Intro - Basic Anatomy

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 Cornea
The cornea is a unique transparent and avascular
tissue that is the most important refractive
structure of the eye.

• Anatomy
• Inflammation/Infection
• Dystrophy/Ectasia

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 Cornea - Anatomy
5 Layers:
• Epithelium – Continuous with conj, richly
innervated by CN-V1
• Bowman’s Membrane
• Stroma – The thickest central portion (90%).
This is where LASIK/Refractive surgery happens!
Primarily made up of Type 1 Collagen in
uniformly-spaced lamellar bundles.
• Descemet’s membrane
• Endothelium – pumps the water out of the cornea
and keeps it clear
 Cornea

The uniform spacing of the stromal collagen bundles at a

distance of approx ¼ wavelength light allows transparency.
Cornea - Refractive Surgery

• Excimer Laser is applied to the stromal bed,

underneath a reflected corneal flap (LASIK).
• The tissue is ablated precisely to counteract the
refractive error
Cornea – Inflammation/Infection
Keratitis – inflammation of cornea
• Bacterial ulcer – Frequent in contact lens
users, Pseudomonas most common
• Viral – Herpes (HSV) is a frequent etiology
• Autoimmune, Syphilis, Fungal, ameobic,
and many other types
MICROBIAL KERATITIS

• BACTERIAL INFECTION

• FUNGALE INFECTION

• VIRAL INFECTION

• PARASITIC INFECTION
BACTERIAL INFECTION

Most common microorganism

• Staphylococci G+
- aureus
- epidemidis
• streptococci G+
- pneumoniae
- pyogenes
• Pseudomonas aeruginosa
• Neisseria
Signs and symptoms
 painful red eye with a localised abscess in
the cornea
 accompanied by stromal ulceration
should arouse clinical suspicion.
 There may be an acute uveitis with
hypopyon.
 Photophobia.
 Diagnosis
 Clinical history.
 Physical examination.
 Cultures of corneal scrapings(for
identification the organism)
 Corneal biopsy .
Treatment
 Hospitalization
 Topical administration
 Subconjuntival injection .
 I . V antibiotic .
 O r a l antibiotics (lowefficacy)
 FUNGALE
INFECTION
 A fungal keratitis is an
inflammation of the eye's cornea that
results from infection by a fungal
organism.
Symptoms of Fungal Keratitis
Symptoms of fungal keratitis include:
 E y e pain and redness
 Blurred vision
 Sensitivity to light
 Excessive tearing ordischarge
 Risk factors
Fungal keratitis most commonly occurs in tropical and
sub-tropical regions of the world. In temperate areas
of the world, risk factors for developing fungal
keratitis include:

 Recent eye trauma.

 Underlying ocular (eye) disease.
 Weakened immunesystem.
 Contact lens use.
Fungal Keratitis Diagnosis

 History.

 Physical examination.

 culture from corneal scrapings is

considered to be the standard for
definitive diagnosis of fungal keratitis.
Fungal Keratitis
Treatment for Fungal Keratitis
 Fungal keratitis must be treated with prescription antifungal
medicine for several months.
 Natamycin is a topical ophthalmic antifungal medication that
works well on superficial corneal infections, particularly those
caused by filamentous fungi such as Aspergillus and
Fusariumspecies.
 However, corneal infections that are deeper and more severe
usually require treatment with systemic antifungal medication
such as amphotericin B, fluconazole, or voriconazole. Patients
who do not get better after topical and oral antifungal
medications may require surgery, including corneal
transplantation.
 VIRAL INFECTION

Herpes simplex Herpes zoster

 T h e DNA viruses, herpes simplex and herpes zoster,

are the commonest viral infections of thecornea.
Herpes simplex

Clinical presentation

 Primary infection

usually in children, involving the eyelids and

lips. Corneal involvement is rare. A minor
follicular conjunctivitis may occur.
 Recurrent infection

1 Acute stage:

a unilateral painful red eye with superficial

ulceration taking the form of club shaped
finger-like processes (dendritic /dendritiform).
Fluorescein stains the epithelial defect and
Rose Bengal identifies dead epithelial cells
along the edge of the defect.
2 Chronic stage:

the disease may progress to ulceration,

scarring, or perforation.
 Cornea - HSV Keratitis

• Epithelial “dendritic” • Stromal Keratits (note the

Keratitis (acute) vessels and clouding)
(chronic)
Symptoms:
• Red eye.
• Pain.
• Photophobia.
• Epiphora (tearing).
• History of previous episodes.
• May complain of blurred vision.
Diagnosis
 Assess visualacuity.
 Examine lids and conjunctiva for evidence of
inflammation. Involvement here is less common in
secondary infection although conjunctival injection
(red eye) is almost universal. There may be erosions
around the lid margin with the presence of small
vesicles or pustules.
 Observe cornea: any opacities or haziness? Thismay
suggest stromal involvement.
 Te s t corneal sensation this can be reduced n i
epithelial disease.
 S t a i n the cornea and look for evidence of ulcers by
staining with fluorescein.
Treatment
 Antiviral medications including:
acyclovir (the drug of choice )
trifluridine, vidarabine, and idoxuridine.

 Steroids in chronicoedema.

 keratoplasty for perforations and

scarring.
Herpes zoster

The pathological features of herpes

zoster infection of the cornea are
very similar to those described for
chronic.
 PARASITIC INFECTION

Various parasitic infections are important

causes of ophthalmic diseasesworldwide.

Most parasitic infections are spread by

insect vectors or consuming orgetting
contact with contaminated water
Various organisms producing
keratitis are the following

 Acanthamoeba
 Microsporidia
 Onchocerca
 Leishmania-
 Trypanosoma bruci
Acanthamoeba keratitis
 Acanthamoeba was first established as a case
of human disease in 1973
 T h i s vision threatening corneal disease was
first recognized in contact lens wearers.
 T h e re was a sharp increase in the
recognition(and perhaps incidence ) of this
disease in the late 1980’s.
 First case of Acanthamoeba keratitis from
India was reported in 1987 from Aravind Eye
Hospital, Madurai
Clinical signs
 are discussed in three stages
1. Early stage / Epithelial defects, epithelial
haze pseudodendrites

2. Late stage / Epithelial defects, stromal infiltrates,

nummular keratitis

3. Advanced stage/ Ring infiltrate, satellite lesions,

stromal abscess
 Other features
- Severe anterior and posterior uveitis
- Nodular or Diffuse scleritis

- Corneal stromal infiltrates

(single,multiple,ring shape)

- Anterior uveitis (transient

hypopyon)

- Radial keratoneuritis
Clinical characteristics that help to
distinguish Acanthamoeba keratitis from
other keratitis include the following:

1. Ring infiltrate

2. Elevated epithelial lesion

3. Relative lack of vascularisation even in chronic

and severe cases
 Treatment
 T h e re is no consensus on treatment.
Various regimens are described.

 Treatment is required for 6-12 months.

 Prolonged medication results in corneal

vascularisation and toxic keratitis.
 Cornea - Bacterial Ulcer

Epithelial defect, infiltrate of white cells into the cornea, and

a layered leukocyte collection in the AC (Hypopyon)
 Cornea – Stromal Dystrophy
• Dystrophy – a heritable disorder resulting in
abnormal tissue morphology, function, or
abnormal depositions of material into the
cornea.
• MANY types, affecting each specific layer.
 Cornea – Stromal Dystrophy

• Granular Dystrophy • Hyaline material deposited

in stroma
 Cornea – Stromal Dystrophy

• Amyloid deposition with

• Lattice Dystrophy “apple-green” birefringence,
with Congo Red staining
 Cornea - Ectasia

• Progressive deformation of cornea is an ectasia.

Keratoconus is the most common ectatic dystrophy.
Ectasia can also be a complication of refractive surgery…
THE UVEA
 The Uvea

“The uvea” is:

1. The Iris
2. The Ciliary body
3. The Choroid
Each has a function
1. Iris is a diaphragm for light
2. Ciliary body suspends and “flexes” the lens, and
makes the aqueous humor
3. The choroid helps nourish the outer retina
 The Uvea - Angle

• The “angle” is a special region of the uvea where the iris meets the
cornea
– Regulates the outflow of Aqueous humor through the Canal of
Schlem
– Determines the Intraocular pressure (Important in Glaucoma)
 The Uvea - Inflammation
• “Uveitis” is inflamation of any combination of the
iris, ciliary body, or choroid.
• Many etiologies (autoimmune, syphilis, sacrcoid,
TB, HLA-B27, infectious, idiopathic, etc…)
• Many names (iritis, anterior uveitis, iridocylitis,
choroiditis, etc…) depending on the location
• Sometimes associated with SERIOUS systemic
inflamatory diseases (eg. arthritic diseases),
inflamatory bowel disease, and vasculitis.
 The Uvea – Anterior Uveitis

• Anterior uveitis/iritis • WBCs floating in the aqueous

 Uvea – Posterior Uveitis

• Active Toxoplasmosis Choroiditis, and old scar (above)

 The Uvea - Tumors
• The Choroid is a highly perfused vascular
“net” feeding the outer retina
• It is a potential target site for metastasis for
carcinoma, such as breast and lung.
 The Uvea - Tumors

• The uvea (especially choroid) is also richly pigmented, and primary

melanocytic tumors are common.
• Nevi and malignant melanomas are both relatively common, and can
be difficult to distinguish, clinically.
• Tumors with “spindle-B” or epithelioid histologic patterns are
malignant