Vitreous

MARC P. JAPITANA MD
Department of Ophthalmology
CLMMRH

APPLIED ANATOMY
VITREOUS HUMOR

 is an inert, transparent, jelly-like structure that
fills the posterior 4/5 of the cavity of the eyeball
 normal volume – 4 mL
 hydrophilic gel with optical functions
 mechanically stabilizes the volume of the globe
 pathway for nutrients to reach the lens and
retina

APPLIED ANATOMY
STRUCTURE OF THE VITREOUS

 composed of a network of randomly-oriented
collagen fibrils interspersed with numerous
spheroidal macromolecules of hyaluronic acid
 colapse = conversion of gel into sol
 can be divided into: cortex and nucleus (main
vitreous body)

APPLIED ANATOMY
CORTICAL VITREOUS

 lies adjacent to the retina posteriorly & to the
lens, ciliary body and zonules anteriorly
 density of collagen fibrils is greater in the
peripheral part
 condensation of these fibrils form false anatomic
membranes: anterior hyaloid membrane and
posterior hyaloid membrane

APPLIED ANATOMY
CORTICAL VITREOUS

 anterior hyaloid membrane is attached to the
posterior lens
 posterior hyaloid membrane is loosely attached
to the internal limiting membrane of the retina

APPLIED ANATOMY
MAIN VITREOUS BODY (NUCLEUS)

 it has less dense fibrillar structure
 true biological gel
 site where liquefaction of the vitreous gel starts
first
 Hyaloid canal (Cloquet’s Canal) – Hyaloid artery
of the fetus

APPLIED ANATOMY
Attachments

 VITREOUS BASE – part of the vitreous about 4
mm across the ora serrata where the attachment
is strongest.
 other firm attachments – around the margins of
the optic disc, foveal region and back of the
crystalline lens (ligament of Wieger)

DISEASES OF THE VITREOUS
 Vitreous Liquefaction
 Vitreous Opacities
 Vitreous Detachment
 Vitreous Hemorrhage
 Vitreo-Retinal Diseases

VITREOUS LIQUEFACTION
 most common degenerative change in the
vitreous
 on SLE, absence of normal fibrillar structure and
visible pockets of liquefaction
 appearance of coarse aggregate material which
moves freely in the free vitreous
 associated with collapse (synersis) and opacities
in the vitreous --- black floaters in front of the
eye

VITREOUS LIQUEFACTION
Causes of Liquefaction

 Degeneration (senile, myopic, retinitis
pigmentosa)
 Post-inflammatory (following uveitis)
 Trauma to the vitreous (blunt or perforating)
 Thermal effects (following diathermy,
photocoagulation and cryocoagulation)
 Radiation

VITREOUS DETACHMENT
 Posterior Vitreous Detachment (PVD)
 Detachment of the Vitreous Base and Anterior
Vitreous

POSTERIOR VITREOUS DETACHMENT

 separation of the cortical vitreous from retina
anywhere posterior to the vitreous base
– vitreous base is 3 – 4 mm wide area of attachment of
vitreous to the ora serrata

 PVD with vitreous liquefaction (synchysis) and
collapse (synersis) is of common occurrence in
majority of the normal subjects above the age of
65 years


 occurs in eyes with senile liquefaction,
developing a hole in the posterior hyaloid
membrane
 the synchytic fluid collects between the posterior
hyaloid membrane and the internal limiting
membrane of the retina, and leads to PVD up to
the base along with collapse of the remaining
vitreous gel (synersis)
 more common among aphakics and myopes


CLINICAL FEATURES

 associated with flashes of lights and floaters
 SLE – collapsed vitreous behind the lens
 optically clear space between the detached
posterior hyaloid phase and the retina
 Weiss ring or Fuchs ring – pathognomic sign


COMPLICATION

 retinal breaks
 vitreous hemorrhage
 retinal hemorrhage
 cystoid maculopathy

VITREOUS BASE & ANTERIOR VITREOUS
DETACHMENT
 occurs following blunt trauma
 may be associated with

– vitreous hemorrhage
– retinal hemorrhage
– anterior retinal dialysis
– dislocation of crystalline lens

VITREOUS OPACITIES
 vitreous is a transparent structure
 – any non-transparent structure present in it will
form an opacity and cause symptoms of
FLOATERS

VITREOUS OPACITIES
MUSCAE VOLITANTES

 physiologic opacities
 residues primitive hyaloid vasculature
 perceived as fine dots and filaments, which drift
in and out of the field against bright background

VITREOUS OPACITIES
PERSISTENT HYPERPLASTIC PRIMARY
VITREOUS

 failure of the primary vitreous structure to
regress combined with the hypoplasia of the
posterior portion of vascular network
 white pupillary reflex (leucocoria) seen after birth
 associated with other anomalies such as
congenital cataract, glaucoma, long and
extended ciliary processes, micropthalmos and
vitreous hemorrhage.

VITREOUS OPACITIES
VITREOUS

Differentials

 retinoblastoma, congenital cataract and ROP
 CT Scan helps in diagnosis

VITREOUS OPACITIES
VITREOUS

Treatment

 pars plana lensectomy
 excision of the membranes with anterior
vitrectomy
 visual prognosis is poor

VITREOUS OPACITIES
INFLAMMATORY VITREOUS OPACITIES

 exudates poured into the vitreous in

– anterior uveitis (iridocyclitis)
– posterior uveitis (choroiditis)
– pars planitis
– pan uveitis
– endophthalmitis

VITREOUS OPACITIES
VITREOUS AGGREGATES AND
CONDENSATION WITH LIQUEFACTION

 commonest cause of vitreous opacities
 condensation of collagen fibrillar network
 maybe senile, myopic, post-traumatic or post-
inflammatory in origin

VITREOUS OPACITIES
AMYLOID DEGENERATION

 rare condition
 amorphous amyloid material is deposited in the
vitreous
 part of generalized amyloidosis

VITREOUS OPACITIES
ASTEROID HYALOSIS

 small, white rounded bodies suspended in the
vitreous gel
 formed due to accumulation of calcium
containing lipids
 unilateral, asymptomatic condition usually seen
in old patients with healthy vitreous

VITREOUS OPACITIES
ASTEROID HYALOSIS

 genetic relationship between this condition,
diabetes and hypercholesterolemia
 genesis is unknown
 effective treatment

VITREOUS OPACITIES
SYNCHYSIS SCINTILLANS

 vitreous is laden with small white angular and
crystalline bodies with formed of cholesterol
 seen in damaged eyes that suffered trauma,
vitreous hemorrhage or inflammatory disease in
the past
 vitreous is liquid and crystals sink in the bottom
and stirred up with every movement

VITREOUS OPACITIES
SYNCHYSIS SCINTILLANS

 “beautiful shower of golden rain” on
ophthalmoscopy
 symptomless
 untreatable

VITREOUS OPACITIES
RED OPACITIES

 caused by small vitreous hemorrhages or left-
outs of the massive vitreous hemorrhage

VITREOUS OPACITIES
TUMOR CELLS OPACITIES

 maybe seen as free-floating opacities in some
patients with retinoblastoma, and reticulum cell
sarcoma

VITREOUS HEMORRHAGE
 usually occurs from the retinal vessels
 may present as pre-retinal (sub-hyaloid) or an
intragel hemorrhage
 intragel hemorrhage may involve anterior,
middle, posterior or the whole vitreous body

VITREOUS HEMORRHAGE
CAUSES

 Spontaneous vitreous hemorrhage from retinal
breaks especially those associated with PVD
 Trauma to eye (blunt or perforating)
 Inflammatory disease
 Vascular disorders (HPN retinopathy or CRVO)
 Metabolic diseases (DM retinopathy)
 Blood dyscrasias

VITREOUS HEMORRHAGE
CAUSES

 Bleeding disorders
 Neoplasms
 Idiopathic

VITREOUS HEMORRHAGE
CLINICAL FEATURES

 sudden development of floaters – small
hemorrhage
 painless loss of vision – massive vitreous
hemorrhage

VITREOUS HEMORRHAGE
SIGNS

 Distant direct ophthalmoscopy reveals black
shadows against the red glow in small
hemorrhage and no red glow in large
hemorrhage
 Direct and indirect ophthalmoscopy may show
presence of blood in the vitreous cavity
 UTZ with B Scan is particularly helpful

VITREOUS HEMORRHAGE
FATE OF VITREOUS HEMORRHAGE

1. Complete absorption may occur without
organization and the vitreous becomes clear
within 4-8 weeks

2. Organization of hemorrhage with formation of a
yellowish-white debris occurs in persistent or
recurrent bleeding

VITREOUS HEMORRHAGE
FATE OF VITREOUS HEMORRHAGE

3. Complications like vitreous liquefaction,
degeneration and khaki cell glaucoma (in
aphakia) may occur

4. Retinitis proliferans may occur which may be
complicated by tractional retinal detachment

VITREOUS HEMORRHAGE
TREATMENT

1. Conservative treatment consist of bed rest,
elevation of patient’s head and bilateral eye
patches -- to allow the blood to settle down

2. Treatment of cause. Once the blood settles
down, indirect ophthalmoscopy should be done
to locate and further manage the causative
lesion such as retinal break, phlebitis, etc.

VITREOUS HEMORRHAGE
TREATMENT

3. Vitrectomy by pars plana route should be
considered to clear the vitreous, if the
hemorrhage is not absorbed after 3 months

Vitreous

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