▃Anatomy of Vitreous

Vitreous is a transparent gel, a jelly-like structure filling the space bounded by lens, ciliary body, and retina. It is an avascular structure and has a volume of approximately 4 mL. It consists of water (99%), network of collagen fibrils, hyaluronic acid, peripheral cells (hyalocytes) which synthesize hyaluronic acid, and mucopolysaccharides. Its refractive index is 1.336. Importance of vitreous lies in the following functions:

•It serves optical functions.

•It provides structural integrity to the eye.

•It is a pathway for nutrients to be utilized by the lens and retina.

The interaction between hyaluronic acid and collagen fibrils is responsible for the gel form of vitreous. It possesses all the properties of a hydrophilic gel.

Inorganic ion content of vitreous contains sodium (146.7 mmol/L), potassium (5.73 mmol/L), chloride (121.6 mmol/L), calcium (1.13 mmol/L), and magnesium (0.9 mmol/L).

Unlike aqueous humor, which is continuously replenished, the gel in the vitreous chamber is stagnant. Therefore, if blood, cells, or other byproducts of inflammation get into the vitreous, they will remain there unless removed surgically. These are known as floaters.

After death, the vitreous resists putrefaction longer than other body fluids. The vitreous potassium concentration rises so predictably within the hours, days and weeks after death that vitreous potassium levels are frequently used to estimate the time-of-death (postmortem interval) of a corpse.

■Parts

Vitreous has three parts: Peripheral cortical vitreous, definitive vitreous, and vitreous base.

Peripheral Cortical Vitreous

The density of collagen fibrils is greater in the peripheral part. The condensation of these fibrils on the surface gives rise to the appearance of a boundary membrane called hyaloid membrane.

Internal limiting membrane (ILM) separates retina from vitreous and there exists a potential space between the two called subhyaloid space.

Main Mass of Vitreous (Definitive Vitreous)

It consists of collagen fibrils which are less dense. Sodium hyaluronate molecules fill the space between fibrils. Developmentally, primary (primitive) vitreous is a vascular structure having a hyaloid system of vessels. Secondary (definitive) vitreous is an avascular structure. When secondary vitreous fills the cavity, primary vitreous is concentrated into the center and forms the canal of Cloquet. Primary vitreous with hyaloid vessels ultimately disappears.

Vitreous Base

It is the part of vitreous 4 to 6 mm wide across the ora serrata. It is firmly attached to posterior 2 mm of the pars plana and the anterior 2 to 4 mm of retina. An incision through the midpart of pars plana will usually be located anterior to vitreous base. The cortical vitreous is strongly attached at the vitreous base.

■Vitreous Attachments

The peripheral cortical vitreous is loosely attached to the ILM. The firm attachment occurs at following sites:

•Vitreous base—Attachment is very strong at the vitreous base around ora serrata.

•Margin of optic disc—Attachment is fairly strong, forming a ring around optic disc.

•Around fovea—Attachment is fairly weak, forming a ring.

•Along peripheral blood vessels—Attachments are usually weak.

Anteriorly, it is attached to the posterior surface of the lens by hyaloidocapsular ligament of Wieger in childhood and adolescents, but later a concave space, Berger’s space, separates the lens and the vitreous.

■Changes in Vitreous with Age

Vitreous gel shows the following changes with age:

•Liquefaction of gel (synchysis).

•Contraction and shrinkage (syneresis).

•Separation of cortical vitreous from ILM of sensory retina (vitreous detachment).

▃Vitreous Detachment

Detachment of vitreous occurs as shown in Flowchart 12.1.

Vitreous detachment may be:

•Posterior vitreous detachment (PVD).

•Basal vitreous detachment.

•Anterior vitreous detachment.

■Posterior Vitreous Detachment (PVD)

It is the separation of cortical vitreous from ILM of sensory retina posterior to vitreous base (Fig. 12.1).

Aetiopathogenesis

1.Degenerations:

•Senile vitreous degeneration.

•Myopic degeneration.

2.Ocular trauma

3.Inflammations:

•Intermediate uveitis.

•Chorioretinitis.

The above causes may result in liquefaction of vitreous gel (synchysis). Some eyes with synchysis develop a hole in the posterior hyaloid membrane, and the liquefied vitreous gains access to newly formed retrohyaloid space through this defect. Posterior vitreous surface detaches from ILM of sensory retina up to posterior margin of vitreous base.

It is more common among diabetics and elderly patients. People with myopia > 6D are at higher risk of PVD. PVD may also occur in cases of cataract surgery.

Types

PVD is of two types:

•Acute PVD (sudden onset).

•Chronic PVD (develops gradually).

Clinical Features

When PVD occurs, there is a characteristic pattern of symptoms:

•Flashes of light (photopsia)—It is common in the temporal visual field and occurs due to vitreoretinal adhesions and provoked by ocular movements.

•Floaters—If PVD occurs over optic nerve head (optic disc), patient complains of a ring-like opacity (Weiss ring).

Complications

In PVD, sensory retina is no longer protected by stable vitreous cortex. Detached vitreous may cause dynamic traction on retina during ocular movements, resulting in retinal tear. The risk of retinal tear associated with vitreous detachment is higher in patients with myopic retinal degeneration and lattice degeneration. Retinal tear may cause:

•Retinal detachment (RD):

a.Rhegmatogenous RD—is associated with acute rhegmatogenous PVD (acute PVD).

b.Tractional RD—is typically associated with chronic, incomplete, nonrhegmatogenous PVD.

c.Exudative RD—is usually unassociated with PVD.

•Vitreous hemorrhages if retinal tear involves the retinal vessels. If a retinal vessel is torn, the leakage of blood into the vitreous cavity is often preserved as a “shower of floaters.”

Therefore, patients with a history of floaters or photopsia must be carefully examined.

Treatment

•If PVD is not associated with retinal tear (i.e., uncomplicated PVD), patient must be reassured and treatment is not required.

•If there is evidence of retinal tear, prophylactic barrage laser photocoagulation or cryopexy of retina is performed.

■Detachment of Vitreous Base and Anterior Vitreous

These usually occur secondary to trauma. These are often associated with vitreous hemorrhage.

▃Vitreous Opacities

The fibrils of vitreous gel become condensed within liquefied vitreous, so that they are less transparent than the rest of the vitreous. These appears as black spots floating before eyes and mistaken for small flying insects. These are called muscae volitantes or floaters.

■Causes

•Developmental: Developmental opacities are located in Cloquet’s Canal and represent remnants of hyaloid system.

•Degenerations such as old age or myopia. Some of the other degenerative conditions are asteroid hyalosis, synchysis scintillans, and amyloid degeneration (amyloidosis).

•Inflammation such as pars planitis and chorioretinitis.

•Vitreous hemorrhage.

•Neoplasms—Neoplastic cells in retinoblastoma and reticulum cell sarcoma form the vitreous opacities.

Asteroid Hyalosis

It is often unilateral and found in elderly individuals. It is characterized by multiple, white round bodies in vitreous gel. The condition is asymptomatic but may cause difficulty in fundus examination. These are composed of calcium-containing phospholipids attached to collagen fibrils in vitreous. These are suspended throughout the vitreous and unaffected by gravity. If it causes impairment of vision, vitrectomy may be considered, otherwise treatment is rarely required.

Synchysis Scintillans

This degenerative condition is characterized by multiple, yellowish white, crystalline bodies floating in the vitreous. These are composed of cholesterol crystals. It occurs in eyes which have suffered from trauma, vitreous hemorrhage, or inflammatory disease in the past, so it may occur at any age. Vitreous in such cases is liquefied, so the bodies float in vitreous and settle down in vitreous cavity due to gravity but can be thrown up by ocular movements and appear as shower of golden crystals. No treatment is indicated. Differentiating features between asteroid hyalosis and synchysis scintillans are listed in Table 12.1.

Amyloid Degeneration (Amyloidosis)

It is a heredofamilial disease.

Inheritance

It is transmitted as an autosomal dominant trait. It is a systemic disease with amyloid deposition in the collagen fibers of heart, thyroid, pancreas, peripheral nerves, and muscles, and produces symptoms related to affected organs.

Ocular Features

Both eyes are involved and the ocular features include the following:

•External ophthalmoplegia.

•Proptosis.

•Diplopia.

•Diminution of vision.

•Perivasculitis.

•Retinal hemorrhages and exudates.

•Vitreous opacities which are classically linear with footplate attachments to retina and posterior surface of lens, which is a diagnostic feature. These cause severe visual impairment.

Treatment

Pars plana vitrectomy with guarded prognosis.

▃Vitreous Bands and Membranes

Vitreous bands and membranes often develop after PVD or massive vitreous hemorrhage. They originate from hyalocytes or endothelial cells of capillaries.

If a band is adherent to retina, traction on retina is likely, producing photopsia and retinal edema/hemorrhage, and may produce retinal break or detachment.

Preretinal or epiretinal membrane (ERM) lines the inner surface of retina. It may be thin and look like a sheet of cellophane or resemble a sheet of tissue when it is thick. Contraction of ERM results in macular pucker.

Treatment includes vitrectromy. ERM may cause impairment of central vision and metamorphopsia and may be removed by vitrectomy, that is, pars plana vitrectomy + epiretinal membrane stripping which is effective especially in treating macular pucker.

▃Persistent Hyper Plastic Primary Vitreous

It is a developmental disorder of vitreous. In PHPV, structures within primary vitreous fail to regress, that is, there is persistence of fetal vasculature.

■Presentation

•It is unilateral and usually associated with microphthalmos.

•It typically presents with white pupillary reflex (leucocoria), seen shortly after birth in full-term infant.

■Types

It is seen in two forms:

•Anterior PHPV.

•Posterior PHPV– less common.

Anterior PHPV

It is characterized by presence of retrolental mass with long and extended ciliary processes. Later, contraction of retrolental tissue pulls the ciliary processes inward.

It may later be associated with the following:

•Cataract.

•Glaucoma.

•Vitreous hemorrhage.

Diagnosis

It is diagnosed by ultrasonography and CT scan.

Treatment

If diagnosed early, treatment consists of aspiration of lens (pars plana lensectomy)

+

Pars plana anterior vitrectomy

+

Excision of retrolental membrane

Visual Prognosis

It is poor.

Differential Diagnosis

It must be differentiated from other causes of leucocoria, especially:

•Retinoblastoma.

•Congenital cataract.

•Retinopathy of prematurity (ROP).

Posterior PHPV

It is characterized by persistent hyaloid artery with a large stalk extending to the peripheral retina from the optic disc. It does not reach the lens, thus usually not causing cataract. It may be associated with tractional retinal detachment.

▃Vitreous Hemorrhage

Vitreous hemorrhage may be located in preretinal or subhyaloid space, vitreous cavity, or both.

Common causes of vitreous hemorrhage are depicted in Fig. 12.2.

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