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OptiExpert™ | Efronin asteikko

Blepharitis

Pale lid margin
Openings of meibomian glands visible
Clean lashes
Pale lid margin
Openings of meibomian glands less visible
Clean lashes
Red lid margin
Openings of meibomian glands barely visible
Yellow crust at base of lashes
Some lashes stuck together
Telangiectasis of lid margin
Increased crusting
More lashes stuck together
Bulbar conjunctival redness
Severe telangiectasis of lid margin
Excess yellow crusting
Lashes stuck together
Increased bulbar conjunctival redness
Skin irritation

Signs

Redness
Telangiectasis
Scaling of lid margins
brittle, leaving bleeding ulcer when removed
Lashes stuck together
Lash collarette
Madarosis
Poliosis
Tylosis

Symptoms

Burning
Itching
Mild photophobia
Foreign body sensation
Dry eye - worse in morning
Lens intolerance

Pathology

Staphylococcal endotoxin-induced complications include:
low grade conjunctivitis
toxic punctate epitheliopathy

Aetiology

Staphylococcal infection of eyelash follicle

Treatment

Antibiotic ointments
Promote lid hygiene
Steroids
Artificial tears
May need to suspend lens wear during acute treatment phase

Prognosis

Variable: expect periods of remission and exacerbation

Differential Diagnosis

Need to differentiate from seborrhoeic anterior blepharitis

Meibomian gland dysfunction

Pale lid margin
Openings of meibomian glands visible
Clean lashes
Pink lid margin
Cloudy expression at some gland orifices
Red lid margin
Milky expression at most gland orifices
Increased tearing
Red lid margin
Yellow expression at all gland orifices
Expressions becoming continuous
Thick creamy yellow expression at all gland orifices
Expressions continuous
Bulbar conjunctival redness

Signs

Cloudy, creamy, yellow expression
Inspissated discharge
Poorly wetting lenses
Tear meniscus frothing
No secretion if blocked
Distended or distorted meibomian glands seen in retroillumination

Symptoms

Smeary vision
Greasy lenses
Dry eye
Lens intolerance

Pathology

MGD is a form of posterior blepharitis
Blocked meibomian orifice
Increased keratinisation of duct walls

Aetiology

Increased turnover of ductal epidermis
Abnormal meibomian oils
- more keratin proteins
Absence of lid rubbing

Treatment

Warm compresses
Heating devices
Lid scrubs/hygiene
Mechanical expression
Antibiotics
Tears/lipid supplements
Essential fatty acids
Sex hormones
Surfactant lens cleaning
Intraductal probing

Prognosis

Excellent if good control can be achieved

Differential Diagnosis

External hordeolum
-localised swelling at lid margin
Internal hordeolum
-tender localised swelling
Chalazion
-chronic form of meibomian gland dysfunction

Superior limbic keratoconjunctivitis

Clear conjunctiva
Clear superior limbus
Clear cornea
Clear reflex
Increased conjunctival redness
Slight limbal redness
Clear cornea
Conjunctival redness and staining
Increased limbal redness
Corneal staining and infiltrates
Greater conjunctival redness and staining
Increased limbal redness
2–3 mm fibrovascular pannus
Greater corneal staining and infiltrates
Severe conjunctival redness and staining
Severe limbal redness
5 mm fibrovascular pannus
Severe corneal staining and infiltrates

Signs

Superior limbic redness
Infiltrates
Micropannus
Corneal staining
Conjunctival staining
Hazy epithelium
Papillary hypertrophy
Corneal filaments
Corneal warpage

Symptoms

Lens awareness
Burning
Itching
Photophobia
Slight vision loss
- with extensive pannus

Pathology

Cornea
-epitheliopathy
-infliltrates
Conjunctiva
-epithelial keratinization
-epithelial oedema
-inflammatory cells

Aetiology

Lens deposits
-posterior lens surface
Mechanical irritation
Immunological reaction
Hypoxia under lid
Thimerosal
-hypersensitivity
-toxicity

Treatment

Cease lens wear until inflammation subsides
Reduce wearing time
Improve solutions
Ocular lubricant
Mast cell stabilizers
Non-steroid anti-inflammatory agents
Increase frequency of lens replacement
Surgery if severe

Prognosis

After ceasing lens wear
-redness resolves rapidly
-epithelium resolves slowly
-can take from 3–40 weeks to resolve

Differential Diagnosis

Superficial epithelial arcuate lesion
-conjunctiva not involved
Bacterial conjunctivitis
Infiltrative keratitis
Theodore's superior limbic keratoconjunctivitis

Corneal infiltrates

Clear cornea
Clear conjunctiva and limbus
Clear reflex
Single small grey infiltrate at 10 o’clock near limbus
Adjacent limbal redness
Five small grey infiltrates at 9–10 o’clock near limbus
Adjacent limbus more red
Numerous small hazy grey infiltrates at 8–10 o’clock in peripheral cornea
Adjacent limbus very red
Hazy grey confluent infiltrates that cover left half of cornea
Adjacent limbal redness from 5 to 11 o’clock
Mild conjunctival redness

Signs

Any condition whereby there are infiltrates in the cornea
Ranges from minute, barely-detectable infiltrate to full-blown corneal ulcer
Often used in the literature to denote a mild event

Symptoms

Depends on severity
Ranges from asymptomatic to suicidal pain
Treat as suspected microbial keratitis if:
-patient is wearing contact lenses
-patient reports ocular discomfort
-infiltrates are observed in the uncomfortable eye

Pathology

Infiltrates in the epithelium and/or stroma
Infiltrates can include one or more of the following:
-polymorphonuclear leucocytes
-other inflammatory cells
-oedema
-microorganisms
By definition, Pseudomonas, Acanthamoeba and Fusarium keratitis are all CIEs

Aetiology

Varies: can be
-toxic
-allergic
-inflammatory
-traumatic
Risk factors:
-contaminated lenses
-solution inefficacy
-patient non-compliance
-poor hygiene
-hypoxia
-swimming
-overnight use
-overnight ortho-K
-mechanical trauma
-smoking
-diabetes
-warm climates
-male gender
-socio-economic class

Treatment

Depends on cause
Cease lens wear immediately
If discomfort persists after lens removal, scrape to test for offending microorganisms
Assume bacterial until proven otherwise:
-prescribe fluoroquinolones
Cold compresses
Analgesics
Continue appropriate treatment when scrape outcome is known
Avoid risk factors if lens wear is to resume

Prognosis

Depends on cause; see various form of microbial keratitis below
-sterile CIEs may be self-limiting and resolve within 7 days
-microbial keratitis can rapidly progress to corneal perforation within hours

Differential Diagnosis

Sterile vs microbial keratitis
Sterile keratitis is usually self-limiting
Microbial keratitis can advance rapidly
In the early stages, it is IMPOSSIBLE to differentially diagnose sterile vs microbial keratitis

Corneal ulcer

Clear cornea
Clear conjunctiva and limbus
Clear reflex
<1 mm corneal ulcer at left pupil margin
Stains with fluorescein
Mild limbal redness at 7–11 o’clock
2–3 mm corneal ulcer
Haze around ulcer
Intense limbal redness at 7–11 o’clock
Ciliary flush
6 mm corneal ulcer
Haze around ulcer
General corneal haze
Intense circumlimbal redness
Conjunctival redness
Increased ciliary flush
White pan-corneal ulcer
Cornea opaque
Intense circumlimbal and conjunctival redness
Intense ciliary flush

Signs

Small rounded peripheral ulcer
0.5 to 1 mm in diameter
Slight infiltration surrounding
There may be mild involvement of the anterior chamber
The ulcer and surrounding area may be stained with fluorescein
Limbic and bulbar redness
May be seen in patients who sleep in their lenses

Symptoms

Eye redness
Tearing
Moderate to severe pain
Foreign body sensation
May be asymptomatic
The patient may report that they see a white spot on their eye
May show just after waking

Pathology

Excavation focal epithelium
Background:
-Polymorphonuclear leukocytes (PMN)
Anterior stromal necrosis
Bowman's layer is intact

Aetiology

Toxins from gram-positive bacteria
Eye closure
Hypoxia

Treatment

Remove the lens
Prescribe:
-fluoroquinolones
-Antibiotic ointment
Saline in single dose
Cold packs
Analgesics
Corticosteroid eyedrops
Fit 1 day lenses
Remove trauma
Improve maintenance regimen
Improve hygiene
Fit rigid lenses
Fit low water content lenses
Increase Dk/t

Prognosis

Excellent:
-21% of cases resolve within 7 days
-All cases are resolved within 2-3 months

Differential Diagnosis

Microbial keratitis
Viral epidemic keratoconjunctivitis:
-Typically bilateral
Stromal opacities
Stromal citcatrices

Endothelial polymegethism

Cells same size
Hexagonal shape
Coefficient of variation (COV) = 0.15
Small variance in cell size
COV = 0.25
Increased variance in cell size
COV = 0.35
Some five-, six- and seven-sided cells
Considerable variance in cell size
COV = 0.45
Some three-, four-, five-, six- and seven-sided cells
Substantial variance in cell size
COV = 0.55
Some three-, four-, five-, six-, seven-, eight- and nine-sided cells

Signs

Large variation in endothelial cell size
Small: large cell ratio:
-normal: 1 : 5
-polymegethism: 1 : 20

Symptoms

Asymptomatic
Corneal exhaustion syndrome:
-reduced wearing time
-discomfort

Pathology

Altered lateral cell walls
Straightening of interdigitations
Cell volume unchanged
Cell organelles normal
Poor oedema recovery

Aetiology

Acidic pH shift at endothelium due to
-hypercapnia: carbonic acid
-hypoxia: lactic acid
Chronic response

Treatment

General strategy
-alleviate acidosis
-higher Dk materials
Corneal exhaustion syndrome
-reduce wearing time
-fit higher Dk/t lens

Prognosis

Possible long-term recovery (many years) after ceasing lens wear

Differential Diagnosis

Guttae
Endothelial dystrophy

Endothelial blebs

Cells same size
Hexagonal shape
No blebs
One bleb
Three single blebs
Two double-cell blebs
Large number of blebs
‘Thickened’ cell borders
Very large number of blebs
Increased spacing between cells

Signs

Black non-reflecting areas
Apparent separation of cells

Symptoms

None

Pathology

Oedema of cell nucleus
Intracellular vacuoles
Extracellular vacuoles
Posterior surface bulging

Aetiology

Acidic pH shift at endothelium due to
-hypercapnia: carbonic acid
-hypoxia: lactic acid
Acute response

Treatment

Not necessary

Prognosis

After inserting lens
-peak response in 10 min
-low level blebs continue
After removing lens
-disappear in 2 minutes

Differential Diagnosis

Guttae
-permanent
Bedewing
-lasts months
Blebs
-last minutes

Corneal distortion

Bright, sharp, circular keratometer mire
Slightly distorted keratometer mire
Variation in thickness of circle
Distorted keratometer mire
Variation in thickness of circle
Loss of focus of right and top +/– signs
Very distorted keratometer mire
Greater variation in thickness of circle
Loss of focus and distortion of all +/– signs
Extremely distorted keratometer mire
Greater variation in thickness of circle with some gaps
Loss of focus and distortion of all +/– signs

Signs

Can manifest as change in corneal:
-curvature
-symmetry
-regularity
Corneal indentation
-may be associated with corneal binding

Symptoms

Spectacle blur
Haze
-if associated with excess oedema

Pathology

Surface Asymmetry Index
-more likely with rigid lenses
-decentred lens flattens cornea
Surface Regularity Index
-distortion may be symmetrical
-more likely with rigid lenses
Corneal indentation
-pressure from lens edge

Aetiology

Oedema
-increased fluid
Physical moulding
-pressure from rigid lenses
-supplementary pressure from eyelids
Associated pathology, e.g. keratoconus

Treatment

Alleviate rigid bearing
Alleviate hypoxia
Corneal indentation
-patient-dependent
-likely to recur again in same patient
Keratoplasty for keratoconus

Prognosis

Rigid lens warpage
-full recovery in 5 to 8 months
Rigid lens binding
-full recovery in 24 hours
Soft lens warpage
-resolves in 7 days

Differential Diagnosis

Keratoconus
-other signs present such as stromal thinning, Vogt’s striae and Fleischer’s ring

Conjunctival redness

‘White’ bulbar conjunctiva
One major vessel
Clear cornea
Small increase in conjunctival redness
Major vessel more engorged
Further increase in conjunctival redness
Limbal redness
Slight ciliary flush
Conjunctiva very red
Increased limbal redness
Ciliary flush
Conjunctiva extremely red
Limbus very red
Intense ciliary flush
Reflex on major vessel

Signs

Conjunctival redness
May be regional variation
Specify location
Depends on lens type:
-no lens: grade 0.78
-rigid lens: grade 0.96
-soft lens: grade 1.54

Symptoms

Often none
Itchiness
Congestion
Warm feeling
Cold feeling
Non-specific mild irritation

Pathology

Vasodilatation due to:
-relaxation of smooth muscle
-vessel blockage

Aetiology

Hypoxia & hypercapnia
Mechanical irritation
Immunological reaction
Infection
Inflammation
-acute red eye
Solution toxicity
Change in tonicity
Change in pH
Neural control

Treatment

Remove cause
-see aetiology
Decongestants
If > grade 2 cease wear

Prognosis

Excellent
-recovery from acute redness within hours
-recovery from chronic redness within 2 days

Differential Diagnosis

Cease lens wear
-rapid resolution implicates lens wear
-slow resolution suggests other cause
‘Push test’:
-for conjunctival vs. scleral involvement
Haemorrhage
-redness between vessels

Limbal redness

‘White’ limbus
White corneal reflex
Slightly increased limbal redness
White corneal reflex
Increased limbal redness
Increased conjunctival redness
White corneal reflex
Limbus very red
Increased conjunctival redness
Speckled corneal reflex
Limbus extremely red
Conjunctival redness
Hazy corneal reflex

Signs

Limbal redness
May be regional variation around limbus
Specify on record card
-virtually absent with silicone hydrogel lenses

Symptoms

Depends on aetiology
-often none
-can be severe pain, e.g. with keratitis
Associated pathology may cause discomfort or pain

Pathology

Vasodilatation of terminal arcades and associated vascular forms:
-recurrent limbal vessels
-vessel spikes

Aetiology

Hypoxia & hypercapnia
Mechanical irritation
Immunological reaction
Infection
Inflammation
-acute red eye
Solution toxicity

Treatment

Remove cause
-see aetiology
Consider whether:
-acute or chronic local limbal redness
-acute or chronic circumlimbal redness
Fit silicone hydrogel lenses

Prognosis

Excellent
-recovery from acute redness within hours
-recovery from chronic redness within 2 days

Differential Diagnosis

Re-vascularization
Vascularised limbal keratitis
Superior limbal keratoconjunctivitis

Corneal neovascularisation

Clear cornea
White reflex
Vessels encroach <1 mm from lower left quadrant (LLQ)
Vessels encroach 2–3 mm from LLQ
Limbal redness
Reflex less crisp
Central corneal haze
Vessels encroach 4–5 mm from LLQ
Corneal haze around vessels
Speckled reflex
Vessels encroach 6 mm from LLQ
Lipid at leading edge of vessels
Very diffuse reflex

Signs

Superficial vessels
-from conjunctiva
‘Normal’ responses:
-no lens: 0.2mm
-Silicone hydrogel: 0.2mm
-Daily wear hydrogel: 0.6mm
-Extended wear hydrogel: 1.4mm

Symptoms

No discomfort
Vision loss if extreme

Pathology

Sprouting or budding
Solid cord of vascular endothelial cells at growing tip
Thin vessel wall
Pericytes
Cell migration
Surrounding inflammatory cells
Disruption of stromal lamellae
Lipid material may surround vessels

Aetiology

Stromal softening
-hypoxia-induced oedema
Triggering agent, e.g.:
-epithelial damage
-solution toxicity
-infection

Treatment

If severe
-cease lens wear permanently
If mild
-improve care system
-increase Dk/t
-reduce wearing time
-monitor carefully

Prognosis

On ceasing lens wear
-vessels empty rapidly
-ghost vessels remain
-years to resolve
On reintroducing lens
-ghost vessels rapidly refill

Differential Diagnosis

Nerve fibres
-any orientation
-’solid’
Striae
-always vertical
-white, whispy
Ghost vessels
-start at limbus
-relatively thick

Epithelial microcysts

High magnification view of pupil margin
Clear cornea
Single microcysts at pupillary margin
Microcyst displays reversed illumination
16 microcysts
Some appear faint (newly formed)
About 70 microcysts
Some microcysts at the surface stain with fluorescein
About 180 microcysts
Many at the surface stain with fluorescein

Signs

Minute scattered dots
Spherical or ovoid shape
5–30µm diameter
Reversed illumination

Symptoms

Can cause slight discomfort
Can reduce vision slightly

Pathology

Intraepithelial sheets
Disorganised cell growth
Pockets of dead cells
Slowly pushed to surface

Aetiology

Possible factors:
-prolonged hypoxia
-mechanical irritation
-reduced oxygen uptake
-reduced mitosis
-typically hydrogel extended wear

Treatment

If ≤ grade 2 microcysts
-no action
-monitor carefully
If ≥ grade 3 microcysts
-cease wear (1 month)
-reduce wearing time
-change to daily wear
-increase lens Dk/t

Prognosis

After ceasing wear
-increase during first 7 days
-decrease thereafter
Full recovery in 2 months
Microcysts will not recur with silicone hydrogel lenses

Differential Diagnosis

Tear film debris
-move on blink
Mucin balls
Vacuoles
-unreversed optics
Bullae
Bedewing
-endothelial
Dimple veiling
-very large

Corneal oedema

Clear cornea and 3 mm wide parallelepiped
Left: endothelium
Centre: stroma
Right: epithelium
Single vertical stria in posterior cornea
Three vertical striae in posterior cornea
Many vertical striae in posterior cornea
Folds in endothelium
Many vertical striae in posterior cornea
Many folds in endothelium
Epithelial bullae

Signs

EPITHELIAL OEDEMA
Slight haziness of epithelium seen in optic section
Can occur during adaptation to rigid lens wear
STROMAL OEDEMA
<2% oedema: undetectable; safe
>5% oedema: vertical striae; caution
>8% oedema: posterior folds; danger
>15% oedema: loss of corneal transparency; pathological

Symptoms

EPITHELIAL OEDEMA
Asymptomatic
Appearance of haloes
STROMAL OEDEMA
<10% oedema: none
>10% oedema: discomfort

Pathology

EPITHELIAL OEDEMA
Disruption to epithelial cells
Extracellular oedema around basal epithelial cells
STROMAL OEDEMA
Oedema
-increased fluid
Striae
-separated collagen fibrils
Folds
-physical buckling

Aetiology

EPITHELIAL OEDEMA
Hypotonic tears, as occurs during lacrimation
Adaptation to rigid lens wear
Fluid enters epithelium
Fluid forms between basal epithelial cells
STROMAL OEDEMA
Primarily hypoxia – 50%
-lactate build-up
Other factors – 50%:
-tear hypotonicity
-hypercapnia
-increased temperature
-increased humidity
-mechanical

Treatment

EPITHELIAL OEDEMA
Modify rigid lens adaptation wear regimen
STROMAL OEDEMA
Alleviate hypoxia
-increase material Dk
-reduce lens thickness
-increase lens movement
-increase edge lift
Alleviate hypercapnia
-as per hypoxia

Prognosis

EPITHELIAL OEDEMA
Rapid recovery upon ceasing of hypotonic stress, i.e. when tearing stops
STROMAL OEDEMA
Acute oedema
-resolves in 2-3 hours
Chronic oedema
-resolves in 7 days
Chronic oedema thins stroma

Differential Diagnosis

EPITHELIAL OEDEMA
Generalised epitheliopathy
STROMAL OEDEMA
Striae
-nerve fibres
-ghost vessels
Folds
-seen in diabetes
Haze
-scarring
-epithelial oedema

Corneal staining

Clear cornea
No staining
Fluorescein in eye
Cobalt blue reflex
Light punctate staining
Slight conjunctival redness
More punctate staining
Increased redness
Light pan-corneal punctate staining
Diffuse reflex
Heavy pan-corneal punctate staining
Very diffuse reflex

Signs

3 & 9 O’CLOCK CORNEAL STAINING
Punctate or diffuse staining at the 3&9 o’clock limbal locations
Triangular patterns:
-apex away from central cornea
-‘base’ corresponds to lens edge
-only seen in rigid lens wearers
INFERIOR EPITHELIAL ARCUATE LESION ('SMILE STAIN')
Inferior arcuate stain parallel to limbus
Punctate form
SUPERIOR EPITHELIAL ARCUATE LESION (SEAL)
Superior arcuate stain parallel to limbus
Full thickness lesion
Also known as ‘epithelial splitting’

Symptoms

3 & 9 O’CLOCK CORNEAL STAINING
Slight discomfort
Dryness
INFERIOR EPITHELIAL ARCUATE LESION ('SMILE STAIN')
Slight discomfort
SUPERIOR EPITHELIAL ARCUATE LESION (SEAL)
Asymptomatic

Pathology

3 & 9 O’CLOCK CORNEAL STAINING
Epithelial disruption at limbus
INFERIOR EPITHELIAL ARCUATE LESION ('SMILE STAIN')
Disruption to epithelium
Cells damaged or dislodged
SUPERIOR EPITHELIAL ARCUATE LESION (SEAL)
Full thickness splitting of epithelium

Aetiology

3 & 9 O’CLOCK CORNEAL STAINING
Rigid lens bridges lid away from ocular surface
Ocular surface adjacent to lens edge not properly wetted
INFERIOR EPITHELIAL ARCUATE LESION ('SMILE STAIN')
Metabolic
Desiccation
-insufficient post-lens tear film
-lens adherence
-lens dehydration
SUPERIOR EPITHELIAL ARCUATE LESION (SEAL)
Mechanical chafing of superior cornea
Inward pressure of upper lid
Contributing factors:
-corneal topography
-rigid lens modulus
-mid-peripheral lens design
-lens surface

Treatment

3 & 9 O’CLOCK CORNEAL STAINING
Alter lens design
-reduce thickness of lens edge
-smaller lens diameter
Blinking instructions
INFERIOR EPITHELIAL ARCUATE LESION ('SMILE STAIN')
Alter lens fit
-more movement
-thicker lens
Alter lens type
-different material
SUPERIOR EPITHELIAL ARCUATE LESION (SEAL)
Alter lens design
-less mid-peripheral bearing
Alter lens type
-lower modulus material
-better surface characteristics

Prognosis

3 & 9 O’CLOCK CORNEAL STAINING
Following lens removal
-recovery: <24 hours
While wearing lenses
-slower recovery: 4–5 days
INFERIOR EPITHELIAL ARCUATE LESION ('SMILE STAIN')
Following lens removal
-rapid recovery: <24hours
While wearing lenses
-slower recovery: 4-5 days
SUPERIOR EPITHELIAL ARCUATE LESION (SEAL)
Following lens removal
-recovery in 3 days

Differential Diagnosis

3 & 9 O’CLOCK CORNEAL STAINING
Vascularised limbal keratitis
INFERIOR EPITHELIAL ARCUATE LESION ('SMILE STAIN')
Lens edge stain
Lens insertion/removal trauma
SUPERIOR EPITHELIAL ARCUATE LESION (SEAL)
Lens edge stain
Lens insertion & removal trauma

Conjunctival staining

Clear cornea
Fluorescein pooling in some folds
Cobalt blue reflex
Increased fluorescein pooling in folds
Slight staining at position of lens edge
More fluorescein pooling in folds
Interrupted lens edge staining
Increased conjunctival redness
Widespread fluorescein pooling in folds
Continuous lens edge staining
Conjunctival redness
Widespread fluorescein pooling in folds
Heavy lens edge staining
Conjunctival redness
Limbal staining

Signs

Normal eye: curved lines of staining in conjunctiva parallel to limbus; furrow staining
Lens-wearing eye:
-diffuse stain
-coalescent stain
-‘lens edge’ stain

Symptoms

Often none
‘Lens edge’ stain may be associated with ‘tight lens syndrome’

Pathology

Normal eye
-fluorescein pools in natural conjunctival folds
Lens-wearing eye
-superficial epithelial cells traumatised or dislodged

Aetiology

‘Lens edge’ stain caused by physical trauma of lens edge
Diffuse stain due to other physical trauma
-trauma induced by excessive movement of loose fitting lens

Treatment

‘Lens edge’ stain:
-fit flatter lens
Lens trauma stain:
-improve care regimen to alleviate deposit formation
-improve lens fit

Prognosis

Excellent
-recovery within 2–4 days

Differential Diagnosis

Physiological ‘furrow staining’ vs. pathological staining

Papillary conjunctivitis

Pale conjunctiva
Vessels clearly visible
Slight roughness at tarsal fold
Pink conjunctiva
Vessels visible
Increased roughness at tarsal fold
Red conjunctiva
Vessels less visible
Papillae at tarsal fold
Reflexes on some papillae
Very red conjunctiva
Vessels barely visible
Large papillae
Bright papillary reflexes
Single mucus strand
Extremely red conjunctiva
Vessels not visible
Very large papillae
Bright papillary reflexes
More mucus strands

Signs

Papillae on tarsal conjunctiva
-‘cobblestone’ appearance
-‘giant’ papillae uncommon
Conjunctival redness
Conjunctival oedema
Excess lens movement
Coated contact lens
Mucus discharge

Symptoms

Early – grades 1&2
-lens awareness
-mild itching
-slight blur
Late – grades 3&4
-lens discomfort
-intense itching
-blur
-reduce wearing time

Pathology

Thickened conjunctiva
Distorted epithelial cells
Altered goblet cells
Inflammatory cells
-mast cells
-eosinophils
-basophils

Aetiology

Lens deposits
-anterior lens surface
Mechanical irritation
Immunological reaction
Hypoxia under lid
Solution toxicity
-thimerosal
May be related to meibomian gland dysfunction

Treatment

Cease lens wear until inflammation subsides
Reduce wearing time
Improve solutions
Ocular lubricant
Mast cell stabilisers
Non-steroid anti-inflammatory agents
Change to a lens material that deposits differently
Increase frequency of lens replacement
Improve ocular hygiene

Prognosis

Papillae can remain for weeks, months or years
Lenses can still be worn
Treat according to symptoms

Differential Diagnosis

Follicle
-vessels on outside
Papilla
-central vascular tuft
This content is based on the book: CONTACT LENS COMPLICATIONS, Author NATHAN EFRON Ed: Butterworth-Heinemann, 1999.

Efronin asteikko * on käytännöllinen kliininen referenssi optikoille.

Se kuvailee seuraavien silmän etuosan piilolinsseihin liittyvien komplikaatioiden vakavuusasteet asteikolla 0 – 4.

  • Blefariitti
  • MGD (Meibomin rauhasen toimintahäiriö)
  • Sarveiskalvon tulehdus
  • Sarveiskalvon infiltraatit
  • Sarveiskalvon haavaumat
  • Endoteliaalinen polymegetismi
  • Endoteliaaliset rakot
  • Sarveiskalvon vääristymä
  • Sidekalvon punoitus
  • Limbaalirenkaan punoitus
  • Sarveiskalvon vaskularisaatio
  • Epiteliaaliset mikrokystat
  • Sarveiskalvon turvotus
  • Sarveiskalvon värjäytyminen
  • Sidekalvon värjäytyminen
  • Papillaarinen sidekalvotulehdus

Kussakin tilassa on viisi kuvitusta. Valitse numero asteikolta vastaavalle kuvalle ja visuaalisille merkeille vakavuusasteesta. Valitsemalla info-painikkeet saat näkyviin oireet, patologian, hoitovaihtoehdot ym.

* Efron-asteikko on tarkoitettu apuvälineeksi optikoille. Se ei korvaa optikon suorittamaa ammattimaista tutkimusta.