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Refers to the fluid-like gel, composed of approximately 98–99% water with trace amounts of hyaluronic acid, glucose, anions, cations, ions, and collagen, and a small population of resident macrophages.
It is predominantly composed of interpenetrating networks of collagen fibrils and hyaluronan molecules forming a clear hydrogel.
It supports the surrounding structures, absorbs mechanical trauma, and is involved in the circulation and regulation of oxygen, metabolites and nutrients.
The anterior face of the vitreous closest to the lens has a more robust collagen structure.
It is an optically clear, viscoelastic, gel-like extracellular matrix that fills the vitreous cavity.
The vitreous space that spans the distance from the posterior pole of the lens to the inner aspect of the retina.
The vitreous has matrix attachment points to the retinal inner limiting membrane, helping to maintain the retina in place.
The vitreous body is an optically clear, viscoelastic, gel-like extracellular matrix that fills the vitreous cavity
The vitreous space spans the distance from the posterior pole of the lens to the inner aspect of the retina.
It is located in the posterior chambers of the eyes.
The vitreous body is large and transparent.
The fundus is normally gray or reddish in color with the choroidal vessels not always visible.
Vitreous humor samples of approximately 2–3 mL can be collected from each eye for analysis.
Drugs distributed into the vitreous humor undergo little, if any, synthesis or degradation, and the vitreous humor can be studied for the detection of drugs when other samples are unavailable due to trauma or putrefaction.
The vitreous humor is largely unaffected by embalming, is an excellent alternative to blood in bodies that have been embalmed.
Several drugs and metabolites such as cocaine, morphine, codeine, phencyclidine, and benzodiazepines are detectable in vitreous humor.
Vitreous humour is pref2241ed to blood for most post-mortem biochemistry evaluations.
After death the retina leaks potassium and vitreous potassium is not a reliable indicator of ante-mortem plasma potassium.
Vitreous sodium and chloride concentrations may fall after death, at rates of up to 1 mmol/L per hour.
Potassium increases at a rate of 0.14–0.19 mmol/L per hour after death.
Urea and creatinine are relatively stable in post-mortem vitreous humor analysis.
If vitreous humor levels of sodium, chloride and urea are > 155, > 115 and > 10 mmol/L, respectively, this may indicate ante-mortem dehydration.
It can be suggested the uremia is present prior to death if the urea concentration is > 20 mmol/L and creatinine > 200 μmol/L with sodium and chloride concentrations within the normally accepted range.
The average vitreous volume is 4.5 mL, and fills the large cavity between the lens–iris diaphragm and the retinal surface.
During youth the vitreous exhibits a gel-like consistency.
In early years the vitreous is attached to the retina at the retinal periphery, the optic disc, and the macula.
With age the vitreous becomes increasingly liquefied.
Eventually the liquidity of the vitreous humor leads to a vitreous detachment, to the formation of a peripheral retinal hole, allowing fluid to enter the subretinal space, thus leading to retinal detachment.
Light flashes and floaters are reported with vitreous detachment, followed by progressive loss of peripheral visual field depending on the location of the progressing retinal detachment.
If the macular region is involved, central visual acuity is also lost as well.
The diagnosis of retinal detachment can only be made by dilated fundus examination.
Surgical reattachment of the detached retina is the only means of improving vision and visual field.
Success of surgical retinal reattach,ent depends mainly on timely repair.
Myopic eyes) are at higher risk for retinal detachment.
Poor cohesion of the vitreous gel in adults can result in mobility of the vitreous components manifested as vitreal floaters, which are of no clinical significance.
Inflammatory matter may accumulate in the vitreous due to uveitis, and progressive organization of inflammatory tissue may result in vitreoretinal detachments.
Uveitis treatment is aimed at controlling intraocular inflammation using systemic and locally administered corticosteroids.