Posterior Vitreous Detachment: A Common Process with Potential for Ocular Morbidity
November 30, 2011
Posterior vitreous detachment (PVD) is a frequent consequence of aging. Understanding the anatomical makeup and biochemical properties of the vitreous are critical in the diagnosis of PVD as well as associated vitreoretinal conditions.
Diana L. Shechtman, O.D. and Diane E. Calderon, O.D.
This course is COPE approved for 1 hour of CE credit. COPE ID is 23658-PS. Please check your state licensing board to see if this approval counts toward your CE requirement for relicensure. There is a $30 fee to take this course.
This continuing education course is joint-sponsored by the University of Alabama School of Optometry.
Dr. Shechtman is on the speakers’ bureau of VSP, MSS and Alcon.
POSTERIOR VITREOUS DETACHMENT
(PVD) is a frequent consequence of
aging. With age, the vitreous degenerates, leading to a PVD. A posterior
vitreous detachment is described as
a separation of the posterior cortex
of the vitreous from the internal limiting membrane of the retina.
Vitreopapillary separation is the
most common location. (Figure 1)
This is described as an annular ring,
known as a Weiss’ ring, attached to
the posterior hyaloid and located
anterior to the optic nerve. (Figure 2) This process is readily observed in
the elderly population, affecting
65% of patients over the age of 65.1,2 Even though a PVD is usually detected in an older female both genders
may be affected and it is believed
that the process starts much earlier.3 Conditions, such as
myopia, trauma, inherited vitreoretinal disease, surgery, and
inflammation may accelerate the process.4 Floaters are the most
described as “cobwebs,
flies or hair-like-structures.” Flashes, or photopsias, may also be
associated with an acute PVD.
Flashes do not always specify the
presence of a retinal break or retinal
detachment. Flashes indicate traction upon the retina, resulting in
stimulating of the photoreceptors.
Although we have recognized the
vitreous as an important ocular structure for more than a century,5 we are
only recently beginning to understand its pathogenic role in various
vitreoretinal diseases. PVD is typically described as a benign process;
however, the location of firm vitreo-retinal adhesions plays a critical role
in various pathological vitreoretinal
There are a number of firm posterior vitreoretinal attachments, which
include areas along retinal vessels,
the vitreous base, macula and optic
nerve. Depending on the site of firm
vitreoretinal attachment, an incomplete PVD may lead to the development of a vitreous hemorrhage, retinal break (RB), rhegmatogenous
retinal detachment (RRD), or vitreomacular traction syndrome (VMT).
Understanding the anatomical makeup and biochemical properties of the
vitreous are critical in the diagnosis
of PVD as well as associated vitreoretinal
Vitreous Anatomy & Biochemistry
The vitreous is considered to be a transparent gel, primarily composed of water. A small
but vital component of
the vitreous consists of collagen and hyaluronic acid, which contributes to
the “gel-like” consistency of the vitreous.6,7 Collagen is
a structural protein, which is connected to hyaluronic
acid.1 As we age, there is alteration between the
hyaluronic-collagen complex, causing vitreous liquefaction and shrinkage. In addition, with age, the internal limiting membrane becomes thickened, causing a
decrease in vitreoretinal adhesion throughout the fundus.7 This weakening further facilitates the migration of the liquid vitreous into the subhyaloid space. The
vitreous volume displacement causes
a forward collapsing of the vitreous
and a complete separation of the vitreous cortex from the retina, a PVD. This entire process commonly runs a
complete and benign course with no
During the PVD process, if vitreous liquefaction surpasses the extent
of weakening of vitreoretinal adherence, tractional forces will ensue
upon areas of firm attachments.7 Depending on the site of the firm vitreoretinal attachment, a number of pathological events can occur during the PVD process, invariably attributing to retinal
disturbances, such as a vitreous hemorrhage, VMT or
retinal break which potentially can lead to a RRD.4,7,8 (Table 1)
Table 1. Complications Associated with PVD
|VR traction site
||Retinal hemorrhage or VH
Avulse retinal vessel
What Happens in the Vitreous?
Vitreous Hemorrhage (VH)
A VH is characterized by the presence of blood posterior to the crystalline lens and anterior to the internal limiting membrane. (Figure 3) Since the vitreous
is an avascular structure, blood found within the vitreous must come from the superficial retinal vasculature. The main causes of a vitreous hemorrhage
include superficial retinal neovascularization, trauma and a PVD (with or without associated retinal
breaks). A firm vitreoretinal attachment is maintained along the retinal vessels. During the PVD
process sufficient traction along a vessel can lead to
a vessel tear, resulting in a vitreous hemorrhage.
A VH can present as a large, dense, diffusely disperse
hemorrhage within the vitreous cavity or a localized
hemorrhage without characteristic borders or as a single streak of blood. Vitreous hemorrhages tend to clot
quickly while resolving slowly. Patients may present
with a history of multiple floaters or smoky vision, typically described as a “red” haze. Decrease in visual acuity is dependent upon the density and location of the VH. Since the VH is situated in a gel
within a cavity, it will shift with head
movements. Thus, patients may
experience intermittent visual
obstruction with head movement.
PVD without retinal breaks
account for less than 10% of VH
cases.9,10 Although PVD may be associated with a VH in the absence of a
retinal break, the presence of a vitreous hemorrhage is considered a
risk factor for the presence of a
coexisting retinal break.11 Vitreous
hemorrhages are indicative of vitreoretinal traction and potential
impending retinal break. Since many VHs settle inferiorly due to gravity, location of VH does not aid in
detecting the possible site of an accompanying RB. In
the presence of a VH, it is imperative to scrutinize the
retina for any evidence of retinal breaks. In cases of
dense VH, ultrasonography (B-scan) may aid in ascertaining the presence of retinal detachment, retinal
tear, or any other associated etiologies. In the
absence of a retinal break, VH should be followed
until complete resolution has occurred.
What Happens in the Periphery?
Retinal Break (RB)
Retinal breaks commonly result from the vitreous
pulling on the retina, causing a full-thickness retinal
defect. This is common following the evolution of a
partial PVD with associated continuous localized traction onto the retina. Up to 15% of all patients who
present with acute symptomatic PVD have at least one
retinal break.9,10,12 Since the strongest vitreoretinal
attachment is at the vitreous base, most retinal breaks
are located between the equator and the ora.12,13 There is a downward gravitational force exerted on the
remaining attached vitreous base, causing a greater
prevalence for superior retinal breaks. Vitreoretinal
traction induced by a PVD increases the risk for a RRD.
Ominous accompanying signs include symptomatic
breaks, as well as the presence of vitreoretinal traction,
a vitreal or preretinal hemorrhage, pigmented vitreal
cells (Schaffer’s sign) and a large retinal cuff of fluid.
It is not uncommon for patients to present with an
asymptomatic retinal break, which is only discovered
during a routine eye exam.
The most common types of retinal breaks include
atrophic retinal holes, operculated retinal holes and
flap tears. Pathogenesis of each is associated with distinct mechanisms, contributing to variable propensity
toward the progression to a RRD. Since atrophic retinal holes are not typically associated with vitreoretinal
traction, this entity will not be discussed in this article.
A retinal break provides a passage for the vitreous into
the retina, thus the potential for a RRD. Management
depends on the type of RB, associated findings, and
risk factors (Table 2). For example, myopia (>6.00D)
and aphakia are considered risk factors for retinal
breaks to progress to RRD.14,15
Table 2. Predisposing Risk Factors
- High myope
- History of previous RD
- Cataract surgery
Categorizing the type of retinal break, in addition to
identifying associated signs and symptoms, is imperative. Not all retinal breaks progress to a RRD. Proper
management relies on determining which RB may
progress to RRD: in other words, which retinal breaks
would benefit from prophylactic treatment.
Operculated Retinal Hole
An operculated retinal hole represents a round, red
full-thickness retinal defect with an associated avulsed
piece of retinal tissue in the vitreous cortex.
Operculated retinal holes are thought to be a sudden
occurrence rather than a progressive change and most
often occur at the same time as a PVD and or associated with retinal tufts.16 Due to their close association
with PVD, operculated retinal holes are found more
commonly in older people.16 Operculated retinal
holes are a result of increased focal vitreoretinal adhesion in the periphery, pulling a plug of retinal tissue
onto the cortex of the vitreous. This avulsed retinal tissue (operculum) is often found directly overlying the
retinal break, but can be found elsewhere depending
on the direction of the force of the vitreous traction at
the time of the separation. The operculum is noted to
be smaller than its associated retinal break due to
degeneration that has occurred over time from vascular insufficiency previously supplied by the underlying
retinal layers. An operculum can be distinguished
from a vitreous floater due to its disc-shaped appearance as compared to the spherical appearance of a vitreous floater.16 Operculated retinal holes may be symptomatic in the initial stages, but symptoms subside
once the traction is released and the operculum is
finally formed. Since
they are not associated with continuous
vitreoretinal traction, most are followed on an annual
Retinal Flap Tear (Horseshoe tear)
A retinal flap tear,
also known as a
horseshoe tear, commonly occurs in association with an incomplete PVD.
During the PVD process, traction at this site may lead
to the development of a flap tear. The cardinal feature of a retinal flap tear in a “U” or “Horseshoe”
shape, representing an incomplete full thickness
retinal tear associated with partial vitreoretinal
adherence. As the vitreous is displaced forward, the
flap assumes a triangular shape, with the apex oriented toward the posterior pole and the attached base
parallel with the peripheral retina. (Figure 4)
Horseshoe tears are the leading cause of rhegmatogenous retinal detachments (RRD). Even an asymptomatic horseshoe tear can result in RRD, making the
timely diagnosis of this condition extremely important.
Symptomatic retinal flap tears are prophylactically treated, creating retinal scars (chorioretinal adhesions) in
order to seal down the detached retina.
Management of Retinal Breaks
The decision to refer for a treatment is anecdotal,
depending on variable factors, such as the type of retinal break, risk factors, and accompanying symptoms
and signs.17 Various studies have confirmed that symptoms are the single most likely predictor that a retinal
break will progress to a RRD.18,19 A retinal consult is
typically considered for acute symptomatic retinal
breaks. An acute symptomatic PVD can co-exist with a
longstanding retinal break. Clinical trials have not
aided in determining whether these retinal breaks
would benefit from prophylactic treatment.18 The presence of a retinal or vitreal hemorrhage, along with
Schaffer’s sign can further help determine the acute
nature of a retinal break.
Retinal break with accompanying subclinical retinal
detachment (associated fluid cuff <2.00DD) should
also be referred for a retinal consult. While fluid cuff
surrounding a retinal break is an inauspicious sign,
retinal pigment epithelial changes are considered a
sign of chronicity and decrease the likelihood that the
retinal break will progress to a RRD.
Most retinal holes only require a yearly dilated fundus exam. Asymptomatic retinal holes are routinely
monitored. On the other hand, a symptomatic operculated hole with persistent vitreoretinal traction may
benefit from a retinal consult, although most have not
been reported to progress to a RRD.10
Retinal flap tears carry the highest risk for progression, but there is some controversy as to whether a non-symptomatic retinal flap tear should be treated.18 Only 5% of asymptomatic retinal breaks progress to
RRD.20,21 At the site of a retinal flap tear, the retina is
incompletely pulled away and vitreoretinal traction
exerts tractional forces upon the edge of the tear.
Since retinal tears have a predisposition to evolve to a
RRD, one may consider that all flap tears, at the very
least, deserve a retinal consult. This is especially true in
the presence of other risk factors such as aphakia,
myopia, or history of RD in the fellow eye.
What Happens in the Macula?
Vitreomacular Tractional Syndrome (VMT)
Vitreomacular traction is described an incomplete
posterior vitreous detachment with continuous
adherence as the macula.22-24 (Figure 5) This continuous vitreomacular adherence induces
VMT is commonly described as a
hyaloid in a “dumbbell” configuration. The clinical
picture is variable with symptoms ranging from mild
blurred vision and metamorphopsia to severe
decrease in visual acuity and accompanying photopsias. The typical patient is older with no history of
cataract surgery. The nature of the vitreomacular
attachment has been associated with a number of maculopathies, including cystoid macular edema, macular
hole formation and epiretinal membranes.24-26 The dynamic nature of the traction, strength of remaining
attachment and extent of vitreoretinal separation may
all contribute to the distinct type of associated maculopathy.27 The clinical course is unpredictable with a
few cases remaining stable for years or associated with
spontaneous posterior vitreous detachment. A spontaneous PVD is typically associated with alleviation of
both the associated symptoms and maculopathies, but
the occurrence is low.28 The classic course is one of progression associated with further deterioration. Thus, in
many cases, pars plana vitrectomy is a necessity.28
Many PVDs result in a complete detachment from the
retina without any further complication. Yet, depending on the site of firm vitreoretinal attachment, the
PVD process may lead to the development of vitreoretinal traction resulting in a vitreous hemorrhage,
retinal break, which may be associated with a retinal
detachment, or vitreomacular traction syndrome
(VMT). The vitreoretinal conditions reaffirm the
importance of further evaluation of every patient presenting with an acute PVD. A dilated fundus exam
should be performed in all patients who present with
signs and/or symptoms of a PVD. Scleral depression
should also be considered, in order to rule out the
presences of a retinal break or retinal detachment.
The vitreous should be carefully scrutinized for the
presences of hemorrhages or pigment.
In the absence of any complications, patients should
be followed-up on a one–two week basis (depending
on risk factors and associated signs or symptoms), until
complete detachment of the posterior vitreous is
noted. This commonly occurs within six weeks and is
typically associated with resolution of photopsias. Any
changes or progression in signs or symptoms, warrants
prompt re-examination. Accompany risk factors, signs
and symptoms, in addition to a complete clinical evaluation can aid in the appropriate management of a
patient presenting with a PVD.
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- Hikichi T, Trempe CL. Relationship between floaters, light flashes, or both and complications of PVD.
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- Hayreh SS. Jonas JB. PVD: Clinical correlations. Ophthalmologica 2004; 218: 333-343.
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- Brodley WW. Risk of retinal tears in patients with vitreous floaters. AJO 1983: 96: 783-7.
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- Austin KL. Palmer JR. Seddon JM, et al. Case-control study of idiopathic RD. Int J Epi 1990;
- National guidelines clearinghouse. RD and related peripheral vitreoretinal diseases.
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- Jones W. Reidy RW. Atlas of peripheral ocular fundus. MA: Butterworth Publ 1985.
- Colyear BH. Pischel D. Preventive treatment of RD by means of light coagulation. Trans Pac
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- Wilkinson CP. Evidence-based analysis of phrophylactic treatment of asymptomatic RD and LD.
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- Reese AB, Jones IR, Cooper WC. VMT syndrome confirmed histologically. AJO 1970; 69:975-977.
- Jaffe. NS. Vitreous traction at the posterior pole of the fundus due to alterations in the vitreous
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- Smiddy WE, Michels RG, Green WR. Morphology, pathology, and surgery of idiopathic vitreo-retinal macular disorders. Retina 1990; 10:288-296.
- Hotta K, Hotta J. Retinoschisis with macular retinal detachment associated with VMTS. Retina
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