(1)
St. Johns, FL, USA
(2)
Helen Keller Foundation for Research and Education, International Society of Ocular Trauma, Birmingham, AL, USA
(3)
Consultant and Vitreoretinal Surgeon, Milos Eye Hospital, Belgrade, Serbia
(4)
Consultant and Vitreoretinal Surgeon, Zagórskiego Eye Hospital, Cracow, Poland
RD1 is defined as a condition in which the neuroretina is separated from the RPE. Based on the etiology and characteristics, several types are distinguished; these are summarized in Table 54.1.
Table 54.1
Detachment of the retina: types and characteristics*
Detachment | Comment |
|---|---|
Rhegmatogenous (“RD”) | A retinal break (“rhegma”) is present, but the primary culprit is VR traction, which is dynamic a The configuration is convex |
Tractional (“TRD”)b | There is very strong VR or subretinal traction, but no break. The traction is static c The configuration is concave |
Combined rhegmatogenous and tractional | The tractional component dominates, even though a break is also present. The tractional element precedes the development of the break The configuration is concave |
Central (posterior, staphyloma spanning)d | Although VR traction is presente, the main culprit is the staphyloma; the rigid ILM does not allow the otherwise elastic retina to conform to the scleral bulge A macular hole may be present, but it is likely to be the consequence, not the cause of the RD The configuration is convex or concave, depending on the size of the staphyloma and the height of the RD |
Exudative/serous | There is no traction, simply secretion of fluid into the subretinal space. The fluid is either too voluminous or too viscous for the RPE to remove. Examples include optic pit (surgical intervention is worth considering, see Chap. 51) and central serous chorioretinopathy (not a surgical indication) The configuration is convex |
Hemorrhagic | There is no traction; the bleeding is typically traumatic in origin or associated with AMD The configuration is initially convex but can become uneven as the blood start to absorb |
54.1 The Pathophysiology of RD2
Separation of the neuroretina from the RPE is used to be a blinding condition.3 It is thus not surprising that so many misconceptions related to this condition have been born. Many of these live on, even though our knowledge of the pathophysiology of RD has greatly expanded since (see Table 54.2).
Table 54.2
RD pathophysiology and treatment: traditional and revised concepts*
Variable | Traditional concept | Revised concept |
|---|---|---|
PVD in old age in an eye with attached retina | Very likely to be present | May or may not be present |
PVD progressing in an eye with attached retina | The highest risk for RD development | True – except that the PVD may be anomalous |
If VR traction is not seen at the slit lamp or on OCT | There is no VR traction | VR traction still may be present, but it is undetectable with current methodology and technology |
PVD as a preoperative diagnosis | Straightforward to make as at least one of the following is present: 1. On biomicroscopy (or on OCT) a surface, distant from the posterior retina 2. Weiss ring | Impossible to make with any kind of certainty: 1. The distant surface seen on biomicroscopy (or on OCT) may indeed be PVD but may also be the anterior wall of a vitreoschisis cavitya 2. The Weiss ring indicates that the vitreous is detached at the disc, but not necessarily that it also detached elsewhere in the posterior pole |
PVD in an eye with RD | Always present | May be complete, partial, or completely absent |
Primary causative pathology in RD | The retinal break (the RD is “retinogenic”) | VR traction (the RD is “vitreogenic”); the retinal break is secondary to the traction |
The initial element in the cascade leading to break/RD development | PVD | Syneresis |
Whether a retinal break leads to RD | Depends on the size of the break (and possibly the strength of the VR traction) | Depends on the strength of the VR traction as well as on the RPE pump, the strength of the IPM, and the resistance (tensile strength) of the retina itself The volume of the incoming fluid must exceed the capacity of the RPE to remove it |
Presence of an operculumb | Signals strong traction and thus significant RD risk | Signals strong past traction and thus reduced RD risk |
PVD in a highly myopic eye with posterior RDc | Present | What is seen as a PVD is in reality a vitreoschisis |
PVD in PDRd | Present, anteriorly (“table-top RD”) | A vitreoschisis is present, not a PVD |
The VR interface in an eye with RD | There is a complete PVD posterior to the break but complete vitreous adherence to the retina anterior to the break | The “PVD posterior to the break, but no PVD anterior to the break” statement may hold true for the eye just examined However, the PVD may also be incomplete (anomalous) or nonexistent |
PVD-associatede retinal tear | Located at the posterior edge of the vitreous base | Located between the vitreous base and the equator, occasionally even more posteriorly |
Primary target of treatment | The retinal break | The VR traction |
Gas use for RD in PPV | The effect is a tamponade, with two goals in mind: Prevent fluid from getting under the retina Press the retina against the RPE until the “pexy” takes effect | The effect is partially a tamponade but also a reduction in fluidic shearing By occupying space in the vitreous cavity, limit the shearing the fluid would cause on the retinal surface, thereby reducing the risk of retinal separation from the RPE Press the retina against the RPE until the “pexy” takes effect |
Vitreous removal in an eye with RD | It is crucial to do a complete (total) vitrectomy in the periphery | Several steps are crucial Creation of a PVD if it has not occurred before Total vitrectomy in the periphery Removal of the anterior vitreous face |
In the vast majority of cases, regardless of the etiology, the cascade of events leading to RD development is identical4 (see Sect. 26.1.2 and Fig. 54.1). While dynamic VR traction is the cause of break formation, the type of the break has important implications regarding the events to come, including management (see Table 54.3), as does the condition of the vitreous and the VR interface (see Figs. 26.1 and 54.2).
Fig. 54.1
The cascade of events leading to RD. 5 (as a reminder, rhegmatogenous, not tractional, RD is discussed here). In areas of VR adhesion, a syneretic vitreous will cause VR traction, but it does not inevitably lead to the formation of a retinal break because the RPE pump and the IPM (plus the retina’s own tensile strength and the IOP, not shown here) are able to overcome the effect of the dynamic traction. Even if a break does develop, the RPE pump and the IPM may be able to counter the effect of the dynamic traction. If the torn retina becomes operculated, the risk of RD is dramatically reduced but not completely eliminated since there still may be VR traction on the retina surrounding the break. RD results only when the traction force overpowers the effect of the RPE pump and the IPM
Table 54.3
Classification of retinal breaks and its implications for treatment
Breaka | Comment | Management implication |
|---|---|---|
Hole, round | A necrotic type: the retina dissolves. Clinically detectable traction may also be present – this is the case when the hole is in an area of lattice degeneration | SB is an efficient method of treatment |
Hole, macular | It is not perceived as a true RD since only of a small ring of subretinal fluid is present around the hole (“fluid cuff”)b | A unique operation is needed (see Sect. 50.2.4) |
Hole, macular, in a highly myopic eye | There is a high risk of central RD; in fact, the RD often – if not always – precedes the formation of the hole | A unique operation is needed (see Sect. 56.2) |
Dialysis | Usually caused by contusion, the retina separates at the ora serrata; since the vitreous is healthy at the time of the injury, the progression to RD is usually slowc | SB and PPV are equally efficient methods of treatment; both have their own advantages, risks, and side effects |
Tear, horseshoe/flap | Caused by VR traction, the opening in the retina faces the posterior pole (the base of the flap is anterior). This is the most common cause of RD | Depending on the location, strength of traction, pigment content in the vitreous and many other variables, SB and PPV may or may not be equally efficient methods of treatment. If PPV is performed, the flap must be removed to completely alleviate the traction that caused it (see the text for more details) |
Giant tear | A tear that runs parallel to the limbus and exceeds 3 clock hours in length; the central edge is often inverted | PPV is the treatment of choice; adding a buckle may increase the risk of slippaged. The curled central edge must be completely cut and silicone oil implanted due to the high risk of PVR |
Fig. 54.2
Relationship between the vitreoretinal interface, a retinal break, and RD. (a) If the vitreous is a healthy gel and there is no retinal break, RD does not occur. (b) Even if a retinal break (arrow) does occur, as long as the vitreous is a healthy gel, RD does not occur.6 (c) Even if a retinal break does occur, should a total PVD also be present, RD does not occur. (d) In the presence of a retinal break and a syneretic gel, there is a risk of traction at the edge of the break. (e) If the VR traction overcomes the sum of forces holding the retina in place (mainly the RPE pump and the IPM), an RD develops.7 V vitreous, R retina, C choroid, B retinal break
54.1.1 RD Due to a Horseshoe or Giant Tear
The initial step is a change in the structure of the vitreous gel (see Sect. 26.1.2). With the vitreous cavity containing both gel and fluid-filled pockets, it becomes possible for the gel to become mobile. With every movement of the eyeball or head, traction forces act on the retina at all sites of vitreoretinal adhesion (see Sect. 26.1.1).8
Traction that caused a retinal tear is also able to keep the break open so that fluid from the vitreous has direct access to the (so far virtual) subretinal space.9 Once the volume of fluid entering exceeds the capacity of the RPE to remove it, an RD ensues.
Pearl
The operculation of the retinal tear means that traction in the area of the break itself has ceased to exist. The torn-out piece of the retina is suspended in the gel or is “swimming” in a pool of fluid in the syneretic pocket (see Fig. 54.3). The retina remains attached if there is no remaining traction in the vicinity but may detach if there is sufficiently strong traction on the retinal edge. The operculum is thus a relative, not an absolute, contraindication against prophylactic laser (see below, Sect. 54.2.4).
Fig. 54.3
The operculum in the vitreous cavity. The operculum is visible as a little gray spot; the shadow it casts on the retina is seen just above the port of the probe. The area of degeneration where the small piece of retina was torn from is obvious from the pigmentation there
A giant tear develops in the same way but is defined as one of at least 3 clock hours in length. Its significance lies in the different surgical technique required to treat it10 and its increased PVR risk.
54.1.2 RD Due to a Dialysis
Seen most commonly after contusion, the retina is torn at the ora serrata where it is inseparable from the vitreous. The vitreous gel may appear healthy initially, but with time, it starts to degenerate, slowly detaching the adherent retina as the dynamic traction grows.
54.1.3 RD Due to a Round Hole
54.2 Additional Information About RD
Any ophthalmologist but especially the VR surgeon should keep in mind the following during the decision-making process.
54.2.1 History
The typical – and the only one that is pathognomic – complaint is that of a curtain, due to the visual-field loss corresponding to the quadrant that has detached.
Loss of the entire visual field suddenly occurs if a VH accompanies the tearing of the retina. ~20% of RDs are accompanied by VH.
Flashes are spontaneously communicated by relatively few patients, although often confirmed by them when asked (see below). The flashes are caused by dynamic VR traction (see below), whether as part of a PVD or not.14
The small floater that is occasionally described by the patient is rarely the operculum; it is usually a small hemorrhage or simply a vitreous opacity.
~10% of the patients have bilateral RD, but only 20% of these occur simultaneously. These are the numbers that justify treating the fellow eye prophylactically (see below, Sect. 54.2.4.2).
54.2.2 Examination15
Even before the ophthalmologist looks at the retina, the presence of pigment clumps in the anterior vitreous (see Fig. 53.1) should raise the possibility of a retinal break, even an RD.
In a fresh RD, the retina can be very bullous and its surface rather smooth; however, it may be folded, too. The latter gives the false appearance of subretinal strands. Even intraoperatively, the distinction, at least until the surgeon touches the retina with an instrument, may be very difficult (see Sect. 32.4.1).
Chronic RDs are recognized by the presence of the following:16
High-water marks: lines of pigmentation, signaling the temporary stoppage of the progression of the detachment in the past.
Intraretinal cysts.
Calcium oxalate crystals in the posterior pole.17
Multiple breaks, present in ~40% of eyes.
The IOP is characteristically low, due to increased uveal outflow.
Retinal thinning – resembling retinoschisis.18
The configuration of the RD suggests the location of the break (see Fig. 54.4).
Fig. 54.4
The configuration of the RD and the expected location of the retinal break. (a) If the detachment is inferior and reaches only somewhat higher on one side of the disc, the break is likely to be found inferiorly, close to the center, on the side where the RD is higher. (b) If the detachment is mostly inferior and much higher on one side, the break is likely to be found superiorly on the high side. It is rare that the break is at the border of detached–attached retina; it is usually surrounded by detached retina completely19. (c) Occasionally the retina does not show a wide area of detachment and remains attached central to the break; the bilateral, inferior detachment has a fingerlike, peripheral protrusion, pointing superiorly. This makes discovery of the break difficult and shows why the laser treatment must always be extended all the way to the ora serrata. D optic disc, M macula, B break (the area is shown by a black area with white dots). The red shows the attached, the blue the detached retina
54.2.3 Clinical Course
Faster progression is expected in the following cases:
Superior break (the effect of gravity20).
Large break (more traction, increased amount of incoming fluid).
Vitreous gel that has massive structural breakdown (more traction).
Vitrectomized eye (no gel tamponading the retina).
Poor efficacy of the RPE pump and the IPM (reduced fluid outflow and retinal adhesion).21
Lack of strong chorioretinal adhesions (e.g., scars fixating the retina).
Occasionally the RD progression stops spontaneously. It is, however, much more common for the RD to not just progress but lead, if untreated, to PVR development (see Chap. 53).
54.2.4 Using Laser to Prevent RD Development
Treatment with laser is defined as sealing the edge of a retinal break. Prophylaxis is interpreted as lasering areas with a pathology that might in the future lead to RD or lasering retina that is healthy.22
54.2.4.1 Prophylaxis in the Affected Eye (RD, Current or Past)
The surgeon may elect to treat only the visible retinal lesion/s. The argument for this approach is that retinal breaks are detected in up to 20% of eyes with attached retina. Especially if the break remains asymptomatic, long-term follow-up proves that the risk of RD remains small.
“Observing” these patients after such focal treatment typically means a detailed fundus examination every 3 months. This is taxing for patient, ophthalmologist, and facility. It is also without any sound scientific basis: why 3 months and not 2 or 5?23
The argument that a break does not necessarily justify treatment is false for another reason. In an eye that has, or has had, an RD, the risk of a future RD may be elevated if the VR traction has not been eliminated.
My preference is to always perform a 360° laser cerclage (see Sect. 30.3.3) during surgery, and I offer this option to each patient who presents with an attached retina but a history of RD. The presence or absence of a retinal tear does not influence this protocol since the RD often originates in an area that appeared healthy previously. This is the final argument against the “focal laser only” type of prophylaxis (see below).
54.2.4.2 Prophylaxis in the Fellow Eye
If one eye had an RD and the fellow eye has the same risk for RD,24 it is akin to playing Russian roulette not to perform prophylactic laser in the fellow eye as well. My personal guidelines regarding prophylactic laser treatment are summarized in Table 54.4.
Table 54.4
RD prophylaxis in persons with a retinal break in one eye and various conditions in the fellow eye*
Variablea | Fellow eye | Commentb |
|---|---|---|
Round hole, asymptomaticc | No pathology/history | No treatment |
RD | Laser cerclage, focal laser, observation | |
Round hole, symptomatic | No pathology/history | Laser cerclage, focal laser, observation |
RD | Laser cerclage | |
Dialysis | No pathology/history | Laser walling-off |
Flap (horseshoe) tear, asymptomatic | No pathology/history | Focal laser, observation |
RD | Laser cerclage | |
Flap (horseshoe) tear, symptomatic | No pathology/history | Laser cerclage, focal laser, observation |
RD | Laser cerclage | |
Giant tear | No pathology/RD | Laser cerclaged |
Pearl
Unless the patient has a unilateral condition (such as pseudophakia, high myopia, trauma), the fellow eye has the same risk for RD development and should always be carefully examined. The patient needs to be informed about the risk, and the issue of prophylactic treatment (see Sect. 30.3.3) must be raised, detailing the risks and benefits.
54.2.4.3 The Patient with a History of a Retinal Tear (No RD)
My rationale is identical to that outlined above. Even in the absence of a history of an RD, a retinal tear signifies traction, and there is a risk of RD.25 Laser cerclage has a high enough success rate to more than offset its complication risk. I therefore offer the prophylaxis to the patient, but accept it if he declines the treatment – as long as he understands the implications. First, the focal treatment does not decrease the RD risk; second, he is supposed to undergo a detailed fundus examination every few months for the rest of his life.
Q&A
Q
Why laser cerclage and not focal laser?
A
Clinical experience shows that the RD often originates in areas that had appeared normal in prior examinations. Focal treatment does not offer extra protection when compared to observation.
54.3 Treatment Principles
54.3.1 The Timing of Surgery26
In principle, as soon as possible, but certain other factors must also be incorporated into the decision-making process.
Q&A
Q
What if the patient with an RD arrives Friday afternoon?
A
With rare exceptions (see below), surgery can safely be postponed until Monday morning, when all is available to give it the best chance of success. The patient has to understand the risks if he is unwilling to remain in bed until the operation (counseling, see Chap. 5).
Patching both eyes is highly inconvenient for the patient, but it eliminates eye/head movement and thus greatly reduces the height of the detachment – less crucial if PPV is performed, but very helpful in bullous RDs if the surgeon plans to do SB.
If the macula is on, the patient should be positioned so that the fluid does not get in the macula.
The rods recover rather well,27 even if the RD is long standing.
The cones do not recover that well, but even if the macula is off for a few days, the chance of recovering reading vision is still 70%.
The most urgent situation is an RD that is just about to reach into the fovea.
54.3.2 The Goals of Surgery
The surgeon’s goals with surgery, irrespective of its type, are the following:
The surgeon can choose between 3 different treatment options.30 Of these SB and pneumatic retinopexy are mostly exterior31 procedures; PPV is solely internal. Table 54.5 presents a comparison between SB and PPV, which are occasionally used in combination.
Table 54.5
Comparison of SB versus PPV for RD*
Variable | SB | PPV |
|---|---|---|
Surgery rational? | No: an internal problem is addressed by an external procedure. The eyewall is pushed toward the detached retina, causing a permanent deformation in the contour of the eyewall | Yes: an internal problem is addressed by an internal procedure. The detached retina is pushed toward its normal resting place, maintaining the original contour of the eyewall |
Main purpose of surgery | Weakening of the traction force to the point that the traction becomes ineffective | Elimination of the traction force |
Able to address nonrhegmatogenous RD? | No, or with significant morbidity (posterior break or staphyloma-spanning RD in high myopes) | Yes |
Can be employed if severe PVR or subretinal component is present? | No | Yes |
What if the sclera is thin? | Thin sclera must not be sutured; if the ectatic sclera cannot be avoided, SB is either contraindicated or a scleral patch needs to be placed first | The thin area should not be selected as a sclerotomy site |
Need for detailed preoperative examination (to identify the VR traction and the location of the retinal break/s) | Yes | No |
Surgery doable if significant VH present? | No | Yes |
Difficulty of intraoperatively identifying VR traction | Somewhat to very difficult | Easy |
Multiple breaks in multiple quadrants | Causes decision-dilemma and technical difficulties | Does not change the surgical planning or the essence of surgery |
Difficulty of intraoperatively identifying retinal break | May be impossible in pseudophakic eyes with capsular opacity, especially if the break is small | Virtually always possible |
Separation of hyaloid from the retina | Not needed | A major goal of surgery but impossible in some cases |
Draining of subretinal fluid | External – if performed at all | Internal – almost always through the original break |
Complete draining of subretinal fluid | May be difficult or impossible to do and risks subretinal bleeding | Almost always possible (see the text for technical details) |
Possibility of treating concurrent problems such as macular hole, EMP | No | Yes |
Cryopexy | Even though a risk factor for PVR development, it may be necessary if the drainage was incomplete or indirect ophthalmoscopic laser is unavailable (see Chap. 29) | No (laser instead; see the text for more details) |
Intravitreal gas (air) tamponade | Risks causing secondary retinal break/s | Straightforward |
Leftover fluid under fovea | Rather common | No |
PVR risk | Low (if cryopexy is not applied or is done properly) | Low, but may be higher than with SB |
PVR prophylaxis | Not possible
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