2. 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
3. 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)
4. 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
5. 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
6. 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
7. 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)
8.
9.
10. DISEASES OF THE VITREOUS
Vitreous Liquefaction
Vitreous Opacities
Vitreous Detachment
Vitreous Hemorrhage
Vitreo-Retinal Diseases
11. 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
12. 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
14. 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
15. POSTERIOR VITREOUS DETACHMENT
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
16.
17. POSTERIOR VITREOUS DETACHMENT
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
20. VITREOUS BASE & ANTERIOR VITREOUS
DETACHMENT
occurs following blunt trauma
may be associated with
– vitreous hemorrhage
– retinal hemorrhage
– anterior retinal dialysis
– dislocation of crystalline lens
21. VITREOUS OPACITIES
vitreous is a transparent structure
– any non-transparent structure present in it will
form an opacity and cause symptoms of
FLOATERS
22. 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
23. 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.
25. VITREOUS OPACITIES
PERSISTENT HYPERPLASTIC PRIMARY
VITREOUS
Treatment
pars plana lensectomy
excision of the membranes with anterior
vitrectomy
visual prognosis is poor
26. VITREOUS OPACITIES
INFLAMMATORY VITREOUS OPACITIES
exudates poured into the vitreous in
– anterior uveitis (iridocyclitis)
– posterior uveitis (choroiditis)
– pars planitis
– pan uveitis
– endophthalmitis
27. 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
31. 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
32. VITREOUS OPACITIES
ASTEROID HYALOSIS
genetic relationship between this condition,
diabetes and hypercholesterolemia
genesis is unknown
effective treatment
33.
34.
35.
36. 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
41. VITREOUS OPACITIES
TUMOR CELLS OPACITIES
maybe seen as free-floating opacities in some
patients with retinoblastoma, and reticulum cell
sarcoma
42. 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
43.
44. 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
47. 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
48. 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
49. 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
50. 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.