Posterior vitreous detachment: Minimising complications through collaboration

At the completion of this article, the reader should be able to improve their management of patients  with posterior vitreous detachment, including:

• Recognise the clinical signs and symptoms of posterior vitreous
  detachment (PVD), including indications for immediate versus delayed management
• Identify risk factors associated with increased likelihood of retinal tears following PVD
• Understand the types of retinal breaks, including horse-shoe tears, operculated tears and round (atrophic) holes, and their risks for progression to retinal detachment
• Consider developing a co-management strategy between optometrists and ophthalmologists for patients presenting with acute PVD

Dr Tuan Tran

MBBS, BSc, MMed(OphthSc),
FRANZCO, DRCPSC (Retina)
Medical Retinal & Vitreoretinal Surgeon
KindSIGHT Eye Specialists, Brisbane
Maroochy Eye Specialists, Sunshine Coast
Images: Dr Tuan Tran

All optometrists understand that posterior vitreous detachment often presents with symptoms like floaters and flashes of light, and how to assess for associated retinal tears or detachment. DR TUAN TRAN highlights the latest research on potential complications and emphasises the need for effective co-management between optometrists and ophthalmologists to minimise them.

Acute symptomatic posterior vitreous detachment (PVD) is a common presentation to both optometrists and ophthalmologists. The main concern is the potential development of retinal tears (RT) or retinal detachment (RD).

The general course entails a dilated examination to assess for signs of RT or RD. In the absence of these signs, patients are often reviewed in four to six weeks’ time, or earlier, if there are any worsening or changes to their symptoms.

However, this simple generic approach may not be best for all patients, in particular those with risk factors. This article delves into PVDs and the potential complications of RTs and RDs, and how the co-management between optometrists and ophthalmologists can minimise them.

Causative factors of PVD

The prevalence of PVD increases with age. Ageing of the vitreous occurs by liquefaction of the gel (vitreous syneresis). As the hyaluronic acid content decreases, vitreous collagen fibres release water. Over time, this results in enlarged pools of fluid within the gel.

PVD occurs when there is a spontaneous separation of the cortical vitreous from the posterior pole that advances toward the anterior periphery. A complete PVD is indicated by the presence of a Weiss ring, a partially or completely grayish-brown, mobile ring, which can be observed during a fundus examination.

Complete PVD occurs when the cortical vitreous detaches without leaving a hyaloid remnant layer. In contrast, in ‘incomplete PVDs’ (vitreoschisis), some portions of the vitreous remain attached (incomplete PVDs make up approximately 50% of PVDs).¹ Importantly, when a Weiss ring denotes vitreous separation at the posterior pole, it is still possible for vitreous to still be attached to the retina elsewhere.²

A PVD often precedes rhegmatogenous retinal detachment (RRDs) as traction from the process of PVD are applied on areas where there is strong retinal and vitreous adhesion causing a retinal break, often anterior to the equator.

Where there is adherent vitreous to the flap of the break, a horseshoe tear results and tractional forces may hold open the retinal break allowing subretinal accumulation of liquified vitreous.³ Operculated tears result if the vitreous traction is strong enough to cause avulsion of the retinal flap at the base generally resolving the tractional forces that may hold open the break.³

As expected, the incidence of PVD increases with age. They are prevalent in only 10% of those aged between 50-59 years old, compared to 60-70% of those over 70 years old and 80-90% of those over 80 years old.^4,5

Early PVDs may be seen in myopes, patients with ocular inflammation, vitreous haemorrhage, trauma and cataract surgery. Most PVDs are symptomatic, however 20% may be asymptomatic.¹ In those presenting with a symptomatic PVD, the fellow eye may have an asymptomatic PVD (approximately 15%) or an asymptomatic retinal tear (in approximately 5%).⁶ Thus, when patients present with an acute PVD, it is always advised to perform dilated fundus examination in both eyes.

PVD and the risk of retinal tears

Most studies have found the incidence of retinal tears in patients presenting with an acute symptomatic PVD between 2% and 8%.^7,8 However, some have demonstrated rates as high as 18%.⁹ Retinal tears are most often seen in the superotemporal quadrant (60%), then inferotemporal quadrant (30%), then superonasal quadrant (6%) and finally inferonasal quadrant (4%).

In approximately 50% of cases with retinal tears, more than one tear will be found – on average, 1.4 tears.^4,8 If a tear is found in the inferonasal quadrant, it’s four times as likely that there is another tear elsewhere.

Risk factors for retinal tears

Risk factors¹⁰ for retinal tears include:

• the presence of pigmented retinal pigment epithelial (RPE) cells in the vitreous humor (Schaffer sign)

• PVD-induced vitreous haemorrhage

• peripheral punctate intraretinal haemorrhages

• myopia

• trauma

• pseudophakia/aphakia

• lattice degeneration

• RD in fellow eye

• family history of RD.

In addition, peripheral punctate haemorrhages warrant close monitoring because they indicate areas of transient vitreous traction and could potentially become sites of future retinal tears.¹¹

Clinical examination in assessment of retinal tears is best performed with scleral depressed binocular indirect ophthalmic (SD-BIO) examination. Studies have demonstrated higher rates of identified RTs (8% to 10%) compared to slip lamp biomicroscopy (4.4%).¹² A recent large prospective study based on more than 1,000 community referrals found that slit lamp examination identified 85% of RTs, where 15% were identified by SD-BIO examination but not on slit lamp examination.6 SD-BIO found all cases of RD, 97% of RTs (both symptomatic and asymptomatic) and only 0.5% of patients could not tolerate SD-BIO.

Acute PVD and vitreous haemorrhage

Vitreous haemorrhage (VH) is defined as the presence of blood in the vitreous cavity. The presence of a VH, particularly a dense VH in the setting an acute PVD denotes a more concerning circumstance. The risks of having a RT increases up to 30-90%.^13-16 There are more often multiple and larger tears increasing or hastening the time to progression to RD.

The median time to develop a delayed RT is 14 days, much earlier than without VH.¹⁷ In patients with dense VH, early vitrectomy is often performed as a retinal tear can be found in 50-90% of cases. In contrast, delaying vitrectomy risks unidentified untreated tears progressing into RD in 40-79% of cases with 50% of these RDs being complicated by proliferative vitreoretinopathy (PVR).^13,14

PVD and delayed RT

After the initial examination of an acute PVD without any RTs found, a repeat examination is often performed at four to six weeks due to the risk of delayed (late-onset) RTs. The rate of delayed RTs varies significantly between studies (2.4% to 12%), however, in most studies the rate under 5%.^6,9,17-19

It’s important to identify delayed RTs early. Twenty-five per cent to 41% may develop into RD,^18,19 and 28% of RDs that develop following laser treatment of an initial RT are due to the development of a new delayed RT.¹⁹ So it’s also important to follow up with patients after their laser prophylaxis to not only assess the adequacy of laser, but to assess for new delayed retinal tears. Risk factors for delayed RTs are similar to the risk factors mentioned above for RTs, however, studies have consistently found additional risk factors including males and those less than 60 years old.¹⁷

The timeframe of repeat examination at four to six weeks is based on a historical notion that breaks may occur with vitreous contraction soon after an acute PVD.⁹ However, up to 45-50% of delayed RTs and 68% of delayed RDs may occur after six weeks,^9,17 and only 40% of these delayed RTs or RDs were symptomatic.¹⁹ Furthermore, 29% of those that develop delayed RT may develop further RTs.⁶ This confirms the requirement for further reviews after six weeks, particularly in higher-risk patients, even despite the absence of new symptoms.

Horse-shoe tears, operculated tears and atrophic holes

There are three types of retinal breaks: horse-shoe tears (HST), operculated tears and round (atrophic) holes.

Horse-shoe tears

HSTs are the highest risk: over 50% lead to RRD if left untreated.^{9, 20,21}

It’s also important to be aware that asymptomatic HSTs may also cause RD in five per cent of patients,²² and old HSTs may still cause RRDs in 2.8% of patients.²³ While it has been documented that prophylactic laser reduces the risk of RD to less than 5%,^6,22 these studies did not differentiate the cause of RD from other untreated retinal breaks that developed after laser treatment – up to 7.3-14% of patients with retinal tears who are treated may develop subsequent new breaks.⁶

Operculated tears

Operculated tears make up 6-13% of all RTs. They may lead to RRD but the rate is unclear. Three studies with a small number of patients found that no patients developed RD after long-term follow up.^20,24,25 However, another study found that one in six may lead to RD.²⁶ Presumably, there may be vitreous traction at adjacent areas around the tear explaining the appearance of some operculated tears surrounded by a cuff of subretinal fluid or associated with a subclinical RD. In patients having RD repair by either scleral buckling or vitrectomy, the causative break is not uncommonly seen to be caused from an operculated break. This suggests a potential role of prophylactic laser in operculated tears (both symptomatic and asymptomatic) as the low risks of these tears developing into RD may outweigh the minimal risks of laser retinopexy. It is worth getting an ophthalmic assessment for consideration of retinal laser prophylaxis in these patients.

Round (atrophic) holes

Round (atrophic) holes have a low (approximately 1.5%) potential in leading to RD.²⁰ If they do, they are often slowly evolving, chronic RDs. It’s estimated that only 2.5-5% of all RRDs are due to these round-hole RDs.²⁷ These lesions may be safely monitored on an bi-annually or annual basis.

The American Academy of Ophthalmology (AAO) preferred practice patterns were based on the available evidence and have provided management recommendations for laser prophylaxis of peripheral retinal lesions (see table 1).²²

While the table provides useful guidance on referring to ophthalmologists, it’s important to bear in mind that although many of the lesions have a low risk of developing into RD, they may still be higher than the minimal risks of laser retinopexy. 

Conclusion 

Both optometrists and ophthalmologists play an important role in the setting of acute PVDs and RTs. Successful collaborative care allows improved management of patients and minimises the risks of missed RTs and the development of RD.

Ultimately, the importance lies in recognising risk factors and understanding that RTs may develop earlier in these patients, as well as the potential for delayed RTs beyond the generic four to six week review. 

More reading

Ménière’s disease: a primer for optometrists

Accommodation disorders: Recognising, assessing and managing

Dry eye: Patient identification, product formulation and therapy escalation

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