Vitreous and Vitreoretinal Disorders

Published on 08/03/2015 by admin

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12 Vitreous and Vitreoretinal Disorders


The vitreous cavity is the space bounded anteriorly by the lens and its zonular fibres and more posteriorly by the ciliary body, retina and optic disc. Its volume is about 4 ml, although this may be as much as 10 ml in highly myopic eyes. Normally the space is entirely occupied by vitreous gel a virtually acellular, viscous fluid with 99 per cent water content. Its low molecular and cellular content is essential for maintaining transparency. Major constituents of the vitreous gel are hyaluronic acid and type 2 collagen fibrils. The cortical part of the vitreous gel has more hyaluronic acid and collagen than the less dense central gel. In addition, the gel exhibits ‘condensations’ both within its substance and along its boundaries. Boundary condensations are the anterior and posterior hyaloid membranes. The gel is unimportant in maintaining the shape or structure of the eye; indeed, apart from its role in oculogenesis, the vitreous has no well substantiated function. An eye devoid of gel is not harmed apart from having an increased risk of nuclear cataract, (which is thought to be due to increased partial pressure of oxygen (po2) in the posterior segment after vitrectomy). The vitreous gel is implicated, however, in the pathogenesis of a variety of sight-threatening conditions.

During early development the invaginated optic vesicle (optic cup) contains the primary vitreous, a vascularized tissue supplying the lens and retina, both of which are of ectodermal origin. During the third month of gestation the primary vitreous gradually loses its vascularity and is replaced by the secondary vitreous which is derived from the anterior retina and ciliary body. The principal remnants of the primary vitreous are Cloquet’s canal, a central tubular stucture that stretches sinuously between the lens and the optic disc and some epipapillary gliosis. In later life an exaggeration of the latter is seen as Bergmeister’s papilla and a Mittendorf’s dot is a primary vitreous remnant seen on the posterior lens capsule (see Ch. 17). The most common and severe developmental anomaly of the vitreous is persistent hyperplastic primary vitreous. This usually presents in infancy as a microphthalmic squinting eye with leukocoria. Pupil dilatation may demonstrate dragging of the ciliary processes towards a central plaque of fibrovascular tissue; this invades the lens posteriorly and ultimately causes complete cataract and secondary angle closure glaucoma (see Ch. 8).


The posterior hyaloid membrane adheres to the internal limiting membrane of the retina (the basement membrane of the Müller cells consisting of type 4 collagen) by the insertion of vitreous gel fibrils. The potential space between the internal limiting membrane and posterior hyaloid membrane is the plane at which the gel cleaves from the retina in posterior vitreous detachment.

The vitreous adheres to surrounding structures at various sites; these attachments are responsible for much vitreoretinal pathology. The vitreous base is an annular zone of adhesion 3–4 mm wide straddling the ora serrata. The anterior border is the insertion of the anterior hyaloid membrane. The posterior border forms the anterior limit at which the gel and retina can potentially separate and is surgically important being a common site for retinal tears. Adhesion of the vitreous base to the retina and pars plana is strong and difficult to break even with severe trauma. Weiger’s ligament is a circular zone of adhesion, 8–9 mm in diameter, between the gel and posterior lens capsule. It is the junction between the anterior hyaloid membrane and the expanded anterior opening of Cloquet’s canal. The posterior hyaloid membrane and the slightly expanded posterior limit of Cloquet’s canal meet around the margin of the optic disc to produce another ring of adhesion. During posterior vitreous detachment gliotic tissue is avulsed from the edge of the optic nerve head to produce Weiss’ ring, a sign of posterior vitreous detachment. A circle of relatively increased adhesion to the retina may be present parafoveally and is implicated in macular hole formation.

Vitreoretinal adhesions are exaggerated in areas of lattice degeneration. Oval or elongated areas of retina are thinned with sclerotic vessels and degenerate overlying vitreous. The lesions tend to be oriented circumferentially but may also be radial or directed along postequatorial retinal veins. Lattice degeneration is found in approximately 7 per cent of normal eyes and is frequently associated with retinal tears. Some eyes have abnormally strong vitreoretinal adhesions along retinal veins (paravascular adhesions) which may also result in retinal tears.



Posterior vitreous detachment which occurs when the posterior hyaloid and internal limiting membranes separate is the commonest and most important pathological event affecting the vitreous. It occurs in about 50 per cent of individuals aged between 40 and 80 years and earlier in myopes. Most patients do not have pathological sequelae but acute symptoms of floaters and flashers are associated with a 10 per cent risk of developing a retinal tear, the cause of most retinal detachments. The great majority of tears are associated with visible retinal pigment epithelium (RPE) cells in the anterior vitreous having been released through the tear (Shafer’s sign). Tearing of retinal blood vessels or neovascular complexes causes haemorrhaging into the vitreous cavity. Posterior vitreous detachment is also implicated in the pathogenesis of epiretinal membranes and macular holes.


Vitreous haemorrhage can reduce vision profoundly. Haemorrhage may be in vitreous gel (intragel) or behind a detached gel (retrohyaloid); haemorrhage in both situations tends to be associated with posterior vitreous detachment. Spontaneous vitreous haemorrhage is principally caused by retinal tears, retinal vein occlusion or retinal neovascularization, for example secondary to diabetic retinopathy. Other common causes are posterior vitreous detachment without retinal tear formation or retinal macroaneurysm. Haemorrhage elsewhere in the eye often disperses into the vitreous cavity (e.g. suprachoroidal blood from trauma, subretinal blood secondary to choroidal neovascularization or blood under the internal limiting membrane in Terson’s syndrome).

The blood in the vitreous gel initially forms a localized clot but subsequently disperses throughout the gel following fibrinolysis. During haemolysis biconcave erythrocytes loose haemoglobin to become spheroidal erythroclasts. Biodegraded haemoglobin stains the gel ochre-yellow or orange. Erythroclast clogging of the vitreous cortex produces an ‘ochre membrane’ at the posterior hyaloid face. The mechanisms by which vitreous haemorrhage is spontaneously absorbed are not clear although phagocytosis by macrophages, outflow through the trabecular meshwork and syneretic disintegration of the gel play a part. Erythroclasts in the trabecular meshwork can reduce outflow to produce raised intraocular pressure and ‘erythroclastic glaucoma’ (see Ch. 8). Rarely, vitreous haemorrhage causes ‘synchysis scintillans’, a localized form of cholesterolosis bulbi characterized by cholesterol crystal accumulation in the vitreous cavity. The crystals sediment inferiorly but shower through the vitreous cavity with eye movement.


Strictly speaking, ‘retinal detachment’ is a misnomer. Rather than the retina detaching from choroid the retinal neuroepithelium separates from the RPE to re-establish the original space between layers of the embryonic optic cup. ‘Rhegmatogenous’ retinal detachment is most commonly caused by a ‘break’ or full-thickness discontinuity in the neuroepithelium allowing fluid from the vitreous cavity to enter the subretinal space. Classically breaks are subdivided into ‘tears’ due to dynamic vitreoretinal traction and ‘holes’ secondary to localized retinal disintegration or atrophy.

Most retinal tears occur in association with posterior vitreous detachment from the forces generated by ‘dynamic vitreous traction’. This is the transmission of rotational energy generated by saccadic ocular movement to the vitreous. If the vitreous remains attached to the retina this energy is uniformly dispersed over the whole area of vitreoretinal contact. With posterior vitreous detachment these forces accelerate the posterior gel and cause excessive traction at focal points of vitreo-retinal adhesion. The vitreous base remains anchored anteriorly; such gel movement can result in U-shaped tears at the site of ‘abnormal’ vitreoretinal adhesions. The tongue of retina which produces the U has its base anteriorly and points posteriorly; vitreous first separates posteriorly, tears the retina at the point of adhesion then extends the tear anteriorly back towards the vitreous base. Vitreous adheres to the periphery of lattice lesions so that the traction tears along the posterior border of the lesion and then extends anteriorly around its edge. Multiple tiny flap breaks at the posterior border of the vitreous base are associated particularly with aphakia or pseudophakia. If the flap of the tear is avulsed completely from the retina the piece of avulsed neurosensory retina is seen attached to the posterior vitreous membrane as an operculum and a round tear is produced. Haemorrhage from rupture of a blood vessel that crosses a U tear may produce a floater or shower of floaters.

Rhegmatogenous retinal detachment may also arise from atrophic retinal holes without posterior vitreous detachment, often in young myopic patients, or by dialysis at the ora serrata. In both retinal detachment is of slow onset, often noticed only coincidentally at routine examination or when the condition becomes symptomatic with foveal detachment. Atrophic holes are often equatorial and associated with lattice degeneration. Retinal dialyses are ellipsoid separations of the retina at the ora serrata, usually inferotemporally. They differ from U tears because there is no posterior vitreous detachment and the gel is attached to the posterior rather than the anterior margin of the break.



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