess along medial orbital wall

Orbital abscess :

• Collection of pus within the orbital soft tissue

• Post traumatic or post operative complication

Temporal or parotid abcess

• Due to spread of infection

General septicimea or pyeremia

INVESTIGATION :

• Bacterial culture
• Complete haemmogram
• Xray pns
• Orbital ultrasonography
• CT scan and MRI scan

TREATMENT :

Orbital cellulitis is an emergency and so patient should be hospitalized

 a. Intensive antibiotic therapy
• Used to overcome the infection .
• Intravenous antibiotics should be administred
• For staphylococcus infection high doses of penicillinace – resistant antibiotic
(eg.oxacillin ) combined with ampicillin shoul be given
• Cefotaxime , ciproflaxicin or vancomycin can be used as alternative for oxacillin
and penicillin combination .
• For H.ifluenza especially In children chloramphenicol or clavulinic and should
also be added
• For anaerobes oral metronidazole 500 mg every behaviour should be added .

b.Analgesics and anti-inflammatory drugs

• Helps to relieve pain and fever

c.topical antibiotic eye ointment

d.nasal decongestant drops

e.revaluation

d.surgical intervension:

• Suggested cause of unresponsiveness to antibiotics decrease in vision and pressure

of an orbital or subperiorbital abscess.
• Surgical intervention required are ad follows :
✓ Immediate conthotomy / cantholysis
✓ Free incision into the abscess
✓ Drowning of the thick abcess by a 2-3 cm curved incision .

CAVERNOUS SINUS THROMBOSIS

CAVERNOUS SINUS THROMBOSIS , refers to infected blood clot . it is described along with
infection of the orbit on it alos manifest an acute inflammatory type of proptosis.

CAVERNOUS SINUS ANATOMY :

Cavernous sinus is formed between the meningeal layer and industrial layer of duramater

The contents of cavernous sinus includes the 3rd cranial nerve , 4th cranial nerve ,

ophthalmus divisions and maxillary division of trigeminal nerve and 8th cranial nerve and
internal carotid artery

ETIOLOGY:

Septic thrombosis of the cavernous sinus is a disasterous regular , resulting from spread of
sepsis travelling along its tributaries from the infected sinuses , teeth , ears , nose and skin to
the face .

Very rarely cavernous sinus thrombosis may also occur after trauma .
Communications of cavernous sinuses and sources of infection anterior :

Anteriorly cavernous sinus is bounded by supraorbital fissure … so the superior and the
inferior ophthalmic veins drain into the sinuses and orbits

There fore , infection to cavernous sinuses may spread from infected facial wounds ,
erysipelas , squeezing of stye , furancles orbital cellulitis and sinusitis

POSTERIOR :

The posterior border of cavernous sinus includes the petrays part of the temporal bone . the
superior and inferior petrosal sinuses leave to join the lateral sinus . labyrinth veins opening
into the inferior petrosal sinuses bring infection from the mastoid air sinuses

SUPERIOR :

The cavernous sinus communicates with the veins of cerebrum and may be infected from
meningitis and cerebral abscesses

INFERIOR :

The sinus communicates with pterigoid venus plexus

MEDIALLY :

The two cavernous sinuses are connected to each other by transverse sinuses which
transfers infection from one side to the other .

The other sources of cavernous sinus thrombosis includes :

• Diabetes
• Cancer
• Trauma

SYMPTOMS :

• Unilateral visual loss

• Sudden headache
• Unilateral eye swelling
• Eyelid drooping
• High grade fever

6.damage to 3rd 4th 6th cranial nerve . the 3rd cranial nerve is involved in medial movement of the eye
ball and 6th cranial nerve involved in lateral movement of the eye ball and 4th cranial nerve supplying
the superior oblique muscle resulting in unable to move the eye ball inderiorly.

INVESTIGATIONS :

1. CT scan head and orbit may show involvement of cavernous sinuses and proptosis.
2. Mangentic resonance venography (angiography) in the investigation of choice which shows
an absence of flow void in thrombosed sinuses
3. Blood culture is recommended for sepsis.

COMPLICATIONS :

At any stage hyperpyrexia and signs of meningitis , pulmonary infarction may precude death
TREATMENT :

1. Antibiotics are the sheet anchor of treatment massive doses of modern potent broad
spectrum antibiotics should be injected intravenously
2. Analgesics and anti-inflammatory drugs control pain and fever
3. Anticoagulants role is controversial .

NON-INFECTIVE ORBITAL INFLAMMATION

1. Idiopathic Orbital Inflammatory Disease (Pseudotumor)

2. Tolosa-Hunt Syndrome

Idiopathic Orbital Inflammatory Disease (Pseudotumor)

➢ Pseudotumor – Condition of the orbit which,

o Clinically – present as tumours, but
o Histopathologically – proven as chronic inflammations.

➢ Recently called as Idiopathic Orbital Inflammatory Disease (IOID)

➢ IOID – Can occur throughout the orbit from lacrimal gland to orbital apex.

➢ Common Features:

o Age – Between 40 and 50 years

o Laterality – Unilateral (occasionally bilateral)
o Clinical Presentation – Swelling / puffiness of eyelids,
Congestive proptosis,
Orbital pain,
Restricted ocular movements,
 Diplopia, chemosis & redness
o Optic Nerve dysfunction – When posterior orbit involved
o Remission - Spontaneous after few weeks
o Recurrence - Common
o Frozen Orbit - In severe prolonged inflammation.

➢ Diagnosis:
o USG and CT – diffuse infiltrative lesion with irregular ill-defined margins and
variable density
(CT image of IOID)

o MRI:

▪ T1 MRI – Hypointense lesion c.f muscle.

 (T1 MRI)
▪ T2 MRI – Hyperintense lesion c.f muscle.

(T2 MRI)

o Incisional biopsy – confirm diagnosis in persistent cases.

➢ Treatment:
o NSAIDs
o Systemic Steroids (only after diagnostic biopsy)
o Radiotherapy
o Cytotoxic drugs
o TNF inhibitors.

Tolosa Hunt Syndrome (Non-specific granulomatous inflammation.)

➢ Involves – superior orbital fissure &/or orbital apex &/or cavernous sinus
 ➢ Clinical features:
o Manifestation – Painful ophthalmoplegia.
o Presentation
▪ Superior orbital fissure syndrome.
▪ Orbital apex syndrome.

➢ Superior orbital fissure syndrome:

o Involvement of structures passing through superior orbital fissure
o Features:
▪ Pain – Retro orbital ache.
▪ Sensory loss/Disturbance – along the course of 5th cranial nerve
▪ Ipsilateral ophthalmoplegia – due to involvement of 3rd,4th,6th CN
▪ Ptosis – due to 3rd CN palsy
➢ Orbital apex syndrome:
o Involvement of structures present at the apex of orbit (i.e., superior orbital fissure plus
optic canal)
o Features:
▪ Features of superior orbital fissure syndrome
+
▪ Features of optic nerve involvement (i.e., early visual loss + afferent pupillary
defect)
 ➢ Treatment:
o Systemic steroids.
o Radiotherapy.

ORBITAL TUMOURS

INCIDENCE: tumours of the eye and orbit are rare.

● Male to female incidence is similar.

● In adult melanoma is most common primary intraocular cancer followed by lymphoma.
● In Children retinoblastoma is the most common followed by medulloepithelioma.
● Metastases or secondary intraocular tumours are more common than primary tumours and
typically come from breast or ling cancer.
CLASSIFICATION:

BY ORIGIN-

● Primary- lesions originating from the orbital tissues.

● Secondary- lesions originating from the neighbouring cavities and tissues.
● Metastatic-lesions reach the orbit via hematogenous or lymphatic spread.
BENIGN ORBITAL TUMOURS-

● ptergium
● Chorodial hemangiomas
● Orbital pseudotumors
● Thyroid associates orbitopathy.
MALIGNANT ORBITAL TUMOURS-

● Metastatic carcinoma to the uvea

● Malignant 14frica of uvea
● Retinoblastoma
A)PRIMARY TUMOURS:

1)Developmental tumours

Dermoids- these are developmental tumors

● Arises from the embryonic displacement of the epidermis to a subcutaneous location.

● Lines with keratinizing epithelium and May contains one or more dermal adNeal structure.
● Two types- a)superficial dermoid
b)deep dermoids

● Superficial dermoid- seen in infancy

Firm ,round,localised lesions in the upper temporal or upper nasal aspect of orbit.
 Not extend deep into the orbit and are associated with bony defects.

Deep dermoid-present in adolescence with proptosis or a mass lesions having indistinct posterior
margins.

Associated with bony defects.

Treatment- surgical excision.

Epidermoid: composed of epidermis without any epidermal appendages in the wall of the cyst.

Almost always cyst.

Cyst wall contains keratin debris.

Treatment- surgical excision

Lipodermoid:solid tumours usually seen beneath the 15frica1515iva.

Located adjacent to the superior temporal quadrant of the globe.

Does not require any surgical intervention unless they enlarge significantly.

Teratomas: composed of ectoderm , mesoderm and endoderm.

May be solid , cystic or a mixture.

Bening but some solid tumours in Newborns are Malignant.

Treatment- exoneration is usually performed for solid tumours to effect a permanent cure.

Cystic tumours may be excused without removing the eyeball.

2)Vascular tumours:

Most common primary benign tumours of the orbit

These can be

● Haemangiomas
● Lymphangiomas
Capillary haemangiomas- seen at birth or during the first month.

Appears as periocular swelling in the anterior part of the orbit.

Increases in size on straining or crying.

Treatment- usually not required any treatment.

Indication for treatment are:optic nerve compression exposure keratitis ocular dysfunction or
cosmetic blemish.

Modes of therapy:

● Systemic or intralesional steroids

● Low dose superficial radiations
● Surgery and cryotherapy
● Systemic beta blocker.
CAVERNOUS HAEMANGIOMA:
 ● Commonest BENIGN ORBITAL tumours among adult with female preponderance.
● Locates in the retrobulbar muscle cone.
● Compress the optic nerve without causing proptosis.
Treatment- via lateral orbitotomy approach surgical tumour excision done.

3)LYMPHANGIOMA: uncommon tumour presenting with slowly progressive proptosis in a young

person.

Often enlarge because of spontaneous bleed within the vascular spaces leading to formation of
chocolate cysts which may regress spontaneously.

MESENCHYMAL TUMOUR:

● Highly MALIGNANT tumour of the orbit.

● Arises from the pluripotent mesenchymal cells which have potential to differentiate into
striated muscles.
● Primary orbital tumours among children.
Histopathology:rhabdomyosarcoma May be of three types.

● Embryonal sarcoma
● Alveolar sarcoma
● Pleomorphic sarcoma.
Clinical feature: present with rapidly progressive proptosis of sudden onset in a child of 7-8 yrs

It mimics an acute inflammatory process.

Commonly involved superonasal quadrant.

Ķdiagnosis:supported by x-rays showing bone destruction and CT/MRI scan.

Seen as well defined tumour with adjacent bone destruction.

Confirmed by biopsy.

Treatment:

● Surgical excision
● Chemotherapy regime
● Radiation therapy
● Exenteration.
NEURAL TUMOURS

Optic nerve glioma:

● Slow growing tumour arising from the astrocytes.

● Usually occur at the first decade of life
● Present as solitary or a part of von Recklinghausen’s neurofibromatosis
● Optic nerve alone is affected in cases with involve the optic chasms often mid brain and
hypothalamic involvement.
Clinical features:

● Gradual visual loss

● Painless unilateral axial proptosis occurring in a child between 4 and 8 yrs
 ● Funds EXAMINATION May may show optic atrophy.
Diagnosis:

● X-ray -show uniform regular enlargement of optic foramen.

● CT scan and ultrasonography -fusiform growth in relation to optic nerve.
Treatment:

● Surgical excision
● Radiotherapy
MENINGIOMA

Invasive tumour arising from arachnoid Villi

Two types

● Primary
● Secondary
Primary :also known as optic nerve sheath meningiomas.

● Tumour of meningothelial cells of meninges.

● Associated with neurofibromatosis
● Present with early visual loss associated with limitation of ocular movements optic disc
edema or atrophy and slowly progressive unilateral proptosis.
● Intramural stage-indistinguishable from optic nerve glioma.
Treatment:

● Observation is recommended if visual acuity is good.

● Surgical excision
● Prognosis for life is good.
Secondary orbital meningioma:

● Arises either from sphenoid bone or involve

It enroute to the orbit.

● Occur typically in the middle age.

Clinical feature:

● Greater proptosis and lesser visual impairment

● Biggy eyelid swelling and a ipsilateral swelling in the temporal region of the face.
● Observation is recommended
● Postoperative radiotherapy is advocated to reduce the risk of recurrence of the residual
tumour.
Lymphoprofliterature tumours

WHO classification of lymphoprofilative tumours is

● BENIGN reactive lymphoid hyperplasia

● MALIGNANT ORBITAL lymphoma
● Langerhans cell histocyctosis.
BENIGN reactive lymphoid hyperplasia (BHRL)

● Uncommon polyclonal proliferation of lymphoid tissue

 ● Occurring in the anterior part of superolateral orbit with a predilection for lacrimal gland
Clinical feature:

● Proptosis -painless progressive with medial displacement of the globe.

● Firm rubbery mass-palpable beneath superolateral orbital rim
● Pink subconjunctival infiltrate may also seen
Treatment

● Systemic steroid and loc radiotherapy

● May requires cytotoxic drugs
● Progression to systemic lymphoma.
Atypical lymphoid hyperplasia:

Atypical lymphoid hyperplasia (ALH) is an intermediate between BRLH and malignant lymphoma.

Feature are similar to BRLH except:

● May involve other systemic organs

● Usually does not respond to steroids.
MALIGNANT ORBITAL LYMPHOMA

● Involved by MALIGNANT non-Hodgkin B cell lymphoma.

● Hodgkin’s lymphoma seldom involve the orbit.
According to the REAL (Revised European American Lymphoma) classification

1)Mucosa associated lymphoid tissue (MALT)lymphoma:

● Accounts for 40-70% of all orbital lymphoma

● Usually unilateral but bilateral involvement May occur in 25%cases
● Present with gradual proptosis and palpable firm rubbery masses.
● Systemic involvement occurs in 50% of cases
Treatment includes radiotherapy or chemotherapy

Depending upon the grade and spread of tumours.

1. Chronic lymphocytic lymphoma:

● Low grade lesion of small mature appearing lymphocytes

2. Follicular center lymphoma:

● Low grade lesion with follicular Centers.

3. High grade lymphoma:

● Large cell lymphoma, lymphoblastic lymphoma and Burkitt’s lymphoma

La ngerhans cell histiocytosis:

● Formerly know as histiocytosis s is a group of diseases characterised by an idiopathic

abnormal profileration of histiocyctes with granuloma formation.
● Most commonly affects the children.
1)Hand Schuller Christian disease:

● Chronic disseminated from histiocytosis

 ● Involving both soft tissues and bones in older children of either sex.
● Characterised by triad of proptosis, Diabetes insipidus and bony defects in the skull.
4. letterer siwe disease:

● Diffuse soft tissue histiocytosis

● Characterised by widespread soft tissue and visceral involvement with or without bony
change.
● Slightly male preponderance and often occurs in the first three years of life.
3)unifocal or multifocal Eosinophilic granuloma:

● Solitary or multiple granulomas involving bones

● Occurs in elder children and frequently involves the orbital bones.
SECONDARY ORBITAL TUMOURS:

● Tumours of eyeball- retinoblastoma and malignant melanoma

● Tumours of eyelids-squamous cell carcinoma and basal cell carcinoma.
● Tumours of nose and paranasal sinuses-very commonly involve orbit.
*carcinoma

*sarcomas

*osteomas.

● Tumour of nasopharynx-nasopharynx is the commonest tumour involving the orbit.

*tumour show opthalmoneurological symptoms inClyde proptosis and involvement of fifth
and sixth cranial nerves.

● Tumours of cranial cavity invading orbit are glioma and meningioma.

C)metastatic orbital tumours:

● Hematogenous spread from distant primary focus .

Metastatic tumour in children

1. Neuroblastoma-fro. Adrenals and sympathetic chain.

2. Nephroblastoma-from kidney
3. Ewing’ s sarcoma-from the bones
4. Leukaemia infiltration
5. Testicular embryoral sarcoma and ovarian sarcoma.
Metastatic tumours in adults:

1. Carcinoma from lungs ( most common in male ) breast ( more common in female)prostate
thyroid and rectum.
2. Malignant melanoma from skin.
ORBITAL TUMOURS

TUMOUR CHILDREN ADULT

Primary Benign Dermoid cyst Cavernous haemangioma
Primary Malignant Rhabdomyosarcoma Lymphoma
Secondary Tumour Retinoblastoma Squamous cell carcinoma
Metastatic Tumour Neuroblastoma Carcinoma breast (females)
Carcinoma lungs (males)
 OCULAR INJURY
What you will learn here?

• Mechanical injuries
• Intra ocular foreign
bodies
• Sympathetic
ophthalmitis
• Extra global injuries
• Optic nerve injuries
• Orbit injuries
1) MECHANICAL INJURY
2) NON MECHANICAL INJURY
MECHANICAL INJURY

(1) CLOSED GLOBE INJURY

• Is the one in which eye wall (sclera & cornea) does not have full thickness wound but there is intraocular damage.
• It includes CONTUSION and LAMELLAR LACERATION
• CONTUSION - from blunt trauma
- damage may occur at the site of impact or at a distant site.
• LAMELLAR LACERATION - characterized by a partial thickness wound of the eye wall
- caused by sharp object or blunt trauma.

Causes and pathogenesis of damage

Modes of trauma
Blunt trauma may occur following

• Direct blow to the eyeball example - fist , tennis or other ball , blunt instrument like stick or big stone.
• Accidental blunt trauma to eyeball example – roadside accident , automobile accident , injury by agricultural and
industrial instruments etc,.

Mechanics of forces of blunt trauma

1. Direct impact on the globe
2. Compression wave force
3. Reflected compression wave force
4. Rebound compression wave force
5. Indirect force
Mechanism of damage
1. Mechanical tearing of the tissues of eyeball
2. Damage to the tissue cells sufficient to cause disruption of their physiological activity
3. Vascular damage leading to ischemia , edema and hemorrhage
4. Trophic change due to disturbance of nerve supply
5. Delayed complications of blunt trauma such as secondary glaucoma , hemophthalmitis , late rosette cataract and
retinal detachment.

Lesion of closed globe injury

a) Cornea
• simple corneal abrasion
• recurrent corneal abrasion
• partial corneal abrasion
• tears in descent’s membrane
• acute corneal edema
• blood staining of cornea
b) Sclera
partial thickness scleral wound may occur alone or in association with other lesion of closed globe injury.
c) Anterior chamber
• Traumatic hyphema
• Exudates ; may occur following traumatic uveitis
d) Iris, pupil & ciliary body
• Traumatic miosis
• Traumatic mydriasis
• Rupture of pupillary margin
• Radiating tears in the iris stroma
• Iridodialysis
• Antiflexion of the iris
• Retroflexion of the iris
• Traumatic aniridia or iridemia
• Angle recession
• Inflammatory change
e) Lens
• Vossius ring
• Concussion cataract
• Traumatic absorption of the lens
• Subluxtion of the lens
• Dislocation of the lens
f) Vitreous
• Liquefaction & appearance of cloud
• Detachment
• Vitreous hemorrhage
• Vitreous herniation
g) Choroid
• Rupture of the choroid
• Choroidal hemorrhage
• Choroidal detachment
• Traumatic choroiditis
h) Retina
• Commotio retinae
• Retinal hemorrhages
• Retinal tears
• Traumatic proliferative retinopathy
• Retinal detachment
• Concussion change at macula
i) Intraocular pressure change in closed globe injury
• Traumatic glaucoma
 • Traumatic hypotony
j) Traumatic change in the refraction
• Myopia
• Hypermetropia
OPEN GLOBE INJURY

• Refers to the full thickness wound of the sclera or cornea of both.

• Ti incudes RUPTURE & LACERATION of eye wall
• RUPTURE - refers to the full thickness wound of eye wall caused by the impact of blunt trauma.
• the wound occurs due to markedly raised intraocular pressure by an inside-out injury mechanism
• LACERATION - refers to the full thickness wound of eye wall caused by a sharp object.
- the wound occurs at the impact site by an outside-in mechanism.
- it include penetrating & perforating injuries.

Globe rupture
Type of globe rupture
1. DIRECT RUPTURE – may occur , though rarely , at the site of injury
2. INDIRECT RUPTURE - is more common
- occurs because of the compression force
- result in momentary increase in IOP
- result in an inside-out injury at the weakest part of eye wall

Clinical feature
Rupture of the globe may be associated with

• Prolapse of uveal tissue, vitreous loss, introcular hemorrhage & dislocation of the lens.
• IOP may be raised initially , but ultimately it is decreased.
• Accompanying signs include irregular pupil, hyphema, commotio retinae, choroidal rupture & retinal tears.

Treatment
• Repair of tear in the eye wall should be done meticulously under general anesthesia to save the eyeball whenever
possible.
• Postoperative treatment should include antibiotics, steroids and atropine.
• Enucleation may be required in a badly damaged eye where salvation is not possible.

Global laceration
Full thickness wound of eye wall caused by sharp object.

It include

• Penetrating injury
• Perforating injury
• Intraocular foreign bodies

(A) Penetrating and perforating injuries

Can cause severe damage to the eye and so should be treated as serious emergencies.

Modes of injury
a) Trauma by sharp and pointed instrument like needle,knives,nails,arrow,screw-driver,pens,pencil,compass,glass pieces etc,.
b) Trauma by foreign bodies travelling at very high speed such as bullet injury and iron foreign bodies in lathe worker

Mechanism of damage
a) Mechanical effect of the trauma or physical changes.
b) Introduction of infection
c) Post traumatic iridocyclitis

Traumatic lesions with management

a) Wound of the conjunctiva – wound more than 3mm should be sutured
b) Wound of the cornea
• Uncomplicated corneal wound - SMALL WOUND ; pad & bandage with atropine & antibiotic treatments. LARGE
WOUND; more than 2mm should always be sutured.
• Complicated corneal wound- 𝐶̅ iris prolapse should be sutured ; 𝐶̅ lens injury & vitreous loss,lensectomy & anterior
vitrectomy along with repair of corneal wound.
c) Wound of sclera- in corneo-scleral tear suture should be applied at limbus.
d) Wound of the lens-treated on general line
e) A badly (severely) wounded-such eye should be exercised.

INTRAOCULAR FOREGIN BODIES

Intraocular foreign bodies Penetrating injuries with foreign bodies are not infrequent. Seriousness of such injuries is
compounded by the retention of intraocular foreign bodies (IOFB).

• Common foreign bodies responsible for such injuries include: chips of iron and steel (90%), particles of glass, stone,
lead pellets, copper percussion caps, aluminium, plastic and wood.
For ex :
While chopping a stone with an iron chisel, it is commonly a chip of the chisel and not of the stone which enters the eye.

Modes of damage and Lesions

A penetrating/perforating injury with retained foreign body may damage the ocular structures by the following modes:
A. Mechanical effects
B. Introduction of infection
C. Reaction of foreign bodies
D. Post-traumatic Iridocyclitis
E. Sympathetic Ophthalmitis

Mechanical effects :
Common sites for retention of an intraocular foreign body
1. anterior chamber
2. iris
3. lens
4. vitreous
5. retina
6. choroid
7. sclera
8. orbital cavity

Mechanical effects depend upon the size, velocity and type of the foreign body.
Foreign bodies greater than 2 mm in size cause extensive damage.
The lesions caused also depend upon the route of entry and the site up to which a foreign body has travelled.

Traumatic lesions produced by intraocular foreign bodies include

• Corneal or/and scleral perforation, hyphema, iris hole
• Rupture of the lens and traumatic cataract,
• Vitreous hemorrhage and/or degeneration,
• Choroidal perforation, hemorrhage and inflammation
• Retinal hole, hemorrhages, edema and detachment.
1. Introduction of infection
• Introduction of infection Intraocular infection is the real danger to the eyeball.
• Fortunately, small flying metallic foreign bodies are usually sterile due to the heat generated on their commission.
However, pieces of the wood and stones carry a great chance of infection. Unfortunately, once intraocular infection is
established it usually ends in endophthalmitis or even panophthalmitis.
2. Reactions of the foreign body
Reactions of Inorganic foreign body depending upon its chemical nature following 4 types of reactions are noted in the
ocular tissues:
• No reaction is produced by the inert substances which include glass, plastic, porcelain, gold, silver and platinum
• Local irritative reaction leading to encapsulation of the foreign body occurs with lead and aluminium particles.
• Suppurative reaction is excited by pure copper, zinc, nickel and mercury particles.
• Specific reactions are produced by iron (Siderosis bulbi) and copper alloys (Chalcosis). Siderosis bulbi It refers to the
ocular degenerative changes produced by an iron foreign body. Siderosis bulbi usually occurs after 2 months to 2 years
of the injury. However, earliest changes have been reported after 9 days of trauma.
Mechanism:
• The iron particle undergoes electrolytic dissociation by current of rest and its ions are disseminated throughout the eye.
• These ions combine with the intracellular proteins and produce degenerative changes. In this process, the epithelial
structures of the eye are most affected.

Clinical manifestations include:

1. Anterior epithelium and capsule of the lens are involved first of all. Here, the rusty deposits are arranged radially in a
ring. Eventually, the lens becomes cataractous.
2. Iris. It is first stained greenish and later on turns reddish brown (heterochromia iridis).
3. Retina develops pigmentary degeneration which resembles retinitis pigmentosa. Electroretinography (ERG) shows
progressive attenuation of the b-wave over time.
4. Secondary open angle glaucoma may occur due to degenerative changes in the trabecular meshwork.
5. Chalcosis It refers to the specific changes produced by the alloy of copper in the eye.

Mechanism of chalcosis:
- Copper ions from the alloy are dissociated electrolytically and deposited under the membranous
structures of the eye.
- Unlike iron ions these do not enter into a chemical combination with the proteins of the cells and thus
produce no degenerative changes.

Clinical features include:

• Kayser-Fleischer ring.
• It is a golden brown ring which occurs due to deposition of copper under peripheral parts of the Descemet’s membrane
of the cornea.
• Sunflower cataract. It is produced by deposition of copper under the posterior capsule of the lens.
• It is brilliant golden green in colour and arranged like the petals of a sunflower.
• Retina- It may show deposition of golden plaques at the posterior pole which reflect the light with a metallic sheen.

3. Reaction of organic foreign bodies

• The organic foreign bodies such as wood and other vegetative materials produce a proliferative reaction by the
formation of giant cell
• Caterpillar hair produces ophthalmia nodosum, which is by a severe granulomatous iridocyclitis with nodule formation.

Management of Retained intraocular foreign Bodies (IOFB) diagnosis-

It is a matter of extreme importance particularly as the patient is often unaware that a particle has entered the eye. To come to
a correct diagnosis following steps should be taken
1) History - A careful history about the mode of injury may give a clue about the type of IOFB.
2) Ocular examination - A thorough ocular examination with slit-lamp including gonioscopy should be carried out.

The signs which may give some indication about IOFB are,

- subconjunctival hemorrhage, corneal scar, holes in the iris, and opaque track through the lens. With
clear media, sometimes IOFB may be seen on ophthalmoscopy in the vitreous or on the retina. IOFB
lodged in the angle of anterior chamber may be by gonioscopy.
3) Plain X-rays orbit - Anteroposterior and lateral views are still being recommended for the location of IOFB, as
most foreign bodies are radio opaque. However, many workers feel there is no use of plain film radiology (PFR), as
CT images are required for suspected IOFB, even if PFR is negative.
4) Localization of IOFB - Once IOFB is suspected clinically and later confirmed, on fundus examination and/or X-rays,
its exact localization is mandatory to plan the proper removal.

Following techniques may be used -

1) Radiological localization - Before the advent of ultrasonography and CT scan different specialized radiographic
techniques were used to localize IOFBs; which are now obsolete. However, a simple limbal ring method which is still
used (most centers have discarded it is described below:
- Limbal ring method. It is the most simple but nowadays, sparingly employed technique. A metallic ring
of the corneal diameter is stitched at the limbus and X-rays are taken
 - One exposure is taken in the anteroposterior view. In the lateral view three exposures are made one
each while the patient is looking straight, upwards and downwards, respectively.
- The position of the foreign body is estimated from its relationship with the metallic ring in different
positions. Ultrasonographic localization. It is being used increasingly these days. It can tell the position
of even non-radiopaque foreign bodies. CT scan. With axial and coronal cuts, CT scan is presently the
best method of IOFB localization.
- It provides cross-sectional images with a sensitivity and specificity that are superior to plain
radiography and ultrasonography
- Magnetic resonance imaging (MRI) is not recommended as a general screening tool, since it can cause
further damage by producing movement of a magnetic IO foreign body. However, after the CT has
excluded the presence of a metallic IO foreign body; MRI has a special role in localizing small plastic or
wooden IO foreign bodies
- Treatment IOFB should always be removed, except when it is inert and probably sterile or when little
damage has been done to the vision and the process of removal may be risky and destroy sight (e.g.,
minute FB in the retina
- Removal of magnetic IOFB is easier than the removal of non-magnetic FB. Usually a hand-held
electromagnet is used for the removal of magnetic foreign body. Method of removal depends upon the
site (location) of the IOFB as follows:
• Foreign body in the anterior chamber. It is removed through a corresponding corneal incision
directed straight towards the foreign body. It should be 3 mm internal to the limbus and in the
quadrant of the cornea lying over the foreign body.
• Magnetic foreign body is removed with a handheld magnet. It may come out with a gush of
aqueous.
• Non-magnetic foreign body is picked up with toothless forceps.
3. Sector iridectomy - foreign body entangled in the iris tissue (magnetic as well as non-magnetic) is removed by
performing sector iridectomy of the part containing foreign body
4. foreign body in the lens
- Magnet extraction is usually difficult for intralenticular foreign bodies. Therefore, magnetic foreign body
should also be treated as nonmagnetic foreign body. An extracapsular cataract extraction (ECCE) with
intraocular lens implantation should be performed.
- The foreign body may be evacuated itself along with the lens matter or may be removed with the help of
forceps.

Foreign body in the vitreous and the retina is removed by the posterior route as follows:
i. Magnetic removal- This technique is used to remove a magnetic foreign body that can be well localized and removed
safely with a powerful magnet without causing much damage to the intraocular structures.
ii. An intravitreal foreign body is preferably removed through a pars plana sclerotomy (5 mm from the limbus).
iii. A preplaced suture is passed and lips of the wound are retracted. A nick is given in the underlying pars plana part of the
ciliary body. And the foreign body is removed with the help of a powerful hand-held electromagnet. Preplaced suture is
tied to close the scleral wound. Conjunctiva is stitched with one or two interrupted sutures.
iv. For an intraretinal foreign body, the site of incision should be as close to the foreign body as possible. A trapdoor scleral
flap is created, the choroidal bed is treated with diathermy, choroid is incised and foreign body is removed with either
forceps or external magnet. Ii. Forceps removal with pars plana vitrectomy
v. This technique is used to remove all non-magnetic foreign bodies and those magnetic foreign bodies that cannot be
safely removed with a magnet. In this technique, the foreign body is removed with vitreous forceps after performing
three-pore pars plana vitrectomy under direct visualization using an operating microscope
 Sympathetic Ophthalmitis

- Sympathetic ophthalmitis is a serious bilateral granulomatous panuveitis which follows a penetrating ocular trauma.
The injured eye is called exciting eye and the fellow eye which also develops uveitis is called sympathizing eye. Very
rarely, sympathetic ophthalmitis can also occur following an intraocular surgery
- incidence Incidence of sympathetic ophthalmitis has markedly decreased in the recent years due to meticulous repair
of the injured eye utilizing microsurgical techniques and use of the potent steroids.
- Etiology of sympathetic ophthalmitis is still not known exactly
- However, the facts related with its occurrence are as follows:
Predisposing factors
a. It almost always follows a penetrating injury.
b. Wounds in the ciliary region (the so-called dangerous zone) are more prone to it.
c. Wounds with incarceration of the iris, ciliary body or lens capsule are more vulnerable.
d. It is more common in children than in adults.
e. It does not occur when actual suppuration develops in the injured eye.

Pathogenesis
Most accepted one is allergic theory, which postulates that the uveal pigment acts as an allergen and excites plastic uveitis
in the sound eye. Pathology It is characteristic of granulomatous uveitis, i.e., there is:

- Nodular aggregation of lymphocytes, plasma cells, epitheloid cells and giant cells scattered throughout the uveal
tract.
- Dalen-Fuchs’ nodules are formed due to proliferation of the pigment epithelium (of the iris, ciliary body and
choroid) associated with invasion by the lymphocytes and epitheloid cells.
- Sympathetic perivasculitis. Retina shows perivascular cellular infiltration.

Clinical features
Exciting (injured) eye.
- It shows clinical features of persistent low grade plastic uveitis, which include ciliary congestion, lacrimation and
tenderness. Keratic precipitates may be present at the back of cornea (dangerous sign).
- Sympathizing (sound) eye. It is usually involved after 4–8 weeks of injury in the other eye. Earliest reported case is
after 9 days of injury.
- Most of the cases occur within the first year. However, delayed and very late cases are also reported.
- Sympathetic ophthalmitis, almost always, manifests as acute plastic iridocyclitis. Rarely it may manifest as
neuroretinitis or choroiditis. Clinical feature of the iridocyclitis in sympathizing eye can be divided into two stages:

Prodromal stage

Symptoms

- Sensitivity to light (photophobia) and transient indistinctness of near objects (due to weakening of
accommodation) are the earliest symptoms.
- Signs
• In this stage, the first sign may be presence of retrolental flare and cells or the presence of a few keratic
precipitates (KPs) on back of cornea.
• Other signs includes mild ciliary congestion, slight tenderness of the globe, fine vitreous haze and disc
oedema which is seen occasionally.
Fully-developed stage

- It is clinically by typical signs and symptoms consistent with acute plastic iridocyclitis

Treatment
a. Prophylaxis
i. Early excision of the injured eye. It is the best prophylaxis when there is no chance of saving useful vision.
 ii. When there is hope of saving useful vision, following steps should be taken:

- A meticulous repair of the wound using microsurgical technique should be carried out, taking great care that uveal
tissue is not incarcerated in the wound
- Immediate expectant treatment with topical as well as systemic steroids and antibiotics along with topical atropine
should be started.
- When the uveitis is not controlled after 2 weeks of expectant treatment, i.e., lacrimation, photophobia and ciliary
congestion persist and if KPs appear, this injured eye should be excised immediately

b. Treatment when sympathetic ophthalmitis has already supervened

I. Early excision (enucleation) should be done when the case is seen shortly after the onset of inflammation (i.e., during
prodromal stage) in the sympathizing eye, and the injured eye has no useful vision, this useless eye should be excised at
once.

II. Conservative treatment of sympathetic ophthalmitis on the lines of iridocyclitis should be started immediately, as follows:

1. Corticosteroids should be administered by all routes, i.e., systemic, periocular injections and frequent instillation of
topical drops.
2. Immunosuppressant drugs should be started in severe cases, without delay.
3. Atropine should be instilled three times a day in all cases.
Note : The treatment should be continued for a long time.
Prognosis
• If sympathetic ophthalmitis is diagnosed early (during prodromal stage) and immediate treatment with
steroids is started, a useful vision may be obtained. However, in advanced cases, prognosis is very poor,
even after the best treatment.
EXTRAOCULAR LESION
Extraocular lesions caused by blunt trauma are as follows:

Conjunctival lesions include:

• Subconjunctival haemorrhage occurs very commonly. It appears as a bright red spot.

• Chemosis and lacerating wounds of conjunctiva (tears) are also not uncommon.

Eyelid lesion include:

- Ecchymosis of eyelids is of frequent occurrence. Because of loose subcutaneous tissue, blood collects easily into the
lids and produces ‘black-eye.’
- Ecchymosis of the eyelids may characteristically appear as bilateral ring hematomas (panda eye) in patients with basal
skull fracture.
- Laceration and avulsion of the lids.
- Traumatic ptosis may follow damage to the levator muscle.

Lacrimal apparatus lesions include:

- Dislocation of lacrimal gland

- Lacerations of lacrimal passages especially the canaliculi.

Optic nerve injuries

• These are commonly associated with fractures of the base of skull. These may be in the form of traumatic papillitis,
lacerations of optic nerve, optic nerve sheath hemorrhage and avulsion of the optic nerve from back of the eye

Orbital injury
• There may occur fractures of the orbital walls; commonest being the ‘blow-out fracture’ of the orbital floor
• Orbital hemorrhage may produce sudden proptosis.
• Orbital emphysema may occur following ethmoidal sinus rupture