vitreous

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VITREOUS MARC P. JAPITANA MD Department of Ophthalmology CLMMRH

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Marc P. Japitana, MDCLMMRH - Department of Ophthalmology

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Page 1: Vitreous

VITREOUS

MARC P. JAPITANA MDDepartment of Ophthalmology

CLMMRH

Page 2: Vitreous

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

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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)

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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

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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

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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

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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)

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DISEASES OF THE VITREOUS

Vitreous Liquefaction Vitreous Opacities Vitreous Detachment Vitreous Hemorrhage Vitreo-Retinal Diseases

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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

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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

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VITREOUS DETACHMENT

Posterior Vitreous Detachment (PVD) Detachment of the Vitreous Base and

Anterior Vitreous

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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

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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

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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

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POSTERIOR VITREOUS DETACHMENT

COMPLICATION

retinal breaks vitreous hemorrhage retinal hemorrhage cystoid maculopathy

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VITREOUS BASE & ANTERIOR VITREOUS DETACHMENT

occurs following blunt trauma may be associated with

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

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VITREOUS OPACITIES

vitreous is a transparent structure – any non-transparent structure present in

it will form an opacity and cause symptoms of FLOATERS

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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

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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.

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VITREOUS OPACITIES

PERSISTENT HYPERPLASTIC PRIMARY VITREOUS

Differentials

retinoblastoma, congenital cataract and ROP

CT Scan helps in diagnosis

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VITREOUS OPACITIES

PERSISTENT HYPERPLASTIC PRIMARY VITREOUS

Treatment

pars plana lensectomy excision of the membranes with anterior

vitrectomy visual prognosis is poor

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VITREOUS OPACITIES

INFLAMMATORY VITREOUS OPACITIES

exudates poured into the vitreous in

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

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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

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VITREOUS OPACITIES

AMYLOID DEGENERATION

rare condition amorphous amyloid material is deposited

in the vitreous part of generalized amyloidosis

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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

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VITREOUS OPACITIES

ASTEROID HYALOSIS

genetic relationship between this condition, diabetes and hypercholesterolemia

genesis is unknown effective treatment

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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

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VITREOUS OPACITIES

SYNCHYSIS SCINTILLANS

“beautiful shower of golden rain” on ophthalmoscopy

symptomless untreatable

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VITREOUS OPACITIES

RED OPACITIES

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

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VITREOUS OPACITIES

TUMOR CELLS OPACITIES

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

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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

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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

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VITREOUS HEMORRHAGE

CAUSES

Bleeding disorders Neoplasms Idiopathic

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VITREOUS HEMORRHAGE

CLINICAL FEATURES

sudden development of floaters – small hemorrhage

painless loss of vision – massive vitreous hemorrhage

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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

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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

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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

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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.

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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

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THANK YOU!