Vitreous Humor Composition and Function

• The vitreous is a clear, avascular gel that fills two-thirds of the eye's volume and weight.
• Attachment to the lens capsule and optic nerve head is firm early in life but diminishes, or after intraocular inflammation.

Vitreous Composition

• The vitreous is composed of 98.5% to 99.7% water.
• Contains Type II collagen fibers and glycosaminoglycans (GAGs), mostly hyaluronic acid.
• Vitamin C levels are higher than in plasma which prevents opacity.
• Amino acid levels are lower than in plasma.
• Hyalocytes are cells within the vitreous, possibly originating from monocytes.
• Hyalocytes are located in the anterior cortical vitreous near the ciliary body.
• Hyalocytes produce hyaluronic acid and have a half-life of about a week.

Vitreous Functions

• It serves as a medium to maintain a clear path of light between the lens and the retina.
• It lacks diffusing and absorbing elements.
• It occupies 60% of the globe.
• Its refractive index is equivalent to the aqueous humor (n = 1.334).

Vitreous Attachments

• Anteriorly, Berger’s space is located behind the crystalline lens and in front of the vitreous body.
• The Wieger’s hyaloideo-capsular ligament attaches the hyaloid to the lens capsule.
• This attachment is strong in young patients but weakens with age.
• Egger’s line/Weiger’s ligament is the line on the posterior lens capsule marking Weiger’s adhesion.
• The anterior vitreous base is at the ora serrata.
• Posteriorly, the vitreous is attached to the optic nerve head (ONH) and blood vessels of the retina and macula.
• The strongest connection is at the vitreous base (vitreoretinal symphysis), straddling the ora serrata, holding the vitreous cortex, sensory retina, and pars plana together.
• Disturbances to this adhesion can result in giant tears or retinal dialysis.
• Posterior vitreous attachment at the optic disc margin forms a ring.
• When detached here, it becomes an annular opacity called a Weiss ring, a sign of complete posterior vitreous detachment.
• Attachment at the macular area is weak and detaching can cause macular edema.
• Weak connections also exist at retinal vessels, and PVD may cause pre-retinal or retrovitreal hemorrhages.

Vitreous Development

• The primary vitreous develops at the end of the third embryonic week.
• It is formed by mesoderm migrating between the optic cup and lens vesicle.
• Primarily the hyaloid vasculature supplies nutrients and is the precursor to the central retinal artery.
• The secondary vitreous develops by the ninth week.
• It is mostly acellular and fibrous, synthesized by primary vitreal and retinal glial cells.
• The secondary vitreous fills the globe, compacting the primary vitreous and is neuroectoderm in origin.
• The tertiary vitreous (zonular fibers) develops at 6 months embryonically.
• The fibrous structure of the secondary vitreous condenses, forming zonules.
• Zonules merge with the lens capsule and the ciliary body's basement membrane.
• Hyaloid vasculature dissolves before birth via an autolytic process.
• The canal left is called the canal of Cloquet or the hyaloid canal.
• Post-birth the canal runs straight, becoming more serpentine with age.
• With liquefaction, it becomes more mobile (ascension phenomenon).

Vitreous Anomalies

• Mittendorf’s Dot: A remnant of Cloquet’s canal's lenticular attachment, slightly nasal to the posterior pole of the lens.
• Bergmeister Papillae: A remnant of the hyaloid artery/Cloquet’s canal, attached only to the optic nerve.
• Vitreous Cysts: Rare congenital remnants of the primary hyaloidal system or ciliary body pigment epithelium.
  • Usually no treatment is required unless symptomatic.
  • Issues can arise during procedures like LASIK or cataract surgery YAG, as breaking the cyst can tear the vitreous and macula.
• Persistent Hyperplastic Primary Vitreous (PHPV): A congenital anomaly resulting from the failure of the primary vitreous and hyaloid vasculature to regress.
  • Occurs in full-term infants without oxygen therapy exposure.
  • Characterized by persistence of embryonic hyaloid vascular system portions, with hyperplasia of connective tissue.
  • Associated with microphthalmia, cataracts, or glaucoma.
  • Anterior PHPV: Remnant vascular stalk attached to the back of the lens but not reaching the optic nerve.
    • Causes leukocoria and is typically unilateral.
    • May present with microcornea, strabismus, retrolental membrane, congenital glaucoma, and microphthalmia, but a normal retina.
    • Ciliary processes drawn to the lens periphery.
    • Traction on the ciliary body compromises aqueous formation, leading to hypotony and potentially phthisis bulbi.
    • May cause NVI leading to NVG and possible hyphema
    • Treatment includes early surgical intervention if the visual axis is occluded, A/C is shallow, or progressive traction is evident.
    • Standard treatment includes observation, lensectomy, and glaucoma management.
    • Glaucoma treatment in babies is usually surgery.
  • Posterior PHPV: Remnant vascular stalk arises from the optic nerve but doesn't reach the lens.
    • Usually doesn't cause cataracts.
    • Associated with abnormal retina, optic nerve, and macula development and may show stalk elongation.
    • Also known as a falciform retinal septum.
    • Treatment: Monitor yearly for retinal breaks or detachments and glaucoma.
    • Lensectomy and membranectomy via vitrectomy may be necessary, prognosis for vision remains poor.
  • Complete PHPV: A combination of anterior and posterior PHPV is the most common clinical presentation.
  • Differential Diagnosis for PHPV: Other causes of leukocoria that might be life and sight-threatening need to be ruled out.
    • Norrie’s disease: X-linked, hearing impairment, similar ocular signs to PHPV, and cerebral dysplasia, requiring a retinal consultation when vitrectomy or retinal repair is necessary.

Vitreous Pathology and Age-Related Changes

• Syneresis: Conversion of the vitreous gel into a more liquid form.
  • 65% of individuals over 60 experience it.
  • Higher incidence in myopes.
  • Hyaluronic acid molecules release water, forming fluid-filled cavities or lacunae.
  • Can lead to posterior vitreous detachment (PVD).
  • Suspect PVD if patients report a significant increase in floaters.
  • Vitreous liquefaction and syneresis are known as fibrillary degeneration and are prerequisites for PVD.
  • Results in opacification (floaters) and shrinkage of the vitreous, collapsing inward and detaching from the retina.
• Floaters: Coalescence of collagen filaments into fibrils causes further breakdown of the vitreous gel structure, may "float" within the liquid vitreous, leading to the sensation of floaters.
• Posterior Vitreous Detachment (PVD): Vitreous behind the vitreous base and hyaloid membrane separates from the sensory retina.
  • Common in women over 45, rare before this age.
  • Younger patients may experience this related to trauma or inflammation.
  • Up to 90% of aphakic patients experience this.
  • Complete PVD involves a Weiss ring.
  • Partial/incomplete PVD involves the attachment to the optic nerve head.
  • Symptoms include sudden onset of floaters (cobwebs, bugs, or spots that change position).
  • Often associated with photopsia, with metamorphopsia suggesting macular edema characteristic of vitreomacular traction

Vitreous Pathologies

• Weiss ring is a pre-ONH annular ring indicative of complete PVD.
• Transient pre-retinal hemorrhage may occur around the optic nerve or in the retinal periphery, between the hyaloid membrane and ILM.
• Retrovitreous hemorrhage is associated with approximately 75% of retinal breaks.
• Retinal breaks occur in about 10% of PVD cases.
• Incipient breaks (70%) are characterized by pigment granules (tobacco dust / Schafer’s sign).
  • Schafer’s sign indicates retinal detachment secondary to vitreous traction.
  • Distinguish hyperechoic retinal detachment vs hypoechoic RD.
• Asteroid Hyalosis: Characterized by hundreds of small spheres of calcium soaps in the vitreous attached to vitreous fibers, moving with the eye but returning to the same position.
  • Theories suggest aging collagen within the vitreous or depolymerization of hyaluronic acid as causes.
  • More common in the elderly and in whites, with a prevalence of 1-2%.
  • Usually unilateral.
  • Does not affect vision and has no clinical significance.
• Synchysis Scintillans: Usually bilateral, involves cholesterol crystals in the vitreous that are not attached.
  • Crystals settle inferiorly at rest and float freely with eye movement.
  • Not associated with systemic conditions and does not cause vision loss.
  • Usually occurs before age 40.
• Vitreous cells: Composed of WBCs in the presence of a posterior inflammatory condition, originates from the uvea.
• Vitreous Inflammations: Typically the result of posterior inflammatory conditions

Vitreous inflammations

• Endophthalmitis is a painful condition associated with photophobia, redness, and edema of the conjunctiva and lids.
  • Rare - Usually caused by a penetrating injury that introduces Bacillus subtilis into the vitreous, often destroying the eye despite antibiotics.
• Secondary inflammations are mostly caused by inflammatory infections of the choroid or retina.
  • White blood cells in the vitreous cause blurring of the retina and decreased vision. Symptoms generally resolve with treatment of the primary infection.
  • A vitrectomy may be needed if the vitreous doesn't clear
• Vitreous hemorrhage can be minimal or can fill the entire vitreous.
  • Can result from trauma, diabetes, HBP, or blood dyscrasias like leukemia.
  • Treatment depends on the primary cause including trauma, diabetes, retinal break, ARMD, hypertension etc.
  • May resolve independently or require a vitrectomy.
• Symptoms of vitreous hemorrhage is a sudden, painless loss of vision or sudden appearance of black spots, cobwebs, or haze.
• Severe vitreous hemorrhage obliterates fundus visualization, with RBCs in the anterior vitreous.
• Chronic vitreous hemorrhage may show a yellow ochre appearance with a mild RAPD possible based on the etiology.
• Vitreous Hemorrhage Differential Diagnosis: Differentiate from vitritis, retinal detachment.
  • Diabetic retinopathy, diabetic retinopathy is usually evident in the contralateral eye
  • Commonly superior with retinal break, needs scleral depression to examine/diagnose and ultrasonography if poor view.
  • Retinal vein occlusion (usually a BRVO) commonly occurs in older patients with a history of high BP.
  • Recent trauma or exudative ARMD may cause bleeding

Vitreous Hemorrhage Etiology

• Sickle cell disease in the contralateral eye will have seafan NV and salmon patches.
• Subarachnoid or subdural hemorrhage (Terson Syndrome) frequently presents with bilateral preretinal or vitreous hemorrhages caused by trauma.
• Eales disease (idiopathic inflammatory venous occlusive disease) typically occurs in men aged 20 to 30 years with peripheral retinal ischemia and NV.
• Others include Coats disease (exudative retinitis), retinopathy of prematurity, and retinal capillary angiomas of von Hippel–Lindau syndrome.
• In Infancy or Childhood VH- Consider birth trauma, shaken baby syndrome, traumatic child abuse, congenital X-linked retinoschisis, and pars planitis
• Exam for vitreous hemorrhages includes case history, VA's, pupils, IOP (tends to be lower in recent retinal detachments), SLE (looking for anterior vitreous), and D.O. examination which show a loss of fundus detail.
• BIO: Use a stronger magnification, illumination, and stereopsis.
• Scleral depression or use of a 3-mirror lens is required to exclude retinal tears of the periphery
• B scan– FA if necessary and if there is a view if fundus is not visible, examine B-scan

Vitreous Treatment (VT)

• Surgical removal of the blood (vitrectomy) is usually performed for: Vitreous hemorrhage accompanied by RD or break seen on B-scan, no clearing VH, usually persisting >3 to 6 months, Vitreous hemorrhage with NVI
• Vitrectomy and cataract surgery are done at the same time
• Ghost cell glaucoma occurs when degenerated red blood cells pass from the vitreous to the anterior chamber with cells that are khaki colored typically 1 or 3 months of the VH
• Treatment: POAG treatment, filtering surgery or tube shunt if persist elevation IOP
• Follow-up includes the patient is evaluated daily for the first 2 to 3 days, if there is a Total vitreous hemorrhage persists, and the etiology remains unknown follow up with B-scan ultrasound every 1 to 3 weeks to rule out an RD
• Amyloidosis is a systemic condition due to extracellular deposition of a fibrillary protein.
• Vitreous opacification occurs in familial amyloidosis, characterized by polyneuropathy and prominent corneal nerves.
• Opacities may attach to the posterior lens by thick footplates, dense opacities result in significant VA loss, requiring vitrectomy.