RETINAL DETACHMENT types, etiology and diagnosis

RETINAL DETACHMENTDr. Neeraj Agarwal

ANATOMICAL CONSIDERATIONPars PlanaThe ciliary body starts 1mm from the limbus and extends posteriorly for about 6mm.

The first 2mm consist of the pars plicata and the remaining 4mm comprises the flattened pars plana.

In order not to endanger the lens or retina, the optimal location for a pars plana surgical incision is 4mm from the limbus in phakic eyes and 3.5mm from the limbus in pseudophakic eyes.

Ora SerrataThe ora serrata forms the junction between the retina and ciliary body.Ora serrata is 2.1 mm wide temporally and 0.7-0.8 mm wide nasally.Its distance from limbus is 7mm temporally and 6mm nasally.

At the ora, fusion of the sensory retina with the retinal pigment epithelium (RPE) and choroid limits forward extension of subretinal fluid.However, there being no equivalent adhesion between the choroid and sclera, choroidal detachments may progress anteriorly to involve the ciliary body (ciliochoroidal detachment).

Vitreous baseThe vitreous base is a 34mm wide zone straddling the ora serrata.The cortical vitreous is strongly attached at the vitreous base, so that following acute posterior vitreous detachment (PVD), the posterior hyaloid face remains attached to the posterior border of the vitreous base. Pre-existing retinal holes within the vitreous base do not lead to RD. Severe blunt trauma may cause an avulsion of the vitreous base.

The vitreous base

MICROSCOPIC LAYERS OF RETINARetinal pigment epitheliumRods and Cones layerExternal limiting membraneOuter nuclear layerOuter plexiform layerInner nuclear layer- 1st order neuron(bipolar cells)Inner plexiformGanglion cell layer- 2nd order neuronNerve fibre layerInternal limiting memb.

DEFINITIONS

Retinal Detachment

A Retinal Detachment (RD) describes the separation of the neurosensory retina (NSR) from the retinal pigment epithelium (RPE).

This results in the accumulation of subretinal fluid (SRF) in the potential space between the NSR and RPE. The main types of RD are:

1Rhegmatogenous(rhegma break), occurs secondarily to a full-thickness defect in the sensory retina, which permits fluid derived from synchytic (liquefied) vitreous to gain access to the subretinal space.

2Tractionalin which the NSR is pulled away from the RPE by contracting vitreoretinal membranes in the absence of a retinal break.

3Exudative(serous, secondary) is caused neither by a break nor traction; the SRF is derived from fluid in the vessels of the NSR or choroid, or both.

4Combined tractional-rhegmatogenous, as the name implies, is the result of a combination of a retinal break and retinal traction. The retinal break is caused by traction from an adjacent area of fibrovascular proliferation and is most commonly seen in advanced proliferative diabetic retinopathy.

Vitreoretinal traction

Vitreoretinal traction is a force exerted on the retina by structures originating in the vitreous. it may be dynamic or static. The difference between the two is crucial in understanding the pathogenesis of the various types of RD.

1Dynamictraction is induced by eye movements and exerts a centripetal force towards the vitreous cavity. It plays an important role in the pathogenesis of retinal tears and rhegmatogenous RD.

2Statictraction is independent of ocular movements. It plays a key role in the pathogenesis of tractional RD and proliferative vitreoretinopathy.

Posterior vitreous detachment

A posterior vitreous detachment (PVD) is a separation of the cortical vitreous from the internal limiting membrane (ILM) of the NSR posterior to the vitreous base. PVD can be classified according to the following characteristics:

1Onset.Acute PVD is by far the most common. It develops suddenly and usually becomes complete soon after onset. Chronic PVD occurs gradually and may take weeks or months to become complete.

2ExtentaCompletePVD in which the entire vitreous cortex detaches up to the posterior margin of the vitreous base.bIncompletePVD in which residual vitreoretinal attachments remain posterior to vitrous base.

COMPLICATION OF PVDNO COMPLICATION occur in most eyes because vitreo-retinal attachment are weak.RETINAL TEAR may occur at same time at the site of abnormally strong adhesion. Sometimes may be delayed upto weeks so pt. should be reexamined after 1-6 weeks.AVULSION OF PERIPHERAL BLOOD VESSEL resulting in vitreous haemorrhage.

Retinal break

A retinal break is a full-thickness defect in the sensory retina. Breaks can be classified according to (a)pathogenesis, (b)morphologyand (c)location.

1PathogenesisaTearsare caused by dynamic vitreoretinal traction and have a predilection for the superior fundus.bHolesare caused by chronic atrophy of the sensory retina and may be round or oval. They have a predilection for the temporal fundus.

2Morphology

aU-tears(horseshoe, flap or arrowhead) consist of a flap, the apex of which is pulled anteriorly by the vitreous, the base remaining attached to the retina.

bIncomplete U-tears,which may be linear, L-shaped or J-shaped, are often paravascular.

cOperculated tearsin which the flap is completely torn away from the retina by detached vitreous gel.

dDialysesare circumferential tears along the ora serrata with vitreous gel attached to their posterior margins.

eGiant tearsinvolve 90 or more of the circumference of the globe. They are most frequently located in the immediate post-oral retina or, less commonly, at the equator..

Retinal tears.(A)Complete U-shaped; (B) linear;(C) Lshaped;(D) operculated; (E)dialysis

(A)Giant retinal tear involving the immediate post-oral retina;

(B)vitreous cortex is attached to the anterior margin of the tear

3Location

aOralbreaks are located within the vitreous base. bPost-oralbreaks are located between the posterior border of the vitreous base and the equator.cEquatorialbreaks are at or near the equator.

dPost-equatorialbreaks are behind the equator.eMacularbreaks (invariably holes) are at the fovea.

Finding the primary breakThe primary break is the one responsible for the RD. A secondary break is not responsible for the RD because it was either present before the development of the RD or formed after the retina is detached. Finding the primary break is of paramount importance and aided by the following considerations.

1Distribution of breaksin eyes with RD is approximately as follows: 60% in the upper temporal quadrant; 15% in the upper nasal quadrant; 15% in the lower temporal quadrant; 10% in the lower nasal quadrant.It should also be remembered that about 50% of eyes with RD have more than one break, and in most eyes these are located within 90 of each other.

2Configuration of SRFis of relevance because SRF spreads in a gravitational fashion, and its shape is governed by anatomical limits (ora serrata and optic nerve) and by the location of the primary retinal break.

If the primary break is located superiorly, the SRF first spreads inferiorly on the same side as the break andthen spreads superiorly on the opposite side of the fundus.

The likely location of the primary retinal break can therefore be predicted by studying the shape of the RD.

aA shallow inferior RD in which the SRF is slightly higher on the temporal side points to a primary break located inferiorly on that side.

bA primary break located at 6 oclock will cause an inferior RD with equal fluid levels.

cIn a bullous inferior RD the primary break usually lies above the horizontal meridian.

dIf the primary break is located in the upper nasal quadrant the SRF will revolve around the optic disc and then rise on the temporal side until it is level with the primary break.

eA subtotal RD with a superior wedge of attached retina points to a primary break located in the periphery nearest its highest border.

fWhen the SRF crosses the vertical midline above, the primary break is near to 12 oclock, the lower edge of the RD corresponding to the side of the break .

The above points are important because they aid in prevention of the treatment of a secondary break whilst overlooking the primary break. It is therefore essential to ensure that the shape of the RD corresponds to the location of a presumed primary retinal break.

3History. Although the location of light flashes is of no value in predicting the site of the primary break, the quadrant in which a visual field defect first appears may be of considerable value. For example, if a field defect started in the upper nasal quadrant the primary break is probably located in the lower temporal quadrant.

UltrasonographyB-scan ultrasonography (US) is very useful in the diagnosis of RD in eyes with opaque media, particularly severe vitreous haemorrhage that precludes visualization of the fundus.

B-scan image showing vitreous haemorrhage and flat retina; B-scan image showing vitreous haemorrhage and funnel-shaped retinal detachment

RHEGMATOGENOUS RETINAL DETACHMENT

Symptoms

1Photopsiais the subjective sensation of a flash of light.In eyes with acute PVD it is probably caused by traction at sites of vitreoretinal adhesion. The cessation of photopsia is the result of either separation of the adhesion or complete tearing away of a piece of retina (operculum). In PVD the photopsia is often described as an arc of golden or white light induced by eye movements and is more noticeable in dim illumination. It tends to be projected into the patient's temporalperipheral visual field. Occasionally photopsia precedes PVD by 2448 hours.

2Floatersare moving vitreous opacities which are perceived when they cast shadows on the retina.

Vitreous opacities in eyes with acute PVD are of the following three types:aWeiss ringis a solitary floater consisting of the detached annular attachment of vitreous to the margin of the optic disc.bCobwebsare caused by condensation of collagen fibres within the collapsed vitreous cortex.cA sudden showerof minute red-coloured or dark spots usually indicates vitreous haemorrhage secondary to tearing of a peripheral retinal blood vessel. Vitreous haemorrhage associated with acute PVD is usually sparse due to the small calibre of peripheral retinal vessels.

(A)Weiss ring;

(B)B-scan shows a Weiss ring associated with posterior vitreous detachment

3A visual field defectis perceived as a black curtain.In some patients it may not be present on waking in the morning, due to spontaneous absorption of SRF while lying inactive overnight, only to reappear later in the day. A lower field defect is usually appreciated more quickly by the patient than an upper field defect. The quadrant of the visual field in which the field defect first appears is useful in predicting the location of the primary retinal break, which will be in the opposite quadrant. Loss of central vision may be due either to involvement of the fovea by SRF or, less frequently, obstruction of the visual axis by a large upper bullous RD.

SignsGeneral 1Marcus Gunn pupil(relative afferent pupillary defect) is present in an eye with an extensive RD irrespective of the type.2Intraocular pressureis usually lower by about 5mmHg compared with the normal eye. If theintraocular pressure is extremely low, an associated choroidal detachment may be present.3Iritisis very common but usually mild. Occasionally it may be severe enough to cause posterior synechiae. In these cases the underlying RD may be overlooked and the poor visual acuity incorrectly ascribed to some other cause.4Tobacco dustconsisting of pigment cells is seen in the anterior vitreous.

5Retinal breaksappear as discontinuities in the retinal surface. They are usually red because of the colour contrast between the sensory retina and underlying choroid. However, in eyes with hypopigmented choroid (as in high myopia), the colour contrast is decreased and small breaks may be overlooked unless careful slit-lamp and indirect ophthalmoscopic examination is performed.6Retinal signsdepend on the duration of RD and the presence or absence of proliferative vitreoretinopathy (PVR) as described below.

Fresh retinal detachment

1The RDhas a convex configuration and a slightly opaque and corrugated appearance as a result of retinal oedema. There is loss of the underlying choroidal pattern and retinal blood vessels appear darker than in flat retina, so that colour contrast between venules and arterioles is less apparent.

2SRFextends up to the ora serrata, except in the rare cases caused by a macular hole in which the SRF is initially confined to the posterior pole. Because of the thinness of the retina at the fovea, a pseudohole is frequently seen if the posterior pole is detached. This should not be mistaken for a true macular hole, which may give rise to RD in highly myopic eyes or following blunt ocular trauma.

3B-scan ultrasonographyshows good mobility of the retina and vitreous.

Fresh retinal detachment.(A)U-tear in detached retina;(B)superior bullous retinal detachment;(C)shallow temporal retinal detachment;(D)B-scan shows a totally detached retina with linear echogenic structures inserting onto the optic nerve head to form an open funnel

Long-standing retinal detachment

The following are the main features of a long-standing rhegmatogenous RD: 1Retinal thinningsecondary to atrophy is a characteristic finding which must not be mistaken for retinoschisis.

2Secondary intraretinal cystsmay develop if the RD has been present for about 1 year; these tend to disappear after retinal reattachment.

3Subretinal demarcation lines(high water marks) caused by proliferation of RPE cells at the junction of flat and detached retina are common and take about 3 months to develop. They are initially pigmented but tend to lose this with time.Demarcation lines are convex with respect to the ora serrata and, although they represent sites of increased adhesion, they do not invariably limit spread of SRF.

Long-standing retinal detachment.(A)Secondary retinal cyst;(B)B-scan shows a retinal cyst;(C)high water mark in an eye with an inferior retinal detachment

Proliferative vitreoretinopathy

Proliferative vitreoretinopathy (PVR) is caused by epiretinal and subretinal membrane formation. Cell-mediated contraction of these membranes causes tangential retinal traction and fixed retinal folds. Usually, PVR occurs following surgery for rhegmatogenous RD or penetrating injury. However, it may also occur in eyes with rhegmatogenous RD that have not had previous vitreoretinal surgery. The main features are retinal folds and rigidity so that retinal mobility induced by eye movements or scleral indentation is decreased.

TRACTIONAL RETINAL DETACHMENT

The main causes of tractional RD are

(a)proliferative retinopathysuch as diabetic and retinopathy of prematurity, and

(b)penetrating posterior segment trauma

Pathogenesis of diabetic tractional retinal detachment

1Pathogenesis of PVD. Tractional RD is caused by progressive contraction of fibrovascular membranes over large areas of vitreoretinal adhesion. In contrast to acute PVD in eyes with rhegmatogenous RD, PVD in diabetic eyes is gradual and frequently incomplete. It is thought to be caused by leakage of plasma constituents into the vitreous gel from a fibrovascular network adherent to the posterior vitreous surface.

Owing to the strong adhesions of the cortical vitreous to areas of fibrovascular proliferation, PVD is usually incomplete. In the very rare event of a subsequent complete PVD, the new blood vessels are avulsed and RD does not develop.

2Static vitreoretinal tractionof the following three types is recognized.

aTangentialtraction is caused by the contraction of epiretinal fibrovascular membranes with puckering of the retina and distortion of retinal blood vessels.

bAnteroposteriortraction is caused by the contraction of fibrovascular membranes extending from the posterior retina, usually in association with the major arcades, to the vitreous base anteriorly.

cBridging(trampoline) traction is the result of contraction of fibrovascular membranes which stretch from one part of the posterior retina to another or between the vascular arcades, tending to pull the two involved points together.

Tractional retinal detachment associated with anteroposterior and bridging traction

Diagnosis

1Symptoms.Photopsia and floaters are usually absent because vitreoretinal traction develops insidiously and is not associated with acute PVD. The visual field defect usually progresses slowly and may become stationary for months or even years.

2Signs. The RD has a concave configuration and breaks are absent.Retinal mobility is severely reduced and shifting fluid is absent.The SRF is shallower than in a rhegmatogenous RD and seldom extends to the ora serrata.The highest elevation of the retina occurs at sites of vitreoretinal traction.If a tractional RD develops a break it assumes the characteristics of a rhegmatogenous RD andprogresses more quickly (combined tractional-rhegmatogenous RD).

(A)Tractional retinal detachment in severe proliferative diabetic retinopathy;

(B)B-scan image of another patient shows incomplete posterior vitreous detachment and a shallow tractional retinal detachment

3B-scan ultrasonographyshows incomplete posterior vitreous detachment and a relatively immobile retina

EXUDATIVE RETINAL DETACHMENT

Pathogenesis

Exudative RD is characterized by the accumulation of SRF in the absence of retinal breaks or traction.

It may occur in a variety of vascular, inflammatory and neoplastic diseases involving the NSR, RPE and choroid in which fluid leaks outside the vessels and accumulates under the retina.

As long as the RPE is able to compensate by pumping the leaking fluid into the choroidal circulation, no fluid accumulates in the subretinal space and RD does not occur.

However, when the normal RPE pump is overwhelmed, or if the RPE activity is decreased, then fluid starts to accumulate in the subretinal space

The main causes are the following: 1Choroidal tumourssuch as melanomas, haemangiomas and metastases; it is therefore very important to consider that exudative RD is caused by an intraocular tumour until proved otherwise.

2Inflammationsuch as Harada disease (Part of VKH syndrome) and posterior scleritis.

3Bullous central serous chorioretinopathyis a rare cause.

4Iatrogeniccauses include retinal detachment surgery and panretinal photocoagulation.

5Subretinal neovascularizationwhich may leak and give rise to extensive subretinal accumulation of fluid at the posterior pole.

6Hypertensive choroidopathy,as may occur in toxaemia of pregnancy, is a very rare cause.

7Idiopathicsuch as the uveal effusion syndrome.

Diagnosis

1Symptoms.Photopsia is absent because there is no vitreoretinal traction, although floaters may be present if there is associated vitritis. The visual field defect may develop suddenly and progress rapidly. Dependingon the cause both eyes may be involved simultaneously (e.g. Harada disease).

2Signs The RD has a convex configuration, just like a rhegmatogenous RD, but its surface is smooth and not corrugated.

The detached retina is very mobile and exhibits the phenomenon of shifting fluid in which SRF responds to the force of gravity and detaches the area of retina under which it accumulates. For example, in the upright position the SRF collects under the inferior retina, but on assuming the supine position for several minutes, the inferior retina flattens and the SRF shifts posteriorly detaching the superior retina.

The cause of the RD, such as a choroidal tumour, may be apparent when the fundus is examined, or the patient may have an associated systemic disease responsible for the RD (e.g. Harada disease, toxaemia of pregnancy). Leopard spots consisting of scattered areas of subretinal pigment clumping may be seen after the detachment has flattened.

Exudative retinal detachment with shifting fluid.(A)Inferior collection of subretinal fluid with the patient sitting;(B)the subretinal fluid shifts upwards when the patient assumes the supine position

Exudative retinal detachment caused by a choroidal melanoma

Leopard spot pigmentation following resolution of exudative retinal detachment

PROPHYLAXISProphylaxis of retinal detachment is best done by identifying predisposing retinal break and treating them with cryotherapy and laser.i/c- vitroretinal traction, h/o trauma, myopia, positive family history, prior cataract surgery or detachment in the fellow eye.

CRYOTHERAPYIt is used to produce chorioretinal inflammation around the edges of retinal break.It may break down blood ocular barrier.In this chorio retinal adhesion take 2-6 weeks to form.

LASER PHOTOCOAGULATIONIt cause less morbidity and is the treatment of choice for prophylaxis except in very peripheral retinal break.It require close chorioretinal apposition for at least one week and cannot be used in the presence of detachment.

TREATMENT

PNEUMATIC RETINOPAXYIt is a Minimally invasive and quick and office based procedure.In this intravitreal expanding gas bubble is used to seal a retinal break and reattach the retina without scleral buckling.Most frequently use gases are Sulphur hexafluride (SF6) and long acting Perfluoro propane (C3F8).

it is used for fresh single retinal break or a group of braks that are clustered within 1 clock hour in the superior two third of fundus.Success rate is slightly less than conventional scleral buckling surgery.

SCLERAL BUCKLINGIt is a procedure in which material sutured on sclera create an inward indentation.Its purpose are to close retinal break by apposing RPE to neurosensory retina and to reduce vitroretinal traction.

EXPLANTSExplants are made from soft or hard silicone.in this a silicone encircling band or sectoral buckle is sutured to sclera and indents the outside of the eye towards the detached retina.The entire break should ideally surround by 2mm of buckle.

BUCKLE CONFIGURATIONRADIAL- placed at right angle to the limbusCIRCUMFERNTIAL- placed in parallel with limbus to create a segmental blockENCIRCLING- explants are placed around the entire circumfernce of the globe to create a 360 degree buckle and may be augmented by local explants.

DRAINAGE OF SRF2 routes-External scerotomy or Internally by a flute needle(soft, blunt, silicone tipped needle).It is indicated in eyes with bullous retinal detachment or when a more marked elevation of the buckle is required.Complications are choroidal hemorrhage, retinal perforation, retinal incarceration, choroidal neovascularisation and endopthalmitis.

VITRECTOMY INDICATIONS- Rhegmatogenous RD- in which retinal break cant be visualized and in which break cant be closed by scleral buckling.Tractional RD- which threatning or involving macula and combined tractional rhegmatogenous RD.

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