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11.6 Post-surgical Macular Oedema
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a
c
b
d
Fig. 11.13 Fundus photograph (a) and uorescein angi-
ography (b) showing media haze due to senile cataract.
Six weeks following cataract surgery, the media clarity
reous surgery with or without phacoemulsication have a signicantly higher risk of ME than
the scleral buckle alone. In more than two-third
of the patients, the CME resolved within
12months of the surgery [172, 173].
11.6.1 Historical Perspective: Role
ofVitreous Traction
It was believed that post-surgical vitreoretinal
traction on the macula due to vitreous incarceration in the cataract surgery wound resulted in
ME.Irvine [171] noted a rupture of the anterior
hyaloid face and late adhesions of the cortical vitreous bres to the cataract wound following
was restored (c), but uorescein angiography showed petaloid pattern (red arrows) of CME (d)
uneventful intracapsular cataract surgery. He
noted ‘macular degeneration’ in 19% of eyes that
did not show any rupture of the anterior vitreous
face vs 45% of those with a rupture of the vitreous face. He showed late adhesions of the vitreous strands to the corneal wound [171]. Tolentino
and Schepens [174] described the incidence of
ME in 1.7% of all cataract surgeries. They found
that the area of macular oedema was often larger
than the size of the adhesion of vitreous strands
to the macula and that spontaneous release of the
traction often led to the resolution of the ME.The
posterior vitreous face is rmly adherent to the
macula and margins of the optic disc. Cataract
surgery precipitates a posterior vitreous detachment. However, the vitreous may remain attached
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11 Macular Oedema
to the macula via a thin strand or a broader adhesion [174].
Traction on the macula and the optic disc may
cause uid leakage from the perifoveal capillaries [175]. Based on extensive anatomical and
clinical studies of the vitreous anatomy, it was
hypothesized that cortical vitreous bres directly
transmit traction on the Muller cells. They also
speculated that inammation or noxious anterior
uveal agents might also play an essential role in
the pathogenesis of ME [176].
11.6.2 Clinical Picture
andFluorescein Angiography
inCME Following Cataract
Surgery
The patients typically become symptomatic
4–12 weeks after uneventful cataract surgery.
The patients complain of blurring of vision. The
visual acuity (VA) may vary from 20/30 to
20/70. Macular oedema associated with VA better than 20/40 is not clinically signicant. On
biomicroscopic examination, the ME is characterized by an absent foveal reex, forward bulging of the macula, with a yellowish spot in the
fovea. It is surrounded by a few intraretinal cystoid spaces [177]. During FFA, there is leakage
of dye from the perifoveal capillaries. The dye
accumulates in the cystic spaces in a petaloid
pattern. It may take 5–15min and sometimes up
to 30min in some cases to show the full extent
of the CME.The ne retinal vessels stand out as
dark lines against the accumulated dye
(Fig.11.13). Using FFA, Gass, and Norton, for
the rst time, showed that the ME resulted from
uid leakage from the perifoveal retinal capillaries. In the late phases of FFA, dye accumulates in the cystic spaces [177]. The eosinophilic
material-lled cystic spaces were found on
pathology in Henle’s outer plexiform layer and
the INL.Contrary to the observation of Tolentino
and Schepens [174], Gass did not nd any signicant vitreous traction on pathological examination of the eyes [177].
11.6.3 Objective Measurement
ofPseudophakic Cystoid
Macular Oedema (PCME)
Clinical biomicroscopic examination, the FFA
and now the OCT can detect PCME.The OCT is
a non-invasive tool to measure the retinal thickness accurately, reproducibly, and, importantly,
the CST. It yields results similar to the FFA,
which, until recently, was the standard of care in
diagnosing pseudophakic cystoid macular
oedema (PCME) [178]. However, the VA does
not always correlate with the measurement of
CST.It is fairly common to see a minor increase
in the perifoveal thickness [179], which resolves
spontaneously. Generally, a 30% increase in CST
over the baseline is signicant. PCME in the
presence of VA >20/40 is generally considered
non-signicant.
OCTA could help in differentiating DME and
PCME.Both show a larger FAZ at the level of
DCP, which is signicantly reversible in patients
with PCME compared to the DME. There are
capillary abnormalities and capillary nonperfusion in DME, which is not seen in
PCME. Disruptions of the parafoveal capillary
network and cystoid spaces in the DCP are seen
more frequently in eyes with DME compared to
PCME [180]. The OCTA studies have shown
decreased vessel density in both the SCP and the
DCP in PCME [181].
11.6.4 Incidence andRisk Factor
forPost-surgery Macular
Oedema
Dening a signicant CME (Irvine-Gass) syndrome as a 30% increase in the CST on SD-OCT,
the incidence of signicant CME was 2.3% following phacoemulsication and non-signicant
in 6.8%. The major risk factors were diabetes,
capsular dehiscence, and the epiretinal membrane [182]. A preexisting epiretinal membrane
(ERM) is a risk factor for pseudophakic CME
[183]. The ERM should be removed before the
11.6 Post-surgical Macular Oedema
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cataract surgery rather than afterwards. The former technique improves visual outcomes [184].
Following uneventful phacoemulsication, the
development of PCME is not an uncommon
cause of visual disturbance. The incidence has
varied depending on the technique of cataract
surgery, the post-surgery interval, the type of
intraocular lens implant, and the technique used
to diagnose [185]. The visual acuity may or may
not be signicantly affected. Preexisting uveitis,
ERM, retinal vascular occlusion, post-retinal
detachment surgery eyes, or posterior capsular
dehiscence with or without vitreous loss during
surgery increases the risk of CME [186].
Patients with DM, especially those with
NPDR, are at a higher risk of developing
PCME.In one of the largest real-world series of
nearly 82,000 consecutive cataract surgeries, the
incidence of PCME in uneventful cataract surgery without any other predisposing factor was
1.17% and was signicantly higher at 1.56% in
eyes with at least one risk factor other than
DM.Nearly 4% of patients with DM developed
PCME, irrespective of the presence or absence of
diabetic retinopathy [187].
The risk and severity of oedema increased
with the increasing severity of diabetic retinopathy [187]. These patients should receive nonsteroidal anti-inammatory agents (NSAIDs)
starting before cataract surgery and continuing
for several weeks. Those with DME should also
receive preoperative IVT anti-VEGF or corticosteroid treatment before cataract surgery.
11.6.5 Role ofInammatory
Mediators andProstaglandins
inSurgical Trauma
ated. Arachidonic acid, a fatty acid, is released
from the cell plasma membrane by phospholipase. The arachidonic acid is metabolized by the
cyclooxygenase (COX) to generate prostaglandins. The prostaglandins are generated even
before the recruitment of the inammatory cells
into the wound. The level of prostaglandins is
low in healthy tissues but increases immediately
following trauma, even before the recruitment of
the leukocytes. PGE2 is the primary prostaglandin involved in inammation. In cataract surgery,
the prostaglandins are released from the iris and
the lens epithelium [188]. The primary function
of prostaglandins is to increase blood ow and
vascular endothelial permeability through their
action on histamine. Applying topical prostaglandins was shown to cause the breakdown of the
blood-aqueous barrier and cause miosis of the
pupil [189]. The prostaglandins are much smaller
molecules, quickly diffuse into tissues, and nd
receptors on practically all tissues in the eye.
Once they diffuse into the vitreous cavity and
reach the retina, prostaglandins cause the breakdown of the blood-retinal barrier, resulting in
uid leakage in the OPL and the INL [188]. Nonsteroidal anti-inammatory agents block the
action of COX-1 and COX-2 and thus prevent the
generation of prostaglandins [190, 191]. Apart
from the prostaglandins, other mediators of
inammation may also play a signicant role in
the formation of CME. In a mouse model of
extracapsular lens extraction, IL-1β and chemokine CCL2 were upregulated in the retina, and
the complement pathway was activated within
30 min of the surgery. The IL-1β is known to
cause the breakdown of the blood-retinal barrier.
Both are acute innate immune responses to injury
and may play a role in the PCME [192].
Any traumatic event, including surgical trauma,
is followed hours later by the initiation of the process of wound healing. Inammation is an integral part of this process. It involves releasing and
recruiting many inammatory cells, namely
platelets, neutrophils, and monocytes, and their
activation into macrophages and broblasts.
Several inammatory mediators, such as chemokines, cytokines, and growth factors, are gener-
11.6.6 Pathogenesis andPrevention
ofPCME
A better understanding of the pathogenesis of
inammation and the mechanism of wound healing has led to a constant evolution of the surgical
techniques in cataract surgery from intracapsular
surgery with almost 15 mm scleral incision to
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11 Macular Oedema
extracapsular surgery (ECCE) to progressively
smaller self-sealing clear corneal incision, phacoemulsication, and placement of the intraocular
lens implants within the capsular bag. The degree
of inammation leading to a breakdown of the
blood-retinal barrier and the release of proteinaceous uid into the anterior chamber can be
objectively measured using the laser are metre.
Compared to the ECCE, the are levels in phacoemulsication were low and lasted for a signicantly shorter time [193]. Likewise, clear corneal
incisions in phacoemulsication produced much
lower are levels than the conventional corneoscleral incisions [194]. Even in patients with DM,
phacoemulsication led to lower inammation
than ECCE in the opposite eye [195]. In a prospective controlled trial, patients preoperatively
received three instillations of eye drops of either
ketorolac 0.45%, uorometholone 0.1% (FML),
or a combination of ketorolac and FML or no eye
drops. In the aqueous samples obtained during
surgery, the IL-6 and the TNF-α values were similar in all four groups. The IL-8 levels were low in
eyes receiving FML alone or in combination with
ketorolac. Likewise, the PGE2 levels were low in
eyes receiving ketorolac alone or in combination
with FML but not in eyes receiving FML or the
control group establishing the role of topical
NSAID in blocking PGE2. Notably, immediately
after the Femto laser application in Femto laserassisted cataract surgery, there was a signicant
rise in the PGE2 levels in the aqueous humour
[196]. A systematic review and meta-analysis of
randomized controlled trials have shown that in
both diabetic and non-diabetic populations,
compared to topical steroids, topical NSAIDs are
more effective in preventing the onset of PCME
after cataract surgery. Adding either the TA or
anti-VEGF agents to the topical NSAIDs was no
additional benet, which remains the standard of
care in preventing PCME [197]. Another topical
NSAID agent, bromfenac, decreased postoperative inammation and CME [198]. Topical use of
nepafenac, another NSAID, in the perioperative
period was highly effective in preventing PCME
in patients with DR [199]. In two large parallel,
randomized vehicle-controlled trials of cataract
surgery in patients with diabetic retinopathy, a
signicant increase in CST (>30% increase over
baseline) was seen in 4% with the use of nepafenac vs 16% in the control group [200].
11.6.7 Treatment ofPCME
Most PCMEs resolve with the continuation of the
topical NSAID within 3 months of the surgery.
However, PCME that persists beyond 6 months is
unlikely to resolve spontaneously. These patients
need intervention beyond a topical NSAID.Posterior
subtenon placement of a single injection of TA
40 mg/mL through a conjunctival peritomy is an
effective treatment modality for PCME.It led to the
resolution of PCME in 90% of the eyes [201]. As
discussed above, patients with DM have a higher
risk of developing PCME, which usually does not
resolve spontaneously and needs denitive interventions in the form of corticosteroids, which can
be prophylactically administered at the time of surgery to thwart the development of PCME.In the
postoperative period, the PCME and the progression of diabetic retinopathy may overlap, emanating
from an exaggeration of downstream inammatory
pathways. The IVT injection of TA 4mg at the time
of cataract surgery in patients with DM resulted in a
signicant reduction in CST and improved visual
outcomes [202, 203]. Similar results were obtained
with the DEXA implant used during surgery [94,
204]. The Dexa implant’s effect lasts at least 3
months [205]. Since the PCME majorly results
from an inammatory pathway, the IVT inj of
Lucentis, an anti-VEGF agent, given simultaneously with cataract surgery in DME eyes, showed
no appreciable difference [206]. However, IVT
injections of 1.25mg of bevacizumab and 2mg of
TA effectively reduced the CST and improved VA 3
months after surgery [207].
11.7 Macular Oedema
inVitreoretinal Traction
The FFA, in a majority of such cases, fails to demonstrate any uid leakage. However, the thickened
retina can be easily diagnosed on OCT.Mechanical
traction on the macula in vitreomacular traction
disorders such as epiretinal membranes, impending
macular holes, diabetic traction maculopathy, and
11.8 Macular Cystic Changes inInherited Macular Dystrophies
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ab
c
Fig. 11.14 Optic disc pallor and macular oedema in a 16-year-old man who had trauma to left eye by a ball 3months
ago (a). OCT showed cystoid macular oedema (b) with a macular hole (c)
20–50% of autosomal dominant or recessive
RP patients may show cystic cavities in the
inner nuclear layer. Some of these patients
may show retinal capillary leakage. Topical
dorzolamide or oral acetazolamide reverses
macular oedema with improvement in central
vision. Interestingly, cystic cavities are not
seen in the X-linked RP.In autosomal reces-
Fig. 11.15 Macular oedema caused by vitreomacular
traction
sive bestrophinopathies, there is a collection
of hyperautofluorescent vitelliform material
and subretinal fluid. In X-linked foveoschisis,
myopic foveoschisis also leads to cystic changes in
the macula [21] (Figs.11.14 and 11.15). The foveal
cysts may disappear on the spontaneous release of
the vitreoretinal traction or require surgical intervention. In some cases, leakage from the retinal
capillaries may also occur.
schisis cavities are seen in the inner nuclear
layer. Patients with enhanced S-cone syndrome, a rare autosomal recessive disorder,
present with night blindness due to loss of rod
photoreceptors, foveomacular schisis
(Fig.11.16), yellow-white dots, and torpedolike lesions [208]. More than 50% of patients
with X-linked choroideremia show topical
11.8 Macular Cystic Changes
inInherited Macular
Dystrophies
dorzolamide-responsive cystoid macular
oedema in the outer plexiform and inner
nuclear layers [209]. For more detailed infor-
mation on the rare inherited macular disorders
Intracellular fluid accumulation may also be
seen in many inherited retinal diseases, especially retinitis pigmentosa (RP). Nearly
that present with cystic changes in the macula,
the readers may refer to recent reviews [21,
22].
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Fig. 11.16 Spoke-wheel pattern (red arrows) of macular oedema in a 12-year-old boy with X-linked retinoschisis,
which is bilaterally symmetrical (a, b). OCT shows schisis cavities in the inner nuclear layer in both eyes (c, d)
11 Macular Oedema
11.9 Drug-Induced Macular
Oedema
[21]. The uid generated from the retina’s nor-
mal cellular metabolism exits via the RMG.Insult
to the K+ channels in the RMG cell’s end feet
The retinal thickness increases most commonly
because of the breakdown of the retinal barriers
with the extravasation of uid from the retinal
vessels. This uid accumulates in the extracellular spaces, and the macular thickening represents the outcome of total ingress and egress of
the uid. The uid is mainly removed from the
inner retinal layer through the retinal Muller
glial (RMG) cells and from the outer retinal layers by an active metabolic pump in the RPE.High
oncotic pressure in the choroid facilitates uid
movement from the vitreous across the retina
and RPE.Fluid leakage from the vessels can be
seen on FFA.The RMG end feet and microglia
processes in the inner retina form intimate contact with the neuronal cells, the capillary endothelial cells, and the pericytes. This
neuro-vascular glial unit is responsible for maintaining normal homeostasis in the retina. It
allows transcellular transportation of nutrients
and oxygen to the retinal cells without going
through the interstitial or extracellular space
may cause a reversal of uid ow from the blood
into the RMG, bringing about swelling of the
RMG and formation of cystic spaces [210]. The
toxic effects of several drugs may lead to intra-
cellular accumulation of uid, causing the thick-
ness of the retina, especially the macula, which
creates cystic spaces [21, 211].
In hormone receptor-positive breast carcinoma, which accounts for nearly third-fourth of
all such patients, the foveal cystic changes on
OCT are estimated to occur in 12% of all who
received tamoxifen. This incidence is much
higher than earlier believed [212]. The changes in
the fovea are similar to the Mac Tel type 2, suggesting tamoxifen toxicity to RMG cells [213].
Several other drugs, including Niacin (used for
dyslipidaemia), Paclitaxel, and Docetaxel (anticancer drugs), are also toxic to the retinal Muller
cells. The uorescein angiogram in these patients
shows no capillary leak, thus labelled as nonvasogenic maculopathy. The macular oedema in
these patients can only be seen on
References
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OCT.Discontinuation of the drug or using acetazolamide may reverse the CME in some patients.
Hydroxychloroquine (HCQ) is often prescribed to patients with autoimmune disorders,
rheumatoid arthritis, and systemic lupus erythematosus as an immunomodulatory drug. HCQ
toxicity has varied from 1.5% to 10% [214].
Patients with HCQ toxicity may have ethnic differences, the white Caucasians showing more
perifoveal and Asians showing a more peripheral
pericentral distribution of changes in the loss of
the photoreceptors. A wide-angle volume OCT
scan was recommended not to miss more peripheral lesions of HCQ toxicity [215]. Cystic
changes may occur in HCQ toxicity even after
drug withdrawal [216, 217]. Occasionally, late
stages of HCQ toxicity may present as macular
oedema and show vessel leakage. Such patients
may respond to oral acetazolamide [216].
Fingolimod used in remitting-relapsing multiple sclerosis may cause cystoid macular oedema
within months. It is an immunomodulatory drug.
It signicantly reduces the relapse rates of multiple sclerosis. It is US FDA-approved for MS.In
the controlled trials, 1.6% of those receiving
1.25 mg/day developed macular oedema, but
none developed ME at a lower dose of 0.5mg/
day. It appears to have dose-dependent toxicity. It
is recommended that patients undergo a baseline
ophthalmological examination and again after
3–4months, at 6 months, and 1 yearly after that
[211, 218]. The oedema is reversible once the
drug is stopped [219].
After many years of use for interstitial cystitis,
pentosan polysulphate sodium used may cause
cystoid macular oedema, areas of complete RPE,
and outer retinal atrophy and needs to be differentiated from geographic atrophy seen in
AMD. The area of atrophy may progress even
after stopping the drug [220].
There are many anecdotal reports of the development of ME following the use of imatinib for
chronic myeloid leukaemia, leunomide for
rheumatoid arthritis, rifabutin for Mycobacterium
avium complex lung disease, and rituximab for
polyangiitis with granulomatous [211].
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