Instructor Dr. Idrees sb

Prep by: Abdul Wasay Baloch

abdulwasay789@gmail.com

OPHTALMOLOGY

Vision System Units

“Curiosity is gluttony. To see is to devour.” ― Victor Hugo, Les Misérables

Unit 1 - Protection :

Orbital Rim

Eye lids

Lacrimal glands

Unit 2 – Transmission of Light

Media

Cornea

Iris

Sclera

Pupil

Lens

Unit 3 – transformation of light

Macula – have only cones, fine vision

Rods – periphery of reitna , crude vision

Unit 4 – axons or nerve fibers

1 million axons in one retina

Optic pathway

Unit 5 – transformation

Takes place in visual cortex, Temporal region

Basic Concept

Refraction

Convergence

FACTORS:

80% - Cornea

20% - lens taking constant

Length of eye ball

Refraction Errors:

1) Myopia

2) Hypermetropia

3) Astigmatism

4) Presbyopia

Myopia

Rays fall short of Retina

Cornea more convex

Length of eyeball increase

Big eye

Disadvantages:

More chances of Retinal Detachment

Treatment:

Concave lens

Hypermetropia

Small eyeball

Converging beyond the retina

Eye ball length may be decreased

Cornea less convex

Convex lens used for treatment

More chances of Acute Narrow Angle Glaucoma

Astigmatism

Irregularity of eyeball

Cornea is irregularly irregular

Spherical lens may be used

Cylinderical no applied having Axis

Presbyopia Loss of accommodation with age

Usually above 40

Accommodation + convergence problems

Ciliary body contracts and lens relaxed

Ciliary body relaxes, zonules contracts – lens become convex

Degeneration of ciliary body, zonules cause loss of accommodation

Need of convex lens

Treatment:

Glasses

Contact Lens

Laser Treatment

Excimer Laser

Applied on Stroma

LASIK: Cornea slicing

IOL implantation

VISION

Uncorrected

Corrected

Pin hole

Lacrimal Apparatus

Lacrimal gland – 90 %

Accessory glands – 10 %

Secretions may increase – wet eye

Secretions may decrease – dry eye

Causes

Congenital – underdeveloped drainage system. Self corrected

Old age

Any cause of irritation of eye – rubbing, infection, allergy

Congenital Causes

Appears during first 6 months of life

Under developed

Massaging the duct 2-3 times

Treatment:

Recurrent infection of sack obstruction flow hinders. In case of bacterial infection, Mucoprulent discharge. Regurgitation test is positive

Treat actively

Treat the cause

Old Age

Stenosis

Hardening of walls, Puncta and canalculi

Entropian – lids inward, Puncta is displaced

Clinical Feature

Blurring of vision

Chances of infection

Discomfort

Treatment:

Massage

Regurgitation for minor block

Puncta dilating

Dacryocystogram – dye injecting – x ray

Treatment:

DCR (Dacrycysto Renotomy)

Artificial passage at sac level, fluid is direct to middle meatus

Dry Eye

Congential problems

Age related – secretion decrease

More common in females

Con tissue disorders Rheumatic dis, SLE

Chemical injuries

Dry eye – infection –

Bells phenomenon

Eye ball rubbing against upper eyelid – corneal ulcer – refraction problems – pain – irritation

Treatment:

Artificial tears

Blockage of Puncta

Conjectival grafting

Avoiding dry atmosphere

Humidifier

Avoiding direct under fan

Dacryocystitis Blockage of Lacrimal sac

Old age

Medial canthus swelling

Pain redness and tenderness

Regurgitation tes is positive

Complication

Infection

Cellulitis

Osteomyelitis

Treatment

Antibiotics

Removal of sac

Cataract

Age related changes

Opacificaition of Lens

Congenital

Maternal disease

Trauma

Presentation:

Gradual decrease of vision

In children, white Pupillary Reflex (also RETINOBLASTOMA, Squint)

Pathogenesis: Lens dehydration

Normally avascular

Media opacified due to metabolic disorders

•Young cataract •Trauma •Steriods •Diabettes •Hypoparathyroidism

Treatment

Phacoemulsification with lens implant

Complication may be Hydration due to rupture of endothelium

Rupture of post capsule with nucleus drop

Infection

Extracapsular Lens extraction Manual compression and aspiration

Incision large

Heal time 2-6 months

Delayed recovery

Astigmatism

Trauma to Iris

LASER

LIDS

Diseases

Ptosis

Entropian

Ectropian

Swelling of lids

Stye

Chalazion

Tumor – BCC , SCC

Blephritis

Swelling of Lids

Stye

Inflammation on the margin of lid

Inflammation of hair follicle and Zeils Glands

Staph, strep, Pneumococci are responsible

Painful swelling

May press cornea – Astigmatism

Palpebral part of conjunctiva is red

Treatment

Medical – pain killer, anti inflammatory, antibiotics, warm compression, Hot Spoon or towel

• Excision after local anesthesia

Chalazion

Inflammation of Mobean gland

Swelling is usually not on lid margin

Non tender

Treatment:

Localized sterilized injection

Incision is vertical, half thickness after everting lid

Not extending upto lid margin

Scooping out

Tumors

BCC

Sun exposed areas

Abnormal growth - ulcer , non healing – bleeding

Localized or may be spread

Treatment surgically

Excision

Radiation

Entropian

Usually of lower lid

Cause :

Congenital

Trachoma

Old age

Trauma

Space occupying lesion

Adhesion of palperbral and Bulbar conjunctiva

Chemical injury

Mechanism

Imbalance between orbicularis occuli

PTOSIS

Drooping of upper eye lid

Due to orbicularis occuli (closure of eye)

Or Levator Palpebral (open the eyelid)

Balance disturbed – Ptosis occur

Cause

Weakness of muscle

Nerve supply disturb

Old age

Trauma

Sympathetic problems – Horner syndrome

3rd nerve Palsy

Myasthenia Gravis

Squint

•Features •In children •Vision problem •Cosmetic defect

Treatment:

Treat the cause

Medical – Botox injection(3-6 months)

Surgical – treated with replacement of fascia

lata Moderate resection – shortening of muscle

•Test : •Ruler test above 6mm normal •Finger on frontalis muscle

Problems:

Exposure of conjunctiva – exposure Keratitis, ulceration, infection

Cosmetic disfigurement

Watery eyes

Treatment :

Essentially surgical

Cauterizing on palperbral Conjuvtiva of mild Entropian

Blephritis

Dandruff cause

Mobean gland dysfunction MGD

Skin abonrmality – dryess – scales

Redness

Deposits onscales

Droping of scales into eyelids

Irritation of eye

Treatment:

Lid hygiene - clean with Na2CO3

Antibiotics oinment

Warm compression

Doxycycline for 3-6 months

RED EYE

Conjunctivitis

Conjuvtiva is red

Causes

Viral - adenovirus

Bacterial – staph , strep

Allergic

Adenovirus

No defect in epithelium (flouroscent stain)

Opacities on cornea ( Sick Epi – Rose bangol stain)

•Features •No pain •No vision loss •Redness more on palperbral part •Discomfort due to chemosis

Keratitis (Bacterial & Fungal) Cause:

Trauma – epithelium breach – entry – infection

Fungal – vegetative injury

Features

Sensory nerve endings below epithelium – painful

Cicumcorneal congestion – limbal area

Treatment

Scrapping after local anaesthesia

Complication :

Infection – abscess

Corneal scarring

Perforation of cornea

Spread of infection to ant chamber – hypopean

Endophthalmitis

•Hyphema : •Blood in anterior chamber •Blunt trauma •Bleeding disorders •Anticoagulants

•Trauma •INR monitoring •Rest for five days – heal •Always examine the FUNDUS •Check IOP •Dialtion of pupil – rest •Steriods •Reexamine

Herpes simplex H. Zoster

Big dendritic patterns

Cold sore of eye

Attack nerve

Red eye

Opacity on cornea

Fluorescent takes

Episcleritic scleritis may be caused

Treat by Acylovior

Loss of sensation of cornea

Small dendritic patterns

Hemi headache, hemi forehead

Vesicles – rash – papule – ulcer

Shingles

Numbness

Pain

Can involve any part of eye

Sterile Corneal Ulcer:

No involvement of org

Breach of epithelium

Treatment:

Antibiotic drops – prophylactic

Lubricants

Pain killers

Interstitial Keratitis

Notorious syphillis

Classical scaring

Saddle shape nose

Keratoconus Cone shaped cornea

10 -30 year

Cause: Cogential weakness of cornea at that place

Aqous pressure rise

Asthama or allergy association

Consequences Astigmatism

Perforation

Treatment Glasses

Hard contact lens

Corneal ring with laser

Corneal graft

•Complications •Acute hydrops •Perforation

•Prevention •Avoid contact sports

Trachoma

Leading cause of death

In between bacterial and viral

Due to unhygienic conditions

Pathology :

New blood vessel formation

And scarring

Limited to upper part of palpebral part of conjunctiva and cornea

Also cause Entropian of upper eyelid – eyelids rub and cause corneal ulcer

Also cause pits called HERBET PITS

Treatment :

Self limited

Erythomycin 1g state, repeat after six months

Tetracycline

3rg generation antibiotics

Entropian – surgical treatment

Scarring – corneal graft

PTERIGIUM

Abnormal growth of fibrovascular tissue

Growth towards cornea

Commonly from Nose side

Hot climate

Dust climate

Sandy climate

Disadvantages:

Corneal pull – astigmatism

Pupillary area – vision problem

Treatment :

Surgical treatment

Excision with Mitomycin on limbal area

Excision with conjunvtival grafting

Corneal graft Removal of cornea and replaced with donor

• Full thickness graft

• Partial thickness graft

• Test for donor:

• Jacob test

• Blood sample

• Indication :

• Scarring • Trachoma

• Trauma

• Abscess

• Pterigium

• Massive endothelial damage

• Post cataract surgery

UVEITIS

Uveal tissue

Most vascular part of eye

Nutrition

Systemic diseases effects

Common inflammation

Infection

Non infective – ankylsing spondyloisosis, HLA

Features

Red eye (congestion more Bulbar part of conjunctiva), Painful, Vision disturbed

Causes: Corneal problems

Uveitis

Acute glaucomma

Cicumcorneal Congestion

Examination

Vision

Redness

Corneal clarity

Pupil may be irregular or small, stick to lens POST Psynechia

Anterior chamber contain Iris cells that mat stick to endothelium of cornea – Keratopreicipitates

Cells visible on slit lamp – Flares

White grayish patches on retina along with blood vessels – Periphlebitis

Fluid oozes out from choroid into macula – Macular edema

Optic nerve inflammation

Retina may also have patches

Vitrous turbid

Causes

Any systemic infection, MS, T.B, Sarcoidosis, septecemia

Treated acc to cause

NON infective – steriods, cytotoxic drugs

INFECTIVE – treat the infection

Complication

Long standing – cataract

Glaucoma

Retinal detachment

Macular edema

Optic nerve dysfunction

Iritis / Uveitis

In acute glaucoma

Perforation of gloe

Corneal propalsion

Penetrating injury

History

Viral (adenovirus)– watery discharge, glands usually involed

Scleritis and Episclretis

Localized and diffused infection

Clinical Feature

Pain

Vision affected

May have systemic assosiation , Autoimmune disorders, Con tissue disorders ( ESR and CRP tests)

Hemiheadache

Nausea vomitting

DD – migraine

Glaucoma

Types

1. Congenital

2. Closed angle glaucoma

3. Chronic open angle glaucoma

4. Secondary glaucoma

Pathogenesis

Ciliary body – lens – pupil – ant chamber – meshwork – canals of Shemn – episcleral vein

Angle between Iris and Cornea

Normal pressure is 10 – 20 mmHg, varies with age

Above 40 considered high

Congenital Glaucoma

Trabecular meshwork or canals of shlemn not developed

Agenesis , disgenesis, fluid drain problem – pressure – BUPHTHALMOS

Due to elasticity – Big eye

Corneal fluid – hazy cornea

Refraction problem

Squint

Diagnosis

EUA

Check IOP

Refraction

Complete examination of eye including Optic Disc

Treatment

Medical Antiglaucoma drops Dimox and Acetazolamide

Surgical Modified trabeculectomy – placement of tube in ant chamber

Prognosis Not very good

Narrow Angle Glaucoma Angle narrow or closed

Fluid obstruct

Back pressure buily

Precipitating factor is CATARACT

Small hypermetric eye

Middle to lat age presentation

Subacute attacks when pupil is Dilated

Hallows around the vision in Evening

Colorful vision

Hydration of cornea

Goneoscopy – examining lens of ant chamber , Gonolens

Treatment

Peripheral iriodotomy

Methods Yag Laser

Making hole at limbal region

Clinical features at extreme conditons

Red

Pain assosiated with nausea vomitting

Pupil semidialted fixed

Cataract may be present

In acute attack, Nerve fibers may damage causing blindness in a day

Treatment of Acute Attack

Maxillon inj for nusea

Acetazolamide 500 mg iv

Antiglaucoma drops Pilocarpine 4%

Beta blockerrs

Steriod drops – reducing swelling and congestion

Ultimate peripheral Iridotomy

And cataract surger ( precipitating factor)

Chronic Open Angle Glaucoma Resistance at trabeculated meshwork

Slowly progress,

Age 20 30 and old age

Pressure increase

Increase Blood Supply of axon

Pressure on axon

patient does not complaint unless get worsen in 60’s

Peripheral patchy field defect

Tunnel vision at end stage (also in Retina pigmentosum

Quality of vision loss

Screening program detection ususally

•White Pupillary reflex •Cataract •Retinoblastoma •Retinopathy

diagnosis Screening program

IOP pilination Tononmeter

Examination of optic nerve

Check the field of vision

Perimetery

OCT of optic nerve

Nerve fiber analysis NFA

Family history of Diabettes Diabetes

Hypertension

Glaucoma

Cholesterol increase

Normal Tension Glaucoma •Pressure is normal •Any pressure damaging nerve of eye •Occular hyper discc

SQUINT

Misalignment of two eye

Types

Paralytic ( CN 3 , 4, 6) 4th nerve damage – diagnosed by Head Tilt, Head Trauma

6th nerve – lateral rectus paralysed – inward eye

3rd and 6th are caused by old age, Diabetes, Hypertension and increase Cholestremia

Non paralytic

Investigations

Assessment

Causes

Clinical Feature

Ptosis

Outward or inward eye

Disfigurement

Double Vision due non fusion of both images in visual cortex

•Aneurysm of PCA •Ptosis •3rd CN paralysis •Dilatation of pupil •painful

Treatment

Blockage of bad eye

Counseling to the patient

Recovery is 6 weeks to 3 months

Prolong one vision cause supression of bad eye

Field of vision loss

Diagnosis

2 feet examination

Eye movements

Botulin toxin in antagonist eye

Accommodating and Non accommodating squint

Squint goes away when covering the bad eye

Partial – half eye corrected

•Monocular and Binocular •Steropsis •Depth of perception •3D imaging

Non Accommodating Squint Eye movements are not restricted

Common in children

Inward turning of eye – ESO

Tropia – when squint is always there

Phoria – when squint is sometime present

Causes Refractive errors

Ptosis

Cataract

Clinical features

Focus problem

Vision reduced

Amblyopic eye – eye sight is normal but eye is tilt

Squint

In children – hypermetropia and ESO deviation

Examination

Preferential looking test

100 and 1000 test

Refraction

K test

Complete examination of eye including fundus Torch corneal reflex

Two feet examination

Cover uncover test

Alternate test

Prism Cover Test

synaptophore

Summary – Check List Examination Refraction

Visual acquity

Check vision

Two feet examination and eye movements

Pupillary reflex

Coves uncover test

Prism cover test

Synatophore

Stereopsis

•Ptosis complete •Corneal examination •Pupil reflex •Refraction •Cataract •Media for opacification •Retina examination •EUA for kids

Management

Cosmetic and vision problem

Treat the cause

Refractive error

Ptosis

Corneal scarring

Cataract

Any congenital problem

Use glasses

Treat cataract

Corneal grafting

Emblopic Therapy : for certain day of time, Patch the good eye

dilate the good eye

Surgical treatment

Recession of eye – weakening of muscle

Resection – strongthe muscle

Retinal Detachment

Retina is separated from Choroid

Pigment epithelium remain attached

Due to Fluid Push or Myopia

Types

Rigmatogenous – tear or hole, common in myopes

Non Rigmatogenous – in acute glaucoma, common in Hypermetropes

Rigmatogenous RD In myopes – BIG EYE - retina thin – more chances

Trauma

Vitrous degeneration

Problems (3F)

Field defect of that area

Retina dead due to low nourishment

Loss of central vision

Vitrous degenerated into pieces – FLOATERS

Retina pull – FLASHES

Bleeding via pulling of vessel

Decreased vision

Treatment –

seal hole or tear, (CRYO and LASER)

Approximate the retina – drainage of fluid OR ( Plomb Or BUCCAL)

•CRYOBUCCAL PROCEDURE •Freezing -200 probe •Scar •Approximate •Plomb and buccal

•VITRECTOMY •ENDOLASER •GAS OR SILICON OIL

Non RG RD Choroidal melanoma

Growth – pigmentation – ulceration – pain

Diabetic retinopathy

Usually upper temporal side defect and upper nasal

Treat the cause

Vascular Problems

Retinal artery occlusion

Systemic

Diabetic retinopathy – ischemia – weak wall- pale – dead axon (cotton wool spots)

Retinal Vein occlusion – back pressure increase – fluid – edema

Hypertiension Retinopathy - pressure increased

New Blood vessel formation Enothelial growth factors

New blood vessel formation

Fragile – tendency to bleed

Causes (inside wall – lumen reduced, Outside – mass occupying lesion) Diabetes

Hypertension

Age factor

hypercholestrol

Sudden Artery Occlusion Sudden loss of vision

Afferent Pupillary pathway defect

Clinical Features:

Pupil – Blue in centre Vision loss depends on area affected

HM +ve – because cilioretinal branch of ophthalmic division is spared

Retina – Pale ischemic Retina, thin arteries

Cherry Red Spots Macular thin, choroidal blood vessels glow

After sometime, disc becomes pale

See the clots in blood vessels

Investigation

Carotid Bruit

Scan pulse feeble

Heart murmur

•Treatment •Lower the IOP •No treatment satisfactory •Aspirin •Treat cause •Prognosis poor

Hypertensive Retinopathy

Hyperemic swellen disc

Macular edema

Treatment

Treat the cause BP

Young hypertensive patien die due to Renal problems

Look for Renal problems

Diabetic Retinopathy

Treat the cause

Argon Laser ( Never do it on Macula and Disc)

Macular edema

New b.v formation

Intravitreal injection of endothelial growth factor inhibitor

Vitrectomy with endolaser

Vein Occlusion

Back pressure – bleeding – SECTORIAL FIELD DEFEC

Central field defect

Treat the occlusion

Macular edema

Argon laser

Endothelial growth factor inhinitor

Antiplatelets

Screening of Diabetes Macular edema

Heamorrhage

Vitrous bleed

Age Related Macular Degeneration Types

Dry ARMD Wear and tear, Choroidal macula

Wet ARMD Exudation – fluid – bleeding –

Clinical Feature Distorsion of vision

O pain or rednes

AMSLER CHART

Complete examination

Investigation Optic Coherence Tomography (OCT)

Layaer by layer examination

Macular fluid – push – macular detachment

Fundus Flourosent Angiography FFA

Leading cause of blindness

•BLINDING CAUSES macular detachemnt •COAG ARMD •DRP •Myopic degenration •Trachoma

Treatment

Dry ARMD – no satisfactory treatment

Wet Intravitreal growth factor inhibitor

Laser treatment

Prevention Fresh green leafy vegetebles

Antioxidants

Multivitamin

UV light precuation

DISC

Raise ICP – pupil edema CSF incr

Head injury

Tumor

Cyst

Optic nerve pressure

Space occupying lesion

Choroditis

Uveitis

Optic nerve inflammation

Diabetes

DRUSEN – bolloid bodies

Venous occlusion

Swelling of Disc

Retina pigmentosa Night blindness

Genetic disease

Rod Cones decreased

Retina destruction

Features ( Classic Triad)

Waxy pale disc

Thin attenuated blood vessels

Bony specules (black pigment around retina)

Macular edema

Cataract

Tunnel vision ( also in COAG)

no satisfactory treatment

Marriage counseling

Steropic glasses

Retinoblastoma

Nerve tissue tumore

2-5 years age comon

White pupillary reflex

Squint , absent red reflex

Treatment

Complete removal of eyeball along with optic nerve

radiation and laser treatment at early stages

May spread to neural tissue

Optica chiasma

Orbital Cellulitis

Inflammation of cellular tissue

Souces

Chalazion clamp

Sinuses

An infection

Clinical features

Sweeling, tenderness and apin

Redness of eye ball

Painful eye movements

Treatment

Local oral antibiotics if eye ball not involved otherwise IV

Optic Nerve Function tests

1. Decreased vision

2. Decreased intensity of light

3. Decreased color vision

4. Field vision defects

5. Pupillary defect

1. Relative Afferent Pupil Defect

Thyrotoxis – squint

Exophthalmus

Inflammatory tissue in retro orbital space

Eye movements restricted LID LAG PHENOMENON

Inflammatory tissue may compress optic nerve - Blindness

IOP raised

Treatment

Treat the cause

Routine management

In emergency – iv steroids and Acetazolamide

Surgery – ORBITAL DECOMPRESSION 1. Lateral canthectomy

2. Medial floor canthotomy

3. Tear drops

4. Treat squint

Temporal Arteritis Inflammatory cells affect medium and small sized arteries

Unknown etiology

Common in old age

Clinical feature

Jaw claudication

Tendeness on scalp

Retinal arteries blockage

Complication

Retinal artery occlusion

CN Palsy

•ESR •TA •TB •MM •Autoimmune dis

Diagnosis

CRP

ESR v. high

Temporal artery biopsy

Slide – lumen blac

Treatment

Steroids high doses

Melanoma

Pigment tumor

Iris may be involeved

Not Normal

Increase in size

Incr in growth

Incr in pain

Incr in ulceration

Accidental finding

Loss of vision

Complication

Locally invasive

Metastatise to liver

Treatment

Local resection

Radiation – palque attack of laser

Cryo Laser

Central Serous Retinopathy Usual age 30 to 40 years

Vision defect

Tense type personality

Blood vessels around macula – leak – fluid – blur vision – retina deachment – field defect

Self restoring about three months

Scarring

Recurrent conditions

Treatment not successful

Laser

IVGHI

Complication

Complication

Scarring

Reoccurrence

Fundus fluorescent angiography

Sudden Loss of Vision

Vitrous haemorrhage

Diabetic retinopathy

Retinal detachment

Bitemporal hemianopia

Pituitary tumor

Nasal fibers representing temporal side after decussation

Headache

Temporal arteritis

PCA aneurysm

Occipital headache in young

Disc swelling – ICP rise – headache

Tumors

Binign –

Intracranial hypertension

Morning sickness

Management

MRI scan

acetazolamide

Nystagmus

Jerky movements of eyes

Constant vision

Visual pathway defect

Cataract may be one of cause

Investigation of eye

Excimer Laser

Cornea refractive surgery

Argon Laser

Retinal problems – sealing

Glaucoma

Laser trabeculoplasty

YAG laser

For narrow angle glaucoma

Periperal ididectomy

Capluletomy – post

RUBIOSIS – blood vessels on Iris

Fundus Flurosent Angiography

Cornel topography for uneven cornea

OCT

Diabetes

ARMD

Corneal ulcer

Fluorescent dye

Rosebangol for sick epithelium

Pupillary reaction

ERG electroretinography

EOG – electro occular gram

Field defect test

Nerve Fiber analysis

Ophtalmoscope

Direct

Indirect – using lens

Refraction

Comp auto ref

Retinoscope

Scans

Alpha scan – length of eye ball

B scans – retina state observe

Cataract power of Lens

Keratometer

A scan