Part 1 described the different types of retinal detachment. We will now concentrate on rhegmatogenous retinal detachments (RRD).
Retinal detachment is a condition that causes concern to optometrists, because it has the potential for permanent reduction of acuity if the early indications are not recognised and treatment instigated soon enough. This is because a detached macula will never regain full function despite successful anatomical reattachment. A survey1 of legal complaints handled by the AOP involving retinal detachment showed that deficient care could often be attributed to not evaluating symptoms, and not paying sufficient attention to risk factors.
Risk factors
Figure 1 shows that the incidence of retinal detachment is highest in axial myopes.
Figure 1: Distribution of refractive error (spherical equivalent D) for rhegmatogenous retinal detachments4 and the population as a whole.20 Myopes have a much higher incidence of RRD than would be expected from their proportion in the population
Practitioners often explain to their myopic patients that this is because they have enlarged eyes which stretch the retina causing it to be less robust and more prone to tears. A post-mortem study2 did show that the peripheral retina photoreceptor density is substantially lower in myopes, but there are other interrelated factors (see table 1) which may be more important. For example, the stretching of the vitreous gel to fill a larger volume could explain the earlier onset of PVD in myopes.
Table 1
It is important to consider age when assessing risk. Most rhegmatogenous retinal detachments (RRDs) are triggered by a PVD and are most likely to occur around the age of 603, but you must remember that there is a much smaller group of myopes, with no PVD, that will have atrophic round hole detachments in their twenties.4
Lattice retinal degeneration5 is a risk factor because of the atrophic round holes and overlying liquefied vitreous. But there is also a risk of horseshoe tears due to the strong attachment of the vitreous cortex at the edge of the lesion.
Direct blunt trauma to the eye causes temporary reduction in the axial length with a compensatory stretching of the equatorial circumference. This is followed by a rebound ‘overshoot’ in axial length.6 These distortions can cause horseshoe tears at the vitreous base or a retinal dialysis at the ora.7 However, this does not account for all the cases that report blunt trauma to the head or eye in the period prior to the detachment.4 It is not possible to prove a link, but a history of trauma should always raise suspicion.
There is increased risk of RRD following cataract surgery, particularly with the posterior capsule rupture.8,9 This is due to leaching out of hyaluronic acid which helps to keep the collagen fibrils apart. This shows that the vitreous gel has a structure which can easily be tipped into a state of collapse, much like the collapse of a house of cards.
Structured approach
Retinal tears need to be referred within 24 hours, so it is important for optometrists to be able to appreciate that a symptomatic PVD has occurred and perform an appropriate examination to exclude a tear. Thus consideration of symptoms is particularly important.1 The SOAP structured approach to clinical decision making provides a good template (figures 3 and 4), for the assessment of patients with flashes and floaters. SOAP stands for subjective, objective, assessment and plan. Subjective includes the patient’s observations and their ocular and medical history. Various factors are known to increase the risk of retinal detachment. Subjective history taking should be directed to revealing these risk factors (see table 1). Objective means the optometrist’s observations which are combined with the subjective information in the assessment to produce a differential diagnosis and a plan.
Subjective
Physiological floaters
Physiological floaters are very common and come about through natural degeneration of the vitreous gel structure. Early in life the vitreous collagen fibrils are kept evenly dispersed by hyaluronate molecules which group around the collagen and are capable of binding a large number of water molecules. This gives the vitreous its structural coherence, but as time goes on photochemically generated free radicals lead to dissociation between the hyaluronate and the collagen strands. This means that they are no longer being held apart in a regular structure and are now free to aggregate (syneresis) to form clumps or strands, which appear to the patient as floaters (figure 2). Floaters created in this way are innocuous and do not indicate an increased likelihood of retinal detachment. They are characterised by gradual onset and can usually be found to some extent in both eyes. However, it should be remembered that this degeneration process also results in the liberation of water (synchisis) which forms into small reservoirs within the gel known as lacunae. Approximately 20% of the vitreous is liquid at the age of 20, rising to 50% by the age of 80-90.21 Remember it is only liquefied gel that will pass freely through a retinal break to cause a detachment.
Figure 2 Syneretic linear floaters
PVD related floaters
In contrast to this, PVD related floaters occur suddenly and only one eye is affected. It would be a great coincidence for a PVD to occur simultaneously in both eyes. The appearance of floaters following an acute PVD comes about through various mechanisms. The sudden appearance of a single floater could be due to a Weiss ring, the peripapillary glial tissue that remains attached to the posterior cortex. When the posterior cortex is no longer held in contact with the entire retina it tends to take on a crinkled appearance which some patients describe as like looking through a cobweb. Sometimes traction by the posterior cortex causes a blood vessel to be ruptured leading to the appearance of a large number of dots (red blood cells or pigment granules in the vitreous). Alternatively streaks of blood congeal in the vitreous which are described as a lace curtain or cobweb. Figure 3 provides a logical framework for decision making for floaters. It should be born in mind that floaters can also result from posterior or intermediate uveitis. These cases are more likely to be characterised by progressive increase in symptoms rather than gradual or sudden. The floaters are more likely to be constant rather than intermittent, with both eyes affected but usually one more than the other. These cases will typically have associated symptoms, such as: eye ache or pain, photophobia, or reduced acuity from cystic macular oedema or vitritis. Objectively these floaters appear as dense aggregations of white material in the vitreous and there are likely to be cells in the anterior chamber.
Figure 3: SOAP approach to differentiating floaters resulting from vitreous syneresis from those due to acute PVD
Flashes in symptomatic PVD
Figure 4 illustrates a systematic approach to flashes. Initial questioning should rule out conditions such as: glare due to media opacities, glare due to spectacle reflections, coloured halos in primary angle closure glaucoma, pressure phosphenes (eye rubbing) and Charles Bonnett syndrome (visual hallucinations in patients with severe visual loss).
Figure 4: SOAP approach to flashes (photopsia), working from subjective clues to confirmation by objective signs. RDW = retinal detachment warning
The key initial questions that will aid identification of flashes due to acute symptomatic PVD are: onset (acute versus chronic or recurrent), duration of flash and whether one or both eyes are affected. These should rule out photopsia that are due to transient ischaemia of the visual cortex. Migraine is the most common example of this but some patients see ‘stars’ when they stand up suddenly or with exercise. This is the phenomenon which is represented by drawing stars orbiting around a dazed cartoon character who has just been hit on the head. Patients can generally tell which eye has the floaters, but this can be more difficult when it comes to reporting photopsia. In particular beware of patients with an homonymous field defect in migraine. Some will describe this as a problem affecting one eye, the eye on the same side as the field change. It is tempting to think that a patient with both flashes (indicating vitreous traction) and sudden onset floaters, is more at risk than one with a single floater. But that single floater could be a Weiss ring, which indicates a symptomatic PVD and therefore examination to exclude a tear is required. Also bear in mind that there are conditions other than vitreous traction that can very rarely give rise to photopsia. These include choroidal neovascular membrane (wet AMD), uveitis (white dot syndromes), and choroidal tumour.
Objective examination
Figures 3 and 4 show the questions that should be asked to determine if an acute symptomatic PVD is the likely cause of the symptoms. The decision-making process then relies on objective observations to confirm the PVD and look for the tears or retinal detachment that could result from it.
Shafer’s sign (tobacco dust)
The presence of pigment granules (figure 5) in the vitreous of an eye that has not previously undergone an intraocular procedure, is an almost certain indication of a retinal break22.
Figure 5: Tobacco dust
Text books direct the clinician to look in the anterior vitreous but you must remember that pigment is liberated at the location of the tear and may not conveniently appear in the vitreous close to the lens. Nor does it escape into the aqueous and present in the narrow channel just posterior to the lens (Berger’s space). Search as much as you can of the vitreous with a narrow oblique beam (no indirect lens), setting the slit lamp to high magnification and illumination. The orange-brown pigment particles in figure 5 are quite obvious, but they can be smaller and fewer in number, making them much more difficult to detect. Furthermore they may have settled in the inferior vitreous, necessitating a dynamic examination. This means agitating the vitreous so that as much as possible passes through the slit beam. This is best done by asking the patient to look up, then immediately down and then immediately straight ahead.
Weiss ring and crinkly membrane
Similar viewing techniques are used to look for a detached posterior cortex which appears as a crinkly membrane drifting in the vitreous (figure 6).
Figure 6: Crinkly membrane
The space in front of this will contain condensed vitreous, while the space behind will appear optically empty because it contains only water (figure 7). Remember that lacunae within the vitreous will also be optically empty, but focusing deeper into the eye will reveal condensed vitreous, once the boundary of the lacuna has been passed. The alternative means of confirming a PVD is to look for a Weiss ring (figure 8), which will generally require the use of an indirect lens. Bear in mind that the ring may appear distorted in shape or broken.
Figure 7: PVD with collapsed vitreous
Figure 8 Weiss ring
Peripheral search
Any break in attached retina appears more red than the surrounding tissue because of the unobstructed view of the choriocapillaris. Figure 9 illustrates a retinal tear, where the vitreous cortex has pulled away a flap of retinal tissue, during the PVD process.
Figure 9: Retinal tear
The key features of a retinal detachment are illustrated in figure 10.
Figure 10: Retinal detachment
These include, a convex shape bulging forward, which is slightly opaque with a corrugated appearance. A recently detached retina will usually be mobile, appearing to drift in the currents created by eye movement. Longstanding detachments can be very shallow so you have to rely on more subtle changes, such as the masking of the pattern of the choroidal vessels, which can be seen in the inferior part of figure 11. The pigment changes at the superior border of this detachment, known as a ‘tide mark’, occur at the border of a detachment that has remained stable for some time.
Figure 11: Chronic RD with tide mark
The SOAP format provides a good template for directing the questioning and examination of a patient who presents with flashes and floaters. The assessment of this information to produce a diagnosis and plan will be covered in part 3, along with referral guidelines.
Dr Graham MacAlister is a specialist optometrist at Moorfields Eye Hospital.
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