Corneal opacity

Corneal opacity
Corneal opacity
Other names	Corneal scarring
	Complete corneal opacity in right eye with normal left eye
Specialty	Ophthalmology
Symptoms	Loss of vision
Complications	Blindness
Usual onset	Congenital or acquired
Treatment	Corneal transplantation
Frequency	4th main cause of blindness globally (5.1%).

Last updated August 09, 2024

Corneal opacification is a term used when the human cornea loses its transparency. The term corneal opacity is used particularly for the loss of transparency of cornea due to scarring. Transparency of the cornea is dependent on the uniform diameter and the regular spacing and arrangement of the collagen fibrils within the stroma. Alterations in the spacing of collagen fibrils in a variety of conditions including corneal edema, scars, and macular corneal dystrophy is clinically manifested as corneal opacity.^[2] The term corneal blindness is commonly used to describe blindness due to corneal opacity.

Keratoplasty also known as corneal transplantation is the main treatment option for visual improvement in corneal opacity. Other treatments which may improve visual outcome includes optical iridectomy, phototherapeutic keratectomy and keratoprosthesises. Corneal tattooing may be used for improving the cosmetic appearance of the opaque eye.

Types

Corneal opacity with neovascularization Corneaneo.jpg — Corneal opacity with neovascularization

Depending on the density, corneal opacity is graded as nebular, macular and leucomatous.

Nebular corneal opacity

Nebular corneal opacity is a faint opacity which results due to superficial scars involving Bowman's layer and superficial stroma. A nebular corneal opacity allows the details of the iris to be seen through the opacity. A thin, diffuse nebula covering the pupillary area interferes more with vision than a strictly localized dense leucoma, so long as the latter does not block the whole pupillary area. This is because the leucoma stops all the light which falls upon it, whereas the nebula refracts it irregularly, allowing many of the rays to fall upon the retina where they blur the image formed by the regularly refracted rays.^[3]

Macular corneal opacity

Macular corneal opacity is a semidense opacity produced when scarring involves about half the corneal stroma.^[4]

Leucomatous corneal opacity (leucoma simplex)

Leucomatous corneal opacity is a dense white opacity which results due to scarring of more than half of the stroma.^[4] A number of different presentations of leucomatous corneal opacity exist:

Adherent leucoma: results when healing occurs after perforation of cornea with incarceration of iris. The iris is adherent to the back of a leucomatous cornea. One of the major complication of adherent leucoma is Secondary glaucoma ^[5]
Corneoiridic scar: if iris tissue is incarcerated and incorporated within the scar tissue, as occurs in healing of a large sloughed corneal ulcer, it is called a corneoiridic scar.^[3]
Corneal facet: corneal surface depressed at the site of healing (due to less fibrous tissue); such a scar is called facet.^[4]
Kerectasia: In this condition, corneal curvature is increased at the site of opacity (bulge due to weak scar).^[4]

Presentation

Signs and symptoms include the following:

Loss of vision or blindness (when dense opacity covers the pupillary area)^[6]
Blurred vision (due to astigmatic effect and light scattering)^[7]
Glare ^[8]

Complications

Congenital corneal opacity that affecting vision will cause amblyopia. That type of amblyopia is known as form-deprivation amblyopia (or amblyopia ex anopsia).^[9]

Secondary changes in corneal opacity

Secondary changes may be seen in long-standing cases include: hyaline degeneration, calcareous degeneration, pigmentation and atheromatous ulceration.^[4]

Causes

Congenital opacities may occur as developmental anomalies or following birth trauma. Causes of congenital corneal opacities include sclerocornea, trauma, ulcer, mucopolysaccharidosis, Peter’s anomaly, congenital hereditary endothelial dystrophy.^[3]
Ocular trauma ^[10]
Corneal ulceration ^[10]
Xerophthalmia, caused by Vitamin A deficiency ^[10]
Trachoma ^[11]
Onchocerciasis ^[12]
Mucous membrane pemphigoid: Ocular form of mucous membrane pemphigoid may cause corneal opacity and loss of vision.^[13]

Genetics

Pediatric corneal opacities may be congenital or acquired.

Congenital corneal opacities

Congenital reasons for this condition include:

Congenital hereditary endothelial dystrophy (CHED): There are 2 forms of congenital hereditary endothelial dystrophy (CHED). Commonest is an autosomal recessive form, which is present at birth, but nonprogressive. Nystagmus is seen in association with this form. Another is an autosomal dominant form that occurs within the first few years of life. This form is progressive, but nystagmus is not seen. Deafness and CHED are seen in Harboyan syndrome. The histologic findings are very similar to those seen in pseudophakic/ aphakic bullous keratopathy. The appearance of the cornea is similar to that in congenital glaucoma but without increased corneal diameter and elevated intraocular pressure.^[14]
Posterior polymorphous corneal dystrophy (PPMD, PPCD)^[15]: PPCD, also known as Schlichting dystrophy, is an autosomal dominant disorder of the corneal endothelium and Descemet’s membrane. It is usually present in the second or third decade of life. It has the same entity as the first form of CHED. Most cases of PPMD are asymptomatic, and these cases generally do not require treatment. PPMD patients with bilateral, corneal opacities that can affect vision, descemet’s membrane endothelial keratoplasty or penetrating keratoplasty are the treatments of choice to improve vision and to avoid amblyopia.
Congenital hereditary stromal dystrophy (CHSD): CHSD is also known as Congenital stromal corneal dystrophy or Congenital stromal dystrophy of the cornea. It is a rare autosomal dominant disease caused by mutations in the DCN gene.^[16] In this bilateral Snowflake, whitish opacities appear throughout the cornea.^[17] The stromal lamellae are abnormal and may be separated by amorphous deposits. Moderate to severe vision loss may occur due to corneal opacity. In case of severe vision loss, treatment of choice is penetrating keratoplasty.^[17]
Peters anomaly:^[18] Peters anomaly, also known as iridocorneal adhesions or keratolenticular adhesions, is a posterior corneal defect with an overlying stromal opacity, often accompanied by adherent iris strands (Peters anomaly type 1). The size and density of the opacity can range from a mild to dense central leukoma.
Congenital anterior staphyloma:^[19] Congenital anterior staphyloma is a rare form of anterior segment dysgenesis that shares similarities with Peters anomaly. It is characterized by an ectatic protrusion of a central opacified cornea lined by uveal tissue. The protrusion extends beyond the plane of the eyelid margins and it can be unilateral or bilateral.
Lattice corneal dystrophy: Lattice corneal dystrophy is an autosomal-dominant characterized by amyloid deposition in the corneal stroma. Due to deposits, lattice-like corneal opacities may occur in stroma. Three types of dystrophies are there, type 1, type 2 and type 3.^[17] Type 1 is also known as Biber-Haab-Dimmer corneal dystrophy, TGFBI type Lattice Dystrophy, or Classic Lattice Dystrophy.^[20] LCD type II is not included in corneal dystrophies.^[20]
Granular corneal dystrophy:^[21] Two types, Type 1 and Type 2 are there. Both have autosomal dominant inheritance. In Type 1, Discrete crumb-like opacities are seen in the central anterior stroma. Visual symptoms such as glare and photophobia may occur early in life. In Type 2, deposits begin to appear in early childhood or adolescence as tiny whitish dots in the anterior stroma. Larger stellate, ring, or snowflake opacities may occur in later stages. Decrease in vision starts earlier in type2 than type1.
Sclerocornea:^[22] Sclerocornea is a congenital disorder in which the cornea is opaque and resembles the sclera, making the limbus indistinct. The central cornea is clearer than the periphery.
Cystinosis: Cystinosis is a rare autosomal recessive metabolic disease characterized by elevated levels of cystine within the cell.^[23] Early deposition of cystine crystals in the cornea cause tinsel-like corneal opacities.^[24]
Ichthyosis: X-linked ichthyosis is a genetic skin disorder caused by the hereditary deficiency of the steroid sulfatase enzyme. Ocular manifestations of XLI include superficial or deep corneal opacities.^[25]^[26]
Trisomy 8 mosaicism (T8M): It is a rare chromosome disorder caused by the presence of an extra chromosome 8 in some cells of the body. Dense corneal opacities may occur in trisomy 8 mosaicism.^[25]
Farber's disease : Nodular corneal opacity may be seen in association with this rare autosomal recessive disease.^[25]

Acquired pediatric corneal opacities

Acquired reasons for this condition include:

Traumatic: Traumatic breaks in Descemet membrane may cause corneal opacity. Injuries to Descemet membrane occur during delivery.^[22] Opacity is commonly unilateral.^[18]
Congenital or infantile glaucoma:^[18] In Congenital glaucoma, the cornea becomes edematous, cloudy, and enlarged. Treatment should be done to reduce Intraocular pressure.
Congenital corneal ulcers: Unilateral corneal opacity may occur in association with conjunctival injection and other signs of inflammation.^[22]
Mucopolysaccharidoses:^[22] The mucopolysaccharidoses are a group of inherited metabolic diseases caused by the absence or malfunctioning of certain enzymes the body needs to break down molecules called glycosaminoglycans.^[27] It is an autosomal recessive disorder. Sometimes, Corneal haze may be present in early life. Treatment options for significant opacities include penetrating keratoplasty and DALK.

Treatment

Keratoplasty

Keratoplasty also known as corneal transplantation is the main treatment option for visual improvement in corneal opacity. In this, the opaque cornea is replaced with donor tissue. Depending on type and density of corneal opacity different types of keratoplasty may be used such as:^[28]

Penetrating keratoplasty: It is the traditional full thickness corneal transplant procedure, in which trephine (a circular cutting device) is used to cut opaque cornea, a similar-sized portion of the donor cornea is removed with a second trephine. The removed part of donor cornea is known as corneal button. The donor tissue is then sutured to the patient eye. Dense corneal opacity which occupies all the corneal layers may be treated with penetrating keratoplasty.^[29]
Superficial lamellar keratoplasty: Superficial lamellar keratoplasty is used to treat superficial corneal opacities, which occupies superficial one third part of stroma. In this technique, the opaque part of the cornea is removed and replaced with donor tissue, leaving healthy part of the cornea including deeper parts of stroma and endothelium.^[29]
Deep anterior lamellar keratoplasty: DALK may be considered in deep opacities with normal endothelium and descemet's membrane. In this procedure, the anterior layers of cornea are removed and replaced with donor tissue, leaving the endothelial layer and the descemet's membrane in place.^[29]

Optical iridectomy

Optical iridectomy creates a clear entrance pupil, improving vision in patients with segmental corneal opacities. An area of clear peripheral cornea can produce retinal images compatible with good visual acuity.^[30]

Phototherapeutic keratectomy (PTK)

Excimer laser phototherapeutic keratectomy (PTK) is useful in superficial (nebular) corneal opacities.^[31]

Tattooing of scar

Keratopigmentation or corneal tattooing is a procedure used for centuries to improve the cosmetic appearance of corneal scars. Tattooing will not improve vision. For tattooing procedure Indian black ink, gold or platinum may be used.^[4]

Techniques

Staining method: In this technique, tattoo ink is directly applied to anterior surface of cornea. Benefits of this procedure include fast procedure with uniform dye application. Risk of fading is a main drawback.^[32]
Femtosecond laser-assisted corneal tattooing: Femtosecond laser-assisted corneal tattooing is a new corneal tattooing technique, with many benefits.^[33]

Keratoprosthesis

Keratoprosthesis is a surgical procedure where damaged or opaque cornea is replaced with an artificial cornea. Artificial corneas currently in commercial use include Boston keratoprosthesis, Osteo-Odonto-Keratoprosthesis (OOKP), AlphaCor, KeraKlear Artificial Cornea etc.^[34]^[35]

Epidemiology

Corneal opacity is the 4th main cause of blindness globally (5.1%).^[1] Using the World Health Organization's (WHO; Geneva, Switzerland) blindness definition,1 45 million people worldwide are bilaterally blind, of which 6 to 8 million are blind due to corneal disease. In some African areas, nearly 90% of the total blindness is due to corneal pathology.^[36]

Europe

The prevalence of congenital corneal opacities (CCO) is estimated to be 3 in 100,000 newborns. This number increases to 6 in 100,000 if congenital glaucoma patients are included. A study of live births in Spain reported that corneal opacities accounted for 3.11% of congenital eye malformations (Bermejo et al, 1998). About 4% of keratoplasties done in the pediatric population in Denmark are due to congenital anomalies (Hovlykke et al, 2014).^[37]

India

In NPCB survey (2001–2002) Corneal opacity was the 6th major cause of blindness in India, which accounts for 0.9% of total blind population. In the RAAB (Rapid Assessment of Avoidable Blindness) survey (2006–2007) Corneal opacity including Trachoma was mentioned as the second major cause of blindness, which accounts for 6.5% of total blindness.^[38]

Related Research Articles

<span class="mw-page-title-main">Cornea</span> Transparent front layer of the eye

The cornea is the transparent front part of the eye that covers the iris, pupil, and anterior chamber. Along with the anterior chamber and lens, the cornea refracts light, accounting for approximately two-thirds of the eye's total optical power. In humans, the refractive power of the cornea is approximately 43 dioptres. The cornea can be reshaped by surgical procedures such as LASIK.

The corneal endothelium is a single layer of endothelial cells on the inner surface of the cornea. It faces the chamber formed between the cornea and the iris.

Corneal transplantation, also known as corneal grafting, is a surgical procedure where a damaged or diseased cornea is replaced by donated corneal tissue. When the entire cornea is replaced it is known as penetrating keratoplasty and when only part of the cornea is replaced it is known as lamellar keratoplasty. Keratoplasty simply means surgery to the cornea. The graft is taken from a recently deceased individual with no known diseases or other factors that may affect the chance of survival of the donated tissue or the health of the recipient.

Fuchs dystrophy, also referred to as Fuchs endothelial corneal dystrophy (FECD) and Fuchs endothelial dystrophy (FED), is a slowly progressing corneal dystrophy that usually affects both eyes and is slightly more common in women than in men. Although early signs of Fuchs dystrophy are sometimes seen in people in their 30s and 40s, the disease rarely affects vision until people reach their 50s and 60s.

Descemet's membrane is the basement membrane that lies between the corneal proper substance, also called stroma, and the endothelial layer of the cornea. It is composed of different kinds of collagen than the stroma. The endothelial layer is located at the posterior of the cornea. Descemet's membrane, as the basement membrane for the endothelial layer, is secreted by the single layer of squamous epithelial cells that compose the endothelial layer of the cornea.

Corneal dystrophy is a group of rare hereditary disorders characterised by bilateral abnormal deposition of substances in the transparent front part of the eye called the cornea.

Iridocorneal endothelial (ICE) syndromes are a spectrum of diseases characterized by slowly progressive abnormalities of the corneal endothelium and features including corneal edema, iris distortion, and secondary angle-closure glaucoma. ICE syndromes are predominantly unilateral and nonhereditary. The condition occurs in predominantly middle-aged women.Iridocorneal Endothelial (ICE) syndrome presents a unique set of challenges for both patients and ophthalmologists, and effective treatment of this group of rare ocular diseases requires a combination of diagnostic and therapeutic complexity. It's important to understand.

<span class="mw-page-title-main">Corneal neovascularization</span> Medical condition

Corneal neovascularization (CNV) is the in-growth of new blood vessels from the pericorneal plexus into avascular corneal tissue as a result of oxygen deprivation. Maintaining avascularity of the corneal stroma is an important aspect of healthy corneal physiology as it is required for corneal transparency and optimal vision. A decrease in corneal transparency causes visual acuity deterioration. Corneal tissue is avascular in nature and the presence of vascularization, which can be deep or superficial, is always pathologically related.

<span class="mw-page-title-main">Bullous keratopathy</span> Medical condition

Bullous keratopathy, also known as pseudophakic bullous keratopathy (PBK), is a pathological condition in which small vesicles, or bullae, are formed in the cornea due to endothelial dysfunction.

Meesmann corneal dystrophy (MECD) is a rare hereditary autosomal dominant disease that is characterized as a type of corneal dystrophy and a keratin disease. MECD is characterized by the formation of microcysts in the outermost layer of the cornea, known as the anterior corneal epithelium. The anterior corneal epithelium also becomes fragile. This usually affects both eyes rather than a single eye and worsens over time. There are two phenotypes, Meesmann corneal dystrophy 1 (MECD1) and Meesmann corneal dystrophy 2 (MECD2), which affect the genes KRT3 and KRT12, respectively. A heterozygous mutation in either of these genes will lead to a single phenotype. Many with Meesmann corneal dystrophy are asymptomatic or experience mild symptoms.

Keratoprosthesis is a surgical procedure where a diseased cornea is replaced with an artificial cornea. Traditionally, keratoprosthesis is recommended after a person has had a failure of one or more donor corneal transplants. More recently, a less invasive, non-penetrating artificial cornea has been developed which can be used in more routine cases of corneal blindness. While conventional cornea transplant uses donor tissue for transplant, an artificial cornea is used in the keratoprosthesis procedure. The surgery is performed to restore vision in patients with severely damaged cornea due to congenital birth defects, infections, injuries and burns.

Macular corneal dystrophy, also known as Fehr corneal dystrophy, is a rare pathological condition affecting the stroma of cornea first described by Arthur Groenouw in 1890. Signs are usually noticed in the first decade of life and progress afterwards, with opacities developing in the cornea and attacks of pain. This gradual opacification leads to visual impairment often requiring keratoplasty in the later decades of life.

Corneal dystrophies are a group of diseases that affect the cornea in dogs.

Congenital stromal corneal dystrophy (CSCD) is an extremely rare, autosomal dominant form of corneal dystrophy. Only 4 families have been reported to have the disease by 2009. The main features of the disease are numerous opaque flaky or feathery areas of clouding in the stroma that multiply with age and eventually preclude visibility of the endothelium. Strabismus or primary open angle glaucoma was noted in some of the patients. Thickness of the cornea stays the same, Descemet's membrane and endothelium are relatively unaffected, but the fibrils of collagen that constitute stromal lamellae are reduced in diameter and lamellae themselves are packed significantly more tightly.

Anterior segment mesenchymal dysgenesis, or simply anterior segment dysgenesis (ASD), is a failure of the normal development of the tissues of the anterior segment of the eye. It leads to anomalies in the structure of the mature anterior segment, associated with an increased risk of glaucoma and corneal opacity.

Congenital hereditary corneal dystrophy (CHED) is a form of corneal endothelial dystrophy that presents at birth.

Dua's layer, according to a 2013 paper by Harminder Singh Dua's group at the University of Nottingham, is a layer of the cornea that had not been detected previously. It is hypothetically 15 micrometres thick, the fourth caudal layer, and located between the corneal stroma and Descemet's membrane. Despite its thinness, the layer is very strong and impervious to air. It is strong enough to withstand up to 2 bars of pressure. While some scientists welcomed the announcement, other scientists cautioned that time was needed for other researchers to confirm the discovery and its significance. Others have met the claim "with incredulity".

Corneal hydrops is an uncommon complication seen in people with advanced keratoconus or other corneal ectatic disorders, and is characterized by stromal edema due to leakage of aqueous humor through a tear in Descemet's membrane. Although a hydrops usually causes increased scarring of the cornea, occasionally it will benefit a patient by creating a flatter cone, aiding the fitting of contact lenses. Corneal transplantation is not usually indicated during corneal hydrops.

Pre Descemet's endothelial keratoplasty (PDEK) is a kind of endothelial keratoplasty, where the pre descemet's layer (PDL) along with descemet's membrane (DM) and endothelium is transplanted. Conventionally in a corneal transplantation, doctors use a whole cornea or parts of the five layers of the cornea to perform correction surgeries. In May 2013, Dr Harminder Dua discovered a sixth layer between the stroma and the descemet membrane which was named after him as the Dua's layer. In the PDEK technique, doctors take the innermost two layers of the cornea, along with the Dua's layer and graft it in the patient's eye.

Descemet membrane endothelial keratoplasty (DMEK) is a method of corneal transplantation. The DMEK technique involves the removal of a very thin sheet of tissue from the posterior (innermost) side of a person's cornea, replacing it with the two posterior (innermost) layers of corneal tissue from a donor's eyeball. The two corneal layers which are exchanged are the Descemet's membrane and the corneal endothelium. The person's corneal tissue is gently excised, peeled off, and replaced with the donor tissue via small 'clear corneal incisions' (small corneal incisions just anterior to the corneal limbus. The donor tissue is tamponaded against the person's exposed posterior corneal stroma by injecting a small air bubble into the anterior chamber. To ensure the air tamponade is effective, it is necessary for people to strictly maintain such a posture that they are looking up at the ceiling during the recovery period until the air bubble has fully resorbed.

References

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↑ J Alroy , M Haskins, D E Birk (2001). "Altered Corneal Stromal Matrix Organization Is Associated With Mucopolysaccharidosis I, III and VI". Experimental Eye Research. 68 (5): 523–30. doi:10.1006/exer.1998.0622. PMID 10328965.{{cite journal}}: CS1 maint: multiple names: authors list (link)
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[WHO-PED-1] 1 2 "WHO -Priority eye diseases". www.who.int. Archived from the original on March 22, 2006.

[2] J Alroy , M Haskins, D E Birk (2001). "Altered Corneal Stromal Matrix Organization Is Associated With Mucopolysaccharidosis I, III and VI". Experimental Eye Research. 68 (5): 523–30. doi:10.1006/exer.1998.0622. PMID 10328965.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[Parson-3] 1 2 3 Ramanjit Sihota; Radhika Tandon (15 July 2015). "The posterior segment". Parsons' diseases of the eye (22 ed.). Elsevier India. pp. 195, 221. ISBN 978-81-312-3818-9.

[Khurana-4] 1 2 3 4 5 6 AK Khurana. "Diseases of the Cornea". Comprehensive Ophthalmology (6 ed.). Jaypee. pp. 121–122.

[5] J Das, S Bhomaj, Z Chaudhuri, P Sharma, A Negi, A Dasgupta (2001). "Profile of Glaucoma in a Major Eye Hospital in North India". Indian Journal of Ophthalmology. 49 (1): 25–30. PMID 15887712.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[Khurana-CO-6] Khurana, AK (31 August 2015). Comprehensive ophthalmology (6th ed.). Jaypee, The Health Sciences Publisher. pp. 133–139. ISBN 978-93-5152-657-5.

[CRST-7] Shachar Tauber. "Help for Patients With Corneal Scarring". CRSToday.

[NCBI-CO-8] Spadea, Leopoldo; Maraone, Giorgia; Verboschi, Francesca; Vingolo, Enzo Maria; Tognetto, Daniele (18 March 2016). "Effect of corneal light scatter on vision: a review of the literature". International Journal of Ophthalmology. 9 (3): 459–464. doi:10.18240/ijo.2016.03.24. ISSN 2222-3959. PMC 4844042 . PMID 27158621.

[9] "Amblyopia".

[WHO-CB-10] 1 2 3 John P. Whitcher; M. Srinivasan; Madan P. Upadhyay. "Corneal blindness: a global perspective" (PDF). www.who.int.

[11] "What is trachoma". Archived from the original on September 22, 2016.

[12] JHubert H Fam (2019-11-21). "Onchocerciasis (African River Blindness)". American Academy of Ophthalmology.

[13] Schonberg, Stacy; Stokkermans, Thomas J. (2020). "Ocular Pemphigoid". StatPearls. StatPearls Publishing. PMID 30252356.

[14] "Congenital Hereditary Endothelial Dystrophy - EyeWiki". eyewiki.aao.org.

[15] "Posterior Polymorphous Corneal Dystrophy - EyeWiki". eyewiki.aao.org.

[GHR-16] Reference, Genetics Home. "Congenital stromal corneal dystrophy". Genetics Home Reference.

[Oxford-17] 1 2 3 "Cornea". Oxford handbook of ophthalmology (4th ed.). Oxford university press. 2018. ISBN 978-0-19-881675-1.

[Medscape-18] 1 2 3 Myra Vita F Ocubillo (2018-10-10). "Congenital Clouding of the Cornea: Background, Pathophysiology, Epidemiology".

[19] Salour, Hossein; Owji, Nasser; Sadeghipour, Alireza (2009). "Congenital Corneal Staphyloma". Journal of Ophthalmic & Vision Research. 4 (3): 182–184. ISSN 2008-2010. PMC 3498567 . PMID 23198071.

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