Lecture :ANATOMY of the EYE

Lecture :ANATOMY OF THE EYE

By Professor Marianne Shahsuvaryan

The tissues and structures surrounding the eye, protecting and supporting the globe:

 Orbit  Extraocular Muscles  Eyelids  Lacrimal Apparatus

The Orbit

- the bony cavity in the scull - contains the globe, the extraocular muscles, the blood vessels, the nerves, fat Fig.1.1.)

The Extraocular Muscles (EOM)

- control the movement of the globe (Fig.1.2)

- four rectus muscles: medial, lateral, superior, inferior

- two oblique muscles: superior, inferior

- medial rectus moves the eye towards the nose

- lateral rectus moves the eye away from the nose

- superior rectus moves the eye up

- inferior rectus moves the eye down

- superior oblique moves the eye down and away from the nose - inferior oblique moves the eye up and away from the nose

Fig.1.1. Sagittal section of the eye in the orbit

1 – Frontal Bone, 2 – Superior Orbital Septum, 3 – Superior Tarsus, 4 – Cornea,

5 – Anterior Chamber, 6 – Pupil, 7 – Lens, 8 – Iris, 9 – Posterior Chamber,

2 10 – Zonules, 11 – Vitreous, 12 – Schlemm’s Canal, 13 - Ciliary Body, 14 – Inferior Tarsus,

15 – Inferior Orbital Septum, 16 – Maxilla, 17 – Levator Palpebrae Muscle,

18 – Superior Rectus Muscle, 19 – Orbital Fat, 20 – Optic Nerve, 21 – Retina, 22 – Choroid,

23 – Sclera, 24 – Inferior Rectus Muscle.

Fig 1.2. The extraocular muscles

The Eyelids

- the outer structures that protect the eyeball and lubricate the ocular surface (Fig 1.3) - join at the medial and lateral canthus - have the space between the two open lids – palpebral fissure - the margin or edge of the eyelid contains: hair follicles for the eyelashes (cilia) – anterior edge

openings of oil – secreting meibomian glands – posterior edge

- consists of the following layers from anterior to posterior: (Fig 1.1 ; 1.3) 1. skin 2. fibrous tissue and muscles – the tarsus containing meibomian glands;

orbicularis oculi – a muscle that closes the eye;

levator palpebral – a muscle that raises the upper eyelid

3. the conjunctiva

The conjunctiva

4 - thin translucent mucous membrane that covers the inner surface of the eyelids (palpebral conjunctiva) and the outer front surface of the eyeball, except for the cornea (bulbar conjunctiva). The Lacrimal apparatus (Fig 1.3) consists of

- lacrimal gland, located in the lateral part of the upper eyelid just under the upper orbital rim, responsible for tears production - the upper punctum and lower punctum located on the upper and lower eyelid margins near the nose - the upper canaliculus and the lower canaliculus join together and connect with the lacrimal sac - lacrimal sac - the nasolacrimal duct, which opens into the nasal cavity in the inferior nasal meatus.

Fig.1.3. External eye and lacrimal system

1 – Lateral canthus, 2 – Lacrimal gland, 3 – Upper Punctum, 4 – Upper Canaliculus,

5 – Medical Canthus, 6 – Lacrimal Sac, 7 – Nasolacrimal Duct, 8 – Lower Canaliculus,

9 – Lower Punctum, 10 - Follicles of Cilia, 11 – Cilia, 12 – Openings of Meibomian Glands

5 The tear film

The tear film is made of 3 layers, from anterior to posterior:

1. The lipid layer; secreted by the meibomian glands in the tarsus of the eyelid

- lubricate the eyelid 2. The aqueous layer; secreted by the main lacrimal gland and the accessory lacrimal glands in the superior fornix of conjunctiva

- provides oxygen and nutrition for the cornea - has antibacterial properties 3. The mucus layer; secreted by goblet cells in the bulbar and palpebral

conjunctiva

- makes the corneal surface hydrophyllic and wettable.

When we remove the eye from the orbit, we can see that the eye is a slightly asymmetrical sphere with an approximate sagittal diameter or length of 24 to 25 mm. and a transverse diameter of 24 mm. It has a volume of about 6.5 cc.

A cross-sectional view of the eye shows:

 Three different layers

1. The external layer, formed by the sclera and cornea. 2. The intermediate layer, divided into two parts: anterior (iris and ciliary body) and posterior (choroid). 3. The internal layer, or the sensory part of the eye, the retina.

 Three chambers of fluid: Anterior chamber (between cornea and iris), Posterior chamber (between iris, zonule fibers and lens) and the Vitreous chamber (between the lens and the retina). The first two chambers are filled with aqueous humor whereas the vitreous chamber is filled with a more viscous fluid, the vitreous humor.

6 The cornea:

- transparent anterior 1/6th of the globe - vertical diameter ~ 11mm, horizontal ~ 11.7mm - central thickness 0.5mm, 1mm peripherally - axial refractive power of 43 diopters - avascular, oxygen supply mainly from the tear film, metabolic requirements from the aqueous humor and perilimbal vascular plexus - composed of 5 distinct histologic layers:

1. Epithelium 2. Bowman’s layer 3. Stroma 4. Descemet’s membrane 5. Endothelium

Bowman’s layer: Does not regenerate after injury.

Stroma: - 90% of thickness of cornea - composed of collagen fibrils of uniform diameter and regular spacing. Fibers in any one lamellae are parallel but perpendicular to fibers in adjacent lamellae.

Descemet’s membrane: Does regenerate after injury

Endothelium: - a single layer of flattened hexagonal cells facing the anterior chamber - highly active in maintaining corneal transparency by regulating the water content of the corneal stroma. Physical or metabolic damage to the endothelium leads to corneal swelling, overhydration and opacification.

The limbus

7 - a transitional zone between the cornea and the sclera - abrupt transition occurs from avascular cornea to vascular limbus - this region contains the outflow apparatus of the aqueous humor (the trabecular meshwork and the canal of schlemn ).

The sclera

- White of the eye, posterior five sixths of the globe.

- Irregular size and arrangement of collagen fibrils.

- Thickness is 1 mm posteriorly near the optic nerve and 0.3 anteriorly where the extraocular muscles (EOM) attach.

- The posterior scleral foramen is a canal which transmits the optic nerve, the central retinal artery and vein, and the sympathetic plexus to eye. This canal is 2 -3 mm in diameter and is bridged by a sieve-like structure called the lamina cribrosa.

The Iris

- a contractile diaphragm that controls the degree of retinal illumination.

- has a central aperature, the pupil, located slightly nasally.

- consists of the following layers from anterior to posterior: Fig 1.4. View of the human eye

1. stroma: contains the sphincter pupillae muscle (parasympathetic innervation). Heavily pigmented in persons with brown eyes, less pigmented in green and hazel irises, and least in blue.

2. pigment epithelium: contains the dilatator pupillae muscle (sympathetic innervation)

The ciliary body (Fig 1.1.)

8 - part of the uvea = choroid + ciliary body + iris

- a band-like structure made of muscle and secretory tissue that extends from the edge of the iris and encircles the inside of the sclera toward the front of the eyem responsible for uveascleral outflow - consists of a posterior portion (pars plana) and an anterior portion (pars plicata).The latter has 60-70 folds called the ciliary processes which secrete the aqueous humor into the posterior chamber.

Contraction of the ciliary muscle relaxes the zonules allowing for increased curvature of the lens, thereby increasing its refractive power in the process of accommodation (near vision).

The choroid

- dark brown vascular sheet, lying between the sclera and the retina.

- consists of large vessels and extensive network of fenestrated vessels, the choriocapillaris which is the major blood supply to the outer layers of the retina and to the whole macula.

Bruch’s membrane

- a relatively thin membrane lying between the choriocapillaris of the choroid and the retinal pigment epithelium (RPE) of the retina.

- In AMD (age related macular degeneration),which is the most common cause of blindness above 65 years of age, there are yellow depositions in Bruch’s membrane called drusens, usually at the macula.

The retina [Fig.1.5; 1.6]

- Most internal layer of the eye, facing the vitreous - ends at the ora serrata anteriorly.

- consists of 10 basic layers

Fig.1.5. Scheme of the human retina.

1. neural retina: inner layer, itself has 9 layers including the photoreceptor layer.

2. RPE (retinal pigment epithelium): outer layer that rests on Bruch’s membrane & choroid.

Fig 1.6. The Retina

- Photoreceptors are the outermost layer of the sensory retina, and are divided into:

1. cones: responsible for color vision and daytime high discrimination vision. They are highly concentrated at the fovea (7 millions). 2. rods: responsible for night vision (black and white) cruder perception and less resolution (120 millions).

The Macula

10 The area of the retina at the posterior pole of the eye responsible for fine, central vision.

Fig 1.7. Normal fundus

The optic nerve (Fig.1.7).

- formed by the axons of the 1.2 million ganglion cells while exiting the eye. - contains within its fibers the central retinal artery and the central retinal vein which emerge from a central depression called the physiologic cup - can be divided into 4 portions:

1. intraocular 2. intraorbital portion extending from the globe until the apex of the orbit 3. intracanalicular portion within the optic canal 4. intracranial portion that merges into the chiasm and then optic tract.

Visual Pathways of the Brain

In order for perception to occur, the physiological signal that starts in the retina must travel to the visual cortex. As we saw in the diagram of the retina, there are several layers of neurons which lead to the optic nerve.

Fig 1.8. Diagram of the Brain

In the diagram of the brain (Fig 1.8) we see that the optic nerve travels from the retina to the lateral geniculate nucleus in the mid brain. The neurons then become the visual radiations which travel to the visual cortex at the back of the brain. The visual cortex is also called the striate cortex and the occipital cortex.

Anterior chamber (Fig.1.1)

- the space that lies between the cornea anteriorly and the iris posteriorly

- contains a wattery fluid called aqueous humor

Posterior chamber (Fig.1.1)

- the small space filled with aqueous humor behind the iris and in front of the anterior lens capsule

The aqueous humor

- secreted actively by the ciliary processes of the ciliary body.

- main metabolic supply for the cornea and lens.

12 - contains glucose, proteins, lactate, ascorbate, and chloride.

The lens

- transparent biconvex structure held in position by the ciliary zonules (of Zinn).

- average refractive power of 19-20 diopters

- very rich in proteins

- metabolic supply from aqueous humor

The zonules:

- hold the lens in position immediately posterior to the iris.

The vitreous

- largest chamber of the eye (4.5ml).

- transparent gel composed of random network of thin collagen fibers in a highly dilute solution of salts, proteins and hyaliuronic acid (99% water)

VASCULAR SUPPLY OF THE EYE (Fig.1.9)

Arterial system

a.ophthalmica from a.carotis interna

13 gives the following branches:

- central retinal artery

- short posterior ciliary arteries (20) - long posterior ciliary arteries (2) - muscular arteries, which give the branches – anterior ciliary arteries - a.lacrimalis - a.supraorbitalis - a.supratrochlearis - a.ethmoidalis

from a.carotis externa

- a.infraorbitalis - a.facialis, which gives the branch – a.angularis

Venous system

The venous drainage:

from central retinal vein and vortex veins into Cavernous sinus

CRANIAL NERVES

Extraocular muscles innervation

- superior oblique m. (Trochlear nerve - Cranial nerve IV) - lateral rectus m. (Abducens nerve - Cranial nerve VI)

14 - the remainder of the extraocular muscles (Cranial nerve III - Oculomotor nerve)

 Optic nerve (cranial nerve II)  Trigeminal nerve (cranial nerve V) sensory innervation divided into 3 branches:

1. Ophthalmic (V1) - lacrimal

- frontal

- nasociliary branches

2. Maxillary (V2)

3. Mandibular (V3)  Facial nerve (cranial nerve VII) for orbicularis oculi muscle

Ciliary Ganglion

- located between optic nerve and lateral rectus muscle - receives three roots:

1. Sensory root from the nasociliary nerve (V1)

2. Motor root from the oculomotor nerve

3. Sympathetic root from the plexus around the internal carotid artery.

Fig.1.9. Vascular Supply of the Eye

Lecture: PHYSIOLOGY OF THE EYE.

BINOCULAR VISION

By Prof. Marianne Shahsuvaryan

In order to get a fuller understanding of why we see things as we do, it helps to learn a little about the physics of light. Light is, after all, that which enters our eyes and causes us to see.

Light is electromagnetic energy. The electromagnetic spectrum is very large ranging from gamma rays to AM waves. The visible part of this range is very small ranging from about 400 nanometers to a little over 700 nanometers.

Light has been considered as energy packaged in particles (the particle theory) or in waves (the wave theory).

That light may come directly from a source like a light bulb and TV screen or it may be reflected light as comes from, say, a piece of paper or from a movie screen.

Light rays are focused through the transparent cornea and lens upon the retina.

The image of the "outside world" is inverted on our retina, even though the world appears right side up.

17 Fig.2.1. Inverted image on the retina

The retina is essentially a piece of brain tissue that gets direct stimulation from the outside world’s lights and images, and sends electrical impulses to the brain.

Photoreceptors can respond to light by virtue of their containing a visual pigment embedded in the outer segment. The visual pigment consists of a protein calls opsin and a chromophore derived from vitamin A know as retinal. The Vitamin A is manufactured from beta-carotine in the food we eat, and the protein is manufactured in the photoreceptor cell.

The opsin and the chromofore are bound together and lie buried in the membranes of the outer segment discs.

Rhodopsin

Light

Vitamin A Retinene + Protein

+ Protein

Photoreceptors transform the light energy into the electric impulses due to abovementioned photochemical reaction

18 In order for perception to occur, the physiological signal that starts in the Retina must travel to the visual cortex. As presented on the diagram of the retina Fig 1.8, there are several layers of neurons which lead to the optic nerve. In the diagram of the brain the optic nerve travels from the retina to the lateral geniculate nucleus in the mid brain.

The neurons then become the visual radiations which travel to the visual cortex at the back of the brain. The visual cortex is also called the striate cortex and the occipital cortex.

Each retina is divided in two halves: the left and the right. The right visual field represented by the red bar at the top is projected to the left half of each retina (Fig 1.8).

The reverse is true for the green bar. The left half of each retina is projected to the left half of the brain and the right half of each retina is projected to the right half of the brain.

This may seem strange considering that the left half of ones body is represented in the right brain and the right half of the body is represented in the left brain. But, we must remember that the retina really is part of the brain. So its representation in the higher centers makes sense.

Stereopsis

Stereopsis refers to our ability to appreciate depth, that is the ability to distinguish the relative distance of objects with an apparent physical displacement between the objects. It is possible to appreciate the relative location of objects using one eye (monocular cues). However, it is the lateral displacement of the eyes that provides two slightly different views of the same object (disparate images) and allow acute stereoscopic depth discrimination.

Stereopsis cannot occur monocularly.

Fusion describes the neural process that brings the retinal images in the two eyes to form one single image.

Clinical Tests used to measure Stereopsis

Four Dot Test and Titmus Fly Stereotest (see Chapter 4. Eye Examination)

CENTRAL VISION

The central point for image focus (the visual axis) in the human retina is the fovea. Here a maximally focused image initiates resolution of the finest detail and direct transmission of that detail to the brain for the higher operations needed for perception.

The foveal pit is an area where cone photoreceptors are concentrated at maximum density with exclusion of the rods, and arranged at their most efficient packing density which is in a hexagonal mosaic. This is more clearly seen in a tangential section through the foveal cone inner segments (Fig.2.2).

Fig.2.2. Tangential section through the human fovea.

CENTRAL VISION is function of CONES

Visual Acuity COLOR VISION

Visual Acuity is the ability of the eye to see fine details.

The Landolt C and the Illiterate E are other forms of detection used in visual acuity measurement in the clinic (Fig.2.3). The task required here is to detect the location of the gap.

Fig 2.3. (a) Landolt C. (b) Illiterate E.

Target recognition tasks, which are most commonly used in clinical visual acuity measurements, require the recognition or naming of a target, such as with Snellen letters (Fig.2.4).

Fig 2.4. The task of recognition. Naming the test objects, in this case, letters of the alphabet (Snellen).

Snellen letters are constructed so that the size of the critical detail (stroke width and gap width) subtends 1/5th of the overall height. To specify a person's visual acuity in terms of Snellen notation,

22 a determination is made of the smallest line of letters of the chart that he/she can correctly identify. Visual acuity (VA) in Snellen notation is given by the relation:

VA = D'/D

where D' is the standard viewing distance (usually 6 metres) and D is the distance at which each letter of this line subtends 5 minutes of arc (each stroke of the letter subtending 1 minute) (Fig.2.5) .

Fig 2.5. For a visual acuity of 6/6, the whole letter subtends an angle of 5 minutes of arc at the eye, and is viewed at 6 metres (20 feet).

What 20/20 or 6/6 or 1,0 means?

Simply, 20/20 means that this person is able to see on an eye chart at 20 feet that which a person with normal visual acuity can see. If VA is 20/60, that means that the person is able to discriminate characters on an eye chart at 20 feet that a person with normal acuity can see at a distance of 60 feet.

6/6 means the same thing only in meters.

COLOR VISION

23 The trichromatic theory of color vision is based on the premise that there are three classes of cone receptors subserving color vision. This theory has a very long history dating back to the 18th century. It was first proposed by Thomas Young in 1802 and was explored further by Helmholtz in 1866.

One of the more important empirical aspects of this theory is that it is possible to match all of the colors in the visible spectrum by appropriate mixing of three primary colors. Which primary colors are used is not critically important as long as mixing two of them does not produce the third.

Modern color scientists have put great effort into determining that there are indeed three classes of cones, that their outer segments contain spectrally selective photopigments and in determining the spectral absorbance of these photopigments.

During the last 15 or so years geneticists have and continue to investigate the genetic basis underlying trichromatic vision. They have indeed been able to identify the genes that are responsible for the receptor photopigments.

Hue Saturation and Brightness

All colors can be fully specified in terms of their hue, brightness and saturation

Fig 2.6. Hue is most closely related to the

wavelength of the stimulus.

Fig 2.7 Saturation depends on the content

24 of main hue. A saturated color has strong hue with little or no white.

Fig 2.8. Brightness is related to how much

white content is in the stimulus

Color Vision Deficiencies

Color Vision Deficiencies (CVD) can be congenital or acquired. Congenital CVD means that the CVD is present at birth and is inherited while acquired CVD occurs secondary to eye diseases.

Congenital CVD comprised of ~ 8% of males and ~ 0.5% of females.

If a person has no cone receptors he is truly color blind. Such people are called achromats and are very rare. Some people have rods and one kind of cone. These people are also unable to make any discriminations based on color and are called monochromats.

Most people have three classes of cone receptors in their retina. These are the short wavelength, middle wavelength and long wavelength receptors. Such observers are called trichromats. Some people are born with only two classes of cone receptors. They are called dichromats. It follows, as noted above, that a person who has only one class of cones is called a monochromat.

There are three classes of dichromats:

1. Those who are missing the long wavelength sensitive cones (red). These observers are called protanopes.

25 2. Those who are missing the middle wavelength sensitive cones (green). These observers are called deuteranopes. 3. Those who are missing the short wavelength sensitive cones (blue). These observers are called tritanopes.

There is yet another class of dichromats called anomalous dichromats. There are three classes:

1. protanomalous, 2. deuteranomalous, and 3. tritanomalous. These observers have somewhat better chromatic discrimination characteristics than dichromats

Multiple tests for color vision have been devised, each with particular strengths and weakness.

• Pseudoisochromatic color plates (see Chapter 4. Eye Examination) Ishihara and Rabkin color plates

• Farnsworth D-100 test • Color anomaloscope. This test allows the patient to directly alter the intensity of red, green, and blue of a color to match tests colors.

PERIPHERIAL VISION is function of RODS

VISUAL FIELD DARK ADAPTATION

The visual field is that portion of a subject’s surroundings that is visible at any one time.

The visual field of each eye is tested separately.

Localising the lesion (Fig 2.9)

• 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 –optic tract. • Binocular quadrantanopias reflect optic tract lesions.

2 2 4 6

5 7 8 9

Fig.2.9. Visual pathway, showing locations of lesions causing visual field disturbances.

1 - Nasal Retina, 2 - Temporal Retina, 3 - Optic Nerve, 4 - Optic Nerve Defect,

5 - Optic Chiasm, 6 - Bitemporal Hemianopia, 7 - Optic Tract,

8 - Homonymous Hemianopia, 9 – Lateral Geniculate Body, 10 – Optic Radiations,

11 – Primary Visual Cortex

DARK ADAPTATION

The eye operates over a large range of light levels.

The sensitivity of our eye can be measured by determining the absolute intensity threshold, that is, the minimum luminance of a test spot required to produce a visual sensation. This can be

28 measured by placing a subject in a dark room, and increasing the luminance of the test spot until the subject reports its presence.

Consequently, dark adaptation refers to how the eye recovers its sensitivity in the dark following exposure to bright lights.

Dark Adaptation test measures the increase in retinal sensitivity with time in the dark-adapting eye and is due to regeneration of rodopsin. The visual threshold to a flash of light is platted against time after bleaching to a standard bright light. Normally, after approximately 10 min of adaptation, the sensitivity of the rods overtakes that of the cones.

After 25-30 min rodopsin has fully regenerated and retinal sensitivity has reached its peak. Defects in rod metabolism, such as retinitis pigmentosa, will produce abnormally high thresholds at this time.

Lecture: EYE EXAMINATION

By Prof. Marianne Shahsuvaryan

The comprehensive eye examination is designed to reveal both existing and potential eye problems, even in the absence of specific symptoms. The procedure thus helps assure that patient will receive timely and appropriate treatment to manage or prevent the development or progression of an abnormal condition. The examination may be divided into two major parts:

1. Patient history 2. Examination and testing to assess the functional behavior and anatomic status of the eye and related structures.

1. PATIENT HISTORY

An accurate history must be obtained before beginning the physical examination.

The purpose of the history is to determine the specific complaint that brought the patient to the doctor and to obtain information on any present illness or past ocular history that may help the physician in evaluating and diagnosing the patient’s condition.

Obtaining a thorough ocular history is a key in making the diagnosis and implementing a treatment plan.

PRELIMINARY OCULAR AND MEDICAL HISTORY

The following are typical questions used to obtain this information:

Chief complaints

What are your symptoms?

When did the problem start?

Does the problem seem to be getting worse?

Additional questions

1. Status of vision: Have both near and far vision been affected? Has the vision been affected in one eye or both? 2. Onset: Did the problem start suddenly or gradually? 3. Presence: Are the symptoms constant or occasional, frequent or infrequent? Does a specific activity trigger the symptoms or make them worse? 4. Progression: has the problem better or worse over the time? 5. Severity: Do the symptoms interfere with your work or other activities? 6. Treatment: Have you ever been treated for these complaints?

OCULAR HISTORY

(Present to past)

Do you wear, or have you ever worn eyeglasses or contact lenses?

Have you ever had eye surgery?

31 Have you ever been treated for a serious eye condition?

Are you taking any prescription or over-the-counter medications for your eyes, including eye-drops?

MEDICAL HISTORY

(Present to past)

Are you taking any prescription or over-the-counter medications for health condition?

Have you ever required treatment for any serious disease? (Ask specifically about diabetes and hypertension).

FAMILY OCULAR AND MEDICAL HISTORY

Does anyone in your family have any significant eye or other health problems?

(glaucoma, cataract, diabetes, heart disease, hypertension, cancer).

ALLERGIES

Do you have any allergies to medication, pollen, food or anything else?

32 2. STEPS IN EYE EXAMINATION A complete eye examination includes the following steps:

 Visual Acuity Measurement (with refraction if necessary)  Determination of best-corrected visual acuity utilizing retinoscopy and refraction  Ocular Motility Examination  External examination, including eyelids, lacrimal system, conjunctiva, sclera, cornea  Anterior segment examination, including anterior chamber depth, pupillary reactivity and size, and status of the lens (possible presence of cataract)  Possible presence of opacity of the media  Tonometry (measurement of intraocular pressure)  Posterior segment examination of the fundus of the eye, including the retina, macula and optic nerve.

Since inspection of the ocular media and the posterior segment require dilation of the pupil with a mydriatic drop (causing blurring of vision), inspection of the internal structures of the eye is usually done last.

2.1. VISUAL ACUITY MEASUREMENT

2.1.1. Distance Acuity Test

The single most important measurement in the ocular examination is visual acuity. Each eye patient must have a visual acuity measurement performed for both eyes and recorded in the medical record.

Visual acuity testing may reveal refractive errors or other optical problems or ocular disease that requires additional testing.

33 An accurate visual acuity can be taken using standard figures or optotypes. The Snellen chart consists of letters or numbers printed in decreasing sizes according to an international standard (Fig. 4.1). The notations on the Snellen visual acuity chart may be in meters or in feet.

Patients are placed at a specified distance, generally 20 feet from the chart and asked to read aloud the line of smallest letters they can discern.

The “normal” visual acuity is 20/20 (feet).

Visual acuity charts may be in printed form for wall display or displayed on a screen from glass slides inserted into a projector. Projection with reflection of the image by mirrors permits use of a shorter actual viewing distance in a small office, although the characters appear to the patient as if viewed from the standard distance of 20 feet. Figure 4.1 The Snellen chart

2.1.2. Pinhole Acuity Measurement

A below-normal visual acuity may be the result of a refractive error. This possibility can be inferred by having the patient read the testing chart through a pinhole occluder (Fig. 4.2).

The pinhole admits only central rays of light, which do not require refraction by the cornea or the lens. The patient can resolve finer detail on the acuity chart in this way, without the use of glasses. If the pinhole improves the patient’s acuity by two lines or more, the chances are that the patient has a refractive error. If poor

34 uncorrected visual acuity is not improved with the pinhole, the patient’s reduced visual acuity is due either to an extreme refractive Figure 4.2 The occluder and pinhole error or to causes other than refractive ones (e.g. cataract).

2.1.3. Low Vision Testing

If a patient is unable to read the largest line of the visual acuity testing chart at the standard distance, acuity testing is repeated at successively shorter distance.

If the patient is unable to read the standard chart even at extremely close distances the examiner can hold up fingers and ask the patient to count. The patient with extremely low vision can also be asked to recognize the examiner’s hand movements or identify the position of penlight.

2.1.4. Near Acuity Test

Near visual acuity is the ability to see clearly at a normal reading distance (14 inches). This test is performed if the patient complains that reading or other close work is difficult (Fig. 4.3). Common causes of decreased near vision in the presence of normal distance vision include presbyopia, uncorrected hyperopia.

Figure 4.3 The printed card used for testing near vision.

COMMON ABBREVIATIONS USED FOR RECORDING VISUAL ACUITY INCLUDE

 VA Visual acuity  cc with correction  sc without correction  RE (right eye) or OD (oculus dexter)  LE (left eye) or OS (oculus sinister)  N Near  D Distance  PH Pinhole  CF Count fingers  HM Hand motion  LP Light perception  NLP No light perception

2.2. REFRACTION

Refraction is the process by which the patient is guided through the use of a variety of lenses so as to achieve the best possible acuity on distance and near vision tests.

Refraction involves both objective and subjective measurements. The objective portion of the process of refraction is called retinoscopy and can be accomplished by manual or automated methods.

2.2.1. Retinoscopy (or objective refraction)

The goal of retinoscopy is to determine the nature of the patient’s refractive error (if any) and the approximate lens power that will diminish (neutralize) that error and approach clear vision.

The handheld streak retinoscope comprises a viewer (peephole), a mirror assembly, and a light bulb with a delicate filament that can be rotated and focused by manipulating a sleeve on the

36 instrument’s handle (Fig. 4.4). It produces a streak of light. To perform retinoscopy, the examiner looks through the retinoscope peephole viewer and aligns the retinoscope streak with the patient’s visual axis. By shifting the position of the instrument, manipulating its light characteristics in specific ways, and observing the reaction of a light reflex from the patient’s eye, the examiner can determine the patient’s refractive state and estimate the corrective needs (Fig. 4.5).

Figure 4.5 Reflexes produced by the streak retinoscope. (A) Normal. (B) “With” motion: the reflex moves in the same direction as the streak of light, indicating a hyperopic eye. (C) “Against’ motion: the reflex moves in the direction opposite to that of the streak, indicating a myopic eye. (D) Neutralization point: there is no apparent movement of the reflex, and the pupil is filled with a red glow.

Figure 4.4 A retinoscope.

The measurements obtained by retinoscopy can be refined by subjective methods to achieve a final prescription for eyeglasses or other optical aids.

2.2.2. Refinement (or subjective refraction)

During refinement, the examiner has the patient look through a variety of lenses until an appropriate optical correction is determined. One way to do this is with the use of trial frames eyeglasses that can held a variety of lenses from a trial set of spheres, cylinders, and prisms.

The Phoroptor, or refractor, provides an alternative to a trial frame and loose lenses. It consists of a face plate that can be suspended before the patient’s eyes. The plate contains a wide range of spherical and cylindrical lenses that the examiner can dial into position

(Fig. 4.6).

Figure 4.6 A Phoroptor.

* * *

38 Both Retinoscopy and Refinement can be done in the presence or absence of cycloplegia. Cycloplegia is the use of eyedrop medication to paralyze accommodation temporarily, enabling the refractionist to determine the patient’s baseline nonaccommodative refractive error.

2.3. Ocular Motility Examination

Testing for normal muscle motility assesses the function of the six extraocular muscles and reveals possible weakness, paralysis, or restriction.

For gross evaluation of ocular motility the examiner holds a small object or displays a finger within the patient’s central field of vision and asks the patient to follow its movement with the eyes in the six cardinal positions of gaze: right and up, right, right and down, left and up, left, left and down (Fig. 4.7).

Proper alignment of the eyes and unrestricted function of the extraocular muscles are necessary for normal vision.

Figure 4.7. The six cardinal positions of gaze used to

evaluate eye movement

Cover-Uncover Test

The cover-uncover test is performed to determine if a patient’s eyes are misaligned. This test requires that the patient fix his or her attention consistently on a target. While a cover is introduced in front of one eye, the other eye is observed. This procedure is repeated, introducing the cover over the other eye. If covering either eye causes the uncovered eye to move to fix on the target, then a manifest deviation or strabismus is present.

2.4. External Examination

2.4.1. General Inspection

A thoughtful and thorough external examination can yield considerable information that directs the course of the rest of the examination.

The purpose of the external eye examination is to provide an assessment of the orbital soft tissues around the eyes, the eyelids, the lacrimal apparatus, the visible portions of the external globe the anterior chamber angle.

Inspection of the eyelids and the external eye can be performed with two simple instruments: a good focal flashlight (torch) and a binocular loupe or hand magnifying glass.

In examining the orbit, the doctor looks for evidence of exophthalmos, inflammation of the orbital tissues, and other visible abnormalities. The extent of proptosis may be measured by a special procedure called exophthalmometry, During inspection of eyelids upper eyelid eversion sometimes required search for conjunctival foreign bodies or other conjunctival signs. Topical anesthetic facilitates this procedure. The patient is asked to look down and the examiner grasps the eyelashes of the upper lid between the thumb and the index finger. A cotton-tipped applicator is used to press gently downward over the superior aspect of the tarsal plate as the lid margin is pulled upward by the lashes (Fig. 4.8). Pressure is maintained on the everted upper lid while the patient is encouraged to keep looking down. If any abnormality is found or the patient’s history and a general examination of the lacrimal system suggest a tear deficiency, biomicroscopy, described later in this Chapter, may be employed for a closer inspection.

Figure 4.8 Eversion of the upper eyelid (A,B)

2.4.2. Anterior Chamber Depth Assessment

Evaluating the depth of the anterior chamber is important in assessing a patient’s risk of or predisposition to angle-closure glaucoma. When the anterior chamber is shallow, the iris becomes convex as it is bowed forward over the lens.

To assess anterior chamber depth the flashlight is holding on the lateral (temporal) side of the eye, parallel to the iris, and aimed across the eye (Fig. 4.9). If the anterior chamber is of normal depth, there will be no shadow (darkening) on the nasal iris. If the anterior chamber is shallow, a shadow will be cast on the nasal iris.

Pupillary dilation with cycloplegic eye drops in an eye with a shallow anterior chamber may cause a dangerous rise in intraocular pressure and, possibly, acute glaucoma.

(A) Normal anterior chamber

. (B) Shallow anterior

Figure 4.9 Determining the depth of the anterior chamber

2.4.3. Pupillary Examination

Examination of the pupil is an important element of a thorough ophthalmic evaluation, requiring meticulous attention to detail, because of its potential to reveal a variety of ophthalmic abnormalities: iris muscle or nerve damage, optic nerve or retina pathology, and diseases affecting the visual pathway and the brain.

Pathologic disorders can alter the size, shape, and location of the pupil, as well as the way the pupil reacts to light.

Light-Reflex Test

Shining a light in one eye normally causes both pupils to constrict equally. The pupillary reaction in the illuminated eye is called the direct reflex, and the reaction in the nonilluminated eye

is called the consensual reflex (Fig. 4.10, Normal Reaction).

Swinging Flashlight Test

42 The swinging flashlight test is done after the light-reflex test to compare the direct and consensual responses in each eye individually. This test is used to detect the presence of a relative afferent pupillary defect (also called the Marcus Gunn pupil), a critical neuro-ophthalmic sign. During the swinging flashlight test, the examiner briskly alternates illumination from one eye to the other several times, noting pupillary response. A normal response is for the pupils to become initially constricted and to remain so as the light is swung from eye to eye. However, if one pupil consistently dilates and the other constricts as the light is alternated, a relative afferent pupillary defect is present ipsilaterial to the pupil that dilates (Fig. 4.10, Afferent Defect).

Figure 4.10. Pupillary reflexes.

ANTERIOR SEGMENT EXAMINATION

2.4.4. BIOMICROSCOPY

The biomicroscope commonly called a slit lamp is a unique instrument that permits magnified examination of transparent

or translucent tissues of the eye in cross-section (Fig. 4.11). The slit lamp consists of a magnification viewing system and a source of illumination that delivers an adjustable narrow beam, or slit of light. It enhances the external examination by allowing a binocular, stereoscopic view; a wide range of magnification (6-40x); and illumination of variable shapes and intensities to highlight different aspects of ocular tissue: lid margins and

43 lashes, conjunctiva, sclera, cornea and tear film, anterior chamber, iris, lens, and anterior vitreous. Figure 4.11 The slit lamp

Examination of Cornea

Fluorescein Staining of Cornea

Corneal staining with fluorescein (a yellow-green dye) is useful in diagnosing defects of the corneal epithelium. Fluorescein is applied in the form of a sterile filter-paper strip, which is moistened with a drop of sterile water, saline, or topical anesthetic and then touched to the palpebral conjunctiva. A few blinks spread the fluorescein over the cornea. Areas of bright-green staining denote absent or diseased epithelium (Fig. 4.12 and Fig. 4.13). Viewing the eye under cobalt-blue light enhances the visibility of the fluorescence.

Figure 4.13 Staining with with Figure 4.12 Typical dendritiform fluorescein in abrasion or erosion staining fluorescein in herpes (gross). simplex keratitis

Gonioscopy

Gonioscopy is examination of the angle of the anterior chamber (where the peripheral cornea

44 meets the peripheral iris) by means of a refracting or reflecting contact lens (gonioprism, or goniolens) that is placed against the patient’s anesthetized cornea (Fig. 4.14).

Figure 4.14 Goldmann three-mirror contact gonioscopy lens (A,B,C).

The goniolens allows light from the slit lamp to enter and exit the angle, which would otherwise not be possible. A careful examination of the structures of the anterior chamber is important for the detection of conditions producing, or likely to produce, glaucoma.

2.5. Tonometry

Tonometry is a technique for measuring intraocular pressure (IOP). Instruments used for this purpose are known as tonometers. Tonometers measure intraocular pressure by one of two principles: appalanation, measurement of the force required to flatten a small area of the central cornea; or indentation, measurement of the amount of corneal indentation produced by a fixed weight. By convention, IOP is expressed in millimeters of mercury (mm Hg).

While all methods and instruments used for tonometry produce satisfactory measurements of intraocular pressure, each system has advantages and disadvantages.

45 2.5.1. Applanation Tonometry

Goldmann Applanation Tonometry is the current gold standard for measuring IOP. Mounted on a slit-lamp it measures the force required to flatten a constant corneal area

(Fig. 4.15), based on the law which states that the pressure of a sphere is equal to the force needed to flatten a given surface area divided by the area flattened. It also takes into account the cornea’s

modulus of elasticity based on the assumption that the cornea is approximately 0.5mm thick.

Figure 4.15 The Goldmann applanation Figure 4.16 Applanation tonometry with tonometer the Goldmann tonometer

The device is mounted on a slit-lamp and has a bi-prism tonometer head, with illumination provided by a cobalt-filtered blue light (Fig. 4.16). A glass plate serves as the applanation surface and is perpendicular to the microscope. Fluorescein placed in the conjunctival sac prior to measurement enables visualization of the periphery of the superficial corneal flattering, while the flattering of the inner cornea is defined by the reflected image of the endothelium. To determine IOP, the examiner turns a scaled knob on the side of the instrument until the two hemi circles of tear meniscus visualized through the bi prism just overlap. Normal IOP is 10 to 21mm Hg. Elevated IOP is very often a sign that glaucoma is present, and accurate tonometry is necessary to help diagnose it.

46 Tonopen

Tonopen is a portable electronic device that is used to estimate intraocular pressure. Pen-like in shape, it consists of a stainless steel probe containing a solid-state strain gauge that converts IOP to an electrical signal (Fig. 4.17). A protective, disposable latex membrane is placed on the tip of the Tonopen before use with each patient. The intraocular pressure results are obtained rapidly by lightly touching the patient’s anesthetized cornea with the tip of the Tonopen and correlate rapidly with these obtained by the Goldman applanation tonometer.

Figure 4.17. The tonopen

Pneumatic Tonometry

Pneumatic tonometry is a noncontact tonometry technique which measures IOP based on the amount of time required for a jet of air to flatten a predetermined area of cornea. It is particularly useful in eyes where topical anesthesia cannot be used. The latest version of pneumatic tonometer, the Ocular Response Analyzer has new software which takes into account corneal hysteresis, an overall measurement of corneal resistance.

Indentation Tonometry

Indentation tonometry provides an estimate of IOP by measuring the indentation of the cornea produced by a weight of given amount - 5.5 to 15.0 grams in case of Schiotz tonometer and 10 g in Maklakov tonometer.

The Schiotz tonometer (Fig. 4.18) consists of a cylinder, the bottom of which forms a concave footplate that contacts the cornea. Surrounding the cylinder is a frame with a pair of handles by which the examiner holds the device while positioning it. Through the cylinder passes a plunger. The upper end of the plunger moves a hammer, which, in turn, moves a needle across a calibrated scale fixed to the top of the device. The examiner chooses a weight of a given size (5.5 to 15.0 grams), attaches the weight to the top of the plunger, and gently lowers the device to rest on the patient’s anesthetized cornea (Fig. 4.19). The amount of corneal indentation by the weight is registered on the scale of the tonometer. The units are then converted to IOP in millimeters of mercury by the use of standard conversion tables supplied with the instrument.

48 Figure 4.18 The Schiotz indentation Figure. 4.19. Indentation tonometry with tonometer Schiots tonometry

Maklakov tonometer (Fig. 4.20) consists of a cylinder with two plane footplates which before measurement are covered with special dye containing Colargol. The examiner with special handle gently lowers the device to rest on the patient’s anesthetized cornea

(Fig. 4.21). The amount of corneal indentation by the weight – 10 grams is registered printing on the paper and represents white disc inside of brown one. The units are then converted to IOP in

millimeters of mercury by the use of special table (Fig. 4.22).

Figure 4.20. The Maklakov Figure 4.21. Indentation tonometry with

tonometer Maklakov tonometer

Figure 4.22 The measurement table

50 2.6. Posterior Segment Examination

Examination of the eye posterior to the ciliary body and lens is important in assecing overall ocular health and in diagnosis and monitoring specific optical nerve, retinal, neurologic, and systemic disorders. Ophthalmoscopy is the examination of the posterior segment of the eye, performed with the use of an instrument called an ophthalmoscope. The posterior segment can also be viewed with the slit-lamp biomicroscope if special lences are used. The posterior segment examination, or the fundus examination, is usually performed with the patient’s pupils pharmacologically dilated and therefore follows pupillary examination.

2.6.1. Direct Ophthalmoscope

The direct ophthalmoscope is a handheld instrument, sometimes electrical but usually battery-powered. It consists of a handle and a head with a light source, a peephole with a range of built-in dial-up lenses and filters, and a reflecting device to aim light into the patient’s eye (Fig. 4.23).

Figure 4.23 Ophthalmoscopic examination with the direct ophthalmoscope

The instrument is used to examine the fundus directly. It gives greater magnification (15x) than the indirect ophthalmoscope and provides an errect, virtual image of the retina. The field of view is only about 5°, and stereoscopic vision for the examiner is not possible.

The direct ophthalmoscope is most useful for examining the optic nerve and blood vessels of the posterior pole (Fig 4.24).

Fig. 4.24. Normal posterior pole

The optic disc is a major ophthalmoscopic landmark of the ocular fundus. Special attention is given to the color, the margins, the cup to disc ratio and the neuroretinal rim.

A healthy ONH (optic nerve head) is a yellowish pink one, with distinct well defined margins, nonelevated, with a cup to disc ratio of less than 0.3.

2.6.2. Indirect Ophthalmoscope

The indirect ophthalmoscope (Fig. 4.25) is widely used for posterior segment examination because of its

52 large field, depth of focus, stereopsis, good illumination, and case of use with the scleral indentor (a device used to facilitate examination of the retinal periphery). Indirect ophthalmoscopy produces an inverted and reversed real image on the proximal side of a handheld condensing lens, onto which the examiner accommodates.

Figure 4.25. Ophthalmoscopic examination with the indirect ophthalmoscope

2.6.3. Slit-Lamp Biomicroscopy

Examination of the posterior segment can be performed on patient’s seated at the slit-lamp biomicroscope (Fig. 4.26). As with the indirect ophthalmoscope, the slit-lamp affords the examiner stereoscopic vision.

Handheld plus-diopter condensing lenses can be used, providing the biomicroscopist an inverted and reversed retinal image, a field of view ranging between 30° and 40°, and magnification between 7.5x and 10x.

Slit-lamp examination with a high-plus lens is most useful for examining the optic disc and

the macula.

Figure 4.26. The slit-lamp biomicroscopy

3. FUNCTIONAL TESTS

3.1. Visual Field Testing

The visual field is that portion of a subject’s surroundings that is visible at any one time. The visual field of each eye is tested separately by one or more tests. The visual field is routinely screened with the confrontation fields test. If macular disease is suspected to be causing a central visual field defect, a device called an Amsler grid is used to test the central area of each eye’s visual field. If a visual field defect is detected by screening, further evaluation is conducted by manual or automated procedures known as perimetry. Perimetry is used to document the presence and severity of a visual field defect loss. Perimetry may be either kinetic or static, the latter manual or automated. Kinetic perimetry requires a moving target to be detected whereas static perimetry requires perception of a stationary target of varying brightness.

3.1.1. Confrontation Field Testing

The simplest way to test the visual field is a confrontation technique (Fig. 4.27). The examiner sits opposite the patient at a distance of approximately 1m. The patient and examiner cover opposite eyes with their palms so that the uncovered eyes have mutually congruent fields. The examiner then introduces a test target into the field (fingers, hand, red bottle cap) until the target is perceived Figure 4.27. Confrontation test by the patient (kinetic perimetry). The patient’s and examiner’s fields should be congruent, so the presence of a defect is noted by the absent patient response when the object is visible in the examiner’s field. Confrontation field produces helpful localizing information.

3.1.2. Amsler Grid Testing

The Amsler grid is a field test that assesses the central 10° of vision qualitatively. It is an effective and rapid method for detecting macular abnormalities that cause blurring or distortion. The test is monocular. The patient holds the grid 35 cm away, fixing on the central dot and draws around the area of abnormality (Fig. 4.28). Figure 4.28. Amsler grid

Sequential grids are very useful to follow changes.

3.1.3. Goldmann perimetry

The Goldmann perimeter is usually used for kinetic perimetry but can be adapted for some basic static perimetry. It consists of a hemispherical bowl that is uniformly illuminated and on to which target lights of varying size and brightness are projected (Fig. 4.29). Target size, brightness, color, background illumination and fixation are all controlled. The patient sits at the machine with the eye to be tested fixed on the centre of the hemisphere. Fixation is checked by an observation telescope mounted at the central fixation point. The target lights are then introduced by the projector into the visual field of the patient while a pantograph arm moves across a standard recording chart at the rear. As the patient signals perception of the target the examiner marks the chart and eventually plots the isopter to the particular target. The test is usually undertaken at several isopters of target size and brightness, thus producing a kinetic field that demonstrates the area and density of field loss. A

static assessment can be made by flashing the target light within the appropriate isopter.

55 Figure 4.29 The Goldmann perimeter

3.1.4. Automated Perimetry

The most commonly used computer-assisted static perimeter is the Humphrey analyzer (Fig. 4.30). Static targets of fixed size but variable intensity are presented randomly at different retinal coordinates within a bowl perimeter of constant background illumination. The Octopus machine is another computer-assisted static perimeter. Automation has the ability to compare results statistically with normal individuals of the same group and with previous tests for the same patient

(Fig. 4.31).

Figure 4.30 The Humphrey analyzer

Figure 4.31 Computerized printout record of automated perimetry.

3.2. Color Vision Testing

Evaluation of color vision is often performed with a book that displays circles in multicolored patterns, called pseudoisochromatic color plate – Ishihara plates and Rabcin’s plates (Fig. 4.32). Patients with normal color vision easily detect specific numbers and figures composed of and embedded in the dot pattern, but patients with impaired color vision do not detect the same numbers. Various combinations of colors are used to identify the nature of the color vision deficit. The type of color defect can be determined by recording the specific errors and using the instructions provided with the plates. Another test of color vision, the 15-hul test, consists of 15 pastel-colored chips (Fig. 4.33), which the patient must arrange in a related color sequence. The sequence is obvious to patients with normal color vision, but patients with color deficits arrange the chips differently. The Anomaloscope – special device is also used for the assessment of color vision.

Figure 4.32. The pseudoisochromatic Figure 4.33. The 92-hue test of color vision

color plates

3.3. Dark Adaptation

This test measures the increase in retinal sensitivity with time in the dark-adapting eye and is due to regeneration of rhodopsin. The visual threshold to a flash of light is plotted against time after bleaching to a standard bright light. Normally, after approximately 7 min of adaptation, the sensitivity of the rods overtakes that of the cones. After 25-30 min rhodopsin has fully regenerated and retinal sensitivity has reached its peak. Defects in rod metabolism, such as retinitis pigmentosa, will produce abnormally high thresholds at this time.

3.4. Electrodiagnostic tests

Electrodiagnostic tests are useful in localizing and diagnosing both inherited and acquired retinal and visual pathway disorders and, where appropriate, in monitoring the efficacy of treatment. They can also assess visual function in eyes with opaque media and retinal function from drug toxicity. In addition, they are particularly valuable for diagnosing nonorganic visual loss.

3.4.1. Electroretinography (ERG)

58 The ERG is the mass electrical response of the retina to a luminance stimulus, usually a brief light flush. Stimulation is delivered by a Ganzfeld bowl which provides uniform whole-field illumination as well as a diffuse background light for photoptic adaptation (Fig. 4.34). As the ERG is a mass response it remains normal when retinal dysfunction is confined to small areas; an eye with disease confined to the macula also has a normal ERG despite the high photoreceptor density of the macula.

Figure 4.34. Electroretinography (ERG)

Pattern electroretinography (PERG) allows assessment of both macular and retinal ganglion cell function. Visual loss from maculopathy or optic neuropathy can therefore be distinguished.

3.4.2 . Visual Evoked Potential

The visual evoked potential (VEP) is the electrical response of the visual cortex to visual stimulation and is recorded using posteriorly situated scalp electrodes (Fig. 4.35). It is extracted from the spontaneous higher-voltage background activity of the brain, the electroencephalogram, by using repetitive stimulation and computerized signal averaging.

VEPs can also be stimulated by pattern appearance (onset/offset). VEPs are particularly

59 useful for detecting and diagnosing optic nerve disease .

Figure 4.35. Recording the visual evoked potential (VEP).

Binocular Vision Testing

Titmus Stereopsis Test

Stereopsis is the perception of depth or three dimensionality that occurs when slightly disparate (noncorresponding) retinal elements are stimulated at the same time. To achieve stereopsis, both eye must be used simultaneously. The tests used to measure stereopsis consist of either polarized images or random-dot stereograms that may be nonpolarizes or polarized. Fig.

4.36 illustrates the Titmus (fly) test, which is the most common test for near stereopsis.

Figure 4.36. The Titmus stereopsis test. (A) Light-polarizing eyeglasses and targets.

(B) The patient views the target through polarizing filters and reports perception of depth.

Worth Four-Dot Test

For this test, the patient wears a pair of eyeglasses with a red filter over the right eye and a green filter over the left. The patient’s gaze is directed at a target displaying four lighted dots: two green, one red, and one white (Fig. 4.37). If the images received by the two eyes are adequately aligned, the brain usually fuses the two images into one visual perception. In the presence of an ocular misalignment or other ocular abnormalities that interfere with fusion, the brain may suppress or ignore the image from one eye. From the patient’s responses about the number and color of lights seen, the ophthalmologist can determine whether or not the eyes are normally aligned and whether one eye is being suppressed.

Figure 4.37. The Worth for dot-test (A, B).

4. IMAGING TECHNIQUES

Many types of imaging studies are useful in evaluation and documenting ocular abnormalities. These include fundus photography, angiography, ultrasonography, optical coherence tomography (OCT), computed tomography, and magnetic resonance imaging

Fluorescein Angiography

Sodium fluorescein solution is injected intravenously and fluorescent properties of the dye are captured (using the special filters placed within the fundus camera) as it passes through the retinal and choroidal circulations.

Figure 4.38 (A) Fluorescein angiogram of a normal retina. (B) Fluorescein angiogram of a

diabetic patient. The numerous white dots are tiny outpouchings in abnormal

capillaries (microaneurysms) that are filling up with dye

The endothelium of the retinal vasculature and the tight junctions of retinal pigment epithelium maintain the inner and outer blood ocular barriers, respectively, and are normally impermeable to the dye. The circulation time, or transit time, of the dye can be measured as it sequentially passes through the retinal arterial, capillary, and venous systems. Retinal vascular occlusive disease can delay the transit time, and retinal microvascular disease such as diabetic and

hypertensive retinopathy can cause abnormal leakage of the dye (Fig. 4.38).

4.1. ULTRASONOGRAPHY

Ultrasound is mainly used to visualize intraocular structures through opaque media or to measure intraocular dimensions for intraocular lens biometry or to assess tumor size. Images of the eye can be obtained in one or two dimensions (A or B scan).. It is a rapid, easy method of imaging intraocular contents and also allows dynamic examination, for example, of retinal detachment (Fig. 4.39). High-frequency probes (50 MHz) give much higher resolution but poor issue penetration;

they are very useful for imaging anterior chamber detail (Fig. 4.40).

Figure 4.39 The B-scan sonography Figure 4.40 Anterior chamber sonography

4.3. OPTICAL COHERENCE TOMOGRAPHY (OCT)

OCT obtains images by using back scattering of light in a way analogues to ultrasound B scanning but as the wavelength of light is shorter the resolution is much higher. The degree of reflectivity is displayed in false color giving an “anatomical” display. Cross-sectional imaging is achieved by combyning a sequence of A-scan profiles across the retina, analogues to ultrasound B- scans (Fig. 4.39). OCT has become essential in the clinical evaluation of macular pathology such as macular holes, cystoid ocdema, pigment epithelial detachment and preretinal membranes, and the demonstration of vitreous traction. OCT show great potential for measuring optic disc cupping and nerve fiber layer thickness in glaucoma and anterior segment imaging.

Figure 4.41. OPTICAL COHERENCE TOMOGRAPHY (OCT)

4.4. Computed Tomography (CT)

Computed tomography (CT) is very useful for imaging the orbit and is the technique of choice (in contrast to magnetic resonance imaging) if the bony orbit, optic canal or calcification needs to be seen (Fig. 4.42).

Figure 4.42. Computed tomography (CT)

4.5. Magnetic Resonance Imaging (MRI)

MRI is the imaging investigation of choice for orbital soft tissue disease, optic nerve pathology and combined orbital and intracranial pathology (Fig 4.43).

Figure 4.43. Magnetic resonance imaging (MRI)

65 Lecture:OPTICS and REFRACTION

By Prof. Marianne Shahsuvaryan

The Eye as an Optical System:

(A) REFRACTIVE MEDIA: (Fig.3.1)

1. The Cornea

2. The Aqueous Humor

in the Anterior Chamber

3. The Lens Fig 3.1. Optical System of the Eye

4. The Vitreous

THE CORNEA

Most of the bending of the light rays (refraction) occurs at the cornea.

The cornea contributes to approximately 2/3 of the refracting power of the eye along with the tear film.

It contributes 43 diopters.

THE LENS

The lens contributes to 1/3 of the refractive power of the eye (20 diopters).

66 THE PUPIL

The pupil reduces the amount of light that enters the eye.

It decreases the aberrations.

It increases the depth of focus when constricting.

(B). ACCOMODATION (Fig 3.2)

It is the process by which the eye changes its refractive power to focus on near or far objects. It results from increased curvature of the lens due to contraction of the ciliary muscle. The stimulus to accommodation is a blurred retinal image.

Fig 3.2. Accommodation

When the ciliary muscle is relaxed, the choroid acts like a spring pulling on the lens via the zonule fibers causing the lens to become flat.

When the ciliary muscle contracts, it stretches the choroid, releasing the tension on the lens and the lens becomes thicker.

Fig 3.3. Looking at far object

When looking at an object that is far away the lens is kind of skinny.(Fig.3.3)

Fig 3.4. Looking at near object

When looking at near objects the lens gets fatter, causing the image of the object to be focused on to the retina in the fovea (Fig.3.4).

68 .(C). REFRACTION and REFRACTIVE ERRORS:

Refractive errors are the most common cause of poor vision. They are the easiest to treat. Refraction is a term applied to the various testing procedures employed to measure the refractive error of the eye in order to provide the proper correction.

TYPES OF REFRACTION

(a) Subjective refraction

(b) Objective refraction or Cycloplegic refraction

Cycloplegic refraction is done by applying a cycloplegic agent to the eye (atropine, cyclopentolate or tropicamide) to paralyze the ciliary muscle so that the absolute refractive error can be measured. it is helpful to detect latent hyperopia in children compensating their hyperopia by accommodation.

REFRACTIVE ERRORS:

Emmetropia: Normal eye.

No refractive error. (Fig 3.5)

Anisometropia: A refractive

69 error is present.

1. Myopia

2. Hyperopia

3. Astigmatism

4. Presbyopia Fig 3.5. Emmetropia

1. Myopia (nearsightedness)

If cornea is too steep or anterior-posterior (AP) axis is too long. The focused image is formed in front of the retina (Fig 3.6.)

Fig.3.6. Nearsighted

Nearsighted people see objects clearly when they are close, but cannot focuse well on objects that are far away.

TYPES OF MYOPIA

a. Axial myopia: (Fig.3.7)

The AP axis is longer than normal. Patients may have pseudoproptosis due to the larger globe. b. Curvature myopia:

The eye has a normal AP axis but at the corneal level the curvature may be steeper than normal ex: congenital, or keratoconus.

Fig 3.7. Axial myopia

MYOPIC SHIFT

At the lens level: lens curvature is increased ex in intumescent cataract.

Symptoms of myopia:

I. Blurred vision for distance

2. Squint (due to blepharospasm - like action to act as a pinhole)

3. Headache (rare)

Myopia is usually detected at the age of 9-10 years and keeps increasing till mid-teens when it stabilizes at -5d. or less

71 Progressive myopia:

- rare form of myopia

- may increase at a rate of up to -4d. per year

- is associated with chorioretinal degeneration and vitreous floaters and liquefaction

- usually stabilizes at the age of 20 years but can progress until mid 30’s

- may reach up to -10 or -20d.

- high myopes (more than -7d) are predisposed to retinal detachment and POAG (primary open-angle glaucoma).

Congenital myopia:

- more than —10d. in infants

- generally not progressive

- should be corrected as soon as detected.

Fig 3.8. Myopia correction with concave lens

Treatment:

Always give full correction with concave (-) lenses (Fig 3.8).

2. HYPEROPIA (Hypermetropia, farsightedness)

72 – if cornea is too flat or anterior - posterior (AP) axis is too short

The focused image forms behind the retina (Fig 3.9). Most children are born with some hyperopia (maximum up to 3d.) but this usually resolves by 12 years of age.

Fig.3.9. Farsighted

Farsighted people see distant objects clearly, but are not able to focus on near objects, for example at a distance for reading a book.

a. Axial hyperopia (Fig 3.10):

- It is the most common cause of hyperopia

- AP diameter of the eye is shorter than normal.

- These eyes are more prone to angle closure glaucoma because of shorter anterior segment with crowding of the angle structures.

- The optic nerve is also smaller

- It may be associated with pseudopapilledema:

- usually occurs with more than +4d.

- swollen discs but no other signs of true papilledema such as blurring of the disc margins, hyperemia of the disc, hemorrhages.

Fig 3.10. Axial hyperepia

b. Curvature hyperopia:

When either the lens or cornea has a less than normal curvature, lower refractive power .

Latent hyperopia: is that part of the refractive error completely corrected by accommodation. It can only be measured by cycloplegic refraction and not manifest refraction

With aging, the accommodative power of the eye decreases. This will shift a hyperopic patient from latent hyperopia to greater degrees of absolute hyperopia.

Symptoms of hyperopia:

1. Blurred vision for near

2. Frontal headache aggravated by prolonged use of near vision.

3. Asthenopia: fatigue, burning eye sensation and periorbital pain when fixing at an object for prolonged periods of time.

4. Light sensitivity

5. Decrease in near visual acuity at a younger age than in emmetropic eyes.

74 Treatment of hyperopia:

Convergent or (+) lenses (Fig 3.11)

Fig 3.11. Hyperopia correction with convex lens

3. ASTIGMATISM

The curvature of the cornea varies in different meridians thus refracting the incident light differently in those meridians.

TYPES OF ASTIGMATISM

With-the-rule astigmatism: the vertical meridian is steeper

Against-the-rule astigmatism: the horizontal meridian is steeper

Regular astigmatism: Principle meridians are 90 degrees apart

Irregular astigmatism: Principle meridians are not 90 degrees apart. This type of astigmatism cannot be completely corrected by spectacles and may need contact lenses ex: corneal scarring, keratoconus.

75 Simple: Emetropia in one meridian and myopia or hyperopia in other meridian.

Compound: The same type of Refractive error in both meridians, but with different refractive power.

Mix: Combination of myopia in one meridian with hyperopia in other.

Symptoms of astigmatism:

1 - blurred vision for far and near

2 - squint (for pinhole effect)

3 - asthenopic symptoms

4 - frontal headaches

5 - tilting of the head (for oblique astigmatism)

Treatment is with cylindrical lenses or contact lens.

4. PRESBYOPIA:

It’s the physiologic decrease in the amplitude of accommodation associated with aging.

There is less bulging of the lens with accommodation due to a change in the crystallins of the lens that result in decrease in the elasticity of the lens fibers or hardening of the lens.

Symptoms include:

- larger reading distance required

- inability to focus on close work.

- Excessive illumination required for close work.

Treatment: Add positive lenses to near correction according to age.

5. AMBLYOPIA:

It is decreased visual acuity of one eye (uncorrectable with lenses) in the absence of organic eye disease insufficient enough to explain the level of vision.

It is caused by visual deprivation due to any cause (congenital or acquired) during the critical period of development (up to age 8-9 yrs) that prevents the establishment of normal vision in the involved eye.

Causes include:

- strabismus (most common cause) (Refer to Ch.9. Strabismus and Amblyopia).

- anisometropia

- high hyperopia

- opacities: corneal scars, cataract

- optic nerve disease

- retinal disease

REFRACTIVE ERRORS CORRECTION

1. Corrective Lenses – Glasses 2. Contact Lenses 3. Surgery A. Photorefractive Surgery

B. Intraocular Contact Lenses – phakic IOL

C. Intraocular anterior chamber Lenses with iris fixation (Artisan)

77 D. Refractive Lens Exchange

1. TYPES OF CORRECTIVE LENSES:

(a). Spherical lenses:

All have equal curvatures in all meridians.

(i). Convex, (+) lenses or convergent lenses are used for the correction of hyperopia, presbyopia and aphakia. They make objects look larger in size.

(ii).Concave, (-) lenses or divergent lenses are used for the correction of myopia. They make objects look smaller in size.

(b). Cylindrical or toric lenses (Fig 3.12):

One meridian is curved more than all the other ones. They are used to correct astigmatism.

Fig 3.12. Cylindrical lens

A cylinder lens is different than a spherical lens which is what one normally sees in spectacles.

As can be seen in the above diagram a cylinder lens has power only in one axis. In the above it is the horizontal axis. This lens does not refract light in the vertical direction.

78 c .Prisms:

A prism is an optical device composed of 2 refracting surfaces that are inclined toward one another.

It has an apex and a base. It refracts light toward its base whereas an object seen through a prism appears deviated toward the apex of the prism.

It does not change the size of an object.

Prisms are used to correct strabismus.

2. Contact Lenses

A scleral lens sits on the sclera of the eye. And because the lens is filled with fluid, A corneal lens, which is the type most some of which gets squeezed out when contact wearer use, floats on a tear the lens is applied to the eye it is held in layer of the cornea place by a partial vacuum

Fig 3.13. The scleral contact lens Fig 3.14. The corneal contact lens

Many people wear contact lenses to help image light properly on to the retina (Fig 3.15).

Fig 3.15. Refractive errors correction: contact lens. 79 3. Surgery

Photorefractive surgery

The EXCIMER LASER causes photoablation

corneal epithelium photorefractive

of tissue keratectomy (PRK)

LasikFig 3.16. Fig (A,B) 3.17 (A,B) corneal stroma (laser in-situ keratomilesis) and is used for: a photorefractive surgery to change the surface of the cornea in order to correct errors of refraction

A B Fig 3.16. (A,B). Photorefractive keratectomy

A B

Fig 3.17. (A,B). Lasik

80 STRABISMUS and AMBLYOPIA

Lecture by Professor Marianne Shahsuvaryan

STRABISMUS

- ocular misalignment

may be

• idiopathic

• acquired

• horizontal

• vertical

COMITANT

INCOMITANT or PARALYTIC

Definitions:

Comitant: the deviation is approximately the same in all gazes. Refer to Ch4. Eye Examination.

Paralytic: due to paresis or paralysis of one or more EOM (Fig.9.1).

Paralytic: the deviation is approximately the same in all gazes. Refer to Ch3. Eye Examination.

Comitant = Nonparetic; usually more common in children.

81 Non comitant = Paralytic; usually more common in adults.

Comitant Strabismus

- Esotropia - in - turning eyes (Fig.9.2.)

- Exotropia - out - turning eyes (Fig.9.3.)

Fig.9.1. Paralytic Strabismus, VI Nerve palsy gaze right

Fig.9.2. Esotropia-in-turning eyes

Fig.9.3. Exotropia-out-turning eyes

Infantile Esotropia:

- Most common type of esotropia.

• Usually occurs before the age of 6 months, • Comitant • Etiology: ? faulty innervational control involving the supranuclear pathways for convergence and divergence and their neural connections to the medial longitudinal fasciculus. • Hereditary: Autosomal Dominant • Deviation is often large (>40 prism diopters) • Most common error of refraction is hyperopia. • Frequently associated with nystagmus, overaction of the inferior obliques • Alternate fixation: occurs if at various times either eye is used for fixation аnd vision will be nearly equal in both eyes.

Treatment:

• Correction of hyperopia • Treatment of amblyopia • Surgical treatment: Bimedial rectus recessions or medial rectus recession and lateral rectus resection.

Acquired Non-accomodative Esotropia:

• Usually occurs after the age of 2 years. • Angle of deviation is smaller than in infantile esotropia but may increase with time.

Accommodative Esotropia:

83 • occurs in children who have a hyperopic refractive error and must therefore accommodate to see clearly. As part of this extra accommodative effort, convergence is triggered and esotropia may develop

- usually appears between 2 and 4 years of age.

High Hyperopia: requiring high accommodation and therefore convergence.

Treatment: full cycloplegic correction.

Paralytic (Noncomitant) Esotropia: (Sixth nerve Palsy) (Fig.9.1).

• More common in adults

• Differential Diagnosis:

1. Microvascular diseases: Diabetes and Hypertension

2. Inflammatory and infectious CNS disorders: meningitis, raised ICP

3. CNS tumors

4. Head trauma

• Esotropia is greater at distance than at near.

• Treatment: Wait till 6-8 weeks: Botulinum toxin, injection to the ipsilateral medial rectus

• > 6 months: medial rectus recession + lateral rectus resection.

Pseudoesotropia:

• Occurs in patients with flat broad nasal bridge and prominent epicanthal folds. • Gradually disappears with age. • Cover/uncover test differentiates it from true esotropia.

84 EXOTROPIA (Fig 9.3) .

• Less common than esotropia but incidence increases with age.

• May progress from exophoria to intermittent exotropia to constant exotropia.

• Possibly hereditary: Autosomal Dominant.

- Sensory exotropia

• occurs following loss of vision in one eye (ex. After Trauma).

- Congenital exotropia

• commonly seen in children with underlying neurologic abnormalities.

Treatment : Surgical correction.

AMBLYOPIA

CRITICAL SIGNS:

• Poorer vision in one eye that is not improved with refraction and not entirely explained by an organic lesion.

• The decrease in vision develops during the first decade of life and does not deteriorate or improve thereafter

• Amblyopia

– “lazy eye”

– suppression of vision in 2% of people

– onset prior to age 7

– Block in normal visual development

– Lack of binocular mapping of the environment

85 – Decrease synapses within lateral geniculate body (even atrophy)

– Lack of alignment of eyes

– Lack of fusion, decrease stereovision

– Decreased vision, usually since birth

– Strabismus (misalignment of eyes)

– Visual preference, head tilt .

ETIOLOGY

- Anisometropia (a difference in refractive error between the two eyes).

- Strabismus (the eyes are not straight. Vision is worse in the nonfixating eye. Strabismus can lead to, or be the result of, amblyopia)

Optical imperfection (prevents a clear image from reaching the retina)

• cataract

• corneal scar

• eyelid ptesis

MANAGEMENT

• early detection

• eliminating predisposing factors

- uncorrected refractive error (correct refractive error/glasses

- treat ocular disease - cataract

- strabismus (patching – Fig.9.4, Occlusion, strabismus surgery).

These measures bring about a focused image in the amblyopic eye and eliminate competition with the normal eye.

Treatment is especially effective

- if undertaken within the first years of life.

Fig.9.4. Patching – occlusion.

• Amblyopia

– Preventable cause of blindness

– Risk until age 10

– Earlier treatment, the better the outcome.

88 OCULAR EMERGENCIES AND TRAUMA

Lecture by Marianne Shahsuvaryan

TRUE OCULAR EMERGENCY

 Chemical Burns  Central Retinal Artery Occlusion (CRAO). Refer to Disorders of the retina and Optic Nerve  Acute Angle-Closure Glaucoma. Refer to GLAUCOMA Section

CHEMICAL BURNS (Fig.8.1)

- Ocular tissue destruction including cornea due to chemical (alkali-based or

acid- based) injury

- A true ocular emergency – a vision –threatening emergency that requires immediate treatment

- Alkali burns comparing to acid causes most severe injury and may cause perforation of the eye-ball because alkali penetrate ocular tissue more rapidly. If not treated promptly, alkali burns can cause irreversible damage to the cornea and permanent loss of vision. Burns from acidic agents are also potentially harmful and warrant immediate attention

Common Alkali - based chemicals

• Lime (cement, plaster, whitewash)

• Drain cleaners

• Lye

• Metal polishes

• Ammonia

• Oven cleaners

Fig.8.1. Chemical Burns (Alkali)

Common Acid - based chemicals

• Swimming pool acid (muriatic acid)

• Battery (sulfuric) acid

MANAGEMENT

All chemical burns require immediate and copious irrigation with clean available water or saline for 30 minutes.

 Do not spend time taking a detailed history, start irrigation

Chemical Burns: Irrigation - Refer to Ch.11. Practical skills

First Aid

• Irrigation should begin before and during transportation of the patient to the hospital.

• Immediate copious irrigation essential!

• Saline or water two liters or for 30 minutes

Chemical Burns: OnSite Management

• Topical anesthesia

- Proparacaine

- Tetracaine

• Copious irrigation

- Sterile saline or water

• Check for foreign bodies

Treatment After Irrigation

• Topical Cycloplegic

- Homatropine

- Cyclopentolate

• Topical Antibiotic

- Double check for allergies!

- Antibiotic topical ointment

• Patch affected eye

91 • Prompt referral to an Ophthalmologist

TRAUMA

• a minor trauma can cause the serious consequences

Ruptured Globe (Fig.8.2)

• ALL EYES ARE RUPTURED UNTIL PROVEN OTHERWISE

• A blunt object impacts the orbit, causing globe compression.

- This raises intraocular pressure resulting in sclera tears. (Fig.8.3)

• Ruptures usually occur where the sclera is thinnest.

- Insertions of the extraocular muscles.

- Limbus.

- Around the optic nerve.

Fig.8.2. Globe Injury: Scleral Defect

Penetrating Globe Injury

• Sharp or high velocity objects may penetrate directly.

• Small foreign bodies may penetrate and remain within the globe.

92 - Consider rupture during all evaluations for:

• Blunt and penetrating orbital trauma

• Cases involving highspeed projectiles.

Fig.8.3. Globe Rupture

PENETRATING GLOBE INJURY (Fig.8.4)

LOOK FOR: Peaked pupil, hyphema, subconjunctival hemorrhage, loss of red reflex, APD

Fig.8.4. Penetrating Globe Injury

93 Intraocular Foreign Body

Left in place, intraocular foreign bodies- particularly those than contain copper or iron – may threaten vision

Protective Eye Shield (Fig.8.5) – Refer to CH.11. Practical Skills

Penetrating injures of the globe, whether actual or suspected, necessitate the protection of an eye shield.(Refer to Ch.12. Practical skills). Neither a patch nor an ointment is advisable. The patient should be prevented from eating or drinking anything in anticipation of surgical intervation

Fig.8.5. Protective Eye Shield

Hyphema (Fig.8.6.)

• Post-injury accumulation of blood in the anterior chamber.

• Even a small hyphema can be a sign of major intraocular trauma with associated damage to vascular and other intraocular tissues.

• Secondary to rapid, marked elevation in IOP with sudden distortion of intraocular structures.

94 • Complications include:

- Secondary hemorrhage

- Secondary onset of glaucoma

- Loss of vision

Fig.8.6. Hyphema

MANAGEMENT IN HYPHEMIA

Blunt trauma

may cause

• serious intraocular damage

• rule out rupture - full exam

• use atropine

• watch for glaucoma

• NO ASPIRIN

– Or MOTRIN

– Hyphema

- cataract formation

95 - a partial dislocation of the lens

- vitreous hemorrhage

- retinal hemorrhage

- edema of the retina

- macular damage

- rupture of the choroid

- traumatic optic neuropathy

- retrobulbar hemorrhage

and

the fracture of the orbit walls

Whenever orbital wall fractures are diagnosed, there is the possibility of a serious cranial wall fracture or brain injury.

Orbital Trauma:

Isolated Blow Out Fracture

• Orbital floor fractures can occur as isolated injuries or in combination with other

significant facial bone injuries.

Blow Out Fracture (Fig.8.7; 8.8)

Fig.8.7. Blow Out Fracture

Fig.8.8. Blow Out Fracture, Inferior Rectus Muscle Entrapment on left

Eye Lid Lacerations

Maintain high index of suspicion for occult globe injury.

Rule out rupture

Site: canaliculus, lid margin (Fig.8.9), elsewhere.

Fig.8.9. Marginal Lid Laceration

Superficial Lid Laceration

• Insure tetanus prophylaxis

• Watch for ruptured globe

• Remove superficial foreign bodies

• Consider risk/presence of intraocular foreign bodies

Conjunctival Foreign Body

- on the ocular surface or on the inside surface of the eyelid.

MANAGEMENT

Remove with either vigorous irrigation or by rolling the moistened cotton-tipped applicator across the conjunctival surface.

Evert the upper eyelid to remove a foreign body on the inside surface of the eyelid. Refer to Ch.12. Practical Skills..

CORNEAL FOREIGN BODY (Fig.8.10).

Fig. 8.10. Corneal Trauma

MANAGEMENT

- topical anesthesia

- remove with either vigorous irrigation or a cotton-tipped applicator.

A sharper instrument may be requested if the foreign body remains embedded

• Consider risk/presence of infection

• Complications include:

- Perforation of the cornea

- Bacterial Keratitis (corneal ulcer)

- Endophthalmitis

Treatment

• Topical cycloplegic

• Topical Antibiotic drops and Ointment

99 CORNEAL ABRASION

• the most common eye injury

• Occurs due to disruption in the integrity of the corneal epithelium

• Corneal surface scraped away as a result of external forces

• Can be small or large

• Usually heal without serious complication

• Deep corneal involvement may result in scar formation

• Abrasions are common and frequently missed.

SYMPTOMS

• Foreign Body Sensation

• Pain

• Tearing

• Photophobia

MANAGEMENT

• Stain with fluorescein to enhance the view Fig.8.11. Refer to Ch.12. Practical Skills.

• Topical Cycloplegic

• Topical Antibiotic

• Pressure patch affected eye Refer to Ch. 12. Practical Skills.

100

Fig.8.11. Fluorescein Staining

Contact Lens Injury

• Prolonged wear of hard contact lenses may produce a corneal abrasion.

• Treat as any other corneal abrasion/injury

101

RED EYE: Part 1

Disorders of the Eyelids, Conjunctiva, Lacrimal apparatus and Cornea

Lecture by Professor Marianne Shahsuvaryan THE RED EYE

The red eye is one of the most common presenting symptoms in ophthalmology. It is the manifesting sign of many ocular diseases, affecting the orbit, eyelid, conjunctiva, cornea, sclera, episclera and even the posterior uveal tract.

The Red Eye

 Acute or Chronic  !Vision- threating (“dangerous”) or Non Vision-threating  Mild or Severe  Unilateral or Bilateral

ETIOLOGY

- Infectious - Allergic - Autoimmune - Inflammatory - Traumatic

102 ! CELLULITIS (Fig.5.1)

 infection and inflammation of periocular tissues - located anterior to the orbital septum

Fig.5.1. Cellulitis

PRESEPTAL CELLULITIS

- within the orbital cavity

!!! ORBITAL CELLULITIS

PRESEPTAL Cellulitis may progress to ORBITAL Cellulitis, which is potentially life-threatening or vision-threatening.

!!! ORBITAL Cellulitis may cause cavernous sinus thrombosis, meningitis or intracranial abscess without appropriate treatment due to intracranially spread through orbital veins.

ETIOLOGY

103  infection - from localized hordeola - from sinuses most commonly secondary to ethmoid sinusitis

 causative agent - streptococcus - staphylococcus - Haemophilus influenzae SYMPTOMS

- Eyelid swelling (upper and lower lids

- Periocular pain - Red eye - Fever (sometimes) - Visual loss (only in ORBITAL cellulitis) - Restricted ocular movement (only in ORBITAL cellulitis) - Proptosis (only in ORBITAL cellulitis)

Management

 CT scan of orbits and paranasal sinuses  Consultations of ophthalmologist , otolaryngologist, orbital surgeon  Systemic antibiotics - oral Cefaclor in PRESEPTAL - IV Ceftriaxone 1-2g q 12-24 h

BLEPHARITIS (Fig 5.2)

- inflammation of the eyelid margins - extremely common in the adult population - often coexist with dry eyes

104

Fig 5.2. Chronic blepharitis

ETIOLOGY

- Staphylococcus infection - Demodex mite - Seborrhea

SYMPTOMS

- Itching - Red Eye - Burning - Tearing - Mild pain - Foreign body sensation - Thickened and erythematous eyelid margins  crusting along eyelashes (Fig. 5.3) - “collarettes” in STAPHYLOCOCCAL Blepharitis

 crusting along eyelashes - sleeves in DEMODECTIC Blepharitis

 dandruff-like flakes (“scurf”) in SEBORRHEIC Blepharitis (Fig. 5.3)

105

Fig.5.3. Diagrammatic representations of Blepharitis.

A – Staphylococcal, B – Seborrheic, C - Demodectic

MANAGEMENT

- Warm compresses for 10 minutes in both eyes qd to qid - Daily lid scrubs: a warm solution of baby shampoo and water (50:50 mixture) may be applied rigorously to the lids and lashes using cotton, a fine cloth or cotton-tipped applicator

- Topical antibiotic ointment (Erythromycin) at bedtime for 1-2- weeks. In recalcitrant cases Doxycycline.

STYE / HORDEOLUM ( Fig.5.4)

- acute focal inflammation of the ciliary follicles or sebaceous glands - is common in Blepharitis

106

Fig.5.4. Bacterial infections

ETIOLOGY - Infection

SYMPTOMS

- Painful, tender focal mounding near the lid margin developing over days,

sometimes with pustule formation.

MANAGEMENT

- Warm compresses for 5-10 minutes twice daily - Topical antibiotic - Treatment for blepharitis, if it is the underlying condition

CHALAZION (Fig 5.5)

- chronic inflammation of a meibomian gland in the eyelid - may follow a hordeolum - recurrent chalazion at the same location may be suspicious for meibomian gland carcinoma or squamous cell carcinoma of the lid -

107

Fig 5.5, Chalazion

SYMPTOM

- Nodule that arises on either eyelid.

MANAGEMENT

- resolve spontaneously over time - if the nodule persists, injection of corticosteroids (triamcinolone acetate) is useful - surgical excision

DACRYOCYSTITIS (Fig 5.6.)

 inflammation of the lacrimal sac caused by bacterial infection in case of an obstructed nasolacrimal passage - Congenital due to Congenital nasolacrimal duct obstruction – the result of an imperforate membrane at the distal end of the nasolacrimal duct

- Aquired in adults

- Acute and Chronic

- Females predominate due to narrower, more tortuous nasolacrimal channels

108

Fig 5.6. Dacryocystitis

SYMPTOMS

- Tender swelling of the medial lower lid (overlying the lacrimal sac) - Discharge from the punctum enhanced by pressing on the swollen area - Excessive tearing - Red eye

MANAGEMENT

 For children - Digital pressure to canalicular system by the parent - Erythromycin ointment to control mucopurulent discharge if present - In case of acute dacryocystitis, a systemic antibiotic (Cefalosporin) - This regimen by 1 year of age to open spontaneously - Nasolacrimal duct probing after age 10 months  For adults Acute

Warm compresses

- antibiotics – oral in mild cases (cephalexin); IV in severe cases (Cefazolin)

Chronic

- Dacryocystorhinostomy

109 CONJUNCTIVITIS

- inflammation of conjunctiva  BACTERIAL  VIRAL  ALLERGIC

BACTERIAL CONJUNCTIVITIS (Fig 5.7)

ETIOLOGY

- Streptococcus pneumoniae - Staphylococcus most common - Hemophilus !!! - Neisseria gonorrhea

- Chlamydia

Fig.5.7. Bacterial Conjunctivitis

SYMPTOMS

- Red eye - Grittiness - Burning - Mucopurulent discharge - Crusted eyelids stuck together on waking

110

MANAGEMENT

- Antibiotic eyedrops (Gentamycin, Ciprofloxacin) every 3 to 4 hours with antibiotic ointment at bedtime for 5 to 7 days

!!! GONOCOCCAL CONJUNCTIVITIS

- ophthalmia neonatorum of the newborn - adults

SYMPTOMS

- extremely profuse, purulent discharge - chemosis (edema of conjunctiva) ! Untreated can lead to keratitis and perforation of cornea.

MANAGEMENT

- Systemic antibiotics IV Ceftriaxone

- irrigation of the conjunctiva with normal saline to remove the mucopurulent debris - Chlamydial conjunctivitis - mild mucopurulent discharge - adults and newborn - Antibiotics oral (Doxycycline) or topical (Ciprofloxacine)

VIRAL CONJUNCTIVITIS (Fig 5.8)

111 Fig.5.8. Viral Conjunctititis

ETIOLOGY

- Adenovirus may occur as the highly contagious (epidemic keratoconjunctivitis [EKC]

- Herpes simplex virus - Enterovirus

SYMPTOMS

- Burning - Foreign body sensation - Watery, mucous discharge - Red eye - Red and edematous eyelids - Pinpoint subconjunctival hemorrhages  Palpebral preauricular lymph node-cardinal sign  History of recent upper respiratory tract infection ! Keratitis may develop 1 to 2 weeks after the onset of the conjunctivitis.

MANAGEMENT

- Artificial tears 4-8-times per day - In keratitis topical nonsteroid anti inflammatory drugs or short course of corticosteroid drops

- Frequent hand washing recommended

112 - Use of separate towels

ALLERGIC CONJUNCTIVITIS (Fig 5.9.)

- Hypersensitivity reaction to specific airborne antigens (pollens) -

Fig. 5.9. Allegic Conjunctititis

SYMPTOMS

- Itching - Watery discharge - Chemosis (edema of conjunctiva) - Red and edematous eyelids - Milky appearance of the upper tarsal conjunctiva  Preauricular node is not palpable.

MANAGEMENT

- Cool compresses several times per day - Topical antihistamines and mast cell stabilizers (Olopatadine, Chromolyn)

VERNAL KERATOCONJUNCTIVITIS

- allergic conjunctivitis characterized by seasonal exacerbations most commonly affecting males between 4 and 20 years of age, common in warm dry climates.

SYMPTOMS

113 - Intense ocular itching - Red eye - Watery discharge - Edema of lids and conjunctiva - Boggy conjunctival edema - Giant papillae of the upper palpebral conjunctiva - Limbal papillae

MANAGEMENT

- Mast cell stabilizers - Topical antihistamines - Artificial tears - Systemic allergy treatment

SUBCONJUNCTIVAL Hemorrhage (Fig. 5.10)

- Diffuse or localized area of blood under conjunctiva  Asymptomatic  Cause - Trauma - Cough - Sneezing - Systemic Hypertension - Anticoagulants - Idiopathic No treatment is necessary. Resolves within 10-14 days.

114

Fig. 5.10. Subconjunctival Hemorrhage.

PINGUECULUM (Fig 5.11) and PTERYGIUM (Fig. 5.12)

- Excessive exposure to outdoor conditions especially UV radiation along with heat, dust and wind, may lead to degenerative conjunctival changes, two of which are:

1. pingueculum: a raised yellowish patch of elastotic degeneration that abutts but does not encroach upon the cornea, usually nasally.

2. pterygium: a raised triangular area of bulbar conjunctiva which actively invades the cornea, usually from the nasal side to produce visual symptoms. It may be surgically removed if it is reaching the central pupillary area affecting vision, if it is causing astigmatism, recurrent inflammation, affecting motility, or even for more cosmetic reasons.

115 Fig.5.11. Pingueculum

Fig.5.12. Pterigium

!! KERATITIS

- inflammation of the cornea

Cause

 Infection - Bacterial: Adnexal infection, lid malposition, dry eye, contact lenses (CL) - Viral: Herpes simplex, herpes Zoster - Fungal - Protozoan: A canthamoeba in CL wearer  Mechanical or trauma  Chemical

!! BACTERIAL KERATITIS (Fig 5.13)

116

Fig.5.13. Bacterial Keratitis

SYMPTOMS

- Pain - Discharge - Photophobia - Red eye - Decreased vision - Hyperemia around cornea – “ciliary flush” - May notice white spots on the cornea

MANAGEMENT

- Never patch - Topical antibiotics (Moxifloxacin) or fortified topical antibiotics (Tobramycin and Cefazolin) - Topical cycloplegic agents (Atropine) - Systemic antibiotics for corneal perforation or endophthalmitis

! HERPETIC KERATITIS (Fig 5.14)

- Herpes Simplex Virus (HSV) may cause primary systemic infection with ocular involvement or recurrent ocular involvement due to latent infection

117

Fig.5.14. Herpetic Keratitis

Herpetic dendritic epithelial keratitis

SYMPTOMS

- Pain - Photophobia - Tearing - Redness - Hyperemia around cornea – “ciliary flush” - Blurry vision - Decreased corneal sensation - Dendritic lesion of the corneal epithelium (Fig. 5.14) stained by fluorescein

TRIGGER MECHANISM

- febrile illness - menses - sunburn - “stress”

MANAGEMENT

- Antivirals topical (Acyclovir eye ointment) or oral (Acyclovir or Valtrex)

118

Cataract

Lecture by Professor Marianne Shahsuvaryan

Definition

– An opacity in the normally transparent focusing lens of the eye that, as it becomes denser, interferes with clears site.

Cataract means “waterfall”.

119

Causes

– Most common: aging

– Less common: intraocular diseases, trauma, medications(steroids, etc), and metabolic, endocrine, or congenital abnormalites

Maturity

– Immature Cataract • scattered opacities are separated by clear areas – Mature Cataract (Fig.7.4) • lens is totally opaque

Fig.7.4. Mature Cataract

EPIDEMIOLOGY

• Most common cause of visual loss in the adult population and cause of treatable blindness

• By age 65, >90% of all people have cataracts

120 • May develop at any age (essential to detect in neonatal period to prevent amblyopia)

MANAGEMENT

• Treatment is surgical removal

– Surgery is often deferred until decreased vision interferes with patient’s ability to

perform routine activities

– Surgery not deferred for above reasons:

• In neonates

• When the cataract interferes with the diagnosis or treatment of other ocular diseases, e.g., diabetes mellitus or a tumor

• When the cataract causes other eye diseases, e.g. uveitis or glaucoma

CATARACT SURGERY

– Couching • the first documented cataract surgery from 600BC by inserting a sharp instrument (a needle or lancet) into the lens and dislodging it away from the pupil

– Intracapsular cataract extraction • removing the entire lens and its surrounding capsule

– Extracapsular extraction (The current technique) • removing only the lens nucleous, its surrounding cortex, and a portion of the anterior capsule, leaving the posterior capsule as a support for an intraocular lens (Fig.7.5).

– Phacoemulsification (Fig.7.6) • method of extracapsular extraction using a high-frequency ultrasound device to fragment the hard nucleous of the lens into smaller particles and then aspirate them.

121 Advantage – small incision.

Complications

Complications (rare):

– Retinal detachment

– Macular edema

– Chronic Uveitis

– Keratopathy

PROGNOSIS

– Most cataract surgery is done on an outpatient basis

– After cataract removal eye is aphakic and optical power is restored by an intraocular lens, an eyeglass lens, or a contact lens

– Visual acuity is restored to precataract levels in more than 99% of uncomplicated cases.

Fig.7.5. Extracapsular Extraction (ECCE)

122

Fig.7.6. Phacoemulsification.

123

Red Eye :Part 2 UVEITIS

Lecture by Professor Marianne Shahsuvaryan

! ANTERIOR UVEITIS

SYMPTOMS

- Pain - Photophobia (due to ciliary spasm) - Red eye (redness around the cornea – ciliary flush) Fig.5.16. - Decreased vision - Narrow or irregular pupil, caused by adhesions between the iris and the lens-posterior synechal (Fig 5.17) - Keratic precipitates (KPs) – cellular deposits adherent to the posterior surface of the cornea (Fig. 5.18)

Posterior synechiae

Fig.5.16. Ciliary Flush

Fig.5.17. Posterior Synechal

124

Fig.5.18. Keratic Precipitates (KPs)

MANAGEMENT

- History and review of systems - Sometimes a laboratory work-up for systemic associations - Cycloplegic drops (Homatropine, Atropine) is used to prevent formation or to breake the posterior synechiae and to prevent secondary glaucoma - Steroids (topical, periocular injection or systemic) - Monitoring intraocular pressure (IOP) - Immunosuppresive agents in refractory cases after rheumatologist consultation.

POSTERIOR UVEITIS

BEHCET’S DISEASE

- multisystem syndrome consisting of an occlusive vasculitis, oral and genital ulceration, and arthritis

- ophthalmo-stomato-genital syndrome

125 • More common in men • Occurs in 3rd - 4th decade • Highest incidence in Mediterranean region and Japan • Associated with HLA-B5

ETIOLOGY

• Unknown • Various bacteria and viruses suggested • No good evidence to suggest any of them • Perpetuated by autoimmune response and CD4 + T-cells • Tumour necrosis factor (TNF) thought to be important

Systemic Involvement

Fig. 5.19. Oral aphthous ulceration Fig 5.20. Genital ulceration

126

Fig.5.21. Erythema Nodosum

• Skin lesions – 80% – Erythema Nodosum (Fig.5.21) – Acneiform

• Uveitis 70% (inflammation. of iris, ciliary body or choroid)

• CNS involvement – strokes, fits • Major vessels eg superior Vena cava obstruction • Increased skin response to trauma eg blood taking

Ocular Features

• Acute iritis – Pain, redness & VA – Flare – Inflammatory cells in anterior chamber – KPs (Inflammatory cells at posterior surface of cornea) Fig.5.22.

Fig.5.22 Acute iritis

• Recurrent hypopyon Fig.5.23. (Fluid level of white blood cells)

The red or white eye

127

Fig.5.23. Recurrent Hypopyon

Marked inflammation of the eye

• Retinal vasculitis and haemorrhage (inflammation. of retinal vessels) Fig.5.24 • Occlusive periphlebitis (venous sheathing & occlusion) Fig.5.25. • Retinal microinfarcts • Very damaging to vision: retinal damage and optic nerve atrophy • Cataract or glaucoma

Fig.5.24. Retinal Vasculitis and Haemorrhage

Fig.5.25. Occlusive Periphlebitis

Treatment Systemic Steroids

• Systemic immunosuppressive agents • Interferon-alpha may have immunomodulating effects • Anti-TNF monoclonal antibodies may be of help

128

!!! ENDOPHTALMITIS (Fig.5.26)

- massive ocular inflammation caused by infected or injured intraocular tissue, frequently leading to blindness

Fig.5.26. Endophtalmitis

SYMPTOMS

- marked pain - visual loss - lid and conjunctival edema - hazy cornea - cells and fibrinous exudates in the anterior chamber, hypopyon - cells in vitreous  divided into: - post-op endophthalmitis 1. acute post-op day 1-10 post-op due to Staphylococcus epidermidis

Staph. aureus

Pseudomonas

Proteus

2. delayed post-op weeks to months after surgery due to Propionobacterium acne

Staph. epidermidis

129 - post-traumatic endophthalmitis worse prognosis due to marked structural damage and virulence of organism

- endogenous endophthalmitis causative agents

Most common organisms Candida

Aspergillus

Bacteria

The causative organisms, usually fungi, enter the previously intact eye from a distant focus through the posterior ocular circulation.

The patients: immunocompromised,

debilitated,

on hyperalimentation.

MANAGEMENT

- Antibiotics (Ceftazidime, Amikacin, Cefazolin): intravitreal, subtenon injections, topical.

- Steroids to decrease the inflammatory response - Vitrectomy for patients with vision equal to light perception - Antifungal drugs in case of fungal etiology. !!! ACUTE ANGLE-CLOSURE GLAUCOMA (Fig.5.27.)

130 Fig.5.27. Primary Angle Closure Glaucoma

 An OPHTHALMIC EMERGENCY associated with a sudden elevation of intraocular pressure - See in the GLAUCOMA Section

Some “Red eye” conditions present a potential threat to vision requiring prompt and specialized care. These dangerous red eyes must be differentiated from the less-threatening conditions. Refer to the Table “Differential Diagnosis of “Red Eye”.

Differential Diagnosis of “red eye”

Diagnosis Conjunctivitis Angle Subconjunctival Allergic, bacterial, Keratitis Closure Uveitis Haemorrhage Sign viral Glaucoma Redness Localized + + + + - Pain - Slight irritation if ++ +++ + any) Photophobia - - + - ++ Purulent – bacterial + Discharge - Serous – viral, - - allergic - Yes Itchy - (only Allergic - - - Conjunctitivis) Visual Normal Normal Normal Decreased Decreased Acuity Decreased Fixed, Irregular, Pupils Normal Normal Normal mid dilated small Opacification present Keratic Cornea Clear Clear, no stain positive fluorescein Hazy precipitates staining Anterior Normal Normal Normal Shallow Normal chamber Iris Normal Normal Normal Normal Synechiae High, Intraocular Normal Normal Normal High normal or pressure low

131 GLAUCOMA

Lecture by Professor Marianne Shahsuvaryan

GLAUCOMA

- optic neuropathy, causes optic nerve head changes and visual field changes.

GLAUCOMA IS A MAIN CAUSE OF IRREVERSIBLE BLINDNESS

SIGNS

1. Elevated intraocular pressure is a common, but not necessary feature 2. Optic Nerve Cupping (Fig.7.1) 3. Visual field defects

Fig.7.1. Optic Nerve Cupping

Mechanism:

Most common is impaired outflow of aqueous.

A. Elevated IOP:

Aqueous is produced by the ciliary body, enters the posterior chamber between the iris and the lens and passes through the pupil into the anterior chamber then to the trabecular meshwork to the anterior chamber angle.

132 The major resistance to aqueous outflow from the anterior chamber occurs at the trabecular meshwork and Schlem’s canal.

Normal IOP is 16 +/- 5 mm Hg. It varies during the day with the highest readings in the early morning. Thus a single normal reading does not rule out glaucoma.

B. Optic Nerve Cupping:

Characterized by loss of disc substance (enlargement of the optic cup). Normal is up to 0.4 As cupping develops, the disc vessels are displaced nasally. Asymmetric cupping suggests glaucoma.

C. Visual Field Loss:

Glaucomatous field loss mainly involves the central 30 degrees of vision. The earliest changes are enlargement of the blind spot, nasal scotomas (nasal step) followed by peripheral arcuate defects. With further loss, there is further constriction of the visual field that may end up in "tunnel vision", as can be seen below:

D. Gonioscopy:

 An important step in the assessment of glaucoma is to visualize the angle structures.  Structures seen on gonioscopy of a normal angle include Schwalbe’s line, scleral spur and trabecular meshwork.  The angle is graded according to the number of structures identified on gonioscopy.

Classification of glaucomas:

133 - Primary Open Angle Glaucoma

- Primary Angle Closure Glaucoma

- Congenital Glaucoma

- Secondary Glaucoma

Secondary Glaucoma:

1. Phacogenic 2. Traumatic 3. Neovascular due to Diabetes, Retinal Vascular Occlusion 4. Steroid-induced

Risk Factors for Glaucoma:

1. Age 2. Race : more common in blacks 3. Family history of glaucoma 4. Cardiovascular diseases 5. Myopia 6. Nutritional factors 7. Vasospastic disorders: migraine.

I. PRIMARY OPEN-ANGLE GLAUCOMA:

 Most common form of glaucoma  More aggressive in blacks  Strong familial tendency  Pathology: Degenerative process in the trabecular meshwork, including deposition of extracellular material within the meshwork and beneath the endothelium leading to dysfunction and impaired drainage of aqueous.  Controlling IOP slows disc damage and visual field loss.  Asymptomatic until late in the course of the disease hence the need for early screening of relatives.  Visual field loss may progress in spite of normalized intraocular pressure.

II. NORMAL TENSION GLAUCOMA:

134  Also called low-tension glaucoma  Evidence of glaucomatous optic disc and/or visual field changes with a pressure consistently below 21 mm Hg.  Pathology: Abnormal sensitivity of the disc to intraocular pressure because of vascular or mechanical abnormalities at the ONH.  Disc hemorrhages are more commonly seen.  Associated with other vasospastic disorders such as migraine.  More aggressive than primary open-angle glaucoma  Treatment: Medications that increase blood flow to the ONH are favored ex: betaxolol , dorzolamide.

III. ACUTE ANGLE-CLOSURE GLAUCOMA (Fig.5.27.) !!!

Fig.5.27. Primary Angle Closure Glaucoma

 An OPHTHALMIC EMERGENCY associated with a sudden elevation of intraocular pressure  Occurs when the iris occludes the angle of anterior chamber and blocks the outflow of aqueous humor in eyes with narrow angles - more often occurs in middle-aged or older patients - female predilection associated with:

- hyperopia - nanophthalmos (small eyeball) - shallow anterior chamber (Refer to Ch.4. Eye Examination) - thicker lens - lens subluxation

SYMPTOMS

135 - Sudden onset of severe eye pain - Red eye - Blurred vision - Halos around lights - Headache or brow ache becomes severe - Nausea, vomiting.

SIGNS

- Increased IOP - Shallow anterior chamber - Hazy cornea (corneal edema) - Mid – dilated fixed nonreactive pupil - Redness around cornea (ciliary flush) or entire eye red

MANAGEMENT – OPHTHALMIC EMERGENCY

- Topical β – blocker ( Timolol 0.5% q 15 minutes × 2, then bid) - Topical steroid (Prednisolone acetate 1% q 15 minutes × 4, then q 1h) - Topical miotic (Pilocarpine 1-2% q 15 minutes only 3 times) - Diamox 500 mg po, then bid if the patient does not have allergy on sulfa drugs - IV mannitol or hyperosmotic glycerol 50% po in glass with ice and juice - Laser peripheral iridotomy once the pressure is controlled, to prevent further attacks. - Prophylactic laser peripheral iridotomy in fellow eye with narrow angle to prevent an acute attack in the future - Surgical iridectomy if laser is not available.

IV. CONGENITAL GLAUCOMA:

Types: 1) Primary congenital glaucoma

1. Anterior Segment Developmental Anomalies (associated with congenital glaucoma ex. Axenfeld’s syndrome, Rieger’s syndrome) 2. Associated with other ocular or extraocular anomalies.

 Pathology: Arrest of development of the anterior chamber angle structures.

136  Manifests at birth in 50% of patients but most patients present between the age of 3 and 9 months.  Symptoms include:  Epiphora (most common and earliest sign)  Photophobia  High IOP  Corneal opacities  Buphthalmos

 Differential diagnosis includes nasolacrimal duct obstruction, corneal opacities secondary to other causes such as congenital dystrophies, mucopolysaccharidoses, and traumatic rupture of Descemet’s membrane (birth trauma) as well as megalocornea.

 Treatment:

If early presentation  Goniotomy (may be repeated)

If late presentation  Trabeculectomy

V. SECONDARY GLAUCOMA

NEOVASCULAR GLAUCOMA (Fig.7.2)

- a secondary angle-closure glaucoma in which neovascularization of the iris and angle causes occlusion of the trabecular meshwork.

Fig.7.2. Neovascular glaucoma

137 ETIOLOGY

ocular ischemia due to:

- Proliferative diabetic retinopathy - Central retinal vein occlusion - Carotid occlusive disease - Tumors - Chronic inflammation

SYMPTOMS

• Decreased visual acuity

• Abnormal blood vessels on iris and angle, particularly at pupillary margin

• Increased IOP

• Optic nerve cupping and visual field defects

• May have corneal edema

MANAGEMENT

• Topical steroids (Prednisolone acetate 1% qid)

• Cycloplegic agent (Atropin 1%bid) for inflammation

• Topical glaucoma medication – Refer to Glaucoma Management, excluding prostaglandine analogues (Xalatan, Travatan) and Pilocarpine

• Laser photocoagulation for retinal ischemia (Refer to Ch.10. Ocular Manifestations of Systemic Diseases – Diabetic Retinopathy )

• Surgery - Refer to Glaucoma Management

- Glaucoma filtering surgery - Glaucoma drainage implant - Cyclodestructive procedure

VI. STEROID-INDUCED GLAUCOMA:

138  Both topical and periocular steroids can cause glaucoma in susceptible individuals (systemic steroids less likely)  IOP decreases once the drug is discontinued  The pressure rises because of an increased resistance to the outflow of aqueous due to deposition of glycosaminoglycans in the trabecular tissues that blocks outflow.  Newer generations of topical steroids (ALREX, LOTEMAX) have a much lesser tendency to raise IOP.

GENERAL MANAGEMENT IN GLAUCOMA

- Management of all forms involves lowering the IOP.

TREATMENT include

- Medication (drops) - Laser - Surgery

Medication

1. Prostaglandin Analogs:

Latanoprost (XALATAN); Travaprost (TRAVATAN): facilitates aqueous outflow through the uveoscleral pathway (a secondary pathway for drainage of aqueous).

2. Suppression of aqueous production:

A. Topical beta blockers:

 Timolol (TIMOPTIC) : contraindicated in asthma and cardiac diseases  Betaxolol (BETOPTIC): more beta1 cardioselective.

B. Alpha2 adrenergic agonists:

 Apraclonidine (IOPIDINE)  Brimonidine (ALPHAGAN)

C. Carbonic Anhydrase Inhibitors:

 systemic: Acetazolamide (DIAMOX)  topical : Dorzolamide (TRUSOPT) Brinzolamide (AZOPT) 139 3. Facilitation of aqueous outflow:

 Pilocarpine: acts through contraction of the ciliary muscle thus facilitating outflow.

4. Reduction of vitreous volume:

Hyperosmotic agents: Mannitol, glycerin.

LASER

1. Peripheral Iridotomy or Iridectomy: (Fig.7.3).

 Used in acute angle-closure glaucoma with pupillary block  Creates an opening between the anterior and posterior chambers to relieve the pressure between the two compartments.  Uses the Nd-YAG laser (iridotomy) or can be surgical (iridectomy).

Fig.7.3. Peripheral Iridotomy or Iridectomy

2. Argon Laser Trabeculoplasty (ALT):

 Argon laser application to the trabecular meshwork facilitates outflow of aqueous and enhances the function of the meshwork.  Can be used in adjunction to medical therapy in order to postpone glaucoma surgery.

3. Glaucoma Filtering Procedures:

A. Trabeculectomy:

140  Bypasses the normal drainage mechanisms of the eye by allowing direct access of aqueous from the anterior chamber to the subconjunctival tissue (bleb), either by trabeculectomy or by insertion of a drainage tube  The major complication of trabeculectomy is bleb failure due to fibrosis of the episcleral tissue. Fibrosis more commonly occurs in young patients, blacks, and patients who have previously undergone glaucoma filtering surgery or other surgeries involving the episcleral tissues. In these cases, adjunctive treatment with an antimetabolite ex Mitomycin C or 5-FU is helpful to reduce the risk of bleb failure.

4. Glaucoma drainage implant

 Implantation of a silicone tube is an alternative to trabeculectomy if the latter cannot be performed successfully. (Ahmed glaucoma valve implant or Baerveldt glaucoma implant).

5. Cyclodestructive Procedures

 These are reserved when both medical and surgical therapies are unsuccessful  They involve destruction of the ciliary body to control the IOP by cryotherapy, diathermy, or using the Nd-YAG laser applied just posterior to the limbus through a probe.  They carry a high risk of phthisis thus they should be reserved only for intractable cases.

141 DISORDERS OF THE RETINA AND OPTIC NERVE Lecture by Professor Marianne Shahsuvaryan

SUDDEN PAINLESS LOSS OF VISION

• CENTRAL RETINAL ARTERY OCCLUSION (CRAO) Fig.6.1

– ETIOLOGY – emboli, thrombosis due to vasculitis, reduction of blood flow due to carotid disease

Fig.6.1. Central Retinal Artery Occlusion

Associated diseases

– Hypertension (HTN) 70%

– Carotid stenosis 45% – Valve disease 25% – Diabetes Mellitus (DM) 25%

– Embolus (mural) 25%

SYMPTOMS

- sudden profound loss of vision

may have history of amaurosis fugax (episodes of loss of vision)

- positive afferent deffect

- diffuse retinal whitening and arteriole constriction - cherry-red spot in the macula

Workup:

142 – Carotid

– Cardiac Valve

– Collagen Vascular Disease

– Coagulopathy

– Giant Cell Arteritis

– IV drug abuse

– Migraine

PROGNOSIS

– Poor visual outcome

– 90% with positive workup

– Over 50% die within 10 years

MANAGEMENT

OPHTHALMIC EMERGENCY

Treatment for central retinal artery occlusion should be immediate.

The goals of treatment

- to restore retinal blood flow

- to move a potential retinal embolus distally

1. Lowering the intraocular pressure

- Massage of the globe using enough pressure to dent a tennis ball

- Acetazolamide (500 mg po)

- Topical ocular hypotensive drops: β- blocker (Timolol 0.5% q 15 min x 2)

143 2. Producing arterial dilation

- by having the patient breath into a paper bag

- by IM injection of Papaverine 40 mg

 CENTRAL RETINAL VEIN OCCLUSION (CRVO)

CENTRAL RETINAL VEIN OCCLUSION (CRVO) – occlusion of the central retinal vein usually caused by a thrombus in the area of the lamina cribrosa (Fig.6.2).

Fig.6.2. Central Retinal Vein Occlusion

ETIOLOGY

- Hypertension

- Cardiovascular disease

- Diabetes mellitus

- Peripheral vascular disease

- Hypercoagulable states

- Vasculitis

144 - Drug-induced (oral contraceptive pills, diuretics)

- Primary open-angle glaucoma (most commonly associated ocular disease)

EPIDEMIOLOGY

Usually seen in elderly patients (90% are > 50 years old)

- Slide male predilection Two types: nonischemic and ischemic.

Of the nonischemic cases, however, 54% later go on to develop ischemic CRVO.

Younger patients can get an inflammatory condition, termed papillophlebitis.

SYMPTOMS

Unilateral sudden painless loss of vision

- Dilated, tortuous retinal veins with superficial retinal hemorrhages and cotton-wool spots in all

four quadrants extending to the periphery.

- Optic disk hyperemia - Disc edema - Macular edema - Positive afferent pupillary defect (APD)

Clinical pearls

Initial poor visual acuity 20/200 or worse and a positive afferent pupillary defect (APD) correlates with ischemia and serve to predict neovascular complications due to ischemic type of CRVO.

MANAGEMENT

145 - Panretinal laser photocoagulation (PRP) when rubeosis (=2 clock hours of iris or any angle neovascularization), disk or retinal neovascularization, or neovascular glaucoma develops; NO BENEFIT TO PROPHYLACTIC PRP. - Intravitreal triamcinalone acetonide (Kenalog), antiVEGF (Macugen, Lucentis) has been shown to decrease macular edema and transiently improve visual acuity. - Consider aspirin 80mg po gd. - Treat underlying medical conditions - Unproven complex treatment included antioxidants, rheologic drugs, and vasodilators

 OPTIC NEURITIS (Fig.6.5.)

Fig.6.5. Optic neuritis

ETIOLOGY

- Multiple sclerosis (MS), fungal, viral

- 3:1 women:men

SYMPTOMS

- Optic disk hyperemic - Disc edema (disk margin is blurred) - 75-90 % regain 20/30 vision in 6 months

146

MANAGEMENT

- MRI

- Consider RPR, ESR, Lyme titer, ANA

- IV methylprednisolone

• at 6 months, slight benefit

• at 1 yr, no difference

• at 2 yr, decrease rate of MS

• recurs in 15%

 PAPILLEDEMA (FIG.6.6)

- Non inflammatory edema of the optic disc secondary to increased intracranial pressure (ICP)

Fig 6.6. Papilledema

147

ETIOLOGY

- brain tumors

- brain abscesses

- brain hematomas

- meningitis

BILATERIAL

may be asymmetric

SYMPTOMS

- Headache

- Nausea, vomiting

- Blurred vision

148

- Brief transient obscurations of vision

- Enlarged blind spot

- Variable degree of disc swelling (disc margin is blurred)

- Dilated tortuous vessels, hemorrhages

MANAGEMENT

- neuroimaging study

- CT or MRI

TREATMENT

directed at underlying cause

Prognosis usually good if primary cause of increased ICP is treated.

149 Optic atrophy (Fig.7.8)

Fig.7.8. Optic Atrophy

ETIOLOGY

• Previous optic neuritis or long-standing papilledema

• Compression of the optic nerve by a mass lesion, such as meningioma, or pituitary adenoma

• Ischemic damage to the optic nerve – non arteritic and arteritic Ischemic Optic Neuropathy – Refer to Ch.6. Sudden Loss of Vision

• Glaucoma

• Previous ocular /optic nerve trauma

• Toxic (methanol ingestion)

SYMPTOMS

- Decreased visual acuity - Visual field loss - Afferent pupillary defect APD, if unilateral - Paleness of the optic disc due to progressive loss of axons or

- white optic disc due to extensive damage.

150 PROGNOSIS

Blindness

 RETINAL DETACHMENT (Fig 6.7).

Fig.6.7. Proliferative vitreoretinopathy

ETIOLOGY

- myopia - surgery - trauma

151 - vascular disease • tear in inner retina

• fluid separates the layers of the retina

SYMPTOMS

- Floaters - Photopsia - Curtain over vision - intermittent changes in vision

TREATMENT

- immediate surgery

- laser and gas injection

Keys

- early intervention best success

- macular off implication

- proliferative vitreo-retinopathy (PVR)

OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES

Many systemic diseases have ocular signs and symptoms that may result in serious ocular sequelae.

152

Ocular Manifestations of Systemic Disease

• Vascular

– Hypertension

– Embolism

– Giant Cell Arteritis (Temporal arteritis)

• Endocrine

– Diabetes Mellitus

– Thyroid disease

• Inflammatory

– Collagen Vascular Disease (JRA,SLE)

– Sarcoidosis

– Rheumatoid Arthritis

• Infectious

– AIDS

– Sepsis

– Herpes Simplex/Zoster

– Sinusitis

• Neurological

– Intracranial Tumor

– Migraine

– Myasthenia Gravis

– Optic Neuritis/Multiple Sclerosis

• Cancer 153 – Primary

– Metatstatic

HYPERTENSIVE RETINOPATHY

Hypertensive retinopathy

- a retinal vasculopathy due to systemic hypertension:

• acute

• chronic

Fundus examination is often important in diagnosing the presence of hypertension and following its course.

Acute hypertensive retinopathy (Fig.10.1.)

• Malignant, accelerated, hypertensive crisis

• BP > 200/120

Fig.10.1. Acute hypertensive retinopathy

ETIOLOGY

154 • Renal disease, toxemia of pregnancy, vasculitis.

SYMPTOMS

• Usually associated with vision loss

• Disc edema

• Flame-shaped retinal hemorrhages

• Cotton-wool spot

MANAGEMENT

- immediate medical attention if the patient has symptoms of end-organ damage

• headache

• chest pain

• difficulty breathing

Chronic Hypertensive Retinopathy (Fig.10.2.)

• usually asymptomatic

• chronic essential hypertension BP > 140/90

SIGNS

- arteriolar sclerosis, narrowing (cooper or silver wiring)

- AV nicking, increased tortuosity

- flame-shaped retinal hemorrhages

- cotton wool spots

155

Fig.10.2. Chronic Hypertensive Retinopathy

COMPLICATIONS

- long-term: Retinal Artery Occlusion, Retinal Vein Occlusion. Refer to Ch.6. Sudden Loss of Vision

MANAGEMENT

• Blood pressure correction

- BP should be lowered slowly. Rapid correction may cause ischemic optic neuropathy with permanent loss of vision.

- Avoid giving the antihypertensive medication at night before sleep, since it is a natural, nocturnal drop in BP at night.

DIABETIC RETINOPATHY

Diabetic Retinopathy (DR) is the most common cause of legal blindness in individuals between the age of 20 and 65 years.

The risk factors for DR are:

1. Duration of DM: The most important factor.

156 The longer a person suffers from diabetes, the greater the likelyhood of developing diabetic retinopathy.

2. Metabolic control:

- Doesn't prevent DR, but delays its progression.

3. Miscellaneous factors:

- Pregnancy, systemic hypertension, renal disease, anemia.

Pathogenesis (Fig.10.3):

A. Ischemia: From thickening of the capillary basement membrane, injury and proliferation of the endothelial cells, decreased O2 transport, and abnormally increased platelet adhesion and aggregation. Ischemia causes infarct of the nerve fiber layer, producing what we see on ophthalmoscopy as cotton wool spots.

157

Fig.10.3. Diabetic Retinopathy: Pathogenesis.

Fig.10.4. Non proliferative Diabetic Retinopathy .

Pathogenesis:

B. Leakage: injury to the endothelial cells, together with pericyte drop out would lead to aneurysmal dilatation of the capillaries, leading to thrombosis, as well as rupture with hemorrhage. If the hemorrhage occur in the deep retinal layers ( inner nuclear cell layer), it would appear as dot or blot hemorrhage. If the hemorrhage occur superficially at the nerve fiber layer-typical in hypertension rather than diabetes, it produces a flame shape hemorrhage.

Leakage from the blood vessels will also lead to lipid deposition later on. This is known as hard exudates. They typically appear as yellowish lesions with distinct margins that sometimes encircle an aneurysm (seen as a red dot on ophthalmoscopy, like the hemorrhage).

Diffuse leakage around the macula would produce macular edema from the excess fluid as well as the exudates, which requires laser treatment.

Clinical Classification

A. Non Proliferative Diabetic Retinopathy (Fig.10.4):

158 Diagnosed by the presence of any of the following:

- Dot and blot hemorrhages

- Aneurysms

- Hard exudates

- Macular edema

- IRMAs (intraretinal microvascular abnormalities)

- Cotton wool spots

- Beading and looping of the capillaries

B. Proliferative Diabetic Retinopathy (Fig.10.5)

- Development of frank neovessels in the retina or on the iris ( Rubeosis Iridis) or fibrous tissue extending from the retina into vitreous cavity .

159 B

Fig. 10.5. Proliferative Diabetic Retinopathy (A, B, C).

Factors that lead to progression

• Puberty and pregnancy

• Systolic and diastolic blood pressure

• Hyperlipidemia : hard exudates in the macula and high risk of visual loss.

• Poor control of serum glucose

Evaluation of Diabetic Eye Disease

* May progress without visual symptoms.

* Florid neovascularization and still maintain perfect 20/20 vision.

• Insulin dependent, juvenile onset:

160 – Needs exam during first 4 years, then yearly

• Non insulin dependent, adult onset:

– Needs exam at the time of diagnosis, then yearly

• Diabetes prior to pregnancy:

– Needs exam prior to or early in first trimester, then every trimester

Treatment

A. Metabolic control slows the progression, but does not prevent the development of DR.

B. Blood pressure control slows the progression.

C. Laser treatment - focal Grid laser for Macular edema.

D. Pan-Retinal Photocoagulation (PRP)(Fig.10.6): is to be done in case of neovessel proliferation. The laser is delivered to the retinal periphery, sparing the posterior pole. The rationale behind such a treatment is to literally to kill as much as possible of the ischemic retina, to decrease the production of the angiogenic factors. The neovessels are supposed to shrink back after such therapy, except for the fibrous component.

E. Vitrectomy: in case of a non-resolving vitreous hemorrhage obscuring vision, or if a retinal detachment develops.

Fig.10.6. Panretinal argon laser photocoagulation- laser burns in the posterior pole.

161 AGE - RELATED MACULAR DEGENERATION

 Age-Related Macular Degeneration (AMD)

- slowly progressive binocular loss of central vision due to deterioration of the retinal pigment epithelium in the macula

ETIOLOGY unknown

RISK FACTORS

- smoking - older age - women - family history

 Age-Related Macular Degeneration (AMD) – Dry Form (Fig.7.7)

Fig. 7.7. Dry Macular Degeneration

 AGE-RELATED MACULAR DEGENERATION WET FORM (Fig.6.9) 162

Fig.6.9. Age-related macular degeneration –Wet form subretinal neovascular membrane

SYMPTOMS

• gradual loss of vision

• metamorphopsia – Amsler grid

• scotoma

• no APD

• drusen - hyaline degeneration of RPE – Fig.7.7.

• small yellow-white deposits underneath the retina

• break in Bruch’s membrane

163 Druzen may increase in size, number, and confluence, indicating progression of the disease.

– gradual vision loss cause

• atrophy of the macula due to dead retinal pigment epithelium

MANAGEMENT

• vitamins - A, C, E, zinc delays progression

• fluorescein angiogram

• laser

• newer modalities of laser, intravitreal steroids, anti-angiogenesis agents

PROGNOSIS

• will not go totally blind

• 20/400 endpoint

• use of low vision aids

164

165