VITREOUS ATTACHMENTS TO SURROUNDING STRUCTURES

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.

Fig. 12.3 Diagram of normal vitreoretinal anatomy showing the macroarchitectural features of the gel and the important sites of vitreoretinal attachment.

POSTERIOR VITREOUS DETACHMENT

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.

Fig. 12.4 With ageing vitreous degenerates to cause syneresis (condensation) and lacuna (cavity) formation and collapse. At slit-lamp examination the detached posterior hyaloid membrane looks like a wrinkled hanging curtain moving freely on eye movement. It separates from the retina up to the posterior border of the vitreous base (or the posterior aspect of any vitreoretinal adhesions).

Fig. 12.5 On posterior vitreous detachment epipapillary glial tissue can become avulsed from the disc margin and is seen ophthalmoscopically as a ring of tissue on the detached posterior hyaloid interface situated in front of the optic disc (Weiss’ ring). The patient sees a circular or oval floater (depending on how it tilts) or describes a ‘cobweb’ or ‘spider’ that moves with the eye. Aggregations of collagen fibrils can also produce symptomatic floaters. ‘Lightening flashes’ may be seen in the temporal periphery, each typically lasting for a few seconds and induced by eye movement, possibly because photoreceptors depolarize when the vitreous base tugs on the retina; these flashes are often more noticeable on the transition from light to dark.

VITREOUS HAEMORRHAGE

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.

Fig. 12.6 A bulla of subhyaloid haemorrhage forces the posterior hyaloid face forwards into the vitreous cavity.

Fig. 12.7 B scans show a retrogel haemorrhage moving from side to side with right and left gaze. There is complete vitreous detachment from the optic disc.

VITRITIS

Inflammatory cell infiltration of the vitreous is a feature of posterior uveitis, bacterial, viral, yeast and fungal infections, and intraocular lymphoma (see Ch. 10). Vitreous biopsy or vitrectomy has an increasing role in the management of these patients to obtain specimens for cellular diagnosis, microbial culture, removal of the vitreous scaffold and delivery of therapeutic drugs.

Fig. 12.8 Candidaemia in patients taking broad-spectrum antibiotics or with indwelling intravenous catheters or in intravenous drug users (Candida can grow in the lemon juice that may be used to dissolve heroin), carries a significant risk of metastatic endophthalmitis which manifests as intravitreal white puff-balls. Candida endophthalmitis, although more slowly progressive than bacterial endophthalmitis, usually requires vitrectomy to remove the infected gel, to administer intravitreal medication and to restore vision. Vitreous puff-balls are seen in this intravenous drug user with Candida endophthalmitis.

ASTEROID HYALOSIS

Asteroid hyalosis is a specific form of gel degeneration in which globules of calcium soaps aggregate on vitreous fibrils and move with the gel on eye movement. When dense, asteroid bodies may preclude ophthalmoscopy of the retina although they rarely impair the patient’s vision. They are not associated with any systemic condition and their aetiology is unknown.

Fig. 12.9 Typical white glistening particles are seen in the anterior gel of this patient. B scanning shows the densely reflective echoes in a collapsed gel.

AMYLOIDOSIS

Amyloidosis of the vitreous is a very rare condition usually associated with the primary or familial (dominantly inherited) forms of amyloidosis. Proteinaceous material, probably derived from the retinal circulation, becomes deposited on the collagenous framework of the gel bilaterally to produce a ‘glass-wool’ opacification; associated cellular invasion is conspicuous by its absence.

Fig. 12.10 Slit-lamp photograph showing proteinaceous material coating the retrolental vitreous fibrils.

FORMATION OF RETINAL BREAKS

Fig. 12.11 Diagram illustrating the concept of dynamic vitreoretinal traction after posterior vitreous detachment and how this generates a flap-tear or an operculated tear. In contrast with a dialysis the vitreous remains attached and there is no posterior vitreous detachment.

Fig. 12.12 Lattice degeneration containing round holes is seen in the equatorial retina.

Fig. 12.13 A U-shaped horse-shoe tear is seen surrounded by subretinal fluid.

Fig. 12.14 A peripheral retinal dialysis seen through the indirect ophthalmoscope.

Fig. 12.15 Atrophic round retinal breaks are seen with an attached vitreous gel. They are usually equatorial and often associated with lattice degeneration. Recruitment of fluid with round hole detachment probably occurs by connection of the hole to vitreous lacunae; this may cause a stepwise detachment with multiple demarcation lines in a chronic-looking retinal detachment (see Fig. 12.24). The vast majority will not cause retinal detachment and prophylactic therapy is generally regarded as unnecessary.

Fig. 12.16 Retinal breaks are seen in a patient with retinal vasculitis in whom the vitreous has separated avulsing small discs of retina that remain attached to the posterior vitreous surface as opercula. Round retinal tears result.

Fig. 12.17 Slit-beam photograph of the anterior gel after a retinal break showing RPE cells in the retrolental gel (the ‘tobacco dust’ or Shafer’s sign). Retinal tears are usually associated with release of RPE cells into the vitreous cavity and, when seen, suggest that a retinal break is present. This is of particular value when assessing a patient following an acute posterior vitreous detachment. These cells transform into fibroblast-like cells in proliferative vitreoretinopathy.

Fig. 12.18 Haemorrhage from a ruptured blood vessel crossing a U tear may produce a ‘tadpole’ floater or shower of floaters. Shown here is a U-shaped tear, with a bridging blood vessel, surrounded by laser scars. These breaks may still bleed despite the laser therapy.

SUBRETINAL FLUID ACCUMULATION