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Sclera
Sclera
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Sclera
The sclera, as separated from the cornea by the corneal limbus.
Details
Part ofEye
SystemVisual system
ArteryAnterior ciliary arteries, long posterior ciliary arteries, short posterior ciliary arteries
Identifiers
Latinsclera
MeSHD012590
TA98A15.2.02.002
TA26750
FMA58269
Anatomical terminology

The sclera,[note 1] also known as the white of the eye or, in older literature, as the tunica albuginea oculi, is the opaque, fibrous, protective outer layer of the eye containing mainly collagen and some crucial elastic fiber.[2]

In the development of the embryo, the sclera is derived from the neural crest.[3] In children, it is thinner and shows some of the underlying pigment, appearing slightly blue. In the elderly, fatty deposits on the sclera can make it appear slightly yellow. People with dark skin can have naturally darkened sclerae, the result of melanin pigmentation.[4]

In humans, and some other vertebrates, the whole sclera is white or pale, contrasting with the coloured iris. The cooperative eye hypothesis suggests that the pale sclera evolved as a method of nonverbal communication that makes it easier for one individual to identify where another individual is looking. Other mammals with white or pale sclera include chimpanzees, many orangutans, some gorillas, and bonobos.[5]

Structure

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Goat eye with relatively dark sclera and horizontal pupil
Cow eye with dark sclera
Rare whites in a western lowland gorilla

The sclera forms the posterior five-sixths of the connective tissue coat of the human eyeball. It is continuous with the dura mater and the cornea, and maintains the shape of the eyeball, offering resistance to internal and external forces, and provides an attachment for the extraocular muscle insertions. The sclera is perforated by many nerves and vessels passing through the posterior scleral foramen, the hole that is formed by the optic nerve. At the optic disc, the outer two-thirds of the sclera continues with the dura mater (outer coat of the brain) via the dural sheath of the optic nerve. The inner third joins with some choroidal tissue to form a plate (lamina cribrosa) across the optic nerve with perforations through which the optic fibers (fasciculi) pass. The thickness of the sclera varies from 1 mm at the posterior pole to 0.3 mm just behind the insertions of the four rectus muscles. The sclera's blood vessels are mainly on the surface. Along with the vessels of the conjunctiva (which is a thin layer covering the sclera), those in the episclera render the inflamed eye bright red.[6]

In many vertebrates, the sclera is reinforced with plates of cartilage or bone, together forming a circular structure called the sclerotic ring. In primitive fish, this ring consists of four plates, but the number is lower in many living ray-finned fishes, and much higher in lobe-finned fishes, crocodilians, various reptiles, and birds. The ring has disappeared in many groups, including living amphibians, some reptiles and fish, and all mammals.[7]

The eyes of all non-human primates have been thought to be dark with small, barely visible sclera, but recent research has suggested that white sclera are not uncommon in chimpanzees, and are also present in other mammals.[8]

Histology

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Histologically speaking, it is characterized as dense connective tissue made primarily of type 1 collagen fibers.[9] The collagen of the sclera is continuous with the cornea. From outer to innermost, the four layers of the sclera are:

The sclera is opaque due to the irregularity of the Type I[10] collagen fibers, as opposed to the near-uniform thickness and parallel arrangement of the corneal collagen. Moreover, the cornea bears more mucopolysaccharide (a carbohydrate that has among its repeating units a nitrogenous sugar, hexosamine) to embed the fibrils.

The cornea, unlike the sclera, has six layers. The middle (third in number; provided the first layer being the anterior and outermost and the sixth layer being the posterior and the inner most), thickest layer is also called the stroma. The sclera, like the cornea, contains a basal endothelium, above which there is the lamina fusca, containing a high count of pigment cells.[6]

Sometimes, very small gray-blue spots can appear on the sclera, a harmless condition called scleral melanocytosis.

Function

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Human eyes are somewhat distinctive in the animal kingdom in that the sclera is very plainly visible whenever the eye is open. This is not just due to the white color of the human sclera, which many other species share, but also to the fact that the human iris is relatively small and comprises a significantly smaller portion of the exposed eye surface compared to other animals. It is theorized that this adaptation evolved because of humans' social nature as the eye became a useful communication tool in addition to a sensory organ. It is believed that the exposed sclera of the human eye makes it easier for one individual to identify where another individual is looking, increasing the efficacy of this particular form of nonverbal communication, called cooperative eye hypothesis.[11] Animal researchers have also found that, in the course of their domestication, dogs have also developed the ability to pick up visual cues from the eyes of humans. Dogs do not seem to use this form of communication with one another and only look for visual information from the eyes of humans.[12]

Another hypothesis states that the distinctiveness of the human's sclera is due to genetic drift and sexual selection. A visibly white sclera is perceived as a sign of good health and youthfullness,[13] this could have been a criterion of selection when looking for a mate. In this case, humans' ability to communicate with their eyes (glancing, cluing at others) would only be a consequence of a very visible sclera.[14]

Trauma

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The bony area that makes up the human eye socket provides exceptional protection to the sclera. However, if the sclera is ruptured by a blunt force or is penetrated by a sharp object, the recovery of full former vision is usually rare. If pressure is applied slowly, the eye is actually very elastic. However, most ruptures involve objects moving at some velocity. The cushion of orbital fat protects the sclera from head-on blunt forces, but damage from oblique forces striking the eye from the side is not prevented by this cushion. Hemorrhaging and a dramatic drop in intraocular pressure are common, along with a reduction in visual perception to only broad hand movements and the presence or absence of light. However, a low-velocity injury which does not puncture and penetrate the sclera requires only superficial treatment and the removal of the object. Sufficiently small objects which become embedded and which are subsequently left untreated may eventually become surrounded by a benign cyst, causing no other damage or discomfort.[15]

Thermal trauma

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The sclera is rarely damaged by brief exposure to heat: the eyelids provide exceptional protection, and the fact that the sclera is covered in layers of moist tissue means that these tissues are able to cause much of the offending heat to become dissipated as steam before the sclera itself is damaged. Even relatively low-temperature molten metals when splashed against an open eye have been shown to cause very little damage to the sclera, even while creating detailed casts of the surrounding eyelashes. Prolonged exposure, however—on the order of 30 seconds—at temperatures above 45 °C (113 °F) will begin to cause scarring, and above 55 °C (131 °F) will cause extreme changes in the sclera and surrounding tissue. Such long exposures even in industrial settings are virtually nonexistent.[15]

Chemical injury

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The sclera is highly resistant to injury from brief exposure to toxic chemicals. The reflexive production of tears at the onset of chemical exposure tends to quickly wash away such irritants, preventing further harm. Acids with a pH below 2.5 are the source of greatest acidic burn risk, with sulfuric acid, the kind present in car batteries and therefore commonly available, being among the most dangerous in this regard. However, acid burns, even severe ones, seldom result in loss of the eye.[15]

Alkali burns, on the other hand, such as those resulting from exposure to ammonium hydroxide or ammonium chloride or other chemicals with a pH above 11.5, will cause cellular tissue in the sclera to saponify and should be considered medical emergencies requiring immediate treatment.[15]

Abnormal coloring

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Redness of the sclera is typically caused by eye irritation causing blood vessels to expand, such as in conjunctivitis ("pink eye"). Episcleritis is a generally benign condition of the episclera causing eye redness. Scleritis is a serious inflammatory disease of the sclera causing redness of the sclera often progressing to purple.

Yellowing or a light green color of the sclera is a visual symptom of jaundice.

In cases of osteogenesis imperfecta, the sclera may appear to have a blue tint, more pronounced than the slight blue tint seen in children. The blue tint is caused by the showing of the underlying uveal tract (choroid and retinal pigment epithelium).

In those with Ehlers-Danlos syndrome, the sclera may be tinted blue due to the lack of proper connective tissue.[16]

In very rare but severe cases of kidney failure and liver failure, the sclera may turn black.[citation needed]

See also

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Notes

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References

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Revisions and contributorsEdit on WikipediaRead on Wikipedia
from Grokipedia
The sclera is the tough, opaque, white outer layer of the eyeball, forming approximately 85% of the eye's outer tunic and serving as its primary load-bearing . Composed mainly of dense fibers (predominantly type I, comprising about 28% of wet weight), with smaller amounts of , proteoglycans, and water, it provides structural rigidity, protection for internal ocular components, and maintenance of the eye's shape and refractive status. Anatomically, the sclera is continuous with the transparent at the front of the eye and extends posteriorly to the , enclosing the and while covering about four-fifths of the . Its thickness varies regionally, measuring 1–1.3 mm at the posterior pole, approximately 0.5 mm at the , and around 0.8 mm near the limbus, with fibers arranged in a that is randomly oriented (unlike the cornea's parallel layers), contributing to its characteristic whiteness and opacity. The sclera also serves as the attachment site for the responsible for and helps anchor the head. Functionally, the sclera maintains (IOP), supports the and against mechanical stresses from eye movements and internal forces, and ensures optical stability by resisting deformation. Its biomechanical properties are non-linear and viscoelastic, exhibiting strain-stiffening as fibers recruit under load, with regional that adapts to varying stresses, such as circumferential fiber alignment in the peripapillary sclera to protect the . These attributes make the sclera essential for vision, as alterations in its structure—due to aging, , or —can lead to thinning, increased stiffness, and compromised eye integrity.

Anatomy

Gross Anatomy

The sclera is the opaque, white, fibrous outer layer of the eyeball, forming the posterior five-sixths of the and providing structural support to the eye. It is continuous anteriorly with the transparent at the limbus, creating a seamless fibrous that encases the internal ocular structures. This tough, avascular tissue maintains the eye's shape and serves as an attachment site for surrounding structures, contributing to the overall integrity of the ocular . In terms of dimensions, the sclera varies in thickness from approximately 0.3 mm to 1.0 mm, being thickest at the posterior pole (up to 1.3 mm) and thinnest near the insertions of the rectus muscles (around 0.3 mm) and at the (0.3–0.5 mm). Its shape consists of a spherical posterior portion with a radius of about 12 mm, merging anteriorly with the flatter curvature of the , and the overall has an axial length of 24–25 mm in emmetropic adult eyes. Key anatomical landmarks include the posterior pole, the rearmost point where the exits; the equator, the circumferential midpoint representing the thinnest region; the limbus, the transitional zone with the ; and the scleral spur, a circumcorneal ridge near the limbus that anchors the . The sclera attaches anteriorly to the and , a fibrous sheath that envelops the globe and facilitates movement, while posteriorly it fuses with the via the sheath, approximately 3 mm nasally and 1 mm inferior to the posterior pole. The , including the four rectus and two oblique muscles, insert directly into the scleral surface, typically 5–7 mm posterior to the limbus for the recti. Biomechanically, the sclera exhibits high tensile strength and rigidity due to its dense fiber bundles, which enable strain-stiffening under load and maintain the eye's spherical form against . These properties arise from the organized lamellae of fibrils, providing resistance to deformation while allowing limited viscoelastic adaptation.

Histology

The sclera is composed primarily of type I collagen fibers, which account for approximately 90% of its total collagen content and form the main structural scaffold, supplemented by smaller amounts of elastin, proteoglycans, and resident fibroblasts. These extracellular matrix components provide the tissue with its characteristic firmness and resilience, while the fibroblasts maintain the matrix through synthesis and turnover. Histologically, the sclera consists of three distinct layers: the superficial episclera, a layer rich in vascular and neural elements; the sclera proper (or stroma), featuring dense, interwoven bundles of fibers arranged in interlacing lamellae; and the deep lamina fusca, a thin pigmented layer interfacing with the . Within the sclera proper, the collagen bundles are oriented in multiple planes, conferring multidirectional mechanical strength to withstand and external forces. The primary cellular residents of the sclera are scleral fibroblasts, which produce and remodel the components, ensuring tissue integrity over time. These cells are sparsely distributed, particularly in the sclera proper, reflecting the tissue's low metabolic activity. Regional variations in scleral include a thinner, more elastic structure anteriorly near the limbus, where density is lower, contrasting with the denser, thicker posterior region that enhances around the . The sclera proper is avascular, contributing to its opaque white appearance through diffuse light scattering by the irregularly arranged fibers.

Vascular and Neural Supply

The sclera proper is avascular, lacking intrinsic blood vessels, and relies on diffusion from adjacent vascularized layers such as the episclera and to support its metabolic needs. This -based supply ensures the maintenance of the sclera's structural integrity without compromising its transparency or rigidity in non-corneal regions. Arterial supply to the sclera is derived primarily from branches of the . The anterior portion receives blood from the , which arise from the muscular branches of the near the rectus muscle insertions and course anteriorly to form the anterior scleral circle. Posteriorly, the sclera is supplied by the short and , which penetrate the sclera near the and provide centripetal flow to the outer layers. These vessels form anastomoses, ensuring redundant , particularly at the rectus muscle insertion sites where muscular branches directly supply the underlying scleral tissue, serving as key surgical landmarks during procedures like surgery. Venous drainage of the sclera occurs through a network that parallels its arterial supply. Posterior scleral veins converge into the four vortex veins, which drain into the superior and inferior ophthalmic veins before emptying into the . Anteriorly, scleral vessels drain via the anterior ciliary veins to the superior and inferior ophthalmic veins, facilitating efficient removal of metabolic byproducts from the episcleral and deep scleral plexuses. Lymphatic drainage in the sclera is sparse compared to other ocular tissues, reflecting its avascular core. Anteriorly, lymphatics in the episclera connect to the subconjunctival lymphatic network, allowing superficial drainage toward the conjunctival vessels. Posteriorly, limited lymphatic channels accompany the sheath, draining toward meningeal lymphatics and ultimately into the jugular system. Innervation of the sclera is primarily sensory, with sparse autonomic components for vasoregulation. The anterior sclera receives sensory fibers from the , branches of the ophthalmic division of the (cranial nerve V), which provide pain and touch sensation to the episcleral surface. Autonomic innervation arises from the , where postganglionic sympathetic fibers supply control to the episcleral and conjunctival vessels overlying the sclera, modulating blood flow without direct penetration into the scleral substance.

Development and Function

Embryology

The sclera primarily derives from , which migrates to surround the developing optic cup, with minor contributions from , particularly in the temporal region. This mesenchymal origin ensures the sclera's role as a supportive fibrous layer, distinct from the neural ectoderm-derived and . Embryonic formation begins around week 7 of gestation, when loose condenses adjacent to the optic cup, induced by signals from the . deposition initiates between weeks 8 and 10, transitioning the mesenchyme into organized fibrous bundles that form the primitive scleral framework. By the third month, this loose tissue differentiates into dense fibrous connective tissue, starting anteriorly near the future limbus and extending posteriorly. The limbus, marking the sclero-corneal junction, fully forms by the fourth month as mesenchymal differentiation integrates with corneal stroma development. Developmental interactions involve inductive signals from the optic vesicle and surface ectoderm, which direct cell migration and specification. The transcription factor regulates these processes by promoting mesenchymal migration and eye field patterning, with its expression in the anterior essential for proper tissue integration. Postnatally, the sclera undergoes continued thickening until ages 10-12, driven by remodeling, followed by lifelong adaptations in cross-linking and stiffness. Disruptions in mesenchymal condensation can lead to anomalies such as colobomas, where incomplete closure exposes scleral tissue, or , characterized by underdeveloped ocular structures including the sclera. These defects often stem from genetic factors like mutations, highlighting the sclera's sensitivity to early signaling pathways.

Physiological Roles

The sclera serves as the primary for the eye, maintaining its globular shape against , which normally ranges from 10 to 21 mmHg. This role is essential to prevent collapse of the eyeball under physiological loads, as the sclera constitutes approximately 85% of the outer with a thickness of 1–1.3 mm at the posterior pole and about 0.5 mm at the . As a protective barrier, the sclera shields internal ocular structures, including the and , from external trauma and potential infection by providing a tough, opaque fibrous layer that resists penetration. Its dense composition ensures mechanical integrity, limiting the entry of exogenous substances to the posterior eye. In optical function, the sclera contributes to the eye's refractive status by supporting the and maintaining axial length for proper light focus on the . Its white appearance arises from light scattering by irregularly arranged fibers, which reduces internal glare and stray light transmission while allowing controlled light passage at the limbus with a of approximately 1.38. The sclera's biomechanical properties enable it to absorb shocks from eye movements and pressure fluctuations through its non-linear viscoelastic behavior, primarily governed by collagen fiber organization. This viscoelasticity provides a modulus of elasticity around 3 MPa, allowing deformation resistance without failure under normal conditions. Metabolically, the avascular sclera supports inner ocular layers by facilitating the diffusion of nutrients and oxygen from the overlying episclera and to adjacent tissues like the . Proteoglycans within the further regulate solute and hydration, ensuring metabolic despite low cellularity. With aging, the sclera undergoes gradual stiffening due to increased fibril size, cross-linking, and reduced content after age 20, alongside thinning that alters biomechanical properties. Yellowing occurs progressively from deposition of fat globules and calcium among bundles, contributing to a yellowish hue in older individuals.

Clinical Aspects

Abnormal Coloration

The sclera typically appears white in most adults due to its dense collagenous structure, which scatters light and masks underlying pigmentation. In infants, however, the sclera often exhibits a blue-tinged hue because of its relative thinness, allowing the underlying choroidal vasculature to show through more prominently. With advancing age, the sclera may develop a subtle yellowing, which serves as a visual cue for perceived age and can result from gradual accumulation of pigments or degenerative changes in connective tissues. Pathological alterations in scleral coloration include , or icterus sclerae, characterized by yellowish discoloration from deposition in the elastic fibers of the sclera when serum levels exceed 2-3 mg/dL. This occurs due to impaired hepatic processing or increased production, making the sclera an early indicator of such imbalances. Another age-related change is , a white or grayish lipid deposit forming an annular ring near the , primarily composed of and triglycerides that accumulate in the peripheral . Genetic conditions can lead to distinctive scleral hues, such as the blue sclera observed in , a disorder arising from mutations in COL1A1 or COL1A2 genes that impair synthesis, resulting in thinned, translucent sclera that reveals the underlying bluish uveal tissue. This feature is particularly prominent in milder forms like type I . Racial and ethnic variations influence scleral appearance, with individuals of darker-pigmented ancestry, such as those of Asian or African descent, often exhibiting increased episcleral melanocytes that impart a brownish or grayish tone to the sclera. This pigmentation arises from a higher of melanocytes in the episcleral layer, a benign trait more prevalent in certain ethnic groups. Abnormal scleral coloration holds diagnostic value as an early marker of systemic conditions, notably , where jaundice manifests first in the sclera due to its affinity for . Slit-lamp biomicroscopy enhances detection by magnifying subtle shifts, aiding in the identification of underlying hepatic or metabolic disorders. Non-inflammatory melanosis, such as ocular melanocytosis, presents as localized brown or slate-gray patches on the sclera due to benign proliferation of deep episcleral melanocytes, often congenital and unilateral without associated inflammation. This condition requires monitoring for potential , though it remains typically asymptomatic.

Trauma and Injury

Physical trauma to the sclera can occur through blunt or penetrating mechanisms, each presenting distinct injury patterns and requiring prompt evaluation to prevent vision-threatening complications. , often from high-velocity impacts such as or assaults, induces rapid spikes that may lead to scleral rupture, particularly at the limbus where the sclera meets the , due to the relative weakness of this junction. This can result in ecchymosis or subconjunctival hemorrhage from vessel rupture, with the deforming momentarily before potential decompression. In contrast, , such as from or projectiles, causes full-thickness scleral lacerations that expose intraocular contents, necessitating surgical closure with 9-0 sutures to restore structural integrity and minimize infection risk. Thermal injuries to the sclera, typically from direct heat exposure like flames or hot liquids, induce necrosis by denaturing proteins in the avascular scleral tissue, leading to localized tissue death and potential weakening. These burns can range from superficial, affecting only the episcleral surface with and minimal scarring, to partial-thickness involvement causing , to full-thickness damage risking and globe collapse, requiring urgent tectonic reinforcement. Chemical injuries pose a significant to scleral due to rapid penetration and tissue reaction, with alkalis and acids eliciting different pathophysiological responses. Alkalis, such as , are lipophilic and penetrate deeply through cell membranes, causing , vascular thrombosis, and ischemia that compromises scleral perfusion. Acids, like , provoke protein coagulation forming an barrier that limits deeper spread but still induces inflammatory damage. Extreme pH deviations in either case can destroy limbal stem cells, impairing epithelial regeneration and exacerbating scleral exposure. Immediate responses to scleral trauma include subconjunctival hemorrhage from disrupted episcleral vessels, appearing as bright red patches over the sclera, and decreased (hypotony) due to aqueous humor leakage through disrupted barriers. A key for scleral rupture is scleral thinning associated with high , where elongated axial length reduces tensile strength, increasing susceptibility to deformation under blunt force. First aid for chemical injuries emphasizes immediate and copious with normal saline for at least 20 minutes to neutralize and dilute the agent, preventing ongoing penetration. For perforations from any mechanism, management involves tectonic scleral patch grafts using donor scleral tissue to provide structural support, seal the defect, and preserve globe integrity until definitive repair.

Associated Diseases

The sclera can be affected by various inflammatory conditions, with representing a severe form characterized by deep, boring eye pain, redness, and potential vision loss due to inflammation of the scleral tissue. Anterior , the most common subtype, may present as diffuse, nodular, or necrotizing forms, often associated with systemic autoimmune diseases, with up to 50% of cases linked to underlying systemic conditions such as (RA), the most common association. Posterior involves the deeper scleral layers and can lead to choroidal detachment or exudative , requiring prompt intervention to prevent complications. , a milder inflammation of the episcleral tissues overlying the sclera, is typically self-limiting, resolving within 1-2 weeks without vision-threatening sequelae, though it may recur and is occasionally linked to underlying vascular disorders. Treatment for often involves systemic corticosteroids or immunosuppressants like , while may respond to topical nonsteroidal anti-inflammatory drugs (NSAIDs) or steroids. Degenerative conditions of the sclera include , an ectatic outpouching due to localized scleral thinning, most commonly associated with high where progressive elongation of the leads to uveal protrusion and increased risk of choroidal exposure or rupture. Scleromalacia perforans, a rare and painless form of necrotizing , occurs predominantly in long-standing , resulting in scleral melting and potential perforation without significant inflammatory signs, often necessitating surgical reinforcement with donor sclera or pericardium. Infectious scleritis arises from bacterial or fungal pathogens invading the scleral tissue, frequently following trauma, surgery, or overuse, with being a common bacterial culprit in lens wearers leading to rapid tissue necrosis. Fungal infections, such as those caused by Aspergillus species, are more indolent but aggressive, often requiring surgical alongside therapy. Management typically involves fortified topical antibiotics for bacterial cases or systemic antifungals for fungal ones, combined with intensive monitoring to avert . Neoplastic involvement of the sclera is uncommon, with primary scleral being extremely rare, comprising fewer than 1% of ocular melanomas and presenting as a pigmented nodule with potential for local invasion or . Metastatic tumors to the sclera, often from or primaries, manifest as yellowish-white lesions and require systemic evaluation. Lymphoproliferative disorders, including ocular adnexal lymphoma, may infiltrate the sclera, causing thickening and requiring for , with treatment guided by systemic staging. Systemic associations highlight the sclera's vulnerability in disorders; for instance, Ehlers-Danlos syndrome (EDS) types IV and VI feature scleral fragility due to defects, predisposing to spontaneous rupture or blue scleral hue from thinning. Recent studies in the 2020s have demonstrated the efficacy of anti-TNF therapies, such as , in refractory autoimmune , achieving remission in over 70% of cases while reducing dependence. Genetic factors, like positivity, increase susceptibility to in , with prevalence exceeding 90% in affected cohorts. Diagnostic evaluation of scleral diseases relies on imaging modalities; B-scan ultrasonography is essential for detecting posterior scleritis through visualization of scleral thickening or T-sign from fluid accumulation, offering high sensitivity for deep involvement. (OCT) provides detailed assessment of anterior scleral thinning or , aiding in monitoring treatment response and quantifying structural changes.

References

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