Contact lens related corneal ulcer

1. CONTACT LENS RELATED CORNEAL
ULCER
MEIRONI WAIMIR
INFECTION AND IMMUNOLOGY SUB DIVISION
DEPARTMENT OF OPHTHALMOLOGY
MEDICAL FACULTY OF ANDALAS UNIVERSITY/ DR. M. DJAMIL
HOSPITAL
PADANG
2020
Literatur Review
dokter.ronnie@gmail.com

2.  Corneal ulcers  One of the leading causes of blindness worldwide 
increased incidence of corneal ulcers associated with contact lens (CL).
 Risk factors  Overnight contact lens wear, extended wear and poor
hygiene.
 The use of contact lenses was first reported in 1887 by Adolf Fick.
Hard contact lenses  were marketed in the 1950s,
Soft contact lenses 1970s and
Rigid gas permeable lenses  in the late 1970s
INTRODUCTION

3.  The incidence:
- 2/10,000 per year in rigid contact lens users,
- 2.2-4.1/10.000 per year in daily-wear soft contact lenses,
- 13.3-20.9 /10,000 per year for extended-wear soft contact lens.
INTRODUCTION

4.  Can not be penetrated by oxygen  relying on pumping tears when blinking  Can
not be used while sleeping and only be used daily wear.
 Hydrophobic polymer.
 Does not have oxygen permeability (Dk)  Chronic hypoxia in the cornea.
 The most uncomfortable CL.
CONTACT LENS
Divided into two types  Hard contact lenses and soft contact lenses
 Polymethyl Methacrylat (PMMA) = Hard Contact Lenses

5.  Hydrophilic polymer
 Low oxygen permeability (Dk)
 Silicone hydrogel type has high Dk.
CONTACT LENS
 Hydroxyethyl methacrylat (HEMA) = Soft contact lens
 Rigid Gas Permeable (RGP)
 Air-permeable material  can eliminate complications due to corneal hypoxia.
 More flexible than PMMA .
 High oxygen permeability (Dk) from 15 to greater than 100.
 RGP is made from silicone acrylate.

6. CONTACT LENS
Water Content
- Lens dehydration 
affects lens flexibility
↓, O2 permeability ↓
- CL that are less
dehydrated will give
more comfort.
Contact Lens Parameters
Ionic and Non-ionic
Materials
- Ionity contributes to the
interaction between the
lens and tear film.
- Ionic materials attract
too much protein 
biofilm
- Non-ionic materials do
not rapidly attract
proteins on the ocular
surface.
Oxygen
Permeability (Dk)
-Daily and extended wear
CL with low oxygen
permeability(Dk) create a
hypoxia
-Low Dk can cause cornea
with oxygen deficiency.
Wettability
- Increasing wettability
of the lens surface
will increase patient
comfort throughout
CL usage time.

7. CONTACT LENS
Classification of Soft Contact Lenses According to FDA

8. PATHOPHYSIOLOGY
CONTACT LENS RELATED CORNEA ULCER
Contact Lens
Related Corneal
Ulcer
- Hypoksia and
Hypercapnia
- Mechanical Effects
- Contact Lens Care
Solution
Contamination
- Bacterial Adhesion
- Bacterial Invasion
- Corneal
inflammation and
tissue damage

9. PATHOPHYSIOLOGY
CONTACT LENS RELATED CORNEA ULCER
Corneal is avascular condition, corneal aerobic metabolism depends on gas exchange in tears
Corneal epithelial mitosis ↓, corneal thickness↓and fragility ↑
Increase the risk of bacterial keratitis and corneal ulcers.
A further effect  neovascularization of both the epithelium and the stroma
 Hypoksia and Hypercapnia
Closing eyes and wearing contact lenses  Reduce O2 and CO2 transmission
on the surface of the cornea

10. PATHOPHYSIOLOGY
CONTACT LENS RELATED CORNEA ULCER
 Mechanical Effects
Mechanical effects  abrasion due to improper lens wear or removal. Sharp stiff contact
lenses can cause corneal distortion or abrasion.
 Contact Lens Care Solution Contamination
 Sourced from the user's hand and the environment transmitted on the lens storage
container or directly to the solution when used.
 Normal flora on the skin of the hands and bacteria in the environment  contaminate the
solution.
 Bacterial contamination can come from biofilms formed at the bottom of contact lens
solution containers.

11. PATHOPHYSIOLOGY
CONTACT LENS RELATED CORNEA ULCER
 Bacterial Adhesion
The pathogen 
adhere in damaged
corneal surface
Interaction of
bacterial adhesion
with glycoprotein
receptors on the
ocular surface.
Biofilm production
 increase
bacterial
aggregation
Pili (fimbriae) on
bacterial surfaces
 facilitate
attachment to the
corneal epithelium.

12. PATHOPHYSIOLOGY
CONTACT LENS RELATED CORNEA ULCER
 Bacterial Invasion
Bacterial invasion
into epithelial cells
 mediated by
interactions
between bacterial
cell surface
proteins,
integrins,
epithelial cell
surface proteins
and the release of
bacterial
proteases.
Inoculation  to
surrounding
epithelium and
deeper stroma.
Keratocytes have
phagocytic ability
 but exposed
avascular stroma
cannot protect the
cornea.
Uncontrolled
multiplication of
bacteria in the
corneal stroma

13. PATHOPHYSIOLOGY
CONTACT LENS RELATED CORNEA ULCER
 Corneal Inflammation and Tissue Damage
* kinin-forming system, clotting and fibrinolytic, immunoglobulins, complement components, vasoactive amino
acids, neuropeptides and cytokines
Various
mediators
inflammatory
cells* 
triggered by
bacterial
invasion 
Inflammation
 Tissue
destruction
Production of
cytokines
such as Tumor
Necrosis
Factor (TNF)-
alpha and IL-1
More cytokines
and
complement
components
are produced
to attract more
leukocytes.
Macrophages
will move to
the cornea to
destroy
bacteria and
neutrophils that
have
degenerated.
Severe
stromal
inflammation

14. CLINICAL MANIFESTATIONS
CONTACT LENS RELATED CORNEA ULCER
• A history of contact lens wear
• Progressive pain, limbal and conjunctival hyperemia, photophobia, mucopurulent
exudate and decreased vision.
• Gram-negative bacterial infections  more aggressive, causing stromal necrosis
Pseudomonas corneal
ulcer after contact lens
wear with corneal ring
abscess

15. CLINICAL MANIFESTATIONS
CONTACT LENS RELATED CORNEA ULCER
• Acanthamoeba infection  Severe eye
pain and/or history of using nonsterile
water on CL dendritic epitheliopathy
or peripheral corneal radial neuropathy.
• Fungal corneal infections  subtle
infiltrates in the form of feathered
borders in the presence of satellite
lesions
Acanthamoeba
keratitis: dendritiform
lesions
Acanthamoeba
keratitis: radial
perineuritis

16. CLINICAL MANIFESTATIONS
CONTACT LENS RELATED CORNEA ULCER
Sweeney et al classify the stages of infection associated with contact lens wear into three
Clinically non-
significant
Asymptomatic
Infiltrates
Asymptomatic
infiltrative
keratitis
Clinically
significant
Infiltrative
Keratitis
Contact Lens Related
Acute Red Eye
(CLARE)
Contact Lens Induced
Peripheral Ulcer
(CLPU)
Mikrobial
Keratitis

17. LABORATORY EXAMINATION
CONTACT LENS RELATED CORNEA ULCER
 Corneal scrapings for smears and culture  carried out before starting
antimicrobial therapy.
 Examination of KOH and Gram staining helps identify pathogens such as
Staphylococcus, Pseudomonas and Acanthamoeba as well as fungal elements.
 Culture of lens care solutions  help in diagnosing.

18. MANAGEMENT
CONTACT LENS RELATED CORNEA ULCER
 Initial therapy
Broad-spectrum topical antibiotics
 Monotherapy  Topical fluoroquinolones.
- Every 30-60 minutes  frequency is reduced according to the clinical response.
- In severe cases  every 5 minutes for 30 minutes as a loading dose (can quickly
reach therapeutic concentrations in the corneal stroma).
Medicamentosa
Antibiotics
Contact lens use must be stopped immediately

19. MANAGEMENT
CONTACT LENS RELATED CORNEA ULCER
 Initial therapy
Topical combination therapy 
Active agents against gram-positive bacteria + active agents against gram-
negative bacteria
- Combination therapy is needed if monotherapy fails or extensive ulcer, threaten
vision or atypical.
- Systemic antibiotics expansion of scleral infection and/or intraocular infections.
- Corticosteroid therapy for bacterial corneal ulcers is still controversial.

20. MANAGEMENT
CONTACT LENS RELATED CORNEA ULCER
Initial Therapy in Bacterial Keratitis

21. MANAGEMENT
CONTACT LENS RELATED CORNEA ULCER
Ms. M, 18 years old
Corneal ulcer OS ec susp bacteria
ec contact lens
was treated in M Djamil General
Hospital, VOS ½ / 60
7th day after receiving
initial therapy, VOS 6/9
ph 6/6

22. MANAGEMENT
CONTACT LENS RELATED CORNEA ULCER
 Natamycin 5%  recommended for most cases of filamentous fungal corneal
ulcers especially Fusarium sp
 Amphotericin B (0.15% -0.30%)  effective for treating yeast corneal ulcers.
Also recommended for filamentous corneal ulcers caused by Aspergillus sp.
 Systemic therapy:
Azoles  ketoconazole (200-600 mg/day), fluconazole (200-400 mg/day), or
itraconazole (200 mg /day) can be considered.
Medicamentosa
Anti-Fungal

23. MANAGEMENT
CONTACT LENS RELATED CORNEA ULCER
 Oral Voriconazole (200-400 mg/day) and Posaconazole (800 mg/day) have
replaced other oral antifungals  excellent penetration and wider spectrum.
 Amphotericin B Intrastromal (5-10 mcg/0.1 cc) or Voriconazole (50-100
mcg/0.1 cc) as treatment of fungal corneal ulcers is recommended.
Medicamentosa
Anti-Fungal

24. MANAGEMENT
CONTACT LENS RELATED CORNEA ULCER
 The combination of the following agents:
• Diamidine: propamidine, hexamidine.
• Biguanide: polyhexamethylene biguanide (polyhexanide), chlorhexidine.
• Aminoglycosides: neomycin, paromomycin.
• Imidazole/triazole: voriconazole, miconazole, clotrimazole, ketoconazole,
itraconazole.
 The main pharmacological treatment Biguanide.
Medicamentosa
Amoebicid

25. MANAGEMENT
CONTACT LENS RELATED CORNEA ULCER
 AMT can restore eye surface integrity.
 The role of AMT in corneal ulcers  accelerate epithelialization, reduce
inflammation, anti-scarring and anti-angiogenic on the surface of the eye.
Surgical
Amniotic Membrane Transplantation (AMT)

26. MANAGEMENT
CONTACT LENS RELATED CORNEA ULCER
 Indication:
Progression occurs, descemetocele or perforation, or corneal ulcer that is not
responsive to antimicrobial therapy.
 PK  Considered when the infection spreads to the parasentral corneal stroma
even maximum antimicrobial therapy has been given.
 PK procedure in localized infections  allow total eradication of the organism
by removing the involved tissue and the clean corneal edges around it.
Surgical
Penetrating keratoplasty (PK)

27. Surgical
Penetrating keratoplasty (PK)
MANAGEMENT
CONTACT LENS RELATED CORNEA ULCER

28. CONCLUSION
 The use of CLs that are not released during sleep (overnight wear), prolonged and
continuous use (extended wear) and poor CLs care are the main risk factors for CLs
related corneal ulcers.
 Pathophysiology of corneal ulcers due to CL are hypoxia and hypercapnia on the
cornea, mechanical effects, CLs care solution contamination, adhesion and invasion
of bacterial, and corneal inflammation and tissue damage.
 Laboratory tests with Gram, Giemsa, KOH, and culture stains are important to find
the etiology and selection of the right therapy.

29. CONCLUSION
 Initial therapy consists of broad-spectrum topical antibiotics. Central and/or more
extensive corneal ulcers related CL are treated with aggressive therapy with topical
combination. Antifungal and amoebicid can be given according to microbes that
cause infection.
 Amniotic membrane transplantation can help restore eye surface integrity and
provide metabolic and mechanical support for corneal healing.
 Penetrating keratoplasty is indicated if progression occurs, the presence of
descemetocele or perforation. Penetrating keratoplasty is the last effective surgical
procedure.

30. Thank You
dokter.ronnie@gmail.com