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Marc P. Japitana, MD
CLMMRH - Department of Ophthalmology

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  1. 1. MARC P. JAPITANA MDDepartment of Ophthalmology CLMMRH
  2. 2. APPLIED ANATOMYVITREOUS 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. 3. APPLIED ANATOMYSTRUCTURE 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. 4. APPLIED ANATOMYCORTICAL 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. 5. APPLIED ANATOMYCORTICAL 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. 6. APPLIED ANATOMYMAIN 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. 7. APPLIED ANATOMYAttachments 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. 8. DISEASES OF THE VITREOUS Vitreous Liquefaction Vitreous Opacities Vitreous Detachment Vitreous Hemorrhage Vitreo-Retinal Diseases
  9. 9. 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
  10. 10. VITREOUS LIQUEFACTIONCauses 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
  11. 11. VITREOUS DETACHMENT Posterior Vitreous Detachment (PVD) Detachment of the Vitreous Base and Anterior Vitreous
  12. 12. 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
  13. 13. 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
  14. 14. POSTERIOR VITREOUS DETACHMENTCLINICAL 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
  15. 15. POSTERIOR VITREOUS DETACHMENTCOMPLICATION retinal breaks vitreous hemorrhage retinal hemorrhage cystoid maculopathy
  16. 16. VITREOUS BASE & ANTERIOR VITREOUS DETACHMENT occurs following blunt trauma may be associated with – vitreous hemorrhage – retinal hemorrhage – anterior retinal dialysis – dislocation of crystalline lens
  17. 17. VITREOUS OPACITIES vitreous is a transparent structure – any non-transparent structure present in it will form an opacity and cause symptoms of FLOATERS
  18. 18. VITREOUS OPACITIESMUSCAE VOLITANTES physiologic opacities residues primitive hyaloid vasculature perceived as fine dots and filaments, which drift in and out of the field against bright background
  19. 19. VITREOUS OPACITIESPERSISTENT 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.
  20. 20. VITREOUS OPACITIESPERSISTENT HYPERPLASTIC PRIMARY VITREOUSDifferentials retinoblastoma, congenital cataract and ROP CT Scan helps in diagnosis
  21. 21. VITREOUS OPACITIESPERSISTENT HYPERPLASTIC PRIMARY VITREOUSTreatment pars plana lensectomy excision of the membranes with anterior vitrectomy visual prognosis is poor
  22. 22. VITREOUS OPACITIESINFLAMMATORY VITREOUS OPACITIES exudates poured into the vitreous in – anterior uveitis (iridocyclitis) – posterior uveitis (choroiditis) – pars planitis – pan uveitis – endophthalmitis
  23. 23. VITREOUS OPACITIESVITREOUS 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
  24. 24. VITREOUS OPACITIESAMYLOID DEGENERATION rare condition amorphous amyloid material is deposited in the vitreous part of generalized amyloidosis
  25. 25. VITREOUS OPACITIESASTEROID 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
  26. 26. VITREOUS OPACITIESASTEROID HYALOSIS genetic relationship between this condition, diabetes and hypercholesterolemia genesis is unknown effective treatment
  27. 27. VITREOUS OPACITIESSYNCHYSIS 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
  28. 28. VITREOUS OPACITIESSYNCHYSIS SCINTILLANS “beautiful shower of golden rain” on ophthalmoscopy symptomless untreatable
  29. 29. VITREOUS OPACITIESRED OPACITIES caused by small vitreous hemorrhages or left- outs of the massive vitreous hemorrhage
  30. 30. VITREOUS OPACITIESTUMOR CELLS OPACITIES maybe seen as free-floating opacities in some patients with retinoblastoma, and reticulum cell sarcoma
  31. 31. 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
  32. 32. VITREOUS HEMORRHAGECAUSES 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
  33. 33. VITREOUS HEMORRHAGECAUSES Bleeding disorders Neoplasms Idiopathic
  34. 34. VITREOUS HEMORRHAGECLINICAL FEATURES sudden development of floaters – small hemorrhage painless loss of vision – massive vitreous hemorrhage
  35. 35. VITREOUS HEMORRHAGESIGNS 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
  36. 36. VITREOUS HEMORRHAGEFATE OF VITREOUS HEMORRHAGE1. Complete absorption may occur without organization and the vitreous becomes clear within 4-8 weeks2. Organization of hemorrhage with formation of a yellowish-white debris occurs in persistent or recurrent bleeding
  37. 37. VITREOUS HEMORRHAGEFATE OF VITREOUS HEMORRHAGE3. Complications like vitreous liquefaction, degeneration and khaki cell glaucoma (in aphakia) may occur4. Retinitis proliferans may occur which may be complicated by tractional retinal detachment
  38. 38. VITREOUS HEMORRHAGETREATMENT1. Conservative treatment consist of bed rest, elevation of patient’s head and bilateral eye patches -- to allow the blood to settle down2. 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.
  39. 39. VITREOUS HEMORRHAGETREATMENT3. Vitrectomy by pars plana route should be considered to clear the vitreous, if the hemorrhage is not absorbed after 3 months
  40. 40. THANK YOU!