Vitreous humour

The vitreous humour (also spelled vitreous humor in American English), also known as the vitreous body, is the transparent, gel-like substance that occupies the large central cavity of the eye, situated between the lens at the front and the retina at the back. It plays a crucial role in ocular anatomy by maintaining the eye’s structural integrity, supporting the retina, and enabling the unobstructed passage of light to the photoreceptor cells at the back of the eye.

Unlike many other bodily fluids, the vitreous humour is non-regenerative and remains largely unchanged after birth. It is avascular (lacking blood vessels) and nourishes the surrounding ocular structures through diffusion. Its consistency is firm yet elastic—more gelatinous in younger individuals, gradually becoming more fluid with age due to biochemical changes.

While often overshadowed in clinical importance by the lens or retina, the vitreous humour is integral to healthy vision and serves as a silent but vital component of the eye’s internal environment. Disorders of the vitreous can lead to visual symptoms such as floaters, flashes, or even retinal detachment, underscoring its importance in ocular health.

Composition

The vitreous humour is composed primarily of water, making up about 98–99% of its total volume. Despite this high water content, the vitreous maintains a gel-like consistency due to a sparse but highly organised network of structural macromolecules. The remaining 1–2% consists of collagen, hyaluronic acid, proteins, salts, and trace amounts of cells and metabolites.

Collagen

Collagen is a critical structural protein that forms the scaffolding framework of the vitreous humour. In the vitreous, collagen exists primarily as type II collagen, although types V and IX are also present in smaller amounts. These collagen fibres create a delicate, three-dimensional meshwork that provides the vitreous with its characteristic gel-like consistency and mechanical strength.

The collagen fibrils in the vitreous are arranged in a fine, loosely packed network, which allows the gel to maintain transparency by minimising light scattering. This organisation is essential because dense or disorganised collagen deposits can cause vitreous opacities, leading to visual disturbances such as floaters.

Collagen also interacts with hyaluronic acid, a large glycosaminoglycan molecule abundant in the vitreous. Hyaluronic acid binds water and maintains the gel’s viscosity, while collagen fibrils provide tensile strength and structural integrity. This interaction helps preserve the vitreous in a stable, hydrated gel state.

Over time, with ageing or in certain pathological conditions, the collagen network can undergo degeneration or aggregation. This leads to vitreous liquefaction (syneresis) and the formation of collagen clumps, which may detach from the retina and contribute to floaters or increase the risk of retinal tears.

Furthermore, collagen fibrils anchor the vitreous to key ocular structures, including the vitreous base near the ora serrata, the optic disc, and the macula. These attachment points are crucial for maintaining retinal positioning and stability but may also be sites of vitreoretinal traction, which can cause retinal complications if abnormal.

Hyaluronic Acid

Hyaluronic acid (HA) is a major component of the vitreous humour’s extracellular matrix and plays a key role in maintaining its viscoelastic properties. It is a large, linear glycosaminoglycan composed of repeating disaccharide units of glucuronic acid and N-acetylglucosamine.

In the vitreous, hyaluronic acid binds large amounts of water, helping to retain hydration and give the vitreous its gel-like consistency. This hydration maintains the vitreous volume and allows it to resist compressive forces while remaining flexible.

Hyaluronic acid molecules interact with the collagen fibrils in the vitreous, spacing them apart and preventing their aggregation. This interaction preserves the clarity of the vitreous by minimising light scattering. The balance between collagen and hyaluronic acid concentrations is critical for the vitreous to maintain its transparent gel state.

With ageing or in pathological conditions, the concentration and molecular weight of hyaluronic acid can decrease, contributing to vitreous liquefaction (syneresis). This process results in pockets of fluid formation within the gel, which can lead to the collapse of the vitreous body and increased risk of vitreoretinal traction or detachment.

Hyaluronic acid also contributes to the shock-absorbing capacity of the vitreous, cushioning delicate retinal and lens tissues from mechanical trauma during eye movements.

Proteins

The vitreous humour contains a variety of proteins, although in much lower concentrations compared to blood plasma. These proteins contribute to the vitreous’s structural integrity, transparency, and biochemical environment.

One of the most important proteins in the vitreous is opticin, a small leucine-rich repeat proteoglycan that helps maintain the regular spacing of collagen fibrils, thereby preserving the gel’s transparency and preventing unwanted aggregation of collagen fibres. Opticin also plays a role in protecting the vitreous from pathological neovascularisation.

Other proteins present include:

• Albumin and immunoglobulins: These proteins are present in trace amounts and may enter the vitreous via diffusion from surrounding ocular tissues or systemic circulation. Their roles include maintaining osmotic balance and contributing to immune surveillance.
• Enzymes: Various enzymes such as matrix metalloproteinases (MMPs) are found in the vitreous and are involved in remodelling the extracellular matrix. Dysregulation of these enzymes can contribute to vitreous liquefaction and pathological changes.
• Growth factors and cytokines: These signalling proteins can influence ocular cell behaviour. In pathological conditions like diabetic retinopathy or uveitis, elevated levels of vascular endothelial growth factor (VEGF) and inflammatory cytokines in the vitreous contribute to disease progression.

Collectively, the proteins in the vitreous contribute to maintaining the homeostasis of the ocular environment, supporting the extracellular matrix, and mediating responses to injury or disease.

Cells

The vitreous humour is largely acellular, meaning it contains very few cells under normal, healthy conditions. Its gel-like structure is primarily composed of extracellular matrix components such as collagen and hyaluronic acid, with minimal cellular presence to maintain transparency and prevent immune reactions within the eye.

However, a small number of specialised cells can be found in or near the vitreous, including:

• Hyalocytes: These are specialised, macrophage-like cells located mainly in the peripheral vitreous cortex, particularly near the vitreous base. Hyalocytes are believed to play a role in synthesising and regulating the extracellular matrix, including collagen and hyaluronic acid production, as well as contributing to the maintenance and turnover of the vitreous gel. They may also participate in immune surveillance by phagocytosing debris and pathogens.
• Fibroblasts and fibrocytes: These cells may be present in small numbers near the vitreoretinal interface, particularly at the vitreous base, where the vitreous gel attaches to the retina and ciliary body. They contribute to the structural integrity of the vitreous and can be involved in pathological processes such as vitreoretinal fibrosis or proliferative vitreoretinopathy.
• Macrophages and immune cells: In normal vitreous, immune cells are rare, reflecting the eye’s status as an immune-privileged site. However, during inflammation or infection (e.g., uveitis or endophthalmitis), immune cells such as macrophages, lymphocytes, and neutrophils can infiltrate the vitreous, leading to cellular infiltration visible during ophthalmic examination.
• Pigment cells: Occasionally, pigment-containing cells may be found within the vitreous following trauma or retinal detachment, where retinal pigment epithelial cells can migrate into the vitreous cavity.

Electrolytes and Metabolites

The vitreous humour contains various electrolytes and metabolites that help maintain its physiological environment, support cellular functions of adjacent ocular tissues, and preserve the transparency and stability of the gel.

Electrolytes

The electrolyte composition of the vitreous closely resembles that of the aqueous humour but differs from plasma in certain respects, reflecting selective permeability and local metabolic activity. Key electrolytes include:

• Sodium (Na⁺) and chloride (Cl⁻): These ions are present in high concentrations and play essential roles in maintaining the osmotic balance and electrical neutrality of the vitreous.
• Potassium (K⁺): Present at lower concentrations than sodium, potassium is vital for cellular function in surrounding retinal and lens tissues.
• Calcium (Ca²⁺) and magnesium (Mg²⁺): These divalent cations act as cofactors for various enzymatic processes and contribute to stabilising the extracellular matrix structure.
• Bicarbonate (HCO₃⁻): Important for pH buffering, maintaining the vitreous at a slightly alkaline pH to optimise enzymatic and metabolic functions.

Metabolites

The vitreous contains metabolic substrates and by-products that reflect ongoing biochemical activity in the eye:

• Glucose: Diffuses into the vitreous from the blood via the retinal vessels and ciliary body. Although vitreous glucose concentrations are lower than plasma levels, glucose is a crucial energy source for adjacent tissues like the lens and retina.
• Lactic acid: Produced by anaerobic metabolism in retinal cells and diffuses into the vitreous. Its concentration provides insight into retinal metabolic status.
• Oxygen: The vitreous has a relatively low oxygen tension compared to other ocular fluids, which is protective against oxidative stress in the lens and retina.
• Ascorbic acid (Vitamin C): Present in relatively high concentrations, ascorbate acts as an antioxidant, scavenging free radicals and protecting ocular tissues from oxidative damage.
• Other metabolites: Various amino acids, urea, and metabolic intermediates are present in small amounts, reflecting local tissue metabolism and waste removal.

Maintaining the delicate balance of electrolytes and metabolites within the vitreous is essential for ocular homeostasis, influencing intraocular pressure, transparency, and the health of surrounding tissues. Disruptions in this balance can contribute to pathological conditions such as diabetic retinopathy or oxidative damage.

Function

The vitreous humour performs multiple crucial roles in maintaining the health, structure, and function of the eye. Far from being a passive filler, this transparent gel is integral to proper vision and ocular stability.

Optical clarity and light transmission

The vitreous humour plays a crucial role in ensuring clear and undistorted transmission of light from the lens to the retina, which is essential for sharp vision. Its optical properties stem from its unique composition and structure:

• Transparency: The vitreous is a highly transparent gel composed mostly of water (~98–99%) with a finely organised collagen and hyaluronic acid matrix. This organised structure minimises light scattering and allows photons to pass through without significant absorption or distortion.
• Avascularity: Unlike many tissues, the vitreous contains no blood vessels, which prevents light obstruction and further preserves optical clarity.
• Refractive index: The vitreous has a refractive index close to that of the aqueous humour and lens, allowing seamless passage of light with minimal refraction at the vitreous interface, contributing to focused image formation on the retina.
• Minimising light scatter: The delicate arrangement of collagen fibrils in the vitreous reduces irregularities that could scatter light. This helps prevent haze and ensures high contrast and resolution in the visual image.
• Filtering of harmful wavelengths: The vitreous also absorbs some short-wavelength ultraviolet (UV) and blue light, protecting the retina from phototoxic damage while maintaining overall transparency.
• Dynamic medium: Because it fills the large vitreous cavity, it provides a stable, clear medium through which light travels, helping to maintain consistent optical properties regardless of eye movement or pressure changes.

Disruptions to the vitreous’s clarity—such as degeneration, haemorrhage, or inflammatory debris—can lead to visual disturbances like floaters, blurring, or reduced contrast sensitivity.

Structural support and shape maintenance

The vitreous humour plays a fundamental role in preserving the physical integrity and shape of the eyeball. By filling approximately 80% of the eye’s internal volume, it acts as a gel-like scaffold that supports the globe from within, helping maintain its nearly spherical form, which is essential for proper optical function.

• Mechanical firmness: The vitreous gel exerts a gentle but consistent pressure on the inner surfaces of the eye, providing internal support that counterbalances external forces and helps maintain intraocular pressure. This pressure is vital for sustaining the eye’s shape and preventing collapse or deformation.
• Retinal support: The vitreous is closely adherent to the retina at key locations such as the vitreous base, the optic disc, and the macula. Through these attachments and its volume, the vitreous helps keep the retina firmly apposed against the underlying choroid and retinal pigment epithelium, supporting the metabolic exchange necessary for retinal health and function.
• Shock absorption: Its viscoelastic properties enable the vitreous to absorb and dissipate mechanical shocks and vibrations caused by head movements or minor trauma, protecting delicate internal structures like the retina and lens from damage.
• Maintenance of ocular compartments: By physically separating the anterior (front) and posterior (back) segments of the eye, the vitreous maintains the correct spatial relationships between the lens, retina, and other ocular tissues, which is critical for coordinated eye function.
• Age-related changes and effects: Over time, the vitreous undergoes liquefaction (syneresis), which reduces its structural support and can lead to posterior vitreous detachment (PVD). This loss of support may increase the risk of retinal tears or detachment, highlighting the importance of vitreous integrity for ocular health.

Shock absorption and cushioning

The vitreous humour acts as a vital shock absorber within the eye, protecting delicate ocular structures from mechanical injury. Its gel-like, viscoelastic nature enables it to dampen forces generated by sudden movements or minor trauma to the head and eyes.

• Viscoelastic properties: The vitreous combines fluid and elastic characteristics, allowing it to deform under pressure and gradually return to its original shape. This elasticity helps absorb and dissipate kinetic energy, reducing the risk of damage to the retina, optic nerve, and lens.
• Protection during eye movements: Rapid or forceful eye movements produce inertial forces that could otherwise strain the retina and other sensitive tissues. The vitreous cushions these movements by evenly distributing mechanical stress throughout the eye.
• Trauma mitigation: In cases of blunt trauma to the eye or head, the vitreous gel absorbs impact energy, preventing excessive deformation of the globe and reducing the likelihood of retinal tears, detachment, or haemorrhage.
• Maintaining intraocular pressure stability: By resisting sudden changes in volume or shape, the vitreous helps stabilise intraocular pressure fluctuations, contributing to overall ocular homeostasis.
• Ageing effects: With age, the vitreous progressively liquefies and loses its gel structure, reducing its shock-absorbing capacity. This degeneration can lead to increased susceptibility to vitreoretinal traction and subsequent retinal injury.

Retinal adhesion and stability

The vitreous humour plays an important role in maintaining the position and stability of the retina, ensuring it remains closely apposed to the underlying tissues necessary for proper function.

• Vitreoretinal interface: The vitreous is firmly attached to the retina at several key sites, including the vitreous base near the ora serrata, the optic disc, the macula, and along retinal blood vessels. These adhesion points anchor the vitreous gel to the retina, helping to stabilise the delicate neurosensory tissue.
• Surface tension and physical support: Through its gel-like consistency and attachments, the vitreous exerts gentle pressure that keeps the retina in contact with the retinal pigment epithelium (RPE) and choroid. This contact is essential for nutrient exchange, waste removal, and retinal metabolism.
• Role in retinal health: By maintaining retinal apposition, the vitreous helps prevent retinal folds, detachments, or tears that can arise if the retina separates from its nourishing layers.
• Vitreoretinal traction: While the vitreous normally supports the retina, abnormal or excessive traction—often due to age-related changes like vitreous liquefaction and posterior vitreous detachment—can pull on the retina, causing tears, haemorrhage, or detachment.
• Dynamic interactions: The strength of vitreoretinal adhesion varies across different retinal regions and changes with age and disease. For example, strong adhesion at the vitreous base is generally maintained lifelong, whereas adhesion near the macula may weaken with age.
• Clinical significance: Disorders of vitreoretinal adhesion are central to many retinal pathologies, including retinal detachment, macular holes, and proliferative vitreoretinopathy. Understanding vitreous-retina stability aids in managing these conditions surgically or medically.

Metabolic and biochemical roles

Although the vitreous humour itself is largely acellular and metabolically inert, it plays a vital role in supporting the metabolic environment of the eye through various biochemical functions:

• Medium for nutrient and waste diffusion: The vitreous acts as an intermediary reservoir, allowing diffusion of oxygen, glucose, electrolytes, and metabolic waste between ocular tissues such as the retina, lens, and aqueous humour. This exchange supports the high metabolic demands of the retina and lens, which lack their own blood supply.
• Oxygen regulation: The vitreous helps maintain a low oxygen tension in the posterior segment of the eye, particularly around the lens. This hypoxic environment protects ocular tissues from oxidative stress and photodamage, reducing the risk of cataract formation and retinal degeneration.
• Buffering capacity: The vitreous contains bicarbonate and other buffering agents that help stabilise the pH of the intraocular environment. Maintaining a stable pH is crucial for enzyme activity and cellular function in adjacent tissues.
• Antioxidant functions: It contains relatively high levels of ascorbic acid (vitamin C) and other antioxidants that scavenge reactive oxygen species, thereby protecting the retina and lens from oxidative damage.
• Matrix remodelling and enzymatic activity: The vitreous harbours enzymes such as matrix metalloproteinases (MMPs), which participate in the controlled remodelling of the extracellular matrix. Dysregulation of these enzymes can contribute to vitreous liquefaction and pathological conditions such as proliferative vitreoretinopathy.
• Immune modulation: The vitreous is part of the eye’s immune-privileged status, providing a compartment that limits inflammatory responses. It contains molecules that regulate immune cell activity, helping to prevent damaging inflammation within the eye.
• Storage of growth factors and cytokines: The vitreous can act as a reservoir for signalling molecules such as vascular endothelial growth factor (VEGF) and inflammatory cytokines. These factors influence retinal vascular health and immune responses, playing key roles in diseases like diabetic retinopathy and uveitis.

Barrier and immune modulation

The vitreous humour serves as an important physical and immunological barrier within the eye, helping to maintain ocular homeostasis and protect delicate tissues from infection and inflammation.

• Physical barrier: The gel-like vitreous acts as a physical barrier that limits the movement of pathogens, inflammatory cells, and toxins within the eye. By compartmentalising the ocular environment, it slows the spread of infections and inflammatory mediators between the anterior (front) and posterior (back) segments of the eye.
• Immune privilege: The eye is considered an immune-privileged site, meaning it has specialised mechanisms to suppress excessive immune responses that could damage sensitive ocular structures. The vitreous contributes to this immune privilege by restricting immune cell infiltration and creating a controlled microenvironment that limits inflammation.
• Modulation of immune cell activity: Resident cells in the vitreous, such as hyalocytes, secrete immunomodulatory factors that help regulate local immune responses. These factors can dampen inflammation and promote tissue repair while preventing harmful immune activation.
• Barrier to neovascularisation: The vitreous matrix contains molecules like opticin and other proteoglycans that inhibit abnormal blood vessel growth within the vitreous cavity, helping to prevent complications such as vitreous haemorrhage and proliferative vitreoretinopathy.
• Infection containment: In the event of intraocular infections such as endophthalmitis, the vitreous gel can trap microorganisms and inflammatory debris, localising infection and potentially limiting widespread tissue damage.
• Limitations and clinical relevance: While the vitreous acts as a protective barrier, disruption due to trauma, surgery, or disease can compromise its barrier function, increasing the risk of inflammation, infection, or pathological neovascularisation. Understanding vitreous immune modulation is critical for managing ocular inflammatory and infectious diseases.

Light filtering and protection

The vitreous humour plays a subtle but important role in filtering and protecting the retina from potentially harmful light exposure, contributing to the overall health and function of the eye.

• Absorption of ultraviolet (UV) light: Although the majority of UV light is absorbed by the cornea and lens, the vitreous also absorbs some residual UV radiation. This helps reduce the amount of harmful UV light reaching the sensitive retinal tissues, protecting them from photochemical damage.
• Filtering of high-energy blue light: The vitreous contributes to filtering short-wavelength visible light, especially blue light, which carries more energy and can induce oxidative stress in the retina. By partially absorbing blue light, the vitreous reduces the risk of phototoxic injury.
• Reducing light scatter: The gel-like, homogenous composition of the vitreous minimises light scatter within the eye, ensuring that the incoming light is transmitted as a focused beam to the retina. This reduction in stray light enhances visual contrast and clarity.
• Protection against phototoxicity: By filtering harmful wavelengths and stabilising the optical path, the vitreous helps prevent damage to photoreceptors and retinal pigment epithelial cells, which are highly susceptible to oxidative stress induced by intense or chronic light exposure.
• Support for circadian rhythm regulation: The quality and spectral composition of light reaching the retina influence circadian rhythm and pupil responses. The vitreous’ filtering properties help maintain appropriate light quality for these physiological processes.
• Age-related changes: With ageing and vitreous degeneration, changes in the vitreous structure can alter its light filtering capacity, potentially increasing the retina’s exposure to damaging wavelengths and contributing to diseases such as age-related macular degeneration.

Debris trapping and floaters

The vitreous humour can trap various types of microscopic debris within its gel matrix, which can sometimes lead to visual disturbances commonly referred to as floaters.

• Sources of debris: Debris in the vitreous may include collagen fibril aggregates, cellular remnants, pigment granules, inflammatory cells, and tiny haemorrhages. These particles often originate from normal ageing processes, injury, inflammation, or retinal tears.
• Vitreous gel as a trap: The semi-solid gel structure of the vitreous physically entraps this debris, preventing it from freely moving within the eye and causing widespread irritation or damage. However, this also means the debris can persist for extended periods.
• Floaters and their appearance: Floaters are shadows cast on the retina by this trapped debris. They often appear as small spots, cobwebs, threads, or squiggly lines drifting across the visual field. Their visibility increases against bright backgrounds, such as a clear sky or white walls.
• Ageing and vitreous degeneration: With ageing, the vitreous undergoes liquefaction (syneresis) and collagen fibres may aggregate or clump, increasing the amount of visible debris. This process contributes to the common occurrence of floaters in middle-aged and elderly individuals.
• Posterior vitreous detachment (PVD): When the vitreous gel detaches from the retina, it can pull collagen fibres and debris into the visual axis, often causing a sudden increase in floaters accompanied by flashes of light. PVD is a common cause of new floaters and can sometimes precede retinal tears.
• Clinical significance: While floaters are usually benign and do not significantly affect vision, a sudden onset of numerous floaters, especially with flashes or visual field loss, warrants urgent ophthalmic evaluation to exclude retinal detachment or vitreous haemorrhage.
• Management: Most floaters become less noticeable over time as the brain adapts or debris settles. In rare cases where floaters severely impair vision, treatments such as laser vitreolysis or vitrectomy surgery may be considered.

Development

The vitreous humour develops early during embryogenesis and undergoes significant changes before reaching its mature, transparent gel form present after birth. Its formation involves two primary phases: the primary vitreous and the secondary vitreous.

Embryological origin

The vitreous originates from mesenchymal cells derived from the mesoderm and neural crest surrounding the developing optic cup. These precursor cells differentiate and organise to form the vitreous body within the eye’s optic vesicle.

Primary vitreous

The primary vitreous forms first during the fourth to sixth week of gestation. It is a vascularised, cellular structure that fills the vitreous cavity and provides nutrients to the developing lens and retina. This early vitreous contains the hyaloid artery, which extends from the optic nerve to the posterior lens, supplying the avascular lens with blood.

By around the seventh month of gestation, the primary vitreous and hyaloid vascular system begin to regress and involute, making way for the secondary vitreous. Failure of this regression can lead to persistent vascular remnants.

Secondary vitreous

The secondary vitreous develops around the eighth week of gestation and gradually replaces the primary vitreous. It is a transparent, avascular gel composed mainly of collagen and hyaluronic acid, similar to the mature vitreous in the adult eye. The secondary vitreous provides the structural and optical properties necessary for normal vision.

Persistent foetal vasculature (PFV)

In some cases, the regression of the primary vitreous and hyaloid artery is incomplete, resulting in persistent foetal vasculature (PFV)—a congenital anomaly characterised by the presence of residual blood vessels and fibrovascular tissue in the vitreous. PFV can lead to visual impairment due to cataract formation, retinal traction, or retinal detachment.

Age-related changes

As a person ages, the vitreous humour undergoes several structural and biochemical changes that can affect its function and the health of the eye.

Vitreous liquefaction (syneresis)

Over time, the gel-like vitreous gradually begins to liquefy, a process known as syneresis. This occurs as the collagen fibres aggregate and the concentration of hyaluronic acid decreases, causing the gel matrix to break down into liquid pockets within the vitreous body. Liquefaction typically starts in middle age and progresses with advancing years.

Posterior vitreous detachment (PVD)

As the vitreous liquefies, it can shrink and separate from the retina, a condition called posterior vitreous detachment (PVD). This detachment commonly occurs in people over 50 years old and may be asymptomatic or cause symptoms such as flashes of light and new floaters. While often benign, PVD can sometimes lead to retinal tears or detachments, requiring prompt ophthalmic evaluation.

Vitreous degeneration effects

Age-related changes can also include vitreous opacities, such as collagen clumps and cellular debris, which manifest as floaters in the visual field. The structural weakening of the vitreous increases the risk of abnormal vitreoretinal traction, contributing to various retinal disorders.

Clinical implications

These age-related changes in the vitreous are a major factor in the pathogenesis of common eye conditions, including retinal detachment, macular holes, and vitreomacular traction syndrome. Understanding these changes is essential for timely diagnosis and management of related ocular diseases.

Clinical significance

The vitreous humour plays a central role in a variety of ocular diseases and conditions. Its unique anatomical and biochemical properties mean that alterations in the vitreous can have significant effects on vision and overall eye health.

Vitreous haemorrhage

Vitreous haemorrhage refers to bleeding into the vitreous cavity. This can result from multiple causes, including:

• Trauma: blunt or penetrating injuries to the eye can rupture retinal vessels, leading to haemorrhage.
• Diabetic retinopathy: proliferative diabetic retinopathy causes fragile neovascular vessels to bleed spontaneously.
• Retinal tears or detachment: traction on retinal vessels during detachment can cause bleeding.
• Vascular occlusions and other retinal vascular diseases.

Symptoms typically include a sudden onset of floaters, dark spots, or even marked vision loss if bleeding is dense. Diagnosis is made clinically and often with ultrasonography if the view to the retina is obscured. Treatment focuses on managing the underlying cause, with vitrectomy surgery considered if the haemorrhage does not clear spontaneously.

Vitreous floaters

Floaters are small shadows cast on the retina by opacities within the vitreous gel, commonly caused by:

• Aggregates of collagen fibrils due to vitreous ageing and liquefaction.
• Cellular debris from inflammation or haemorrhage.
• Posterior vitreous detachment causing vitreous collagen clumps.

While generally benign, a sudden increase in floaters—especially when accompanied by flashes of light or peripheral vision loss—can indicate serious retinal pathology, such as a retinal tear or detachment, requiring urgent ophthalmological assessment.

Endophthalmitis

Endophthalmitis is a severe intraocular infection involving the vitreous and aqueous humour. It can occur as:

• A postoperative complication, particularly after cataract surgery or intravitreal injections.
• Post-traumatic infection.
• Haematogenous spread from systemic infection.

This condition leads to intense inflammation, rapid vision loss, and requires prompt intravitreal antibiotics and sometimes vitrectomy to clear infection and inflammatory debris.

Asteroid hyalosis

Asteroid hyalosis is characterised by the presence of calcium-lipid complexes suspended in the vitreous. These appear as bright, refractile particles on fundoscopy but rarely cause symptoms or significant visual impairment. It is generally benign and more common in elderly patients.

Proliferative vitreoretinopathy (PVR)

Proliferative vitreoretinopathy is a complication of retinal detachment characterised by the formation of contractile, fibrocellular membranes on both sides of the retina and the vitreous surface. These membranes exert traction, causing recurrent retinal detachment despite surgical repair. PVR is a major cause of vitreoretinal surgery failure.

Vitrectomy

Vitrectomy is a microsurgical procedure to remove part or all of the vitreous gel. It is indicated in various conditions including:

• Non-clearing vitreous haemorrhage.
• Rhegmatogenous retinal detachment.
• Severe vitreous floaters causing visual disability.
• Endophthalmitis.
• Macular hole repair.

During vitrectomy, the vitreous is replaced temporarily with saline, gas, or silicone oil to maintain ocular structure and facilitate retinal reattachment.

These clinical conditions illustrate the vital importance of the vitreous humour in both maintaining ocular health and contributing to disease processes. Early recognition and treatment of vitreous-related pathology are essential for preserving vision.

Imaging and diagnosis

Accurate assessment of the vitreous humour is essential for diagnosing and managing various ocular conditions. Due to the vitreous’s transparent and gel-like nature, specialised imaging techniques are employed to visualise its structure, detect pathological changes, and guide clinical decisions.

Ultrasonography (B-scan ultrasound)

• Indications: B-scan ultrasonography is indispensable when direct visualisation of the vitreous and retina is obscured by opaque ocular media such as dense cataracts, vitreous haemorrhage, corneal scars, or hyphema.
• Technique: Using high-frequency sound waves, B-scan produces two-dimensional cross-sectional images of the globe, allowing real-time dynamic assessment of the vitreous cavity and adjacent structures.
• Findings:
  • Vitreous opacities: Echogenic areas representing haemorrhage, inflammatory debris, or asteroid hyalosis.
  • Posterior vitreous detachment (PVD): Visualised as a mobile, echogenic membrane separated from the retina.
  • Vitreous membranes and traction: Fibrous bands or membranes that may exert traction on the retina, potentially causing tears or detachment.
  • Retinal detachment: Characteristic “V” or funnel-shaped echogenic membrane attached at the optic disc.
  • Vitreous haemorrhage: Diffuse low-to-medium reflectivity echoes within the vitreous gel.
• Advantages: Non-invasive, widely available, portable, and effective in urgent clinical scenarios.
• Limitations: Lower resolution compared to optical methods; operator-dependent.

Optical coherence tomography (OCT)

• Principles: OCT uses low-coherence interferometry to generate micrometre-resolution cross-sectional images of the retina and vitreoretinal interface.
• Applications:
  • Vitreomacular interface disorders: Detects vitreomacular adhesion (VMA), vitreomacular traction (VMT), macular holes, and epiretinal membranes.
  • Posterior vitreous detachment: Identifies subtle or partial detachments not evident on clinical examination.
  • Assessment of retinal layers: Provides detailed information on retinal morphology and thickness adjacent to vitreous pathology.
• Limitations:
  • Limited ability to image the entire vitreous cavity due to light scattering.
  • Best suited for central retina; peripheral vitreous and retina are less accessible.
  • Requires clear optical media for optimal imaging.

Fundoscopy (Direct and indirect ophthalmoscopy)

• Utility: Clinical examination remains the cornerstone for assessing the vitreous and retina in a cooperative patient with clear media.
• Observations:
  • Detection of floaters or debris within the vitreous.
  • Identification of a Weiss ring, indicating posterior vitreous detachment.
  • Visualisation of vitreous haemorrhage as diffuse haze.
  • Assessment for retinal tears, holes, or detachment.
• Limitations: Opacities such as dense vitreous haemorrhage or cataract may limit view; patient cooperation is necessary.

Additional imaging modalities

• Ultra-widefield imaging: Captures peripheral retina and vitreous pathologies, useful in diabetic retinopathy and peripheral retinal tears.
• Magnetic resonance imaging (MRI): Occasionally utilised in complex orbital or intraocular pathology, particularly tumours or inflammatory disease, but not routinely for vitreous evaluation.
• Fluorescein angiography: Although primarily used for retinal vascular assessment, it may assist indirectly in evaluating vitreoretinal diseases.

In clinical practice, combining these imaging techniques with thorough history-taking and examination enables accurate diagnosis of vitreous disorders and optimises patient management. Early detection of vitreous degeneration, traction, or haemorrhage is crucial to preventing vision-threatening complications.

Comparative anatomy

The vitreous humour is a common feature among vertebrates, serving vital optical and structural roles. However, its anatomy, composition, and functional adaptations vary significantly across species, reflecting evolutionary pressures, habitat, and visual demands.

Mammals

In mammals, including humans, the vitreous humour is a large, transparent gel occupying most of the eye's posterior chamber. It is composed primarily of water (98–99%), collagen fibrils, and hyaluronic acid. The gel structure provides:

• Mechanical support: Maintaining ocular shape and stabilising the retina.
• Optical clarity: Minimal light scattering to ensure high visual acuity.
• Metabolic environment: Facilitates diffusion of nutrients and waste between retina and lens.

The vitreous is largely avascular in adult mammals, with the hyaloid artery regressing during foetal development. The gel consistency tends to be firm to maintain a stable ocular shape, important for precise focusing.

Birds

Birds have smaller vitreous volumes relative to eye size, and their vitreous is generally more liquid compared to mammals. This fluidity supports rapid eye shape changes necessary for accommodation, especially in species requiring sharp vision at multiple distances (e.g., raptors).

A distinctive avian feature is the pecten oculi, a highly vascularised, comb-like structure projecting into the vitreous from the optic disc. It supplies nutrients to the avascular retina and may influence vitreous composition. The pecten's presence reduces the need for vascularisation within the vitreous itself, aiding optical clarity.

Reptiles and Amphibians

The vitreous humour in reptiles and amphibians shows considerable variability:

• Reptiles often have a more gelatinous but less dense vitreous than mammals, sometimes containing higher cellular content.
• Amphibians, such as frogs and salamanders, possess vitreous with more liquid components and retain persistent hyaloid vasculature into adulthood, reflecting their distinct developmental processes.

These adaptations may relate to lower visual acuity demands or differing metabolic needs.

Fish

Fish vitreous varies widely depending on ecological niche:

• Freshwater and shallow-water species usually have vitreous similar to amphibians, more liquid to accommodate rapid eye movements underwater.
• Deep-sea fish may have vitreous adaptations to low-light environments, including specialised proteins or increased gel density to improve light transmission and reduce scattering.
• Some fish maintain persistent vasculature within the vitreous to support retinal metabolism in low-oxygen environments.

Evolutionary and functional considerations

Across species, vitreous composition balances three key functions:

1. Optical clarity: Minimising light scatter to ensure image quality.
2. Mechanical support: Maintaining eye shape against external and internal pressures.
3. Metabolic exchange: Facilitating nutrient and waste transport in avascular regions.

Evolutionary pressures have tailored the vitreous’s consistency, cellularity, and vascular presence to optimise these functions for each species' habitat and lifestyle.

Clinical relevance in veterinary ophthalmology

Recognising interspecies differences is vital in diagnosing and managing vitreous disorders in animals. For instance, persistent foetal vasculature is common in certain species but pathological in humans. Similarly, vitreous degeneration patterns vary and influence prognosis and treatment strategies.

Research and future directions

The vitreous humour remains an active area of research due to its crucial role in ocular health and vision, as well as its involvement in numerous eye diseases. Recent advances focus on understanding its biology, improving clinical interventions, and developing novel therapies.

Vitreous substitutes and biomaterials

• Synthetic and biological substitutes: Since vitrectomy surgery involves removing the natural vitreous, research aims to develop substitutes that mimic its gel-like structure and functions. Materials studied include hydrogels, silicone oils, and collagen-based gels designed to maintain ocular shape, support retinal attachment, and minimise complications.
• Biocompatibility and longevity: A key challenge is creating substitutes that remain stable long-term without inducing inflammation, toxicity, or increased risk of cataracts and glaucoma. Advances in biomaterials science are addressing these issues to produce safer and more effective vitreous replacements.

Drug delivery systems

• Intravitreal injections: The vitreous is a target for delivering medications directly to the retina. Research explores optimising drug formulations and sustained-release implants to improve treatment of retinal diseases like age-related macular degeneration and diabetic retinopathy.
• Nanotechnology: Nanoparticles and microparticles are being investigated to enhance drug penetration, prolong therapeutic effects, and reduce injection frequency.

Understanding vitreous ageing and degeneration

• Molecular and cellular mechanisms: Studies focus on the biochemical changes causing vitreous liquefaction and posterior vitreous detachment, aiming to identify biomarkers or targets to prevent or delay these processes.
• Genetic factors: Research into genetic predispositions to vitreoretinal diseases may inform personalised medicine approaches.

Vitreoretinal interface pathologies

• Vitreomacular traction and macular holes: Improved imaging and understanding of the vitreoretinal interface have led to better diagnostic criteria and surgical techniques.
• Pharmacologic vitreolysis: Investigational treatments aim to enzymatically induce controlled vitreous liquefaction and posterior vitreous detachment, potentially reducing the need for surgery.

Regenerative medicine

• Cellular therapies: Emerging research explores using stem cells or growth factors to repair or regenerate damaged vitreous or retinal tissues.
• Tissue engineering: Efforts are underway to bioengineer vitreous-like materials or entire ocular tissues for transplantation.

These research directions hold promise for advancing the management of vitreous-related diseases and improving visual outcomes for patients. Continuous collaboration between clinicians, biologists, and material scientists is essential to translate laboratory findings into effective therapies.