VITREOUS
MARC P. JAPITANA MDDepartment 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
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
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
POSTERIOR VITREOUS DETACHMENT
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
PERSISTENT HYPERPLASTIC PRIMARY VITREOUS
Differentials
retinoblastoma, congenital cataract and ROP
CT Scan helps in diagnosis
VITREOUS OPACITIES
PERSISTENT HYPERPLASTIC PRIMARY 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
THANK YOU!
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