College of Medicine and Health Science,

Department of Optometry

Refractive Effects of Ocular Disorders

Moderator:- Mr. Dereje Hailu (BSc, MSc).

By:- Bekalu G.( MSc 2nd )1
 Outline
Introduction
Ocular disorders that induce myopic change

Ocular conditions that lead to hyperopic shift

Induced astigmatism

Reference

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 Objective

• After this seminar presentation, we will:-

 Identify the type of refractive changes and their
management that will occur as a result of different
ocular disorders

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 Introduction
 The refractive status of the eye
 Tells whether the patient has an ocular or systemic abnormality,
even a life-threatening disease.
 Different ocular and systemic conditions induce refractive changes
in the eye
 Both a thorough history and a thorough examination are required
to provide the clues for the most likely differential diagnoses.
 Most of the induced refractive changes will spontaneously resolve
after treating the ocular &/or systemic disorder.
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 Induced myopia
Accommodative spasm
Caused by over stimulation of PNS, due to sustained near
demand that results hyper tonicity of CB
Can be functional or psychogenic
May be associated with fatigue
Results pseudo myopia

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 Clinical manifestations
 Low NRA
 Poor distance vision
 Significant reduction in myopia
 Variable VA findings
under cycloplegia
 Variable static and subjective
 Esophoria @near and possibly
RX
@distance
 Fails Monoc and Binoc AF with
 Fluctuating ret reflex
plus lenses
 Over minus acceptance
 Low degree of against the rule
 SNR
cyl

 Low MEM

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Management
Plus lenses for distance and near
Minus lenses for distance with near add

Referral to psychologist, psychiatrist or social worker

 placebo spectacles may help

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CL Induced corneal edema

 CL wear may induce refractive changes during immediate post wear

 Mainly in PMMA and soft CL wearers hypoxia
corneal edema corneal steepening induced myopia
 Changes in posterior corneal surface, corneal thickness, corneal index
& A/C depth may contribute to myopic change
 Patients will be asymptomatic or have significant symptoms

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Clinical features

 Excessive spectacle blur

 Inability to wear spectacle

after CL removal

 Lens intolerance
 Central corneal clouding,
 Reduced VA
 Steep K reading & corneal
 Myopia on over refraction
distortion 9
Management
 Updating the Rx if mild (-0.25 to -1.00Ds) and no corneal
distortion or excessive interruption
 Refit the CL if significant induced myopia with corneal distortion
 Patient education about
 Wearing time

 Regular follow up care

 Discontinue CL in severe cases

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Nuclear sclerosis
 Results myopic shift(≥-0.50Ds) due to “n” increment caused by
condensation of the lens proteins and a loss of water
 Pesudovs and Elliott" reported that 50% of their 22 patients with
clinical nuclear sclerosis had a myopic shift.
 More common in 6th , 7th & 8th decades
 Near VA improves ( second sight of the aged)

 Diagnosed using slit lamp and retinoscopy

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Management
Spectacle Rx

Surgical lens removal with IOL implantation

Follow up care

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Lenticonus
Posterior Lenticonus
 Bulging of the posterior axial lens into the vitreous, non inherited &
usually unilateral
 The capsule in the bulge may be thinned and/or opacified.

 Associated with PHPV, Lowe's syndrome, Down syndrome, optic

nerve hypoplasia, Duane syndrome, retinoblastoma, Microphthalmia,
coloboma, anterior lenticonus and deafness

 Results increased myopia axially

 May cause amblyopia and even strabismus

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Anterior Lenticonus
 Bulging of the anterior axial lens into the anterior chamber,
usually bilateral & inherited.
 Highly associated with Alport's syndrome
 Usually develops in males around age 10-20yrs in patients
with Alport's syndrome.
 Results in high myopia centrally, up to -30.00 Ds
 Patients are at risk of amblyopia and strabismus from the
optical distortion 14
 Features of both lenticonus include :- oil droplet reflex,
scissor movement, cortical opacity.

Management
Daily dilation
Spectacle correction
Cataract extraction
Amblyopia management
Referral for kidney transplant or dialysis--- for anterior
lenticonus with Alport's syndrome 15
Retinal Detachment surgery
 Scleral buckles cause refractive shifts from changes in axial

length, but depends on the type and site of buckle placement

 In 1965, Grupposo reported a refractive shift of -5.00 Ds

 In 1979, Larsen and Syrdalen reported -2.50 D myopic shift.

 Can also cause transient corneal curvature changes which may

lead to transient astigmatism

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 If Silicone oil is in place after vitrectomy, either myopic or
hyperopic shift will occur
 In aphakic eyes, the oil has convex shape --- myopia
 In phakic eyes, the oil has concave shape--- hyperopia
 Patients with silicone oil have fluctuations in refractive
error with head position.
 Spectacle corrections for the induced refractive error after

6 months will be given

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Diabetes mellitus
 A disorder of metabolism caused by a lack of insulin and/or
a decreased effect of insulin, either of which results in
chronic hyperglycemias
 Can be IDDM or NIDDM

 Increases with age, obesity & it is familial

 Hyperglycaemia dehydration of crystalline lens
nucleus myopic shift
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Clinical features
Blur at distance
Horizontal diplopia
Polyuria, polydipsia, polypahgia and weight loss
Elevated blood sugar level
Myopia usually 1- 3.00Ds
Diabetic cataract, 3rd & 6th nerve palsy, DRP

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Management
o Systemic health and Px education

o Appropriate Mx for EOM involvement and DRP

o Refractive care
o Follow up care

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Drug induced
 Very young and patients with kidney and liver abnormalities are more
likely to be affected by certain topical and systemic drugs
 Drugs cause accommodative spasm

 Clinical manifestations
o Blur or improved VA at distance

o Pupillary meiosis
o Specific drug toxicity
o Thickening & forward displacement of the lens with A scan

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Selected drugs that may induce myopia
 Antiglaucoma drugs: Pilcarpine, carbacol, physostigmine, neostigmine,
CAIs
 Antibiotics : sulphonamides, TTC, isoniazid
 Antianginal agents: isosorbide dinitrate
 Antihypertensive drugs: thiazide diuretics
 Antiallerics: antihistamines
 CNS medications: morphine, phenothiazines
 Heavy metals: arsenicals
 Hormonal agents: ACTH, corticosteroid, oral contraceptive
 Analgesics: aspirin 22
Management
 Medication change, dose reduction or discontinuation

 Spectacle Rx

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Night (nocturnal) myopia
Due to dim light conditions
In a 1967 study by Richards, it was common in 20-40 yrs age and patients
benefit from additional up to -0.75Ds lenses for night time
Can range from -0.25 to -6.00 Ds

Caused by
o Spherical aberration in dilated pupil at dim light
o Chromatic aberration
o Peripheral fixation to the perimacular area
o Accommodation shift

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Clinical features
o Long standing driving difficulty at night

 differentiate night myopia from night blindness, disability glare

and anxiety
o Normal or slightly reduced VA

o Poor VA in dim light

o Increased myopia on scotopic conditions

Management
 Night driving glasses
 Follow up care 25
Pregnancy
Manifestations include
 Increased myopia, increase in corneal thickness and curvature,
decrease in night vision, Worsening of DRP
 IOP change, loss of accommodation, Contact lens intolerance
 Central serous Choroidopathy --- hyperopic shift
 Pregnant women with preeclampsia may suffer from blurry vision,
photophobia, diffuse retinal edema, serous retinal detachment,
scotoma and blindness.
 Optical Rx is reserved until delivery unless of greater demand
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 Induced hyperopia
Adie's pupil
Isolated internal ophthalmolplegia

Unilateral in 80-90% of cases

Observed in all ages and both sexes

Caused by orbital/ surgical trauma, viral infections that affect ciliary ganglion
Application of 0.125% Pilcarpine will constrict the adies pupil but not the
normal pupil

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Clinical features
 Blurred near and distance vision, asthenopia, reduced stereopsis,
photophobia, reduced dark adaptation
 Non reactive dilated pupil & slow accommodative response

 Anisocoria which is greatest at bright light

 Vermiform reaction of the iris may be seen
 Reduced AA

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DDX
Physiologic Anisocoria

Horner's syndrome

CN- 3 palsy

Pharmacologic mydriasis

Management
 Optical Rx for induced hyperopia

 Reading glasses (asymmetric near add) or progressive addition with tinted

lenses
 Pilcarpine for young's but it is not long term therapy

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CL induced
 In rigid wearers mainly PMMA with flat fit or secondary to OK

 Patients will be asymptomatic or symptomatic

 Symptoms include
• Improved VA after CL removal, discomfort with CL

• Conjunctival injection, irritation and reduced wearing time

 Lose fit , apical touch and scaring, flat K reading, distorted mires on
slit lamp exam may ne evident

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DDX
Induced hyperopia from
Drugs
Adie's pupil
DM
Retinal elevations
Orbital mass

Management
– Discontinuation of CL
– Refitting CL
– Proper follow up 31
Aging of the Crystalline Lens
 As crystalline lens becomes older, it results hyperopic shift
 Beaver Dam Study found that

– patients 43 to 59 yrs old had a hyperopic shift of +0.54 Ds after 10

yrs.
– Ages of 60 & 69 yrs had a mean shift of -0.03 D after 10 yrs, and
patients older than 69 yrs had a mean myopic shift of -0.41 Dafter
10 yrs.

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Retinal elevations
 Results hyperopic shift by reducing the axial length
 300 µm axial distance at the retina is ≈ to 1.00Ds of
refractive change.
 If optical Rx is required, it is temporary
 Treating the underlying cause will spontaneously correct the
induced hyperopia

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Causes of retinal elevation include:-
 Central serous Choroidopathy
 Uveal effusion syndrome
 Serous elevation of the macula secondary to an optic pit,
tilted disc or papilledema
 VKHS

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Posterior scleritis
 Inflammation of the posterior sclera thought to be a scleral immune
reaction
 Occurs more often in women; it may occur at any age, and it may be
unilateral or bilateral
 Highly associated with systemic disorders and systemic evaluation is
needed
 Results in thickening and swelling of the posterior sclera, causing the

retina to protrude forward and hyperopic shift.

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Intraorbital Tumors: Intraconal lesions
 As the tumor grows, it will cause compression of the optic nerve
with optic nerve head edema, choroidal folds, and elevation of
the retina
 Results shortening of the axial length and hyperopic shift

 Unilateral hyperopia with optic nerve swelling, choroidal folds,

and/or proptosis is highly suggestive of an intraorbital tumor
 Freiberg and Grove found that the intraconal tumors usually cause a
shift of at least +0.50 D hyperopia.

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 Common intraorbital tumors: Intraconal
o Lymphangioma
o Leukemia
o Cavernous Hemangioma
o Orbital Sarcoma
o Orbital Inflammatory Pseudotumor
o Optic nerve glioma

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 Diagnosed using

Hx, Slit lamp , retinoscopy & exophthalmometer/ ruler

Ocular U/S
Biopsy

CT & MRI of the orbit and the brain

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Chronic renal failure and haemodialysis.
 In a series of 18 patients who underwent haemodialysis, Tomazzoli
and colleagues reported that 64% of these patients experienced a
hyperopic shift of +0.25 D to +0.75 D (spherical equivalent) after
their haemodialysis treatment.
 Haemodialysis-induced changes in hydration of the crystalline lens
nucleus causes hyperopic shift.
 Patients will develop also PSC due to postoperative steroid use

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Diabetes mellitus
 Bilateral Hyperopic shift due to a decrease in blood glucose level

Clinical manifestations
 Reduced vision exacerbated at near for presbyopia
 Polyuria, polydipsia & polypahgia

 Sweating, flushing/pallor, headache, dizziness, weakness

 Diabetic cataract, EOM involvement, DRP

Management
 Systemic blood sugar control

 Temporary plus lenses/ Fresnel lenses

 Manage DRP and EOM defect accordingly 40
Drug induced
 Topical /systemic anticholinergic drugs produce pupillary dilation & acc
paralysis that will cause a hyperopic shift
Clinical features
– Blurred vision at distance and near
– Pupil size changes, photophobia, AACG
– Sluggish pupillary Rxn, reduced AA, hyperopia, plus add acceptance at
near
Management
– Patient education
– Plus lenses with tint
– Drug discontinuation, change or dose reduction 41
Selected drugs that may induce hyperopia
 Topical anticholinergics: tropicamide, atropine, cyclopentolate

 Local aesthetics: cocaine

 Antidiabetic agents: chloropropamide

 Oral contraceptives

 NSAIDS: indomethacin

 Antidepressants: imipramine, amphetamine

 Antipsychotic agents: phenothiazines

 Anti inflammatory analgesics: salicylates

 Antihistamines

 Sedatives & hypnotics: chloral hydrate

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 Induced astigmatism
CL induced
 Mainly occurred in extended (≥6-12 month) rigid wearers
who are CL abuse Px's
 Due to induced distortion with the rule astigmatism
and increase in K reading

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Clinical features
– Distorted mires
– Asymptomatic
– Increased K reading post lens
– Reduced Vision
removal
– Spectacle blur
– Corneal imprint
– Mild lens intolerance
– Cylinder power on ret
– Corneal edema, striae, limbal
– difficult subjective refraction
vessel engorgement
&neovascularisation

Management
 Reduce wearing time
 Refitting the CL 44
Chalazion
 Lipogranulomatous inflammation of the eyelid
 Caused by blocked meibomian gland orifices or ducts and stagnation
of the sebum
 Can be small or quite large, reaching ≥10 mm
 Can cause hyperopic astigmatism

Management
 Massage with worm compress
 Injection of triamcinolone
 Surgical removal by incision and curettage 45
Other Lid Tumors
 Hemangiomas, dacryocele, dermoids may indent the cornea

 The deformation of the cornea and the potential refractive

shift depends on
 location & size of the lesion and rigidity of the eye lid

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Pterygium
 Degenerated, fibrovascular conjunctival tissue that grows
from the bulbar conjunctiva onto the cornea.
 Usually results in a decrease in corneal power and an
increase in with-the-rule astigmatism
 Topographical astigmatism is much greater than actual
refractive astigmatism

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 Pterygia reaching 3.2 mm of the visual axis (>45% of the
nasal corneal radius) affects the central cornea significantly.
 Managed by sunglasses, artificial tears, mild steroid drops,
lubricating ointments or surgically.
 Surgical Mx results in a topographical increase in corneal
power and a decrease in topographical astigmatism which
decrease the refractive astigmatism

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Keratoconus
 Progressive ectasia in which the corneal stroma thins
resulting in a localized paracentral bulging of the cornea
 usually bilateral, but it may be asymmetric
 Results progressive irregular myopic astigmatism.

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 Management
 Optical
 Spectacles
 CL:- soft CL, RGP, piggyback, hybrid, scleral, rose K

 Surgical :- PKP, DLK, Epikeratoplasy or Intacs

 Collagen cross linking:-combined riboflavin UVA treatment
 Combinations

 Patient advice

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Pellucid Marginal Degeneration
 1- to 2-mm wide arc of slowly progressive inferior corneal
thinning from 8 - 4 o'clock.
 Results severe, irregular against-the-rule astigmatism.
 Management
 spectacles
Contact lenses
Surgical

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Terrien's Marginal Degeneration
 Idiopathic unilateral/ bilateral thinning of the peripheral cornea.
 More common in ≥ 40 yrs old males

Clinical features
yellow-white lipid line develops superiorly and then spreads around
the corneal periphery
clear space b/n the line & the limbus, and the cornea is thinned
peripheral to the lipid line
Neovascularisation but no pain or inflammation.
Pseudopterygium may grow 52
 Regular & irregular refractive astigmatism can result
 Management
Spectacles
CL
Lamellar corneal grafts
– Polycarbonate or Trivex lenses could be prescribed and safety
frames considered

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Cortical Cataract
 Pesudovs and Elliott" in their study of 77 patients found that
around 25% of patients with cortical cataracts have more
astigmatism as compared with patients with no cataracts.
 They proposed that changes in the index of refraction in the
area of the cortical cataract are responsible for the increased
astigmatism.

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Subluxation or Dislocation of the Lens
 Subluxation:- the crystalline lens has been decentered because of
partial disruption of the zonules and seen within the pupil
 Dislocation:- the lens has been completely displaced out of the pupil
because of complete disruption of the zonules
 Patients will be asymptomatic or highly symptomatic
 Phacodonesis and Iridodonesis are clinical signs
 The amount and type of the refractive change depends on the location
of the crystalline lens as it relates to the visual axis.

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Causes of lens Subluxation
o Trauma
o Ciliary body malignant
melanoma
o Ectopia Lentis
o Ectopia Lentis et pupillae
o Marfan's syndrome
o Homocystinuria
o Weill-marchesani syndrome
o Acquired syphilis
o Aniridia
o Ehler-danlos syndrome
o Hyperlysinemia
o Crouzon syndrome
o Sulfite oxidase deficiency
o Molybdenum cofactor
deficiency
o Stickler's syndrome
o Pathological myopia
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 Diagnosed using Slit lamp and retinoscopy

Management
 Observation
 Optical Rx with pupillary dilation
 Surgical lens removal with IOL implantation & aphakic
refractive correction with bifocals
 Amblyopia management as appropriate

57
Intraorbital Tumors and lacrimal Gland Tumors:
Extraconal lesions
 Press on the equator of the globe, and they may cause
astigmatism or even make the axial length of the eye longer
and cause myopia.
 Causes nonaxial Proptosis and displaced in the direction
opposite the location of the tumor.
 Referral for investigation and appropriate management is
required 58
Common causes – Isolated neurofibroma

– Dermoid cyst – Haematocele Lymphangioma

– Anterior and posterior – Lymphoid tumor

encephalocele – Metastatic tumors
– Capillary hemangioma – Maxillary sinus carcinoma
– Plexiform neurofibroma – Ethmoidal sinus carcinoma
– Rhabdomyosarcoma Neurilemoma

– Metastatic neuroblastoma – Hemangiopericytoma

– Mucocele – Dermoid cyst

– Osteoma

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 References
John F. Hamos. Diagnosis and management in vision care.
Induced refractive and visual changes: 313-367.
William J. Benjamin. Borish's clinical refraction, second
edition. Refractive effects of ocular disease: 1618-1658.
Jack Kanski. A systematic approach to clinical
ophthalmology 7th edition

Advanced pediatric optometry power points

Contact lens power points
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THANK YOU!

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