طب وجراحة العيون Disorders of the Cornea



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الدكتور محمد عبد الله منصور البغدادي

طب وجراحة العيون

Disorders of the Cornea

Have a nice flight in ophthalmology ^_^

Applied corneal anatomy
Anatomically, the cornea consists of the following five layers: -

  1. The epithelium.

  2. Bowman's layer.

  3. The stroma.

  4. Descemet's membrane.

  5. The endothelium


Clinical evaluation of corneal disease

By SLITLAMP BIOMICROSCOPY


The three main techniques of slitlamp biomicroscopy are: -

  1. Direct illumination with diffuse light is used to detect gross abnormalities.

  2. Scleral scatter: - This technique is especially useful in the detection of subtle opacities and mild corneal oedema.

  3. Retroillumination uses the reflection of light from the iris to illuminate the cornea from behind. This allows the detection of fine epithelial and endothelial changes, keratic precipitates and small blood vessels.


CLINICAL SIGNS OF CORNEAL DISEASE

Superficial (epithelial) signs

Punctate epitheliopathy or punctate epithelial erosions (PEE)

It is characterized by tiny, slightly depressed, grey white spots which stain well with fluorescein.

PEE is a non-specific sign which may be seen during the early stages of a wide variety of keratopathies. The location of it serves as a clue to the aetiology of the keratopathy, for example:


  1. Superior PEE occurs in vernal disease and superior limbic keratoconjunctivitis.

  2. Inferior PEE may be seen in trichiasis, entropion, staphylococcal blepharitis, primary meibomitis, keratoconjunctivitis sicca, rosacea and corneal exposure.

  3. Interpalpebral PEE is associated with seborrhoeic blepharitis, neurotrophic keratopathy and exposure to ultraviolet light.


Epithelial oedema

It is an important sign of endothelial decompensation. It is characterized by loss of normal corneal lustre and in severe cases vesicles and bullae may develop.


Corneal filaments

They are composed of mucous threads attached to abnormal receptor sites (comma-shaped opacities).


Punctate epithelial keratitis (PEK) It is the hallmark of viral infections.
A pannus consists of an ingrowth of fibrovascular tissue from the limbus into the subepithelial space.
Signs involving the stroma and Descemet's membrane

Stromal infiltrates They are composed of leucocytes and are indicative of active inflammation
Stromal oedema usually coexists with inflammatory infiltration. Clinically, it is characterized by optically empty spaces between stromal lamellae, associated with increased corneal thickness, and variable decrease in transparency as a result of disruption of the regular arrangement of corneal lamellae. Four important causes of central stromal oedema are disciform keratitis, keratoconus, Fuchs' dystrophy and intraoperative damage to the corneal endothelium.
Stromal vascularization
Breaks in Descemet's membrane

Folds in Descemet's membrane
Special investigations
Pachometry measures corneal thickness which is an indirect indication of the integrity of the corneal endothelium.

Specular microscopy photographs the corneal endothelium and delineates various cellular characteristics such as size, shape, density and distribution.

Keratometry measures corneal curvature.

Keratoscopy detects abnormalities of corneal shape.

Consist of

1. Hand-held Placido's disc is the crudest type.

2. Photokeratoscopes

3. Computer-assisted photokeratoscopes (corneo- scopes)
Laboratory investigations


  1. Scrapings

  2. Corneal biopsy to diagnose problematic corneal diseases.


Principles of management of corneal disease
Antimicrobial agents should be used for corneal infections.
Steroids
Promotion of re-epithelialization in eyes with stromal thinning is important because thinning seldom progresses if the epithelium is intact. The methods of promoting re-epithelialization:

1. Lubrication with artificial tears and ointments.

2. Lid closure is particularly useful in exposure and neurotrophic keratopathies as well as in eyes with persistent epithelial defects.

3. Bandage soft contact lenses


Prevention of perforation can be with one of the following:

1. Tissue adhesive glue.

2. Conjunctival flaps.

3. Immunosuppressive agents.

4. Corneal grafting may be required to restore corneal transparency.

Microbial keratitis
Bacterial keratitis
PREDISPOSING FACTORS

1. Contact lens wear.

2. Ocular surface disease
MANAGEMENT


  • Hospitalization, and Scrapings.

  • Antibiotics choices depend on the result of C/S.

  • The initial therapy should be with a combination of a fortified aminoglycoside and ciprofloxacin.

  • Topical cycloplegics


Methods of administration of the medicine: -

    • Topical

    • Subconjunctival injections of antibiotics

    • Systemic antibiotics



Fungal keratitis

Although rare, fungal corneal infection (keratomycosis) should always be considered if the differential diagnosis of suppurative bacterial keratitis and herpetic stromal necrotic keratitis is suspected.


CLINICAL FEATURES

The clinical appearance of fungal keratitis varies with the infectious agent and stage of the disease. Topical steroids enhance fungal replication and corneal invasion by interfering with the host's inflammatory response; they are often in use at the time of diagnosis.




  1. Filamentous fungal keratitis

It is usually caused by Aspergillus or Fusarium spp. It is most prevalent in agricultural areas and typically preceded by ocular trauma, most frequently involving organic matter such as wood. Filamentous keratitis occurs under these circumstances in previously healthy individuals with no pre-existing eye disease.
The signs are similar to the bacterial keratitis as (corneal abscesses, hypopyon etc) and shows a greyish white ulcer with indistinct margins which may be elevated above the surface of the cornea. The lesion is typically surrounded by delicate, feathery, finger-like infiltrates in adjacent stroma. Less specific associated findings include satellite lesions, ring infiltrate.


  1. Candida keratitis

Candida keratitis usually develops in association with pre-existing chronic corneal disease or in an immunocompromised or debilitated patient. Usually it is acquired endogenously.
TREATMENT

Before starting antifungal therapy, re-culture and corneal biopsy should be considered to establish the diagnosis if this is uncertain.



  1. Topical and broad-spectrum antifungal agent such as econazole 1%.

  2. Systemic antifungal agent such as itraconazole or ketoconazole may also be helpful in severe cases. Antifungal treatment should be continued for 6 weeks.

  3. Therapeutic penetrating keratoplasty may be required in unresponsive cases.

  4. Steroids are absolute contraindication.


Acanthamoeba keratitis


  • It may occur following a minor corneal abrasion.

  • Contact lens wearers who use non commercially saline risk.

  • Misdiagnosed

  • Important clues to the diagnosis includes:-

1. history of soft contact lens wear,

2 .negative cultures for bacteria, fungi and viruses.

3 .lack of response to conventional antimicrobial therapy.

CLINICAL FEATURES

Blurred vision and pain which is severe and disproportionate to the extent of ocular involvement.

O/E shows multifocal, patchy, anterior stromal infiltrates. The infiltrates gradually enlarge and coalesce to form a partial or complete central or paracentral non-suppurative ring which may be associated with variable epithelial breakdown or pseudodendrite formation. Small white satellite lesions may develop peripheral to the ring.

Central corneal oedema, scleritis, hypopyon, stromal thinning and descemetocele.



Investigations: -

  1. The diagnosis can be confirmed by staining corneal scrapings with special media.

  2. Corneal biopsy may be required.


TREATMENT

The initial treatment is with a combination of dipropamidine and polyhexamethylene biguanide drops.

Penetrating keratoplasty may be required if medical therapy fails.
Interstitial keratitis
Interstitial keratitis (IK) is an inflammation of the corneal stroma with no primary involvement of the epithelium or endothelium.
Luetic interstitial keratitis

Presentation is acute bilateral pain and severe blurring of vision.



O/E: - diffuse, midstromal clouding. Within a few weeks deep vascularization. After several months, the cornea begins to clear and the BV become (ghost vessels).

Treatment of active luetic IK is with systemic penicillin, topical steroids and cycloplegics.
Cogan's syndrome

It is in middle age with acute tinnitus, vertigo and deafness.



O/E of the early corneal lesions shows anterior stromal infiltrates.

Treatment of early lesions with topical steroids.

Early diagnosis of Cogan's syndrome is important because treatment of the cochlear symptoms with systemic steroids may prevent permanent and profound deafness. Some patients may have associated polyarteritis nodosa.


Viral keratitis
Herpes simplex keratitis

It (HSV) is a DNA virus with humans as the only host.



HSV-1 mainly causes infection above the waist (face, lips and eyes).

HSV-2 typically causes infection below the waist (genital herpes).

PRIMARY OCULAR INFECTION

Primary ocular infection typically occurs in children between the ages of 6 months and 5 years, and may be associated with generalized symptoms of a viral illness. In most cases primary herpetic infection is self-limited and seldom presents serious problems.



Clinical features

Blepharoconjunctivitis is usually benign and self-limited and, in children, it may be the only manifestation of primary herpetic infection. The skin lesions typically involve the lids and periorbital area. Initially, they consist of vesicles which rapidly form superficial crusts and then heal without scarring. The conjunctivitis is unilateral, acute, follicular, and associated with a watery discharge and preauricular adenopathy. It may occasionally cause secondary canalicular obstruction.

Keratitis develops within a few days in about 50% of patients with blepharoconjunctivitis. A fine epithelial punctate keratitis may be a transient finding. A coarse epithelial punctate keratitis may give rise to a variety of epithelial lesions which subsequently progress to dendritic shapes.

Treatment

Topical antiviral ointment should be applied prophylactically to the eye five times a day for about 21 days to prevent keratitis.


DENDRITIC ULCER

Clinical features

It may be single or multiple is the hallmark of epithelial disease.



O/E: - Early cases shows opaque cells arranged in a dendritic, coarse, punctate or satellite pattern. Central desquamation & a linear-branching ulcer begins to form.

Diminished corneal sensitivity. Geographical ulcer shape (enhanced by injudicious use of topical steroids).


DDx: -

  1. Marginal (catarrhal) ulcer. The differentiation is extremely important because topical steroid therapy, which is very effective for marginal keratitis, may exacerbate a herpetic infection.

Other causes of non-herpetic dendritic ulceration include:

  1. Herpes zoster keratitis (see later).

  2. A healing corneal abrasion.

  3. Soft contact lenses which may rarely give rise to a pseudodendrite in the midperipheral cornea.

  4. Toxic keratopathies usually caused by excessive drop administration.


TREATMENT
Antiviral drugs

  1. Acycloguanosine (3% oint.) (acyclovir, Zovirax).

  2. Trifluorothymidine (1% drops).

  3. Adenine arabinoside (3% oint, 0.1% drops).

  4. Bromovinyldeoxyuridine (1% oint, 0.1% drops).

Débridement

  • Débridement is an effective way of treating dendritic ulcers, especially when combined with antivirals.

  • Not appropriate for geographical ulcers.


STROMAL NECROTIC KERATITIS

Clinical features
Stromal necrotic (infiltrative) keratitis is caused by active viral invasion and destruction. Fortunately it is fairly rare. It may be associated with an intact epithelium or it may follow epithelial disease.

O/E

The stroma shows a cheesy, necrotic appearance, like that of active and severe bacterial keratitis.

There may be an associated anterior uveitis with keratic precipitates underlying the area of active stromal infiltration, vascularization, scarring and perforation.

Treatment

Combined use of steroids, with topical antiviral and antibiotic cover.

If corneal perforation occur, emergency penetrating keratoplasty (PKP)
DISCIFORM KERATITIS

The aetiology is either caused by a reactivated viral infection of keratocytes and endothelium or an exaggerated hypersensitivity reaction to antigen. (+/ -) past history of dendritic ulceration.

O/E: -

Central zone of epithelial oedema and stromal thickening.

The lesion is centric or eccentric.

Other features include folds in Descemet's membrane, a mild-to-moderate anterior uveitis, and small keratic precipitates.

The IOP may be elevated.

Treatment

Topical steroids combined with antiviral cover are required.

Cycloplegics agents (atropine).
TROPHIC KERATITIS

Trophic keratitis is not caused by active viral disease alone but also by elements of denervation, drug toxicity and persistent defects in the basement membrane.

When trying to differentiate a geographical from a trophic ulcer.
Treatment consists of withdrawal of potentially toxic topical therapy and measures to promote epithelial healing.
Herpes Zoster Ophthalmicus


Viraemia



Dorsal root ganglion

Chickenpox



AutoShape 32


Reactivates



migrates back down the sensory nerves

Skin & Eye

characteristic lesions

HZO = 15% of all cases.

1/3 nasociliary nerve (Hutchinson's sign)= ocular complications.


Classified into;

1.ACUTE PHASE

2.CHRONIC PHASE

3.RELAPSING PHASE


1-ACUTE PHASE

An influenza like illness, heralds the neuralgia which precedes the cutaneous lesions of HZO.


Features of skin lesions

Initially it is maculopapular and then becomes pustular. The pustules subsequently burst to form crusting ulcers. Initially, the rash is accompanied by periorbital oedema.



Treatment of skin lesions

Systemic antiviral therapy is with Acyclovir (Zovirax), 800 mg tablets administered five times daily for 7 days. (Other antiviral agents: - Valaciclovir 1gm three times daily or Famciclovir 250mg three times daily).

This significantly diminishes vesiculation, accelerates healing and reduces pain during the eruptive phase, especially in immunosuppressed patients.

Systemic steroid therapy has a beneficial effect on the severity of chronic postherpetic neuralgia.

Topical therapy consists of:-


    • Antiviral creams and paints (acyclovir, idoxuridine) and a

    • Steroid-antibiotic preparation (Neo-Cortef ointment or Terra-Cortril spray).

    • Calamine and starch powder promote crust formation and should be avoided.



Clinical features of ocular lesions

1. Conjunctivitis, is associated with vesicles on the lid margin.

2. Episcleritis.

3. Scleritis, it may involves the cornea (sclerokeratitis).


Corneal lesions include the following:

  1. Punctate epithelial keratitis.

  2. Microdendritic ulcers.

  3. Nummular keratitis.

  4. Disciform keratitis.

  5. Anterior uveitis.

  6. Acute retinal necrosis.

  7. Neurological complications: - CN palsies affecting the III, IV and VI. Optic neuritis, Encephalitis, Contralateral hemiplegia.


Treatment of ocular lesions


  1. Topical steroids.

  2. Topical and systemic acyclovir.

  3. Topical cycloplegics


CHRONIC PHASE
Skin lesions

  1. These are typical 'punched-out' scars associated with varying degrees of hyperpigmentation and hypopigmentation.

  2. Ptosis may occur as a result of scarring of the lids.

  3. Trichiasis,

  4. loss of lashes,

  5. ectropion,

  6. Entropion.

  7. Lid-notching.

Ocular lesions

  1. Mucus-secreting conjunctivitis.

  2. Scleritis and sclerokeratitis may lead to a progressive scarring of the cornea.

  3. Corneal vascularized and infiltrated by lipid.

  4. Neutrophic and exposure keratitis may lead to severe ulceration, secondary infection and even perforation.

  5. Mucous plaque keratitis it is characterized by a sudden onset of ciliary injection and the production of mucous plaque deposits on the surface of a diffusely swollen corneal epithelium.

  6. Post-herpetic neuralgia: -It may be constant or intermittently severe and stabbing as in tic douloureux. The pain may be worse at night and aggravated by touch and heat.


RELAPSING PHASE
Relapsing or recurrent lesions may reappear as long as 10 years after the acute lesions. They are frequently precipitated by the sudden withdrawal or reduction of topical corticosteroids.
The most commonly occurring lesions are:

  1. Episcleritis,

  2. Scleritis,

  3. Iritis,

  4. Glaucoma

  5. Nummular, disciform and mucous plaque keratitis.



Peripheral corneal disorders

  1. Dellen

Dellen consist of localized areas of corneal thinning which occur as a result of localized tear film instability. The three main causes are: (1) raised limbal lesions, (2) hard contact lenses and (3) idiopathic in the elderly.

O/E shows saucer-like thinning of the peripheral cornea.

Treatment involves elimination of the cause, and promoting corneal rehydration by patching and the use of lubricants.


  1. Marginal keratitis

Caused by a hypersensitivity reaction to staphylococcal exotoxins. It is in patients suffering from chronic staphylococcal blepharitis.

O/E: - A subepithelial infiltrate. The 10, 2, 4 or 8 o'clock positions are affected first.

Treatment with a short course of topical steroids is extremely effective in promoting resolution. To prevent recurrence associated chronic staphylococcal blepharitis, should also be treated.


  1. Rosacea keratitis

Acne rosacea is a common, skin disease of unknown aetiology which typically affects women aged between 30 and 50 years. Examination of the skin shows chronic hyperaemia of the face, usually involving the nose, central forehead and upper cheeks. Other features include variable degrees of telangiectasia, papules, pustules and Rhinophyma is the most advanced form of the disease.

KERATITIS

  1. Punctate epitheliopathy involving the inferior two thirds of the cornea.

  2. Peripheral vascularization, especially involving the inferotemporal and inferonasal quadrants. In severe cases pannus formation may obscure the visual axis.

  3. Thinning occurs either by resolution of the infiltrates or by gross ulceration. Perforation may be precipitated by the excessive use of topical steroids.

  1. Chronic posterior blepharitis (primary meibomitis) and recurrent chalazia are very common in patients with rosacea.


Treatment

Topical therapy with steroid drops is a very effective short-term measure.

Systemic therapy is with one of the following antibiotics:


    1. Tetracycline 250 mg 4X daily.

    2. Doxycycline 100mg once daily.


4.Phlyctenulosis

It is caused by a non-specific delayed hypersensitivity reaction to staphylococci or other bacterial antigens.



Presentation: -

    • Photophobia,

      • Lacrimation and

        • Blepharospasm.

O/E:-

    • Conjunctival phlycten shows a small pinkish-white nodule near the limbus, surrounded by hyperaemia.

    • A corneal phlycten starts astride the limbus and it may either resolve spontaneously or extend radially on to the cornea.

Treatment

  1. Short course of topical steroids is usually very effective in promoting resolution.

  2. Systemic tetracycline may be necessary.




  1. Marginal corneal degeneration

It is a thinning of the peripheral cornea. It is usually bilateral and asymmetrical.

O/E early cases show fine, yellow-white, punctate stromal opacities which are frequently associated with mild superficial vascularization. Vision gradually deteriorates as a result of increasing corneal astigmatism.

Treatment for severe astigmatism can be treated by a crescent-shaped excision of the gutter with suturing of the 'healthier' margins.


  1. Mooren's ulcer

It is a rare peripheral ulcerative keratitis thought to be caused by an ischaemic necrosis resulting from vasculitis of limbal vessels.

O/E of early cases shows patches of grey infiltrate near the margin of the cornea. This spreads by slowly undermining the corneal epithelium and superficial corneal lamellae at its advancing border, forming an overhanging edge.
Treatment is frequently difficult and includes the following options:

1. Topical therapy with steroids used at hourly intervals is the initial approach.

2. Systemic therapy with cyclosporin, steroids and cytotoxic drugs (cyclophosphamide, azathioprine or methotrexate).

3. Conjunctival excision, approximately 3 mm from the limbus and parallel to the ulcer, may be effective in some cases resistant to systemic therapy.


Keratitis in systemic collagen vascular disorders
The presence of severe, persistent, peripheral, corneal infiltration, ulceration or thinning unexplained by coexistent ocular disease should prompt a search for an associated systemic collagen vascular disease.
The four main diseases that should be considered are:

    1. Rheumatoid arthritis.

    2. Systemic lupus erythematosus.

    3. Polyarteritis nodosa.

    4. Wegener's granulomatosis.

The ocular lesions may occasionally precede the clinical manifestation of the systemic disease.


Corneal degenerations

  1. Age-related degenerations

    1. ARCUS SENILIS is the most commonly encountered peripheral corneal opacity. It may be associated with familial and non-familial dyslipoproteinaemias but may also occur without any predisposing factors. It is frequently bilateral arcus. The presence of arcus is also age related and is found in virtually all individuals over the age of 80. Unilateral arcus is a rare entity that may be associated with carotid disease or ocular hypotony.

Examination shows bilateral lipid deposition which starts in the superior and inferior perilimbal cornea and then progresses circumferentially to form a band about 1 mm wide.

    1. VOGT'S WHITE LIMBAL GIRDLE bilateral, narrow, crescentic lines composed of chalk-like flecks running in the interpalpebral fissure along the nasal and temporal limbus.

    2. CORNEA FARINATA characterized by the presence of minute, bilateral, flour-like deposits in the deep corneal stroma most prominent centrally.

    3. CROCODILE SHAGREEN

    4. CORNEA GUTTATA




  1. Lipid keratopathy

It is occurs in two settings:

  1. Primary lipid keratopathy (spontaneously in an avascular cornea).

  2. Secondary lipid keratopathy common and associated with previous ocular injury or disease which results in corneal vascularization.


O/E shows white or yellowish corneal stromal deposits consisting of cholesterol, fats and phospholipids. In the secondary type there is associated corneal vascularization. In the absence of treatment, vascularized lipid keratopathy is a progressive condition which causes deterioration of vision.
Treatment

Control of the primary inflammatory disease and then of the lipid deposits. Slow resorption of the lipid infiltrate can be induced by: -



  1. Argon laser photocoagulation to the feeder vessels.

  2. Corneal grafting where laser therapy is inappropriate or ineffective.

Band keratopathy

Deposition of calcium salts in the subepithelial space and Bowman's membrane. The four main causes are:



      1. Chronic iridocyclitis particularly in children,

      2. Idiopathic in the elderly,

      3. Phthisis bulbi and

      4. Increased serum calcium or phosphorus levels.

O/E distribution of the lesions is in the interpalpebral fissure with a clear space separating the sharp margin of the band from the limbus.

Slitlamp examination reveals holes in the calcium plaques which are thought to represent nerve canals in Bowman's layer.


Treatment

Chelation is a simple and effective form of treatment for relatively mild cases.

Excimer laser keratectomy may be used for cases with more extensive and deeper involvement.


  1. Spheroidal degeneration

Spheroidal degeneration is also known under many eponyms, including corneal elastosis. It is a degenerative condition which typically occurs in men whose working lives are spent outdoors. The degree of severity of the degeneration correlates closely with the length of time spent outside.

O/E shows small amber-colored spheroidal granules or droplets composed of protein in the superficial corneal stroma in the interpalpebral strip. It begins in the periphery and spreads centrally. The condition varies in severity from localized mistiness to the development of large nodules and serious visual impairment in later life caused by corneal opacification.

Treatment

  1. Corneal epithelial débridement.

  2. Superficial keratectomy (temporary measure) to improve vision.

  3. Lamellar or penetrating keratoplasty is required for long-term improvement of visually incapacitating cases.


5.Salzmann's nodular degeneration

It is invariably occurs secondary to chronic keratitis, especially trachoma and phlyctenulosis.

O/E shows discrete, elevated grey or blue grey superficial stromal opacities, which form nodules that elevate the corneal epithelium.

These nodules are located either in scarred cornea or at the edges of transparent cornea. The base of a nodule may be surrounded by epithelial iron deposits.



Treatment is similar to that of spheroidal degeneration.
Corneal dystrophies

The corneal dystrophies are a group of spontaneous appearing, usually inherited, bilateral, stationary or slowly progressive corneal alterations that develop in the absence of inflammation. Age of onset, symptoms, mode of progression and inheritance differ in the various dystrophies. Most present by the second decade, but some that have little effect on vision may present in adult life.



Classification

I. Anterior dystrophies

  1. Microcystic

  2. Reis-Bücklers'

  3. Meesmann's

II. Stromal dystrophies

  1. Lattice

  2. Macular

  3. Granular

III. Posterior dystrophies

  1. Fuchs' endothelial

  2. Posterior polymorphous

IV. Ectatic dystrophies

  1. Keratoconus

  2. Posterior keratoconus

  3. Keratoglobus

  4. Pellucid marginal degeneration


Miscellaneous keratopathies

1. Exposure keratopathy

It is caused by improper wetting of the corneal surface by the precorneal tear film because of the inability of the lids to resurface the cornea with each blink. Important causes include facial nerve palsy, severe proptosis and scarring of the eyelids.


2. Neurotrophic keratopathy

It is occurs in an anaesthetic cornea. It appears that the corneal sensory nerves are very important in maintaining the health of the corneal epithelium.

Causes section of the fifth nerve, herpes simplex and herpes zoster keratitis, diabetes and leprosy.
3. Recurrent corneal erosion syndrome

It is a disturbance of the corneal epithelial basement membrane complex which results in defective adhesion and recurrent breakdown of the epithelium. The condition is most commonly caused by superficial corneal trauma, especially from a scratch. It may also occur in certain corneal dystrophies as already described.


Presentation is typically on waking with a sudden onset of unilateral pain, lacrimation, photophobia and blurred vision. It is troublesome in diabetic patients.
O/E: - during the acute stage shows a corneal abrasion. It is also important to examine the fellow eye for evidence of microcystic dystrophy.
TREATMENT OF ACUTE EROSIONS

  1. Pressure patching for 24 hours, combined with a

  2. Mild cycloplegic and a

  3. Prophylactic antibiotic ointment, will usually suffice in most mild cases.

  4. Débridement in severe cases. It provides a smooth basement membrane substrate which can be resurfaced with healthy epithelium.


PROPHYLACTIC TREATMENT

  1. Lubrication with artificial tears four times daily.

  2. Bandage contact lenses with low water content can be tried if lubrication is ineffective.

  3. Superficial epithelial keratectomy may be necessary for severely recalcitrant cases.

  4. Anterior stromal puncture is an alternative treatment for recalcitrant erosions. The Nd: YAG laser can also be used to perform stromal punctures.


4. Metabolic keratopathy

  1. MUCOPOLYSACCHARIDOSES




  1. WILSON'S DISEASE

Wilson's disease (hepatolenticular degeneration) is a rare condition caused by a deficiency of the α2-globulin ceruloplasmin. It is characterized by a widespread deposition of copper in the tissues and becomes manifest in one of three ways: (1) liver disease, (2) neurological involvement of the basal ganglia or (3) psychiatric features.

Corneal copper deposition is present in nearly all patients. The classic Kayser-Fleischer ring is located at the peripheral part of Descemet's membrane and appears as a zone of granules which change colour under different types of illumination. It will be disappear with penicillamine therapy. Some patients also have a green 'sunflower' cataract.


Principles of keratoplasty

Keratoplasty, which is also referred to as corneal transplantation or corneal grafting, is an operation in which abnormal host tissue is replaced by healthy donor corneal tissue. The graft may be partial thickness (lamellar) or full thickness (penetrating).


Penetrating keratoplasty

INDICATIONS:



  1. Optical indications are primarily improvement of visual acuity by replacing opaque corneal tissue with clear donor tissue. Currently, the most common indication is pseudophakic bullous keratopathy, keratoconus, corneal dystrophies and degenerations, and scarring caused by various types of keratitis and trauma.

  2. Tectonic indications are restoration or preservation of corneal anatomy in eyes with severe structural changes such as stromal thinning and descemetoceles.

  3. Therapeutic indication is removal of inflamed corneal tissue in eyes unresponsive to conventional antimicrobial or antiviral therapy.

  4. Cosmetic indication is improvement of the appearance of the eye.

Donor tissue should ideally be removed less than 6 hours after death.


GRAFT FAILURE

Early

Early failure is characterized by cloudiness of the graft from the first postoperative day. It is caused by endothelial dysfunction resulting from defective donor endothelium or surgical trauma at the time of operation.


Late

Late failure is most frequently the result of immune graft rejection.


Treatment is with prompt administration of hourly topical steroids and periocular steroid injections. In severe resistant cases, systemic immunosuppressive agents may be necessary.
Lamellar keratoplasty

The following are the main indications for lamellar keratoplasty.



    1. Opacification of the superficial one-third of the corneal stroma not caused by potentially recurrent disease.

    2. Marginal corneal thinning or infiltration as in recurrent pterygium, marginal cornealdegeneration, and limbal dermoids or other tumours.

    3. Localized thinning or descemetocele formation.

        • who present with scleral necrosis.

Done by Omar Abid ALsamrrae


With best wishes






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