Dr.

Swaby's Notes
Amanda Davis
2K14

Table of Contents
Anatomy and Embryology of the Eye
Eye Anatomy

Diabetes and the Eye

Classification of Diabetes

Cotton Wool Spots

Diabetes Dx

Diabetes and the Eye- Central Retinal Vein Occlusion

10

Diabetic Papillopathy

12

Diabteic Retinopathy- Risk Factors for Progression

15

Diabetic Retinopathy

17

Microaneurysms

19

Mx of Diabetic Retinopathy

22

Pathological Features of Diabetic Angiopathy

26

Dry Eye and Tear Production

Tear Production and Drainage

27

Hypertension and the Eye

Hypertension and the eye

28

Hypertensive Retinopathy

30

Occular Trauma

34

Opthalmic Hx and Examination

Cranial Nerve Assessment

37

Cranial Nerve Palsies that Affect the Eye

50

Opthalmic Hx and Examination

53

Pupil Assessment and Abnormalities

59

Pupillary Light Reflex

64

Relative Afferent Pupillary Defect

65

Squint in a Child
Amblyopia

67

Assessment of a Child with a Squint

70

Mx of a Child with a Squint

74

The Child with a Squint

74

The Red Eye

Causes of the Red Eye

78

Allergic Conjunctivitis

81

Eye Anatomy

1Upper eyelid
2 Lower eyelid

3 Lateral angle

4 Medial angle

5 Lacrimal caruncle

6 Limbus

7 Iris

8 Pupil

9 Lacrimal papilla

10 Sclera

11 Plica semilunaris

Figure 1 The surface anatomy of eye and lids

Figure Sagittal section through the eye

Figure Sagittal section of the eye the arrows show the production of aqueous humour by the
ciliary process and final drainage through the canal of schlemm.

Diabetes - Classification
Classification and causes of diabetes:

Type 1 diabetes is characterized by a lack of insulin production. Without daily

administration of insulin, Type 1 diabetes is rapidly fatal.
o Symptoms include excessive excretion of urine (polyuria), thirst (polydipsia),
constant hunger, weight loss, vision changes and fatigue. These symptoms may
occur suddenly.

Type 2 diabetes results from the bodys ineffective use of insulin. Type 2 diabetes
comprises 90% of people with diabetes around the world, and is largely the result of
excess body weight and physical inactivity. Until recently, this type of diabetes was seen
only in adults but it is now also occurring in obese children.

Gestational diabetes is hyperglycaemia which is first recognized during pregnancy.

Impaired Glucose Tolerance (IGT) and Impaired Fasting Glycaemia (IFG) are intermediate
conditions in the transition between normality and diabetes. People with IGT or IFG are at high
risk of progressing to type 2 diabetes, although this is not inevitable

Etiologic Classifications of Diabetes Mellitus

1) Type 1 diabetes mellitus
2) Type 2 diabetes mellitus
3) Other specific types:

5) Infections

Congenital rubella
Cytomegalovirus

Others

Genetic defects of beta-cell function

Genetic defects in insulin action

Diseases of the exocrine pancreas

Pancreatitis

Trauma/pancreatectomy

Neoplasia

Down syndrome
Klinefelter's syndrome

Cystic fibrosis

Turner's syndrome

Hemochromatosis

Wolfram syndrome

Others

Friedreich's ataxia

Endocrinopathies

Huntington's chorea

Acromegaly

Lawrence-Moon Beidel syndrome

Cushing's syndrome

Myotonic dystrophy

Glucagonoma

Porphyria

Pheochromocytoma

Prader-Willi syndrome

Hyperthyroidism

Others

Somatostatinoma

Aldosteronoma

Others

4) Drug- or chemical-induced

6) Uncommon forms of immune- mediated

diabetes
7) Other genetic syndromes sometimes associated
with diabetes

8) Gestational diabetes mellitus

Vacor
Pentamidine

Nicotinic acid

Glucocorticoids

Thyroid hormone

Diazoxide

Beta-adrenergic agonists

Thiazides

Phenytoin

Alfa-interferon

Others

COTTON WOOL SPOTS

Cotton wool spots result from occlusion of retinal pre-capillary arterioles supplying the nerve
fibre layer with concomitant swelling of local nerve fibre axons.
Also called "soft exudates" or "nerve fibre layer infarctions" they are white, fluffy lesions in the
nerve fibre layer.
They are very common in DR, especially if the patient is also hypertensive

Figure Showing multiple cotton wool spots

COTTON WOOL SPOTS MAY BE SEEN IN THE FOLLOWING CONDITIONS: ("DHL

Always Speed" useful pneumonic)

DIABETES
HYPERTENSION

LEUKAEMIA

AIDS

SLE

SICKLE CELL DISEASE

Diagnosing diabetes mellitus

Positive findings from any TWO of the following three tests on DIFFERENT
days!!!

Symptoms of diabetes mellitus* plus casual plasma glucose concentration >=200 mg per dL (11.1 mmol
per L)

(Casual is defined as any time of day without regard to time since last meal)

or

Fasting Plasma Gluose (FPG)>=126 mg per dL (7.0 mmol per L)

or

2hr Post Prandial Glucose (PPG)>=200 mg per dL (11.1 mmol per L) after a 75-g glucose load

Impaired glucose homeostasis

Impaired fasting glucose: FPG from 110 to <126 (6.1 to 7.0 mmol per L)
Impaired glucose tolerance: 2hrPPG from 140 to <200 (7.75 to <11.1 mmol per L)

Normal

FPG <110 mg per dL (6.1 mmol per L)

2hrPPG <140 mg per dL (7.75 mmol per L)

Diabetes and the Eye

When you think about diabetes and its effect on the eye remember to consider
the extraocular and ocular structures NOT only the retina:

Figure Diabetic retinopathy

Orbit

Increased incidence of Orbital cellulitis

Cranial nerve palsies

3rd, 4th and 6th Cranial nerve may be affected by diabetic neuropathy

Lids

Increased risk of lid infections

Cornea

Increased risk of microbial keratis (Corneal ulcer)

Anterior chamber and uvea

Increased risk of uveitis especially following intra ocular surgery for eg Cataracy
extraction

Glaucoma

Open angle glaucoma

Rubreotic glaucoma (Associated with abnormal vessels in the anterior chamber angle

Lens

Transient myopia - Due to accumulation of sorbitol within the lens

Cataract - Especially cortical cataracts

Vitreous

Vitreous hemorrhage

Retina

Diabetic retinopathy
Central and Branch vein occlusion

Central and Branch artery occlusion

Optic nerve

Diabetic papillopathy - Disc swelling without any

tractional component

Non arteritic optic neuropathy

Central retinal vein occlusion

Figure illustrating CRVO with multiple retinal hemorrhages

Definition
Central retinal vein occlusion (CRVO) is blockage of the central retinal vein by a
thrombus, usually occurring in elderly patients.
Its symptom is sudden, painless vision loss.
fundus findings:

Multiple retinal hemorrhages

Retinal veins appear distended and tortuous

The fundus is congested and edematous and the optic disc and macula
may be swollen

Cotton wool spots may indicate that the retina is ischemic

Retinal neovascularisation in ischemic CRVO with resultant vitreous

hemorrhage

Figure illustrating retinal neovascularisation

The occlusion may be idiopathic however the following risk factors have
been identified:

Glaucoma
Diabetes

Hypertension

Increased blood viscosity

Elevated haematocrit

Main complaications:

Neovascularization of the retina

Iris (rubeosis iridis) with secondary (neovascular) glaucoma can occur
weeks to months after occlusion

Figure illustrating abnormal new vessels on the iris. Their growth is stimluated
by the release of Vascular endothelial growth factor (VEGF)

Vitreous hemorrhage may result from retinal neovascularization.

Symptoms:
Painless visual loss can be sudden or gradual over a period of days to weeks.
Prognosis and Treatment
In patients in whom normal retinal perfusion is re-established, normal vision may
return. The time to vision improvement varies.
Those with poor perfusion are more likely to develop complications and suffer
severe vision loss.
Visual acuity at presentation is a good indicator of final vision. If visual acuity is
at least 20/40, visual acuity will likely remain good. If visual acuity is worse than
20/200, 80% of patients will not improve or will deteriorate.
There is no generally accepted medical therapy unless neovascularization
develops. In this event, panretinal photocoagulation should be initiated, which
may decrease vitreous hemorrhages and prevent neovascular glaucoma.

DIABETIC PAPILLOPATHY

Figure showing diabetic papillopathy with a grossly swollen disc.

Diabetic papillopathy is a form of optic neuropathy occasionally described in patients

with diabetes mellitus. It is rare and the classical presentation is in a young adult with
type 1 diabetes.
Symptoms are usually mild, often seen as a slow progressive

blurring of vision. Signs are usually, but not invariably, unilateral.

It may be an incidental finding in an asymptomatic patient.

Visual acuity is often slightly reduced or normal, with or without an enlarged blind spot.
Optic disc swelling can be striking, with distended surface vessels.

Signs of diabetic macular oedema are often present.

The pathogenesis is unknown. No relationship has been demonstrated between diabetic

papillopathy and either diabetic retinopathy or glycaemic control.

Hypoxia is thought to play a role. Although, diabetic papillopathy has been considered a
form of AION, its presentation and prognosis differ profoundly from arteritic AION in
which visual loss is sudden and profound, with a poor prognosis for recovery

Risk factors for progression of Diabetic Retinopathy

Systemic factors
The risk of macular exudation, edema, and ischemia increases with poor control of:

Blood glucose levels

Blood pressure

High cholesterol

Triglyceride levels

Anemia

diabetic kidney disease.

A) Blood glucose control

Prolonged exposure to hyperglycemia causes microvascular complications, such as retinopathy,
nephropathy, and neuropathy.
Two important studies to remember:
Diabetes Control and Complications Trial:

intensive insulin therapy effectively delays the onset and slows the progression of
diabetic retinopathy in patients with type 1 diabetes.
In the primary prevention cohort (those with no retinopathy at baseline), intensive
therapy reduced the adjusted mean risk for the development of retinopathy by 76%
compared with conventional therapy.
In the secondary intervention cohort (those with mild retinopathy at baseline), intensive
therapy slowed the progression of retinopathy by 54% and reduced the development of
proliferative or severe nonproliferative retinopathy by 47%.

UK Prospective Diabetes Study:

Improved control in patients with type 2 diabetes not only led to a reduction in
retinopathy but also reduced overall microvascular complications by 25%.
A one-point decrease in hemoglobin A (HbA ) was associated with a 35% reduction in
risk of microvascular complications.
1c

1c

The American Diabetes Association advocates an HbA goal of less than 7%.
1c

B) Diet and exercise

Exercise alone reduces the concentration of HbA by about 0.65 point and should be
strongly encouraged.
Risks of progressive nephropathy and neuropathy are also reduced with tight glucose
control.
1c

C) Blood pressure control

Wisconsin Epidemiologic Study of Diabetic Retinopathy and the UK Prospective Diabetes
Study:

Diabetic retinopathy progressed significantly more slowly with more tightly controlled
blood pressure
Risks of progressive nephropathy and neuropathy are also reduced with good blood
pressure control.

EURODIAB Controlled Trial of Lisinopril in Insulin-Dependent Diabetes Mellitus:

Showed that an angiotensin-converting enzyme (ACE) inhibitor (lisinopril) reduced

progression of retinopathy in nonhypertensive patients with type 1 diabetes by 50% in 2
years.
This finding needs to be confirmed on a larger scale, much evidence supports the use of
ACE inhibitors in both hypertensive and nonhypertensive patients with diabetes to
prevent microvascular and macrovascular diabetic complications.

D) Lipid control
Evidence suggests that hyperlipidemia contributes to the progression and morbidity of diabetic
retinopathy.
Wisconsin Epidemiologic Study of Diabetic Retinopathy,

The presence of retinal hard exudates was significantly associated with increased serum
cholesterol levels in patients taking insulin.

Early Treatment Diabetic Retinopathy Study

Subjects who had an elevated total cholesterol or low-density lipoprotein cholesterol

level were significantly more likely than those with normal levels to have retinal hard
exudates.
Accumulation of retinal hard exudates can lead to vision loss either from a foveal lipid
plaque or from the development of fibrosis.
Risks of progressive nephropathy and neuropathy also are reduced with lipid control.

E) Diabetic nephropathy
: This condition may exacerbate diabetic retinopathy in a number of ways:

Erythropoietin-sensitive anemia exacerbates retinopathy if not effectively treated.

Erythropoietin (Epogen, Procrit) treatment of nephropathy-associated anemia has been
shown to result in resolution of diabetic macular edema.

Two factors--hypoalbuminemia associated with diabetic nephropathy-induced

microalbuminuria and the hypertension that often accompanies diabetic nephropathy-shift the Starling forces toward the extravascular compartment, which exacerbates edema.

Diabetic retinopathy
Background Diabetic Retinopathy:

Microaneurysms
Dot and Blot hemorrhages

Hard exudates (Lipid deposition)

FIGURE 1
MICROANEURYSMS HIGHLIGHTED BY YELLOW RINGS

Figure Hard exudates

Pre Proliferative Diabetic Retinopathy

IRMA
FLAME HEMORRHAGES

VENOUS BEADING

COTTON WOOL SPOTS

FIGURE 2 COTTON WOOL SPOTS HIGHLIGHTED IN THE YELLOW CIRCLE

FIGURE 3 Showing IRMA, Cotton wool spots and Flame hemorrhages.

PROLIFERATIVE DIABETIC RETINOPATHY

Neovasculariation of disc (NVD)

Neovasculariation elsewhere (NVE)

FIGURE 4 Neovasculariation of disc (NVD) and elsewhere (NVE) plus hard exudates within the macular region.

Figure illustrating new abnormal retinal blood vessels

which are fragile and may bleed.

MICROANEURYSMS
Retinal microaneurysms are focal dilatations of retinal capillaries, 10 to 100 microns in diameter, and appear as red
dots.

They are usually seen at the posterior pole, especially temporal to the fovea.
Microaneurysms are the first ophthalmoscopically detectable change in diabetic retinopathy.

Fibrin and erythrocytes may accumulate within the aneurysm. Despite multiple layers of basement membrane,

they are permeable to water and large molecules, allowing the accumulation of water and lipid in the retina.

Diabetic Retinopathy - Treatment

Management of Diabetic Maculopathy
Focal laser
Treatment of microaneurysms associated with clinically significant macular edema is essential in
preventing severe vision loss in patients with nonproliferative diabetic retinopathy
Management of the following is also crucial:

Blood glucose levels

Blood pressure

Lipid levels

Renal function

Anemia

Patients with clinically significant macular edema have a 62% chance of moderate vision
loss over a 3-year follow-up period, which is reduced to 28% with focal laser treatment of
microaneurysms.

Periocular steroid injection

Local corticosteroid therapy with periocular or intravitreal administration of triamcinolone has
been shown to reduce macular edema, perhaps by stabilizing the blood-retinal barrier.
Triamcinolone injections may need to be repeated if macular edema persists or recurs.

Management of Proliferative diabetic retinopathy

Treatment of PDR involves Pan Retinal laser photocoagulation

Up to 2000 laser burns are placed on the retina. Further treatment is dependant on the
response.

Figure showing multiple laser burns.

Why do we treat proliferative diabetic retinopathy ?

Vascular endothelial growth factor (VEGF) elaborated by an ischemic retina induces retinal
neovascularization.
These newly formed vessels then erupt through the surface of the retina (internal limiting
membrane) and grow on the vitreous cortex "scaffold". They have the tendency to bleed with
vitreous movements and the synchysis (ie, shrinkage) that occurs normally with age, causing
vitreous hemorrhage.

Such hemorrhage causes subacute and acute loss of vision

and visual field; patients may complain of floaters or
veils, or both, across their central or peripheral field of
vision. Organization of hemorrhage on the vitreous
cortex or formation of fibrovascular tissue on the vitreous

cortex and retina can cause tractional retinal detachment

and permanent loss of vision. As in nonproliferative
retinopathy, macular edema and ischemia can lead to
vision loss as well.
Pathological changes in diabetic blood vessels

1) LEAKAGE

In diabeteic patients the pericytes (diamond shaped cells) detach, destabilizing vessels.
The loss of pericytes leads to weakening of the capillary walls and microaneurysm formation.

The microaneurysm eventually leak blood (Dot and Blot haemorrhages) and lipids (Hard Exudates) This
gives rise to BACKGROUND DIABETIC RETINOPATHY and DIABETIC MACULOPATHY

2) ISCHAEMIA

Diabetes can cause blood vessels to collapse, creating a hypoxic environment that generates vascular endothelial
growth factor (VEGF) and triggers angiogenesis.
The retinal hypoxia leads to ischaemia and the development of the following:

Cotton wool spots - Swollen axons of the nerve fibre layer

Venous beading

Venous omega loops

Intra Retinal Micovascular abnormalities (IRMA) - Colaterals between arterioles and venules

Flame haemorrages

3) PROLIFERATION
"Kazlauskas and Im hypothesize that endothelial cells (rectangles) receive specific instructions during this unstable
state that dictate whether the vessels should grow or regress. In the case of diabetic retinopathy we have proliferation
of blood vessels stimulated by the release of VEGF.
Features of proliferative diabetic retinopathy include:

New vessels at the disc (NVD)

New vessels elsewhere (NVE)

Vitreous and pre retinal hemorrhage

Tractional retinal detachement

Tear production and drainage

The lacrimal apparatus is divided into two components: the secretory system and the excretory
system.

Lacrimal gland
The main lacrimal gland resides in the superotemporal orbit, partially within a shallow bony
fossa in the lateral angular process of the frontal bone (lacrimal fossa).
The Accessory Lacrimal Glands
The accessory lacrimal exocrine glands of Wolfring and Krause structurally resemble the main
lacrimal gland but on a lesser scale. Between 20 and 40 glands of Krause are located in the
superior conjunctival fornix; 2 to 8 are located in the inferior conjunctival fornix. Between 3 and
20 glands of Wolfring can be found along the upper border of the superior tarsus, 1 to 4 below
the lower tarsus and an occasional gland in the caruncle and in the plica semilunaris. The glands
of Wolfring are larger in size than glands of Krause.46

Hypertension and the eye

WHO definition of hypertension

Systolic blood pressure >140 mm Hg

Diastolic blood pressure > 90 mm Hg

Hypertension can affect the eye and vision in several ways:

Hypertensive retinopathy - refers to retinal microvascular signs that develop in response to raised blood
pressure.

A) Arteriolar changes:

generalized arteriolar attenuation

Focal arteriolar constriction

Arteriovenous nicking

Arteriolar wall opacification

B) More advanced retinopathy lesions:

Microaneurysms
Blot and flame-shaped hemorrhages

Cotton-wool spots

Hard exudates

Pptic disc swelling

Signs of hypertensive retinopathy are frequently seen in adults 40 years and older, and are predictive of
incident stroke, congestive heart failure, and cardiovascular mortality--independently of traditional risk
factors.

OTHER EFFECTS ON THE EYE AND VISION:

Retinal vein and artery occlusion

non arteritic Ischaemic optic neuropathy

Cranial nerve palsies

Visual field defects following cerebrovascular accidents (CVA)

Glaucoma

Age related macula degeneration

High blood pressure increases the risk of both development of diabetic retinopathy and its progression.
Adequate control of blood pressure has been proven in randomised clinical trials to reduce vision loss associated
with diabetic retinopathy.

Finally, hypertension has been implicated in the

pathogenesis of glaucoma and age-related macular
degeneration.

Hypertensive Retinopathy

Figure illustrating the main features of hypertensive retinopathy

Elevated systemic blood pressure commonly affects the retina, causing changes that can be
readily seen with the opthalmoscope and which relate to the severity of the hypertension.
Hypertensive retinopathy refers to damage to the retina from chronic and/or acutely elevated
blood pressure.

Features of the hypertensive retinopathy include:

Mild to moderate hypertension:

Variable degrees of arteriolar narrowing

Hemorrhages in the retinal nerve fiber layer flame-shaped hemorrhages

Exudates, including some that fan out around the center of the macula (macular star)

Cotton wool spots

Microaneurysms

Moderate to severe hypertension:

In cases of severe hypertension , the retinal arterioles are much narrower than normal,
and there is edema of the optic nerve head .
Arteriolosclerosis accompanies long standing hypertension and commonly affects the
retinal and choroidal vessels.

The thickened retinal arterioles become attenuated, increasingly tortuous, and of irregular
caliber.

At sites where the arterioles cross veins, the veins may appear kinked (arteriovenous
nicking) , but the venous diameter is not narrower distal to the compression, an
appearance which indicates that the kinked appearance of veins is not due to compression
by a taut sclerotic artery. Instead it reflects sclerosis within the venous walls, because
retinal arteries and veins share a common adventitia at sites of arteriovenous crossings.

Figure illustrating AV nipping

The abnormal retinal arterioles appear clinically as parallel white lines at sites of vascular
crossings (arterial sheathing).
The narrowed lumen of the retinal vessels decreases the visibility of the blood column
and makes them first appear orange on opthalmoscopic examination (copper wiring)

Figure copper wiring

Eventually as the blood column becomes completely obscured, light reflected from the
sclerotic vessels appear as threads of silver wire (silver wiring).

Hypertensive retinopathy has been classified according to severity in Grade 1 through 4, with the
higher numbers having more serious changes and a poorer prognosis.

Small superficial or deep retinal hemorrhages often accompany retinal arteriolosclerosis.

In malignant hypertension, a necrotizing arteriolitis, with fibrinoid necrosis and
thrombosis of the precapillary retinal arterioles, occurs.

Hypertensive Retinopathy:
Modified Scheie Classification

Grade 0 - No changes
Grade 1 - mild generalized retinal arteriolar narrowing

Grade 2 - more severe generalized narrowing, focal areas of arteriolar narrowing

and arteriovenous (AV) nicking

Grade 3 - grade 1 and 2 signs plus the presence of microaneurysms, retinal

hemorrhages, hard exudates and cotton-wool spots

Grade 4, - accelerated (malignant) hypertensive retinopathy, consists of signs in

the preceding three grades plus optic disc swelling and macular edema

Whereas the 3 year survival of persons with grade 1 hypertensive retinopathy was 70%, the
survival was only 6% in those with grade 4 hypertensive retinopathy.
Retinal microvascular abnormalities, such as generalized and focal arteriolar narrowing,
arteriovenous nicking and retinopathy, reflect cumulative vascular damage from hypertension,
aging, and other processes. Epidemiological studies indicate that these abnormalities can be
observed in 2-15% of the nondiabetic general population and are strongly and consistently
associated with elevated blood pressure. Generalized arteriolar narrowing and arteriovenous
nicking also appear to be irreversible long-term markers of hypertension"
Why is it important to identify and document hypertensive retinopathy?

Hypertensive retinopathy has long been regarded as a risk indicator for systemic morbidity and
mortality.

New population-based studies show that hypertensive retinopathy signs are strongly
associated with blood pressure, but inconsistently associated with cholesterol and other
risk factors of atherosclerosis.
Mild hypertensive retinopathy signs, such as generalized and focal retinal arteriolar
narrowing and arteriovenous nicking, are weakly associated with systemic vascular
diseases.

Moderate hypertensive retinopathy signs, such as isolated

microaneurysms, haemorrhages and cotton-wool spots, are strongly
associated with subclinical cerebrovascular disease and predict incident
clinical stroke, congestive heart failure and cardiovascular mortality,
independent of blood pressure and other traditional risk factors.

Ocular Trauma
The eye may be traumatised by several conditions:
Chemical - Chemical eye injuries are potentially blinding injuries. If chemicals are
splashed into the eye, the eye and the conjunctival sacs (fornices) should be washed out
immediately with copious amounts of water. Alkalis are aable to particularly damaging,
and any loose bits such as lime should be removed from the conjunctival sac with the aid
of local anaesthetic if necessary. The patient should then be referred immediately to an
ophthalmic department. If there is any doubt, irrigation should be continued for as long as
possible with several litres of fluid.
Mechanical

Thermal

Radiation - The most common form of radiation damage occurs when welding has been
carried out without adequate shielding of the eye. (Arc Eye) The corneal epithelium is
damaged by the ultraviolet rays and the patient typically presents with pain, photophobia
and increased lacrimation usually several hours after welding. This condition is
commonly known as arc eye.

Electrical

History
How the injury was sustained gives clues about what to look for during the examination.

High velocity injury (particularly a hammer and chisel injury) a penetrating injury must
be excluded.
Forceful blunt injury (such as a punch), signs of a "bowout" fracture should be sought.

Corneal abrasions are the most common result of blunt injury. They may follow injuries with
foreign bodies. Fluoroscein will reveal the abrasion.
The main aims of treatment are to:
Prevent infection apply antibiotic for eg Vigamox
Relieve pain instil a cycloplegic drug (cyclopentolate 1% or Atropine 1%) The cylopegic
drops will relieve ciliary spasm and dilate the pupil

Apply topical steroids if there is a traumatic uveitis eg Pred Forte

Recurrent erosion syndrome

The corneal epithelium may repeatedly break down if the patient has had a previous
injury or has an inherently weak adhesion between the epithelial cells and the basement
membrane.

Treatment is long term and entails drops during the day and ointment at night to lubricate
the eye.

A surgical procedure (such as epithelial debridement or corneal stromal puncture) may

occasionally be required to improve adhesions between epithelial cells and basement
membrane.

Chemical Injuries
Alkali burns to the eye trigger a cascade of proteolytic events, causing varying degrees of
destruction depending on the strength of the alkali. Possible sequelae include:
Opacification of the cornea
Cataract

Secondary glaucoma

Limbal stem cell failure

Management of chemical injuries

Use topical anesthetics liberally to facilitate irrigation and examination. A 1%-4%

solution of lidocaine HCl (Xylocaine) can be used if proparicaine HCl or tetracaine HCl
(Alcaine, Ophthaine, Ophthetic) is not readily available.
Briefly rule out globe perforations. Chemical explosions (eg, those involving a battery)
may also produce an open globe injury or intraocular foreign bodies
Irrigate the superior and inferior cul-de-sacs and remove any foreign bodies that may act
as a depot for the chemical.
o

Intravenous tubing connected to a bag of normal saline or lactated Ringer's

solution makes an ideal irrigation tool.

A lid speculum greatly facilitates irrigation.

Continue irrigation with water or normal saline solution for at least 20 minutes.

After 20 to 30 minutes, perform a brief eye examination, including vision testing.

Five to 10 minutes after stopping irrigation, touch dry litmus paper to the inferior cul-desac to test pH.

Repeat irrigation in 20- to 30-minute intervals until pH is nearly neutral (pH 7) when
checked 5 to 10 minutes after irrigation or until an ophthalmologic consultant assumes
care of the patient.

Whenever possible, identify the chemical.

Cranial nerve assessment

FIRST CRANIAL NERVE---OLFACTORY NERVE
The olfactory nerve is a special afferent cranial nerve composed of sensory fibers only. Its sole
function is to discern smells. Olfaction depends on the integrity of the olfactory neurons in the
roof of the nasal cavity and their connections through the olfactory bulb, tract, and stria to the
olfactory cortex of the medial frontal and temporal lobes. To test olfaction, an odorant, such as
concentrated vanilla, peppermint or coffee extract, is presented to each nostril in turn. The
patient is asked to sniff (with eyes closed) and identify each smell (Fig. 4). Olfaction is
frequently not tested because of unreliable patient responses and lack of objective signs.

FIGURE 4. Testing the olfactory nerve. While occluding each nostril, patient is asked to
sniff and identify various odorants.

SECOND CRANIAL NERVE---OPTIC NERVE

The optic nerve contains special sensory afferent fibers that convey visual information from the
retina to the occipital lobe via the visual pathway. Evaluation gives important information about
the nerves, optic chiasm, tracts, thalamus, optic radiations, and visual cortex.
CN 2 is also the afferent limb of the pupillary light reflex.
The optic nerve is tested in the office by visual acuity measurement, color vision testing, pupil
evaluation, visual field testing, and optic nerve evaluation via ophthalmoscopy and/or stereo
biomicroscopy.

Intracranial lesions affecting the visual pathway can be localized based on the pattern of visual
field defects. Prechiasmal lesions usually cause monocular field defects. Chiasmal lesions
produce heteronymous hemianopsias, and postchiasmal lesions produce homonymous
hemianopsias. The further posterior the lesion, the more alike (congruous) the two fields appear.

THIRD CRANIAL NERVE---OCULOMOTOR NERVE

The oculomotor nerve contains somatic efferent and visceral efferent motor fibers. The somatic
efferent fibers innervate the levator palpebral superioris, superior rectus, medial rectus, inferior
rectus, and inferior oblique muscles of the eye. The visceral efferent fibers convey
parasympathetic innervation for pupillary constriction and accommodation (Fig. 5).

FIGURE 5. Testing the optic and oculomotor nerves. The pupillary light reflex
To begin testing CN 3, it is important to first inspect the eyes. Look for ptosis, note the
appearance of the eyes, and check for ocular alignment (the light source reflection should fall at
the same location on each eyeball).
Next, test extraocular range of motion by having the patient follow a near target through the six
principal positions of gaze ("H" pattern). Note any misalignment of the eyes or complaints of
diplopia. When specifically evaluating CN 3 during testing, note adduction (medial rectus),
depression while abducting (inferior oblique), and elevation (superior rectus and inferior
oblique).
Pupillary constriction is tested by the light reflex, and having the patient focus on a near target
can test accommodation. Loss of CN 3 function may cause diplopia, and an eye that is "down
and out" with ptosis and mydriasis.

FOURTH CRANIAL NERVE---TROCHLEAR NERVE

The trochlear nerve supplies somatic efferent motor fibers that innervate the superior oblique
muscle. The superior oblique is tested, as previously described, by inspection followed by having
the patient track a near target moved in an "H" pattern (Figs. 6 and 7).

FIGURES 6 and 7. Testing CN III, IV, and VI: To test the extraocular muscles, have the
patient follow a target through the six principal positions of gaze ("H" pattern).

Having the patient adduct and look downward to the nose best isolates this nerve. The trochlear
nerve is the only nerve to exit from the dorsal aspect of the brain, and it has the longest
intracranial course of any cranial nerve. For this reason, it is often the most susceptible to
damage from intracranial lesions caused by trauma, inflammatory disease, and compression.
Loss of CN 4 function causes diplopia with a compensating head tilt.

FIFTH CRANIAL NERVE---TRIGEMINAL NERVE

The trigeminal nerve supplies both sensory and motor fibers to the face and periorbital area. The
afferent sensory fibers separate into three divisions and carry touch, pressure, pain, and
temperature sense from the oral and nasal cavities, and the face. Motor efferent fibers function to
innervate several facial muscles, including the muscles of mastication.
The sensory portion of the trigeminal nerve is commonly tested by examining the integrity and
symmetry of pain and light touch sensation from all areas of the face (forehead, cheek, and jaw).
After asking the patient to close his/her eyes, a tissue is lightly touched to one side of the
forehead. The tissue is then touched to the opposite side and the patient is asked to compare
sensations. A sharp object can be used in the same manner when testing for pain symmetry. The
test is then repeated on the cheek (Fig. 8) and jaw line to assess the second and third divisions.

FIGURE 8. Testing the sensory distribution of the trigeminal nerve. Ask the patient to
compare the sensation of light touch on both sides of the forehead, cheek, and chin.
An additional test used to evaluate the trigeminal nerve is the corneal reflex test. Evaluate the
reflex by gently touching each cornea with a cotton wisp and observing any asymmetries in the

blink response (Fig. 9). This tests both the sensory fifth nerve and the motor portion of the
seventh nerve, which is responsible for lid closure.

FIGURE 9: The corneal reflex: Immediate closure of both eyelids should occur as
examiner touches temporal aspect of cornea with cotton wisp.
To test the motor component of CN 5, feel and compare the tone of the masseter muscles during
jaw clench. Next, have the patient open his/her mouth and resist the examiner's attempt to close
it. If there is weakness of the pterygoids, the jaw will deviate towards the side of the weakness.
Sensory loss of CN 5 is usually due to trauma while vascular damage, tumors, and trauma can
result in damage to the motor aspect of the system.

SIXTH CRANIAL NERVE---ABDUCENS NERVE

The abducens nerve supplies somatic efferent motor fibers to the lateral rectus muscle, which
functions to abduct the eye. As in prior discussions regarding extraocular muscles, having the
patient follow a near target and tracing an "H" pattern tests the abducens nerve. Inability to
abduct the eye indicates a possible deficit. Aneurysms, tumors, meningitis, trauma, and
cavernous sinus pathology are all potential causes of abducens deficits. Loss of CN 6 function
can elicit complaints of horizontal diplopia and may cause patients to appear esotropic.

SEVENTH CRANIAL NERVE---FACIAL NERVE

The facial nerve supplies efferent motor innervation to the muscles of facial expression, and
carries sensory afferent fibers from the anterior two thirds of the tongue for taste. To test the
motor division of the facial nerve, start from the top and work down. First, have the patient
wrinkle the forehead and check for asymmetry (Fig. 10). Next, have the patient shut the eyes
tightly while the examiner attempts to open them (Fig. 11). Note any weakness on one side.
Finally, have the patient show his/her teeth or smile and compare the nasolabial folds on either
side of the face (Fig. 12).

FIGURES 10, 11, and 12. Testing the facial nerve. The patient wrinkles her forehead while
the two sides are compared. Patient tightly shuts eyelids while examiner attempts to pry
open. The two sides are compared. Patient smiles and shows her teeth while the examiner
compares the nasolabial folds on either side.
Bell's palsy is a common lower motor neuron lesion of the facial nucleus or its axon. The result
is facial asymmetry with drooping of the eyebrow, a smooth nasolabial fold, drooping of the
corner of the mouth, and a reduced blink reflex on the affected side.
To test the sensory fibers of the facial nerve, apply sugar, salt, or lemon juice on a cotton swab to
the lateral aspect of each side of the tongue and have the patient identify the taste. Taste is often
tested only when specific pathology of the facial nerve is suspected.

EIGHTH CRANIAL NERVE---VESTIBULOCOCHLEAR NERVE

The eighth cranial nerve carries two special sensory afferent fibers, one for audition (hearing)
and one for vestibular function (balance). The cochlear division of CN 8 is tested by screening
for auditory acuity. This can be done by the examiner lightly rubbing his/her fingers together
next to each of the patient's ears and comparing the left and right side responses.
In addition, the Rinne and Weber tests are easy to perform and can help differentiate conductive
deficits from neurosensory lesions. The Weber test consists of placing a vibrating tuning fork on
the middle of the forehead and asking if the patient feels or hears it best on one side or the other
(Fig. 13). The normal patient will say that it is the same on both sides. The patient with unilateral
neurosensory hearing loss will hear it best in the normal ear, and the patient with unilateral
conductive hearing loss will hear it best in the abnormal ear.

The Rinne test (Fig. 14) consists of comparing bone conduction, assessed by placing the tuning
fork on the mastoid process behind the ear, versus air conduction, assessed by holding the tuning
fork in air near the front of the ear. Normally, air conduction volume is greater than bone
conduction sound volume. For neurosensory hearing loss, air conduction volume is still greater
than bone conduction, but for conduction hearing loss, bone conduction sound volume will be
greater than air conduction volume.

FIGURES 13 and 14. Testing of the vestibulocochlear nerve. The Weber test. The tuning
fork is struck and placed in the middle of the patient's forehead. The patient compares the
loudness on both sides. The Rinne test. A tuning fork is held against the mastoid process
until it can no longer be heard. It is then brought to the ear to evaluate patient response.
Vestibular testing is can be used to assess brainstem function in comatose patients or in patients
who report vertigo/dizziness.
Damage to CN 8 can be caused by trauma, tumors, or infection and can lead to hearing loss,
dizziness, loss of balance, tinnitis, and deafness.
(More information on this topic is provided in another Pacific University On-Line CE course:
Sensory Conflict and Other Causes of Dizziness: Etiology Differential Diagnosis, and
Management by Robert L. Yolton, PhD, OD.)

NINTH CRANIAL NERVE---GLOSSOPHARYNGEAL NERVE

The ninth cranial nerve supplies motor fibers to the parotid gland and the pharynx. It also carries
sensory fibers from the carotid body and taste sensation fibers from the posterior third of the
tongue.
The gag reflex tests both the sensory and motor components of CN 9 and CN 10. This
involuntary reflex is obtained by stroking the back of the pharynx with a tongue depressor and
watching the elevation of the palate (as well as causing the patient to gag).
The motor division of CN 9 and CN 10 is tested by having the patient say "ahh" or "kah" (Fig.
15). The palate should rise symmetrically in the back of the oral cavity (Fig. 16). Paralysis of the
ninth nerve causes a pulling of the uvula to the unaffected side. The ninth, tenth, and eleventh
cranial nerve pathways are physically so close together that isolated lesions are rarely seen.

FIGURES 15 and 16. Testing the glossopharyngeal and vagus nerve. The patient sticks out
her tongue and says "ahh." The palate and uvula should elevate symmetrically without
deviation.

TENTH CRANIAL NERVE---VAGUS NERVE

The vagus nerve carries sensory afferent fibers from the larynx, trachea, esophagus, pharynx, and
abdominal viscera. It also sends efferent motor fibers to the pharynx, tongue, thoracic and
abdominal viscera, and the larynx. Testing of the vagus nerve is performed by the gag reflex and
"ahh" test as described above.
A unilateral lesion affecting the vagus nerve can produce hoarseness and difficulty swallowing
due to a loss of laryngeal function. Causes of unilateral lesions include trauma from surgical
procedures of the neck, aortic aneurysm, and compression due to enlarged paratracheal lymph
nodes caused by metastatic carcinoma.

ELEVENTH CRANIAL NERVE---ACCESSORY NERVE

The accessory nerve carries efferent motor fibers to innervate the sternomastoid and trapezius
muscles. The accessory nerve is tested by asking the patient to shrug the shoulders (trapezius
muscles) and turn the head (sternomastoid muscles) against resistance (Figs. 17 and 18). Palpate
the patient's sternocleidomastoid muscles and feel for tension as the patient attempts to turn
his/her head.

FIGURES 17 and 18. Testing the accessory nerve. Patient is instructed to shrug their
shoulders against resistance. The patient turns her head against the examiner's hand while
the sternomastoid muscle is palpated. The muscle tone on both sides is compared.
Loss of CN 11 function causes a drooping of the ipsilateral shoulder and trapezius on the
affected side. The patient may also have difficulty turning his head to the side opposite the
lesion. Damage usually occurs secondary to surgery or trauma.

TWELFTH CRANIAL NERVE---HYPOGLOSSAL NERVE

The twelfth cranial nerve supplies efferent motor fibers to the muscles of the tongue. To test the
hypoglossal nerve, have the patient stick out their tongue and move it side to side. If there is
unilateral weakness, the protruded tongue will deviate towards the side of the weakness.
Further testing includes moving the tongue right to left against resistance (Fig. 19), or having the
patient say "la, la, la."

FIGURE 19. Testing the hypoglossal nerve. Patient is instructed to stick out the tongue and
then move it laterally against resistance.

Summary of Cranial Nerve Functions

Table 3 summarizes the cranial nerves and their functions.
Cranial Nerve

Innervation

Primary Function(s)

Test(s)

Olfactory

Sensory

Smell

Identify odors

Optic

II

Sensory

Vision

Visual acuity, fields, color,

nerve head

Oculomotor

III

Motor

Upper lid elevation, extraocular eye

movement, pupil constriction,
accommodation

Physiologic "H" and near

point response

Trochlear

IV

Motor

Superior oblique muscle

Physiologic "H"

Trigeminal

Motor

Muscles of mastication

Corneal reflex

Trigeminal

Sensory

Scalp, conjunctiva, teeth

Clench jaw/palpate, light

touch comparison

Abducens

VI

Motor

Lateral rectus muscle

Abduction, physiologic
"H"
Smile, puff cheeks,
wrinkle forehead, pry open
closed lids

Facial

VII

Motor

Muscles of facial expression

Facial

VII

Sensory

Taste-anterior two thirds of tongue

Vestibulocochlear

VIII

Sensory

Hearing and balance

Rinne test for hearing,

Weber test for balance

Glossopharyngeal

IX

Motor

Tongue and pharynx

Gag reflex

Glossopharyngeal

IX

Sensory

Taste-posterior one third of tongue

Vagus

Motor

Pharynx, tongue, larynx, thoracic and

abdominal viscera

Vagus

Sensory

Larynx, trachea, esophagus

Accessory

XI

Motor

Sternomastoid and trapezius muscles

Hypoglossal

XII

Motor

Muscles of tongue

Gag reflex

Shrug, head turn against

resistance
Tongue deviation

Cranial nerve palsies that affect the eye

Cranial Nerve Palsy
Each of the cranial nerve palsies that may result in limitation of eye movement is presented
below.
Fourth Cranial Nerve Palsy
The double vision is vertical, that is, the two images are vertically misaligned and sometimes
tilted.
The causes of fourth cranial nerve palsy are many, but the two most common are head trauma
and a vascular infarct, which is usually secondary to hypertension or diabetes.
The diagnosis is confirmed by evaluating the patient's eye movements in all fields of gaze. The
findings are often subtle, even to the ophthalmologist, but one eye is found to be slightly higher
than the other and improves or worsens in specific head positions. If head trauma appears to be
the cause of the nerve palsy, a CT scan of the brain may be in order if not already completed. In
acquired cases in which diabetes or high blood pressure is present, a CT scan is usually not
necessary unless other neurological abnormalities are present. In congenital fourth cranial nerve
palsy, a CT scan of the brain may or may not be ordered depending on whether the child is
symptomatic or other neurological findings are present. In acquired fourth cranial nerve palsy in
which diabetes or high blood pressure is present, the prognosis is good for recovery of single
vision. The process of resolution, however, may take 6 months or longer. During this period of
time, prisms applied to glasses may be particularly helpful in restoring single vision, at least in
straight-ahead gaze. The prisms are usually of the temporary type, being applied to the surface of
the glasses, and perhaps, requiring different powers every few weeks as the condition resolves.
Alternatively, in adults, a patch may be applied over one eye until resolution if the patient
desires. If double vision persists beyond the sixth month following onset, strabismus surgery
may be indicated in attempt to restore single vision. Young patients with congenital fourth nerve
palsy must be observed for signs of amblyopia (lazy eye), though no other treatment is usually
required.
Sixth Cranial Nerve Palsy
Sixth Cranial Nerve Palsy presents with horizontal double vision, that is, the two images are
horizontally misaligned. Again, the double vision resolves when one eye is closed. In adults, the
cause is usually a vascular infarct (diminished blood flow) of the nerve secondary to underlying
diabetes or high blood pressure. Head trauma may also result in sixth cranial nerve palsy. In
children, the condition usually follows a viral syndrome, though more serious intracranial
inflammatory conditions and tumors must be considered. The diagnosis is usually easily
confirmed by an ophthalmologist after observation of the eye movements in all fields of gaze.
The affected eye will be unable to abduct (turn outwards beyond the midline). In adults with

diabetes or high blood pressure and the sixth nerve palsy is the only other abnormal finding, a
CT scan is usually not necessary. If there are any other concomitant neurological findings, pain,
or a history of cancer, however, a CT scan will usually be obtained. In children, a CT scan is
usually obtained to rule-out intracranial pathology. The prognosis for a full recovery in adults
with diabetes or high blood pressure is good. However, recovery usually takes 3 to 6 months.
Adults may elect to patch the eye to avoid double vision. In many cases, however, a temporary
prism applied to the glasses may help restore single vision. The prism power may need changing
every few weeks as the condition improves. For both children and adults in whom the condition
fails to resolve, strabismus surgery may be considered.

Third Cranial Nerve Palsy

Third Cranial Nerve Palsy usually presents with sudden onset of double vision, which may be
horizontal or vertical in character but disappears when one eye is closed. The eyelid is usually
droopy and there may be significant pain. The cause of this condition is usually also related to
diabetes or hypertension, though much more severe and potentially lethal disorders such as
intracranial aneurysms may be present. The ophthalmologist will make the diagnosis based on
the findings of an eye that moves outwardly but is otherwise largely immobile. Whether the pupil
is involved (an afferent pupillary defect is present) will be heavily relied upon in the
ophthalmologist's algorithm guiding the work-up. All patients who have an involved pupil will
undergo neurological imaging (CT or MRI) while those in whom the pupil is spared (normal)
may or may not undergo neuro-imaging, depending on many other factors, the scope of which is
beyond this site. In patients with pupil-spared third cranial nerve palsies and underlying
cardiovascular risk factors, such as diabetes and hypertension, there will likely be resolution of
symptoms over 3 to 6 months. If not, an initial or repeat neuro-imaging study may be obtained.
Because of the severe limitations of eye movement, prisms applied to the glasses may not be
helpful in restoring single vision. However, the droopy eyelid that often accompanies this
condition may act as occlusion, preventing double vision. Patients with pupil-involved third
cranial nerve palsies will often be hospitalized while an intense evaluation is completed. Patients
will be scheduled for a CT or MRI, "blood work," and perhaps cerebral angiography in young
patients. Treatment of these patients depends on the myriad of potential causes for the third
cranial nerve palsy.

OPHTHALMIC HISTORY
It's important to remember that it's not just the ophthalmic history that is important; the patient's
current medical problem and past medical history are often highly relevant to the ophthalmic
diagnosis.

The structure for the ophthalmic history

Presenting complaint (PC)
The acute nature of the symptoms and duration
Painless loss of vision for 2 weeks
Painful red eye for 3 days with blurred vision and green discharge

History of presenting complaint (HPC)

This sections is used to try and elaborate on the symptoms and identify any associated symptoms
that will help point towards the diagnosis.
Painless loss of vision associated with a headache, painful jaw whilst eating, poor
appetite and weight loss This would suggest temporal arteritis
Painless loss of vision with increased floaters and flashing light for 3 weeks This would
suggest a retinal detachment
Painful eyes after welding in a machine shop yesterday for 3 hours, associated with
increased pain eyes in bright light (Photophobia) and increased watering of eyes
(Increased lacrimation) This would suggest arc eye.

Try to focus on the relevant symptoms to try an establish a diagnosis.

Past ophthalmic history (POH)
Include any relevant previous eye problems for example cataract surgery, glaucoma surgery,
laser for diabetic retinopathy.

Past medical history

Remember to mention any conditions that can affect the eye for example:
Diabetes
Cardiovascular disease eg. Atrial fibrillation which may cause emboli
Hypertension
Multiple sclerosis
Collagen vascular disease

Drug history
Remember certain drugs can affect the eyes:
Steroids
o Predispose to glaucoma and cataracts
Anticoagulants and aspirin
o Predispose to hemorrhaging eg sub conjunctival hemorrhage
Diabetic who recently started insulin
o Diabetic retinopathy can paradoxically worsen if the diabetes is brought under
tighter control.
Amiodarone
o Can deposit within the cornea (Corneal verticilata)
Tamoxifen
o Can deposit within the retina
Chloroquine
o Can cause problems with the macula (Bulls eye maculopathy)
Antihistamines
o May trigger an attack of angle closure glaucoma in susceptible patients
Tri cyclic antidepressants
o
This class of medication including amitriptyline can have several ocular side
effects. They can cause a decrease in tearing, which can lead to dry eye problems.
Patients with narrow angles are at risk of developing acute angle closure
glaucoma.
Cimetidine
o
Can rarely lead to angle closure glaucoma in patients with narrow angles
Chlorpromazine
o
If taken in large dosages can lead to cataracts plus increased pigmentation of the
conjunctiva, cornea, and eyelids and retina.
Ethambutal
o
This agent used in the treatment of tuberculosis can rarely lead to a optic atrophy
(Degeneration of the optic nerve.
Viagra
o Ocular side effects include pupillary dilation, redness, dryness, blurred vision, and
a temporary bluish discoloration to the vision. This drug should be used
cautiously in individuals with retinitis pigmentosa, macular degeneration, and
diabetic retinopathy. Some cases of vision loss secondary to an ischemic optic
neuropathy have also been reported.

*Remember to document any drug allergies*

Family history and social history

Smoking
o Nicotine itself probably does not cause ocular damage. However, other chemicals
found in smoked tobacco materials have been shown to lead to ocular
complications
o

Cataract. Studies have proven that smoking tobacco increases the risk of cataract
formation in men, and increases the risk of cataract surgery in women.

Macular degeneration. Studies have shown that smoking tobacco increases the
risk for macular degeneration in men and women.

Vascular disease. Smoking tobacco is known to contribute to arteriosclerosis, or

hardening of the arteries, along with high cholesterol and hypertension. This
arteriosclerosis may contribute to vascular problems of the eye such as vein
occlusions, artery occlusions, and optic nerve damage.

Nutritional optic nerve degeneration. Tobacco is often implicated along with

alcohol (in combination) as to causing a nutritional degeneration of the optic
nerve. "Tobacco alcohol optic neuropathy"

Note Alcohol consumption in units per week

Document any conditions that may be inherited:

Glaucoma
Squint

Other conditions for example

o

Optic atrophy

Retinitis pigmentosa

OPHTHALMIC EXAMINATION
"The eye has been described as the window of the soul"
It is possible to diagnose several medical conditions from AIDS to Zoonoses*
* Zoonoses are diseases that can be spread from animals to humans under natural conditions.
These diseases can include any type of organism, for example, viruses, bacteria, parasites, and
prions. Zoonotic diseases may be spread directly from animals to people, or indirectly through
the environment or vectors such as ticks, mosquitoes, flies, etc

As a medical student you will not be required to perform a detailed

examination of the eye with a slit lamp. You should however be familiar
with the following examination techniques:
Visual acuity
Always make an attempt to measure the visual acuity of each eye separately. You may not have a
full size Snellen chart on the ward, but many pocket clinical handbooks have reduced Snellen
charts that are held at one third of a metre, making them easy to use. If a Snellen chart is not
available, then an assessment of the ability to read standard newspaper print gives an estimate of
near visual acuity. Next, measure the acuity through a pinhole, which can be made by sticking a
pin through a piece of cardboard. Testing with a pinhole is important, as a reduction in vision
with the pinhole can be a sign of ophthalmic pathology rather than a refractive error (the patient
requires distance glasses).
Colour vision
Colour vision is important to assess as it is a sensitive indicator of the function of the optic nerve.
Acquired defects of colour vision can be roughly determined by comparing the depth of colour
of a red target between the two eyes. Hold the target in front of a white background and ask the
patient to look at it with each eye separately. A "duller red" with one eye suggests optic nerve
damage, even though the patient may have good acuity in that eye.
Visual fields
Test the fields by confrontation. You do not need lots of hatpins to do this. Initially, assess for
gross homonymous defects by sitting 1 metre away from the patient. Ask him or her to look at
your nose. Hold one finger of each hand in the superior quadrants and make a small movement
with one finger. Ask the patient to point towards the movement. Repeat with the other finger and

then both fingers together. Assess the inferior quadrant by repeating the process. A normal
response should exclude gross homonymous hemianopia.
Eye movements
The patient may complain of diplopia in varying positions of gaze. Try to establish whether the
diplopia is monocular or binocular by asking the patient to fixate on an object and then covering
one eye. If the diplopia disappears it is true binocular diplopia; if it remains it is monocular.
Repeat this for the other eye. Assess the extraocular movements by asking the patient to follow a
target held 1 metre directly in front of him/her. Slowly move the target in an "H" shape, keeping
it vertical when moving to the left and right, and horizontal when moving up and down.
Pupils
The pupils are often just examined for their reaction to light and accommodation, and "PERLA"
written in the notes. Many other visible signs can give valuable information.

Look at the size and shape of the pupils and the iris.
A difference in iris colour (heterochromia) may be a sign of inflammation, tumour, or congenital
Horner's syndrome.

The pupil may have an odd shape; causes include posterior synechiae where the iris sticks to the
lens due to inflammation, as sometimes seen in anterior uveitis. Ocular trauma or recent surgery
may also lead to an irregularly shaped pupil, illustrating the importance of the history.

Variation in pupil size between the two eyes (anisocoria) may indicate neurological pathology.

Neuro- ophthalmic signs are important to elicit; examples include Horner's syndrome, where
there is a small pupil and a mild ptosis, and a third nerve palsy, where the pupil may be dilated
with a mild or complete ptosis.

Test the pupil's reactions.

Ask the patient to fix on a distant object (to avoid the accommodation reflex that causes
constriction of the pupil).

Shine a pen torch into one eye and assess if the pupil constricts.

Then repeat this in the other eye.

Observe for the direct and consensual response.

Of more significance is the "swinging flashlight" test used to identify a relative afferent pupillary
defect (RAPD).
o

Ask the patient to fixate on an object in the distance, and then direct a bright light to one
eye. Move the light quickly to the other eye and repeat the process, swinging the light
from eye to eye.

A normal reaction would be a brisk pupil constriction of the stimulated eye; as the light is
moved to the fellow eye it should constrict (or stay constricted).

If it dilates rather than constricts, this is known as an RAPD. A positive finding is a

strong indicator of retinal or optic nerve pathology.

External eye examination

It's easiest to be systematic and work from the front to back.

The ophthalmoscope can be used as a magnifying glass by setting the dioptric

power to +10

Eyelids
o

Erythema (Cellulitis/Blepharitis)

Swelling (Chalazion)

Position of the lids (Ptosis)

Conjunctiva
o

The appearance of the skin

It looks red (injected),

Diffuse redness (Conjunctivitis)

Localised pattern (Episcleritis)

Around the iris (Iritis)

Look for evidence of discharge (Conjunctivitis)

Cornea
o

Corneal oedema - Glaucoma

Corneal abrasion/ulcer

Corneal foreign body

Lens
o

Cataract

Subluxed/Dislocated (Trauma, Marfans syndrome, Homocystinuria)

Vitreous (Assessed with use of ophthalmoscope by checking the red reflex)

o

Opacity (Persistent primary hyperplastic vitreous)

Blood (Vitreous hemorrhage)

Ophthalmoscopy

Becoming comfortable with the ophthalmoscope and the close proximity between you
and the patient takes time. Before attempting to get a view of the retina and disc (fundus),
stand at arm's length from the patient and shine the light from the ophthalmoscope into
the pupil. You should see a yellow/orange
glow known as the red reflex; this represents the reflection from the fundus. If you do
not see this, it means there is an opacity in the lens, vitreous, or cornea. The commonest
cause is acquired cataract, but other ocular pathology can also be responsible. If there is
no red reflex, no fundal view will be possible.
If you do get a red reflex, move in closer and try to get a view of the disc. If you are
having trouble locating it, "track" on to a retinal vessel, and follow it back; it should lead
to the disc. If it seems out of focus, turn the lens dial up or down until the image is clear.
Examine the disc, then the retina, moving your head around and asking the patient to
look in different directions to improve the view of the periphery.
Complete the examination by asking the patient to look directly into the light; this
should give a view of the macula.

Pupil assessment and abnormalities

Pupil Evaluation

The pupils function is to control the amount of light entering the eyes, providing the best
visual function under varying degrees of light intensity.

The normal diameter of a pupil is 3 to 4 mm under average lighting conditions. In dim

lighting the pupil size is larger and in bright light it is smaller.

Pupils are usually larger in children and smaller in the elderly. Twenty percent of fibers
in the optic tract are for pupillary function.

Changes of the pupil in accomodation

o

The pupil changes when focusing on near objects. With accommodative effort, a
near synkinesis is evoked, including increased accommodation of the lens,
convergence of the visual axes of the eyes and pupillary constriction or miosis.

How to accurately assess the pupils

The testing conditions for evaluating pupils include:

Evaluate pupils in dim illumination

Have the patient fixate at a distance (eliminates miosis from accomodation)

Use bright light source

Note size of pupils before assessing the responses look for anisocoria (unequal pupil size)
and corectopia (irregular shaped pupil)

Direct light response

In watching the eye receiving the direct light, you can then determine the direct
response by:

Shining the penlight directly in the right, look at the response including speed of
response note (brisk, sluggish)

Repeating for the opposite eye

If the pupils are normal, they will react equally to the direct light.

Indirect light response

Placing the penlight in front of the right eye (OD) The examiner watches the left
eye for a consensual response. In a normal eye the pupils should constrict

Lesions of the parasympathetic system cause a dilated pupil

Acute third nerve palsy
May signal compression of the third nerve due to a posterior communicating artery aneurysm.
A third nerve palsy will be usually associated with other signs of dysfunction including ocular
motility disturbances and ptosis.
o
An isolated dilated pupil does not usually signify a III nerve palsy.

Tonic pupil or Adie's pupil

o Characterized by a dilated pupil with very poor or no light reaction with tonic
constriction to
o near and tonic redilation.
o that cause pupillary constriction to bright light and accomodation).
o Under the slit lamp sectoral palsies of pupillary sphincter may be seen with light
stimulation. Because the abnormality is post-ganglionic (that is, damage to the ciliary
ganglion), one can demonstrate supersensitivity of the sphincter muscle to pilocarpine 1/10%.
Adie's syndrome

consists of a tonic pupil and loss of deep tendon reflexes. The lesion causing pupillary
dysfunction is generally thought to be in the ciliary ganglion and the cause is basically
unknown

o Caused by damage to peripheral pathways to the pupil (parasympathetic neurons in the

ciliary ganglion

Argyll Robertson pupils

o Bilateral small pupils that constrict when the patient focuses on a near object, but do not
constrict when exposed to bright light (they do not react to light). They were formerly known
as "prostitute's pupils" because of their association with syphilis and because, like a prostitute,
they accommodate but do not react.
o The primary lesion is thought to be caused by damage to central pathways for pupillary
constriction. Specifically caused by selective damage to pathways from the retina to the EdingerWestphal nucleus. These light-sensitive pathways allow the pupil to constrict to bright light. The
accommodation pathways (pathways to the Edinger-Westphal nucleus that cause the pupils to
constrict with near vision) are thought to be spared because of their more ventral course in the
brainstem.
o They are a highly specific sign of neurosyphilis.
o Pupils that accommodate to near objects but do not react to light are said to show lightnear dissociation.

Lesions of the sympathetic system cause a small pupil

Horner's Syndrome

Horner's Syndrome, consists of pupillary miosis which is more accentuated in darkness.

Light and near reactions are intact.

There is ipsilateral ptosis due to paresis of Muller's muscle (not the levator muscle of the
eyelid)

There is an pseudo enophthalmos because of the associated ptosis.

Occasionally anhydrosis of the face will also be seen.

Pharmacologic testing, to confirm the diagnosis of a Horner's syndrome:

o
o

Cocaine test (Diagnose horners as a cause of miosis, however cannot distinguish

preganglionic from post ganglionic)
10% cocaine is instilled into the eye

The cocaine prevents the re-uptake of norepinephrine into the normal nerve and
hence the norepinephrine will cause dilation of the pupil

If there is a lesion anywhere along the sympathetic pathway, there will be less
norepinephrine coming down the nerve to be released

COCAINE will NOT DILATE the eye with a sympathetic defect (Horners
syndrome)!!!

Hydroxyamphetamine test (Differentiate between preganglionic and

postganglionic horners)
o

To localize whether the Horner's syndrome is preganglionic (that is before the superior
cervical ganglion) or postganglionic (after the cervical ganglion). Hydroxyamphetamine
(Paredrine) is instilled into both eyes
Hydroxyamphetamine actively releases norepinephrine from the nerve endings. If the
lesion is preganglionic, there will be normal norepinephrine store present at the iris and
therefore the pupil dilates.

A dilation to Hydroxyamphetamine in a Horner's eye means the lesion is preganglionic.

If the pupil does not dilate, the lesion is postganglionic because there is no
norepinephrine to be released.

Parinaud syndrome:

Another cause of light-near dissociation is Parinaud syndrome, also called dorsal

midbrain syndrome

This uncommon syndrome involves vertical gaze palsy associated with pupils that
accommodate but do not react.

The causes of Parinaud syndrome include:

Brain tumors (pinealomas)

Multiple sclerosis

Brainstem infarction.

Pupillary light reflex

Pathway for the pupillary light reflex:

When light first enters the eye, the light reflexes are mediated through axons from ganglion cells
in the retina.
These impulses pass back in the optic nerve and decussate in the chiasm with the other visual
fibers.

Pupillary fibers then leave the optic tract just before the lateral geniculate body, synapse at the
pretectal area of the midbrain and then synapse bilaterally with the Edinger-Westphal nuclei.

The impulse then leaves the midbrain via the third cranial nerve to the ciliary ganglion, (Located
within the muscle cone behind the eyeball).

After synapsing in the ciliary ganglia, the post-ganglionic fibers innervate the pupillary sphincter
muscles to constrict the pupils.

Figure 1

Figure 2
Figures 1 and 2 highlight the pathway for the pupillary light reflex.

Stimulation of one eye by a bright light produces an equal constricting response in both eyes due
to the direct and consensual light reflexes.
Transfer of the light to the fellow eye will maintain the same constriction and tone on this pupil.
However, if an asymmetrical lesion in the pathway on one side exists, the light transfers from the
good eye to the bad eye, which results in less neuronal stimulation of the E-W nucleus from that
eye and a comparative dilation of both pupils, and vice versa.
This is seen as an alternating constriction and dilation of each pupil as the light is swung from
eye to eye.
A relative afferent pupillary defect (RAPD) or optic disk pallor, are the only objective
clinical signs of disease of the afferent visual system.

Relative afferent pupillary defect

Assessment of RAPD (Relative afferent pupillary defect)
For assessing the indirect response, utilize the swinging flashlight test by
Placing the penlight in front of the right eye (OD) The examiner initially watches the Right eye
for a direct response and the left eye for a consensual response. Both pupils should constrict
The light should then be swung to the left eye (OS).
The normal pupil will constrict to the direct light as the light swings back and forth, and the normal pupil
will also constrict to indirect light, having a consensual response. RAPD constricts to consensual light and
not to direct light.
Next repeat the above starting with the left eye and swinging to the right eye.

Abnormalities of the Pupil and Their Characteristics

Relative Afferent Pupillary Defect (RAPD) also referred to as APD and Marcus-Gunn Pupil
Objective sign of an asymmetrical lesion of the anterior visual pathway (retina, optic nerve, chiasm or
optic tract) seen with major retinal lesions or neurological lesions of the anterior visual pathway.

The presence of a RAPD and the absence of gross ocular disease indicate a neurological lesion in the
anterior visual pathway and the importance of this physical sign cannot be over emphasized.

Grading Scale: RAPD

Grade 1+:
Grade 2+:
Grade 3+:
Grade 4+:

A weak initial pupillary constriction followed by greater redilation

An initial pupillary stall followed by greater redilation
An immediate pupillary dilation
No reaction to light Amaurotic pupil

Conditions associated with an RAPD

A) Unilateral optic nerve diseases:
i) Anterior ischemic optic neuropathy:
ii) Arteritic (Giant Cell Arteritis) and Non-arteritic
iii) Optic neuritis
iv) Compressive optic neuropathy:
a) Optic nerve tumor
b) Traumatic optic neuropathy
c) Asymmetric glaucoma
d) Homonymous hemianopsia (Lesions involving pupillary pathway)
B) Retinal conditions:
i) Central retinal arterial occlusion
ii) Branch retinal arterial occlusion
iii) Ischemic central retinal vein occlusion
iv) Retinal detachment, greater RAPD if involving macula
.

Amblyopia
What is amblyopia?
A common vision problem in children is amblyopia, or "lazy eye." It is so common that it is the
reason for more vision loss in children than all other causes put together.
Amblyopia is a decrease in the childs vision that can happen even when there is no problem
with the structure of the eye. The decrease in vision results when one or both eyes send a blurry
image to the brain. The brain then learns to only see blurry with that eye, even when glasses
are used. Only children can get amblyopia. If it is not treated, it can cause permanent loss of
vision.

There are three main causes for amblyopia:

There are several different types and causes of amblyopia: Strabismic amblyopia, deprivation
amblyopia, and refractive amblyopia. The end result of all forms of amblyopia is reduced vision
in the affected eye(s).

Strabismic amblyopia develops when the eyes are not straight. One eye may turn in, out,
up or down. When this happens, the brain turns off the eye that is not straight and the
vision subsequently drops in that eye.

Deprivation amblyopia develops when cataracts or similar conditions deprive young

childrens eyes of visual experience. If not treated very early, these children can have
very poor vision. Sometimes this kind of amblyopia can affect both eyes.

Refractive amblyopia happens when there is a large or unequal amount of refractive error
(very short or long sighted). Usually the brain will "turn off" the eye that has more
farsightedness or more astigmatism.

Treatment of amblyopia
Early treatment is always best. If necessary, children with refractive errors (nearsightedness,
farsightedness or astigmatism) can wear glasses or contact lenses when they are as young as one
week old.
Children with cataracts or other amblyogenic conditions are usually treated promptly in order
to minimize the development of amblyopia.
One of the most important treatments of amblyopia is correcting the refractive error with
consistent use of glasses and/or contact lenses.
Other mainstays of amblyopia treatment are to enable as clear an image as possible (for example,
by removing a cataract), and forcing the child to use the nondominant eye (via patching or
eyedrops to blur the better-seeing eye)

Figure A child wearing a patch

Patching should only be done if an ophthalmologist recommends it. An ophthalmologist should
regularly check how the patch is affecting the childs vision. Although it can be hard to do,
patching usually works very well if started early enough and if the parents and child follow the
patching instructions carefully. It is important to patch the dominant eye to allow the weak eye to
get stronger.

Figure A common design for eye patch - "Band-Aid"

Are there different types of patches?

The classic patch is an adhesive "Band-Aid" which is applied directly to the skin around the eye.
These may be available in different sizes for younger and older children.

Is there an alternative to patching to treat amblyopia?

Sometimes the stronger (good) eye can be penalized or blurred to help the weaker eye get
stronger.

Blurring the vision in the good eye with Atropine eye drops or with extra power in the
glasses will penalize the good eye. This forces the child to use the weaker eye.

What happens if amblyopia treatment does not work?

In some cases, treatment for amblyopia may not succeed in substantially improving
vision. It is hard to decide to stop treatment, but sometimes it is best for both the
child and the family. Children who have amblyopia in one eye and good vision only
in their other eye can wear safety glasses and sports goggles to protect the normal
eye from injury.

Assessment of a child with a squint

Clinical Evaluation

History:
Take a full history identify risk factors:

Family history of squint

Intrauterine infections

Prematurity

Birth trauma

Previous ocular history

Examination:
Visual Acuity
Visual acuity improves with age. All children over age 8 should be able to achieve 20/20 visual
acuity using their best eyeglass correction. Younger children should be referred to an
ophthalmologist if there is a difference between the right and left eyes of two or more lines on a
Snellen chart evaluation.

Figure 1 a) Allen object recognition posters and tumbling E" chart. Both used to assess vision in
children.

Visual screening begins with assessment of visual acuity. The testing method varies,
depending on age.
By five months of age, infants should regard faces or interesting objects with steady,
conjugate gaze through all fields of vision.

Toddlers with some speech skills can use Allen object recognition posters, which present
a series of simple, idealized pictures.

Recognition of each picture at 10 ft (3 m) is roughly equivalent to 20/30 vision.

Children aged three and older can usually perform the "tumbling E" game, in which the
child indicates the cross-bar direction of a series of progressively smaller "E's" presented
with varying orientation.

For children in kindergarten or first grade, the Snellen letter or number charts represent
the gold standard for in-office assessment of visual acuity. Children usually stand 10 ft (3
m) away from the visual chart to minimize the distraction that may occur in a busy office.

Tolerance to occlusion of one eye and intolerance to occlusion of the other may suggest a
significant difference in visual acuity between eyes.

Binocular Alignment
Once visual acuity is established, assessment of binocular alignment is the next step.

In young infants, strabismus must be differentiated from the more common

pseudostrabismus, in which the perception of medial deviation or esotropia is caused by

prominent medial canthal folds and a flat nasal bridge.

Hirschberg corneal light reflex test

The most common method of assessing ocular alignment is the Hirschberg corneal light reflex
test.

Figure 2 Findings during Hirschberg corneal light reflex test. (A) Normal alignment: the light reflections are
centered on both corneas. (B) Left esotropia: the light reflection is outwardly displaced on the left cornea. (C) Left

exotropia: the light reflection is inwardly displaced on the left cornea. (D) Left hypertropia: the light reflection is
downwardly displaced on the left cornea.

In this test, the examiner notes the position of the corneal reflection from a light held
about 3 ft (1 m) from both eyes.
The reflection should fall in the same location in the cornea of each eye, even when the
eyes move.
Displacement of the corneal light reflection in one eye suggests strabismus.

Cover-uncover test and the alternating cover test

The second screening method for evaluating ocular alignment is a combination of the coveruncover test and the alternating cover test.
The cover-uncover test:

the child first focuses on an object about 10 ft (3 m) away. An interesting object such as a
small toy usually holds the child's attention.
The examiner covers one eye with a hand-held occluder or cupped hand, while watching
the other eye for any movement of fixation. (COVER TEST)

The examiner then removes the cover to see if the first eye has deviated. (UNCOVER
TEST)

If no movement is elicited on the cover-uncover test, the alternating cover test is

performed. This will identify the presence of a manifest squint (Tropia)

The alternating cover test:

Again with the child focused on a distant object, each eye is covered in sequence, while
the examiner looks for ocular deviation. This will identify the presence of a latent squint
(Phoria)
A squint that is only present when the eye with the phoria is covered by the occluder and
binocular vision (Vision with both eyes) is lost.

Figure 3 Exophoria is detected by the following procedure:

(top) One eye is covered. That eye will deviate outward.
(bottom) When the cover is removed, it will return to a central position. In this example, the
patient has a left exophoria. The same procedure is then performed on the other eye.

Figure 4 Esophoria is detected by the following procedure:

(top) One eye is covered. That eye will deviate inward.
(bottom) When the cover is removed, that eye will return to a central position. In this example,
the patient has a left esophoria. The same procedure is then performed on the other eye.

Figure 5 Hyperphoria is detected by the following procedure:

(top) One eye is covered. That eye will deviate upward.
(bottom) When the cover is removed, the eye will return to a central position. In this example,
the patient has a left hyperphoria. The same procedure is then performed on the other eye.

Cycloplegic refraction and Retinal Examination:

Dilation with a mydriatic agent that can paralyse the ciliary body (Preventing accomodation) for
example like atropine 1% or Cyclopentolate 1% will aalow for retinoscopy to estimate the
refractive error. percent may aid in the retinal examination. The clinician should then perform
retinoscopy, looking for intraocular pathology such as retinoblastoma.

Mx OF A CHILD WITH A SQUINT

The following basic principles are used to manage children with a squint:

Perform a dilated fundal examination to exclude possible causes of poor vision. eg

Cataract, Retinoblastoma
Correct any refractive error with spectacles or contact lens

Treat any underlying causes of poor vision, for example removal of cataract

Treat any existing amblyopia with patching of the unaffected eye

Consider surgical correction of squint by reposition the extraocular muscles. Provided the
squint is stable and there is no diplopia (Double vision) when both eyes are aligned

The child with a squint

What is Strabismus?
Strabismus is derived from the Greek word to squint.
Strabismus may be classified as:

unilateral

bilateral

alternating

This is based on whether one eye or both eyes are affected.

A unilateral strabismus will consistently have the same eye this is misaligned
Bilateral strabismus is a condition where both eyes are squinting at the same time; either
convergently or divergently (both are subtypes of Concomitant strabismus).
Finally, an alternating strabismic patient can fixate on a target object with either eye. In this case
either eye may be askew while the opposite eye is focused on the target.

We may also describe a squint based on the direction of gaze for the squinting eye:

Esotropia Turning inwards (Nasally)

Exotropia Turning outwards (Temporally)

Hypertropia Turning upwards

Hypotropia Turning downwards

aralytic (Non concomitant) vs Non Paralytic (Concomitant)?

Paralytic Squint:
One of the muscle attached to the eyes is paralyzed and the eye affected may turn in/out/up/down
depending on the muscle involved i.e. the eye movement is restricted in the direction of the
action of the paralyzed muscle. This can be caused by direct trauma to the muscle as for e.g.
injury during forceps delivery or any other injury. It may also be caused by certain nerve palsies,
which in turn may be caused by peripheral neuritis or diseases of the CNS, e.g. meningitis,
encephalitis etc.
"THE ANGLE OF MISALIGNMENT BETWEEN THE TWO EYES VARIES
DEPENDING ON THE POSITION OF GAZE"
Non Paralytic Squint: A loss of coordination between the muscles of the two eyes leads to
misalignment. This misalignment may be the same in all direction of gaze, or in some conditions
the misalignment may be more in one direction of gaze.
"THE ANGLE OF MISALIGNMENT BETWEEN THE TWO EYES IS CONSTANT"

What is pseudostrabismus?
Pseudostrabismus is the false appearance of strabismus. It generally occurs in infants and
toddlers and is associated with flat nasal bridge, prominent epicanthal folds, narrow
interpupillary distance.With age, the bridge of the child's nose narrows and the folds in the
corner of the eyes go away. To detect the difference between pseudostrabismus and strabismus, a
Hirschberg test may be used.

What is the cover-uncover test?

The cover-uncover test to diagnose various types of tropias, which is a medical term for
strabismus.

Figure 1 A child with a left exotropia is seen to staighten the left eye when the right eye is
covered "A cover test"

Phoria vs. Tropia

A phoria is a tendency for one eye to drift which is only noted when that eye is covered. The eye drifts out of
position behind the cover but immediately returns to the normal position as soon as the cover is removed and the
patient is allowed to use binocular (both eyes together) vision. A misalignment which is only brought out under
such circumstances is called latent.

A tropia is a deviation which is there all of the time. It is manifest. No cover test is necessary.

Risks of strabismus
Untreated strabismus can result in the favouring of one eye over the other. This results in
laziness of the vision in one eye, which is referred to as amblyopia.
However, strabismus does not seem to make children perform more poorly in school or
sports. The brain of a child automatically turns off and rewires the vision in the misaligned
eye so that the child has no sense that one eye is turned. Therefore, the child with strabismus
does not have double vision (diplopia). Rather they are using one eye at a time. It is the risk
for amblyopia that causes us to recommend treatment.

Causes of strabismus
There are five major reasons for strabismus.
Restrictive

strabismus, the eye is unable to move in one or more directions because it is

physically stuck. This might be seen after an orbital bone fracture (blowout fracture)
when a patient cannot look up because the tissues below the eye are stuck in the
fracture and the eye cant be pulled up by the elevating muscles. "Paralytic squint"

Paretic

strabismus. This occurs when one muscle is weak due to innervational reasons.
An example would be a 3rd, 4th or 6th nerve palsy. "Paralytic squint"

Myopathy

affecting the extraocular muscles for eg Myositis

The

most common cause of strabismus occurs without restriction or paresis. In these

patients, the eyes can move normally in all directions. However, there is misalignment
either because there is an unexplained eye muscle imbalance such that the brain and
muscles are unable to keep the eyes straight. An example would be congenital
esotropia. "Non Paralytic squint"

Strabismus

due to poor vision in one eye is a subtype called sensory

strabismus. An example would be following vision loss from a
retinoblastoma. "Paralytic squint"

Causes of Red Eye

Eye inspection may give clues to the cause

Figure 1 Schematic diagram illustrating some causes of a red eye.

Note the nature of the red eyes i.e. localized or diffuse redness
o Conjunctivitis has clearly defined vessels that covers the entire sclera
o

Episcleritis and scleritis have larger blood shot vessels and are concentrated
towards the cornea

Iritis has a parallel arrangement of vessels around the periphery of the cornea that
are not clearly defined

Subconjunctival hemorrhage is a beefy red localized hemorrhage with a definite

margin

If pain is present and is relieved by local anesthetic drops, this suggests a surface problem
such as a corneal abrasion, corneal foreign body or corneal ulcer

Pain and photophobia are not typical features of a primary conjunctival inflammatory
process. If these features are present, the physician should consider more serious
underlying ocular or orbital disease processes, including uveitis, keratitis, acute glaucoma
and orbital cellulitis.
If eye pain is unrelieved by the anesthetic drops, a deeper problem must be suspected
such as iritis

View iris for any irregularity:

Intraocular foreign body - Irregular pupil

Acute angle closure glaucoma - Mid dilated pupil

Iritis - Miosis (Small pupil), irregular pupil due to the presence of posterior
synchiae

Stain the surface of the eye with fluorescein eye drops:

o

View the cornea for any corneal abrasion,ulcer or foreign bodies

Note any dendritic (branching) ulceration typical of herpes simplex infection

Evert the eyelids:

o

Foreign bodies eg Sub Tarsal foreign

Follicles eg viral infection

Large papillae eg vernal allergic conjunctivitis

If discharge is very acute or severe, if infection is prolonged or infection is in neonates.

Examination for enlarged lymph nodes just in front of the ears (pre-auricular) characteristic of viral conjunctivitis. (Adenoviral keratoconjunctivitis)

Tonometry (measure of the eye pressure) - if suspect acute or rubreotic glaucoma

Allergic conjunctivitis
Allergic conjunctivitis may be divided into 5 major subcategories.
Seasonal allergic conjunctivitis (SAC) and perennial allergic conjunctivitis (PAC) are commonly
grouped together.
Vernal keratoconjunctivitis (VKC)
Atopic keratoconjunctivitis (AKC)
Giant papillary conjunctivitis (GPC)
Allergic responses are the immune system's overreaction to foreign substances known as
immunogens or allergens.

Figure Mechanism of Type 1 hypersensitivity reaction

Figure Mast cell degranulation

The classic symptoms are ocular itching with mucoid discharge.

Treatment includes the use of ocular anti histamine agents for example Patanol and Ocular
lubricants for example Systane. Occasionally steroids may have to used however these have be
used cautiously to avoid the long term side effects (Cataracts, Glaucoma and secondary
infections)

Pathophysiology:
Seasonal and perennial allergic conjunctivitis
Since conjunctiva is a mucosal surface similar to the nasal mucosa, the same allergens that
trigger allergic rhinitis may be involved in the pathogenesis of allergic conjunctivitis.
Common airborne antigens including pollen, grass, and weeds may provoke the symptoms of
acute allergic conjunctivitis
Ocular itching
Redness
Burning
Tearing.

Figure Seasonal allergic conjunctivitis

Main distinction between seasonal and perennial allergic conjunctivitis, as implied by the name,
is the timing of symptoms.
SAC patients typically have symptoms of acute allergic conjunctivitis for a defined period of
time
In spring when the predominant airborne allergen is tree pollen
In summer when the predominant allergen is grass pollen
in fall when the predominant allergen is weed pollen.
Typically, persons with SAC are symptom-free during the winter months in cooler climates
because of the decreased airborne transmission of these allergens.
PAC patients may have symptoms that last the whole year; thus, PAC may not be caused
exclusively by seasonal allergens, although, they may play a role.

Other common household allergens such as dust mite, cockroaches, and pet dander may be
responsible for the symptoms of PAC.

Vernal keratoconjunctivitis
VKC is a chronic bilateral inflammation of the conjunctiva, commonly associated with a
personal and/or family history of atopy.
The key component of the vernal ocular allergic response is the eosinophil. Vernal conjunctivitis,
which is IgE-mediated, is the only ocular disease to involve solely Type I hypersensitivity.
Symptoms often include severe itching with thick, ropy discharge.
In most cases, patients have a history of allergies or infantile eczema.
The important clinical signs include large conjunctival papillae on the back of the superior tarsus

Figure Papillae
Raised Horner-Trantas dots (gelatinous, white clumps of degenerated eosinophils usually located
at the superior limbus)

Figure Trantas spots

Areas of superficial punctate keratitis (SPK) and,
In severe cases, well-demarcated, sterile corneal shield ulcers, located superiorly.

Figure Shield ulcer

You can differentiate VKC from atopic keratoconjunctivitis (AKC) based on age, location,
dermatitis and lack of seasonal variability.
More than 90% of patients with VKC exhibit one or more atopic conditions such as:
Asthma
Eczema
Seasonal allergic rhinitis.

Atopic keratoconjunctivitis
AKC is a bilateral inflammation of conjunctiva and eyelids, which has a strong association with
atopic dermatitis
It is also a type I hypersensitivity disorder with many similarities to VKC
Association between atopic dermatitis and AKC

Giant papillary conjunctivitis

GPC is an immune-mediated inflammatory disorder of superior tarsal conjunctiva.
As the name implies, the primary finding is the presence of "giant" papillae, which are typically
greater than 0.3 mm in diameter.
It is believed that GPC represents an immunologic reaction to a variety of foreign bodies, which
may cause prolonged mechanical irritation to the superior tarsal conjunctiva. exapmles of
irritants that may precipitate GPC include:
Contact lenses (hard and soft) are the most common irritant
Ocular prostheses
Extruded scleral buckles
Exposed sutures following previous surgical intervention .

Figure The upper lid has been inverted exposing the superior tarsus and the giant papillae

Important facts
Frequency: In the US: Allergic conjunctivitis occurs very frequently and is seen most commonly
in areas with high seasonal allergens
Mortality/Morbidity: Allergic conjunctivitis rarely causes any visual loss
Race: VKC occurs predominantly in areas with tropical and temperate climates such as the
Mediterranean, the Middle East, and Africa
The limbal form of VKC commonly occurs in persons of African and Indian descent.
Sex: VKC has a significant male preponderance
Age: VKC typically affects young males with onset generally in the first decade and duration up
to one decade. Its symptoms usually peak prior to the onset of puberty and then subside

Management
Establish the diagnosis - Itching is a pathognomonic symptom for allergy.
A family history of atopy is common.
Advise patients to avoid rubbing their eyes, as this is a mechanical stimulus for mast cell
degranulation and histamine release. Instead, have the patient use cool compresses to relieve
itching and swelling.
Recommend frequent instillation of preservative-free ocular lubricants.These lubricants are
beneficial in flushing allergens and cytokines away from the ocular surface.
Prescribe antihistamine/mast cell stabilizers. These are an effective first line of treatment eg
Patanol
Look for corneal involvement.
Corneal involvement is an indication of the severity of the disease and the inflammatory
response. Patients with shield ulcers should receive additional treatment involving cycloplegia
for pain relief, atropine 1% and topical antibiotic drops eg Vigamox