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Kanski’s Clinical
Ophthalmology
A SYSTEMATIC APPROACH
EIGHTH EDITION

Brad Bowling
FRCSEd(Ophth), FRCOphth, FRANZCO
Ophthalmologist
Sydney
New South Wales
Australia

For additional online content visit expertconsult

S

Bowling_Title page_main.indd 3 2015-02-25 18:35:53

 Chapter

Vitreous opacities 17  

Introduction  722 Asteroid hyalosis  722 Vitreous cyst  726

Muscae volitantes  722 Synchysis scintillans  722 Persistent fetal vasculature  726
Vitreous haemorrhage  722 Amyloidosis  722
722 Kanski’s Clinical Ophthalmology
Introduction
The vitreous is a transparent extracellular gel consisting of colla-
gen, soluble proteins, hyaluronic acid and water. Its total volume
is approximately 4.0 ml. The few cells normally present in the gel
are located predominantly in the cortex and include hyalocytes,
astrocytes and glial cells. The vitreous provides structural support
to the globe while allowing a clear and optically uniform path to
the retina. Once liquefied or surgically removed it does not
re-form. Vitreous opacities can be caused by a variety of patho-
logical processes primarily involving other ocular sites; apart from
vitreous haemorrhage, the conditions discussed below are those in
which the vitreous gel is the primary site of pathology.
Muscae volitantes
Muscae volitantes (Latin for ‘hovering flies’), commonly referred
to as ‘floaters’, is an almost ubiquitous entoptic phenomenon of
fly-, cobweb- or thread-like lesions best seen against a pale back-
ground. It is thought to predominantly represent tiny embryologi-
cal remnants in the vitreous gel. A sudden exacerbation can occur
due to vitreous haemorrhage or, more commonly, a change in the
conformation of the gel, such as a posterior vitreous detachment
(see Fig. 16.22).
Vitreous haemorrhage
Vitreous haemorrhage is a common condition with many causes
(Table 17.1). Symptoms vary according to severity. Mild haemor-
rhage (Fig. 17.1A) causes sudden onset floaters and diffuse blurring
of vision, but may not affect visual acuity, whilst a dense bleed
(Fig. 17.1B) may result in very severe visual loss. B-scan ultrasono­
graphy in unclotted vitreous haemorrhage generally shows a
uniform appearance, and once cellular aggregates develop, small
particulate echoes become visible (Fig. 17.1C); ultrasonography is
critical in the evaluation of eyes with dense vitreous haemorrhage
to exclude an underlying retinal tear or detachment (Fig. 17.1D).
Treatment is dictated by severity and cause, but an increasingly
low threshold is being adopted for early vitrectomy (see Ch. 16) in
cases of dense haemorrhage.
Table 17.1  Causes of vitreous haemorrhage
• Acute posterior vitreous detachment associated
either with a retinal tear or avulsion of a peripheral
vessel
• Proliferative retinopathy
• Diabetic
• Retinal vein occlusion
• Sickle cell disease
• Eales disease
• Vasculitis
• Miscellaneous retinal disorders
• Macroaneurysm
• Telangiectasia
• Capillary haemangioma
• Trauma
• Systemic
• Bleeding disorders
• Terson syndrome
Terson syndrome
Terson syndrome refers to the combination of intraocular and
subarachnoid haemorrhage secondary to aneurysmal rupture,
most commonly arising from the anterior communicating artery.
However, intraocular haemorrhage may also occur with subdural
haematoma and acute elevation of intracranial pressure from
other causes. The haemorrhage is frequently bilateral and is typi-
cally intraretinal and/or preretinal (Fig. 17.2), although occasion-
ally subhyaloid blood may break into the vitreous. It is probable
that intraocular bleeding is due to retinal venous stasis secondary
to increase in cavernous sinus pressure. Vitreous haemorrhage
usually resolves spontaneously within a few months and the long-
term visual prognosis is good in the majority. Early vitrectomy
may be considered in some cases.
Asteroid hyalosis
Asteroid hyalosis is a common degenerative process in which
calcium pyrophosphate particles collect within the vitreous gel. It
is seen clinically as numerous tiny round yellow–white opacities
of varying size and density (Figs 17.3A and B). These move
with the vitreous during eye movements but do not sediment
inferiorly when the eye is immobile. Only one eye is affected
in 75% of patients; it rarely causes visual problems and the
majority of patients are asymptomatic. An association with diabe-
tes has been suggested, but is unproven. The prevalence of
asteroid hyalosis increases with age and affects 3% of those aged
75–86 years. It is more common in men than in women. OCT
(Figs 17.3C and D) and ultrasonography (Fig. 17.3E) show high
reflectivity foci.
Synchysis scintillans
Synchysis (synchisis) scintillans occurs as a consequence of chronic
vitreous haemorrhage, often in a blind eye. The condition is
usually discovered when frank haemorrhage is no longer present.
The crystals are composed of cholesterol and are derived from
plasma cells or degraded products of erythrocytes, and lie either
freely or engulfed within foreign body giant cells. Numerous flat
golden-brown refractile particles are seen; these tend to sediment
inferiorly when the eye is immobile. Occasionally the anterior
chamber may also be involved (Fig. 17.4).
Amyloidosis
Amyloidosis is a localized or systemic condition in which there is
extracellular deposition of fibrillary protein. Vitreous involvement
typically occurs in familial amyloidosis, also characterized by
polyneuropathy, prominent corneal nerves and pupillary light-
near dissociation. Vitreous opacities may be unilateral or bilateral
and are initially perivascular. Later they involve the anterior gel
and take on a characteristic sheet-like (‘glass wool’) appearance
(Fig. 17.5A). The opacities may become attached to the posterior
lens by thick footplates (Fig. 17.5B). Dense opacification resulting
in significant visual impairment may require vitrectomy.
 17
CHAPTER
Vitreous opacities 723

A B

C D

Fig. 17.1  (A) Mild vitreous haemorrhage seen against the red reflex; (B) severe diffuse vitreous haemorrhage; (C) B-scan
image showing vitreous haemorrhage and flat retina; (D) B-scan image showing vitreous haemorrhage and funnel-shaped
retinal detachment
724 Kanski’s Clinical Ophthalmology

Fig. 17.2  Terson syndrome. (A) Acute intra- and preretinal haemorrhages in a 48-year-old man with subarachnoid
haemorrhage; (B) composite image
(Courtesy of A Agarwal, from Gass’ Atlas of Macular Diseases, Elsevier 2012)

B
A

D
C

Fig. 17.3  Asteroid hyalosis. (A) Clinical appearance of moderate severity; (B) wide-field image; (C) appearance on OCT; (D)
three-dimensional OCT reconstruction;
Continued
 17
CHAPTER
Vitreous opacities 725

Fig. 17.3, Continued  (E) B-scan ultrasonogram

(Courtesy of S Chen – figs B–D)
Fig. 17.4  Synchysis scintillans in the anterior chamber of a
degenerate eye
(Courtesy of P Gili)

A B

Fig. 17.5  Amyloid deposits in the vitreous (see text)

726 Kanski’s Clinical Ophthalmology
Fig. 17.6  Vitreous cyst
Vitreous cyst
Vitreous cysts can be congenital or acquired, acquired cysts being
caused by a range of pathology such as trauma and inflammation.
Congenital cysts are pigmented or non-pigmented, the former
usually arising from the ciliary body pigment epithelium, the latter
from remnants of the primary hyaloid vascular system. They are
generally fixed – non-pigmented cysts are typically attached to the
optic disc – but can be found floating freely in the posterior (occa-
sionally anterior) segment (Fig. 17.6). Treatment is seldom
Fig. 17.7  Bergmeister papilla
required, but laser cystotomy or vitrectomy can be performed for
troublesome symptoms.
Persistent fetal vasculature
In addition to non-pigmented vitreous cysts, remnants of the
hyaloid vessels can form a Bergmeister papilla, seen as a tuft at the
optic disc (Fig. 17.7), a Mittendorf dot on the posterior lens surface,
and the more marked manifestations for which the term persistent
fetal vasculature is generally reserved, previously termed persistent
hyperplastic primary vitreous (see Ch. 12).