Common Ocular Disorders

Dr.K.A.Salvin, MD, FRCS (Glasg)

Senior Lecturer / Consultant
Ophthalmologist
Anatomy of the eye
Visual disorders in elderly
 Aetiology
• Sudden • Gradual
– Retinal – Cataract
• Retinal vascular – Glaucoma
occlusion
– Dry AMD
• Wet AMD
– Neurological
• AION
• Neurological visual
field loss
 Etiology

• Age-related changes in the lens are not the

only cause of cataracts
• Some infants are born with cataracts or
develop them during childhood
• Such cataracts may be the result of the
mother having contracted rubella during
pregnancy
• Metabolic disorders
 Cataract
• Slow, painless decrease of vision
• Glare
• Occasionally, monocular multiple images
• Blurred vision
• Increasing difficulty with vision at night
• Glare, especially at night
• Halos around lights
• The need for brighter light for reading
• Fading or yellowing of colors
Types of Cataract
 Etiology of Pediatric Cataracts

• Hereditary
– Autosomal dominant form most common
• Genetic and Metabolic Diseases
– Down syndrome
– Marfan’s syndrome
– Myotonic Dystrophy
• Maternal Infections
– Rubella, Syphilis, Toxoplasmosis, Varicella
• Ocular Anomalies
– Aniridia-Absence of iris at birth
• Toxic
– Corticosteroids, Radiation
• Trauma
 Risk Factors In Adults

• Exposure to sunlight (UV light)

• Smoking
• Diabetes
• Trauma (blunt or penetrating)
• Family history of cataracts
• Corticosteroid therapy
• Radiation exposure
• Electrical injury
• Myotonic dystrophy
• Uveitis- Ocular inflammation
 Management
• Cataract surgery is
typically an outpatient
procedure that takes less
than an hour
• Most people are awake
and need only local
anesthesia
• On rare occasions some
people may need general
anesthesia if they have
difficulty laying flat or have
claustrophobia
 Complications of Surgery
• Vitreous Loss- 3.1%
• Vitreous Hemorrhage-0.3%
• Uveitis-1.8%
• Increased Eye Pressure- 1.2%
• Retinal Detachment- 0.7%
• Endophthalmitis- 0.13%
Glaucoma
Aqueous Outflow
 Glaucoma
• Primary open angle • Secondary open
– Reduced outflow angle
and poor optic – Ocular disease
nerve perfusion • Ocular
inflammation
• Trauma
• Intraocular
haemorrhage
– Drugs
• Steroids
 Symptoms
• Silent killer of vision
• Often none until extensive loss of V F
• ‘Bumping into things’
• Gradual deterioration of near vision
• Pain very uncommon unless IOP very high
 Treatment
MEDICAL
• ß-Blockers(side effects!)
• PG agonist
• α2 adrenergic agonist
• Parasympathomimetics
• CAIs
• Osmotic agents
SURGICAL
• Trabeculectomy
• Laser
 AION
• Arteritic
– Older patients
– Second eye involved
75%
– Polymyalgia
Rheumatica
• Non-arteritic
– Younger
– HT, DM
 Arteritic IAON
• Headache, scalp
tenderness
• Thickened temporal
artery
• Jaw claudication
• Weight loss, anorexia,
fever, night sweats,
malaise, depression
• Raised ESR
• CRAO, CN palsy
 Retinal Vein Occlusion
• Sudden, painless
– VF defect
– loss of vision
 Retinal Artery Occlusion
• Sudden, painless
– VF defect
– loss of vision
• Amaurosis fugax
• CVA, TIA

Cherry spot
Investigations for retinal vascular disease

• Visual acuity, pupil reflexes, visual field

• BP, pulse, ECG
• BSL, FBC, U/Es
• Protein electrophoresis
• Carotid doppler
 Macular Disease
• Commonest cause of untreatable visual loss
in the elderly
• Distortion
• Deterioration of central visual acuity
• Normal pupil reflexes
Dry AMD

Drusen
Exudative AMD
DIABETES AND THE EYE
 EPIDEMIOLOGY
• Commonest cause of blindness in the
population of working age in developed
countries
• Prevalence of DR of any severity in the
diabetic population is 30% and prevalence
of blindness due to DR is approximately 5%
PATHOGENESIS
 RISK FACTORS
• Duration of DM
• Control of DM. Will not prevent but delays
• Hypertension
• Renal Disease
• Pregnancy
• Obesity, hyperlipidaemia, smoking,
anaemia
 CLINICAL CLASSIFICATION OF DIABETIC
RETINOPATHY

• Background
• Pre-proliferative
• Proliferative
• End-stage diabetic eye disease
 Background
Microaneurism

Exudate
Blot haemorrhage
 Diabetic maculopathy

Hard exudate
 Pre-proliferative
CWS

Vascular
tortuosity
Microaneurism
Proliferative retinopathy

NVD NVE

Pre-retinal
haemorrhage

Laser burn scars

Advanced diabetic eye disease
Preretinal fibrosis and tractional retinal
detachment

Rubeosis iridis
 TREATMENT
• LASER: Light
Amplification by the
Stimulated Emission of
Radiation
– Focal
– Grid
– Panretinal
photocoagulation
 SCREENING
• No retinopathy or BDR with normal vision
– See yearly, or sooner if vision deteriorates

• Refer to ophthalmologist
– BDR with macular changes
– BDR with decrease in vision
– Pre-proliferative retinopathy
– Proliferative retinopathy
• Injections
• Surgery
NEURO-OPHTHALMOLOGY
 Clinical Examination
• Visual Acuity
• Colour Vision
• Visual Fields
• Pupils
 The swollen optic disc

•Papilloedema
•Papillitis
•Malignant hypertension
•Ischaemic optic neuropathy
•Diabetic optic neuropathy
•CRVO
•Intraocular inflammation
The pale optic disc
•Congenital
•Secondary to
• raised ICP
• vascular
retinal disease
• optic neuritis
• optic nerve
compression
• trauma
•Glaucoma
 Papilloedema
Blurred optic
• Disc swelling secondary to raised ICP disc margin

• Headache Haemorrhages
– Worse in the morning
– Valsalva manouver
• Nausea and projectile vomiting
Small optic
• Horizontal diplopia (VI palsy) CWS cup
• Causes
– Space occupying lesion
– Intracranial hypertension Disc pallor
• Idiopathic
• Drugs
• Endocrine
– Severe hypertension

Vessel attenuation
 Pupil

• Constricted • Dilated (mydriasis)

(mioisis) – Parasympathetic
– Sympathetic (pupilloconstrictor)
(pupillodilator) denervation
denervation – Lesion of the third
– Drugs CN
• Pilocarpine – Drugs
• Morphine • Atropine
• Cocaine
 Ocular motility abnormalities
• Third nerve palsy • Sixth nerve palsy
– Double vision – Double vision
– Eye turned down & – Eye turned in
out
– Ptosis
– Dilated pupil &
headache
• Compressive lesion
 Posterior communicating artery aneurysm

Chiasma

Posterior cerebral
artery
III CN
 Internuclear Ophthalmoplegia
• Defective adduction of the
ipsilateral eye
• Nystagmus of the contralateral
(abducting) eye
• NORMAL CONVERGENCE
• Causes
– Young patients
• Bilateral
• Demyelination
– Older patients
• Unilateral
• Vascular, tumours
 Myasthenia Gravis
• Fatigability
• Double vision
• Lid twitch
• Ptosis
• Normal reflexes & sensation
 Localising the lesion
• Monocular visual field defects indicate lesions
anterior to the optic chiasm
• Bitemporal defects are the hallmark of chiasmal
lesions
• Binocular homonymous hemianopia result from
lesions in the contralateral postchiasmal region
• Binocular quadrantanopias reflect optic tract
lesions
Anatomy of Apex of Orbit
LPS

Sup Orbital Fissure

Sup Oblique Mus

Optic Nerve

Med Rectus Muscle

Annulus of Zinn

Lat Rectus Mus

Inf Rectus Muscle

Sketch of Apex of Orbit by Dr Sanjay Shrivastava

 Apex

• Annulus of zinn giving rise to origin to extra

ocular muscles
• Optic canal
• Part of superior orbital fissure
 Openings

• Optic canal- optic nerve with meninges and

ophthalmic artery
• Superior orbital fissure-
Outside tendinous ring – structures passing outside
are:
Lacrimal nerve –V1
Frontal nerve -V2
Trochlear nerve
Superior and inferior veins
 Opening
• Inside tendinous ring- structures passing
inside the ring are -
Oculomotor (3rd cranial nerve) upper division
Nasociliary nerve
Abducent nerve (6th cranial nerve)
Oculomotor lower division (3rd cranial nerve)
Inferior orbital fissure-inferior ophthalmic vein
 Relations

• Frontal sinus
• Sphenoidal sinus
• Maxillary sinus
• Ethamoidal air cells
 Common lesions
• Proptosis
• Exophthalmos- endrocrinal
• Enophthalmos
• Pseudoproptosis-slight prominence of eyes
like myopia, paralysis of extra ocular muscles,
obese people, mullers stimulation by cocain
 Proptosis and Exophthalmos
• Abnormal protrusion of eye ball is called
proptosis or exophthalmos.
• The term exophthalmos is reserved for
prominence of the eye secondary to thyroid
disease
 Proptosis
• Abnormal protrusion of globe
• It may be Unilateral or Bilateral
• Unilateral – caused by orbital cellulitis, idiopathic
orbital inflammatory disease, thrombosis of orbital
vein, arterio-venous aneurysms, tumors of structures
of orbit , orbital haemorrahge , emphysema.
• Bilateral – endocrine exophthalmos , cavernous sinus
thrombosis , symmetrical orbital tumors, oxycephaly
- diminished orbital volume
Proptosis
 Proptosis in children
• Dermoid and epidermoid cyst
• Capillary haemangioma
• Optic nerve glioma
• Rhabdomyosarcoma
• Leukaemias
• Metastatic neuroblastoma
• Plexiform neurofibromatosis
• Lymphomas
Mass lesion in Left orbit
Due Retinoblastoma Stage III
 Proptosis in adults
• Metastases – (of malignancy) from breast,
lung, GIT
• Cavernous haemangiomas
• Mucocele
• Lymphoid tumors
• Meningiomas
 Causes of proptosis in different in different
locations
Extra conal lesions Intra conal lesions Muscular disorders
Dermoid cyst Cavernous haemangioma Thyroid
ophthalmopathy

Rhabdomyosarcoma Optic nerve glioma Pseudo tumor

Extension of nasal Meningioma Cysticercosis

/sinus diseases

A-V malformations Lymphoproliferative

disorder

Rhabdomyosarcoma
 GIANT CELL ARTERITIS
(Temporal or Cranial Arteritis)
• Idiopathic vasculitis
• Same disease spectrum as polymyalgia
rheumatica
• Mainly women 65-80 years old
• Medium and large arteries in head & neck
involved

67
 GIANT CELL ARTERITIS
Presentation
• Headache
• Scalp tenderness
• Thickened temporal arteries
• Jaw claudication
• Acute visual loss
• Weight loss, anorexia, fever, night sweats,
malaise & depression

68
 GIANT CELL ARTERITIS
Ocular Complications
• Transient monocular
visual loss (amaurosis
fugax)
• Visual loss due to
– Central retinal artery
occlusion (CRAO) or
– Anterior ischaemic
optic neuropathy
(AION)
• Visual field defects

69
 GIANT CELL ARTERITIS
Management
• ESR if suspected
• Start high dose steroids immediately to
prevent stroke or second eye involvement
• Temporal artery biopsy within a week of
starting steroids

70
 GIANT CELL ARTERITIS Temporal Artery
Biopsy
• Arteries have skip lesions
• ultrasound/Doppler may
help identify involved
areas
• If positive, confirms
diagnosis – helpful in
management of future
disease
• If negative, doesn’t
exclude diagnosis, but
need to think about an
alternative diagnosis
71
 GIANT CELL ARTERITIS
Histopathology
• Granulomatous cell
infiltration
• Giant cells
• Disruption of internal
elastic lamina
• Proliferation of intima
• Occlusion of lumen

72
 GIANT CELL ARTERITIS
Treatment

• Intravenous and oral steroids – prolonged

course of steroids often necessary

73
Refractive error
 Emmetropia
• Adequate correlation between axial length
and refractive power
• Parallel light rays fall on the retina (no
accommodation)
 Ametropia (Refractive error)
• Mismatch between axial length and refractive
power
• Parallel light rays don’t fall on the retina (no
accommodation)
– Nearsightedness (Myopia)
– Farsightedness (Hyperopia)
– Astigmatism
– Presbyopia
 Accommodation
• Emmetropic eye
– object closer than 6 M send divergent light that focus
behind retina , adaptative mechanism of eye is
increase refractive power by accommodation
• Helm-holtz theory
– contraction of ciliary muscle -->decrease tension in
zonule fibers -->elasticity of lens capsule mold lens
into spherical shape -->greater dioptic power
-->divergent rays are focused on retina
– contraction of ciliary muscle is supplied by
parasympathetic third nerve
 Myopia

• Parallel rays converge at a focal point anterior

to the retina
• Etiology : not clear , genetic factor
• Causes
– excessive long globe (axial myopia) : more
common
– excessive refractive power (refractive myopia)
 Myopia
• Forms
– Benign myopia (school age myopia)
• onset 10-12 years , myopia increase until the child
stops growing in height
– Progressive and malignant myopia
• interchangeable
• myopia increase rapidly each year and is associated
with vitreous opacities , fluidity of vitreous and
chorioretinal change
• rate of increase in amount of myopia generally tapers
off at about 20 years of age
 Myopia
– Congenital myopia
• Myopia > 10 D
• Increase slowly each year
 Myopia

• Special forms : nuclear sclerosis ,

keratoconus , spherophakia
• Symptoms
– Blurred distance vision
– Squint in an attempt to improve uncorrected
visual acuity when gazing into the distance
– Headache
– Amblyopia – uncorrected myopia > 10 D
 Myopia
• Morphologic changes
– deep anterior chamber
– atrophy of ciliary muscle
– vitreous may collapse prematurely -->opacification
– fundus change : loss of pigment in RPE , large disc and
white crescent-shaped area on temporal side , RPE
atrophy in macular area , posterior staphyloma ,
retinal degeneration-->hole-->increase risk of RD
• Treatment : concave lenses, clear lens extraction
 Hyperopia
• Parallel rays converge at a focal point posterior
to the retina
• Etiology : not clear , inherited
• Causes
– excessive short globe (axial hyperopia) : more
common
– insufficient refractive power (refractive hyperopia)
 Hyperopia
• Special forms : lens dislocation , postoperative
aphakia
• hyperopic persons must accommodate when
gazing into distance to bring focal point on to
the retina
• Symptoms
– distance vision is impaired in high refractive
error( > 3 D) and in older patient
 Hyperopia
• Symptoms
– visual acuity at near tends to blur relatively early
• nature of blur is vary from inability to read fine print to near
vision is clear but suddenly and intermittently blur
• blurred vision is more noticeable if person is tired , printing
is weak or light inadequate
– asthenopic symptoms : eyepain, headache in frontal
region, burning sensation in the eyes,
blepharoconjunctivitis
– accommodative esotropia : because accommodation is
linked to convergence -->ET
– Amblyopia – uncorrected hyperopia > 5D
 Hyperopia

• Fundus in axial hyperopia may reveal

pseudooptic neuritis (indistinct disc margin,
no physiologic cup, may elevate disc)
– DDx from optic neuritis by > 4 D , no enlarged
blind spot, no passive congestion of vein
• Treatment : convex lenses, keratorefractive
surgery, refreactive lensectomy with IOL,
phakic IOL
 Astigmatism

• Parallel rays come to focus in 2 focal lines

rather than a single focal point
• Etiology : heredity
• Cause : refractive media is not spherical--
>refract differently along one meridian than
along meridian perpendicular to it-->2 focal
points ( punctiform object is represent as 2
sharply defined lines)
 Astigmatism
• Classification
– Regular astigmatism : power and orientation of
principle meridians are constant
• With the rule astigmatism , Against the rule
astigmatism , Oblique astigmatism
• Simple or Compound myopic astigmatism , Simple
or Compound hyperopic astigmatism , Mixed
astigmatism
– Irregular astigmatism : power and orientation
of principle meridians change across the pupil
 Astigmatism
• Symptoms
– asthenopic symptoms ( headache , eyepain)
– blurred vision
– distortion of vision
– head tilting and turning
– Amblyopia – uncorrected astigmatism > 1.5 D
• Treatment
– Regular astigmatism :cylinder lenses with or
without spherical lenses(convex or concave), Sx
– Irregular astigmatism : rigid CL , surgery
 Presbyopia
• Physiologic loss of accommodation in
advancing age
• deposit of insoluble proteins in lens in
advancing age-->elasticity of lens
progressively decrease-->decrease
accommodation
• around 45 years of age , accommodation
become less than 3 D-->reading is possible
at 40-50 cm-->difficultly reading fine print ,
headache , visual fatigue
 Presbyopia
• Treatment
– convex lenses in near vision
• Reading glasses
• Bifocal glasses
• Trifocal glasses
• Progressive power glasses
 Anisometropia

• Difference in refractive power between 2 eyes

• refractive correction often leads to different
image sizes on the 2 retinas( aniseikonia)
• aniseikonia depend on degree of refractive
anomaly and type of correction
• closer to the site of refraction deficit the
correction is made-->less retinal image changes
in size
 Anisometropia
• Glasses : magnified or minified 2% per 1 D
• Contact lens : change less than glasses
• Tolerate aniseikonia ~ 5-8%
• Symptoms : usually congenital and often
asymptomatic
• Treatment
– anisometropia > 4 D-->contact lens
– unilateral aphakia-->contact lens or intraocular
lens
 Correction of refractive errors
• Far point
– point on the visual axis conjugate to the retina
when accommodation is completely relaxed
• placing an object or imaging an object at far
point will cause a clear image of that object
to be relayed to the retina
• use correcting lenses to form an image of
infinity at the far point , correcting the eye
for distance
 Types of optical correction
• Spectacle lenses
– Monofocal lenses : spherical lenses , cylindrical
lenses
– Multifocal lenses
• Contact lenses
– higher quality of optical image and less influence
on the size of retinal image than spectacle lenses
– indication : cosmetic , athletic activities ,
occupational , irregular corneal astigmatism , high
anisometropia , corneal disease
• Contact lenses
– disadvantages : careful daily cleaning and
disinfection , expense
– complication : infectious keratitis , giant papillary
conjunctivitis , corneal vascularization , severe
chronic conjunctivitis
• Intraocular lenses
– replacement of cataract crystalline lens
– give best optical correction for aphakia , avoid
significant magnification and distortion caused by
spectacle lenses
• Surgical correction
– Keratorefractive surgery :RK, AK, PRK, LASIK,
ICR, thermokeratoplasty
– Intraocular surgery : clear lens extraction (with
or without IOL), phakic IOL