Regional Institute of Ophthalmology, PGIMS, Rohtak

99

Prof. Manisha Nada

Editor-in-Chief, HJO
Regional Institute of Ophthalmology

Pt. B.D. Sharma PGIMS,
Rohtak-124001 (Haryana)

Mobile : 9896007158
E-mail : [email protected]

100

Haryana Journal of Ophthalmology Volume XI (No. 1) June, 2019

HARYANA OPHTHALMOLOGICAL SOCIETY

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101

Clip Sheet
Differential diagnosis of Macular Edema

Aakash Sharma MBBS, Arjun P MBBS, Keerthi Pai MBBS

Regional Institute of Ophthalmology, PGIMS, Rohtak

Macular oedema occurs in a wide variety of 3. On FFA-Macular leakage is the hallmark (except in
pathologic conditions and represents the final typical Nicotinic acid maculopathy) with pooling in cystoid
phenotype of several basic pathophysiologic spaces in later phases (flower petal or spoke-
processes. Pathogenesis of macular oedema depends wheel/honey-comb pattern classically due to radial
on the underlying aetiology. Because it may be arrangement of retinal cells in the macular area
multifactorial, active management is based upon around the foveal center). Degree of leakage doesn't
recognizing and addressing each factor that is correlate with visual acuity; rather macular thickening
operative in a given clinical setting. is a better index of visual impairment. Mild ME may
just produce a faint halo of hyper fluorescence around
Clinical features common to all types of Macular the fovea.
Edemas are-
ME due to RP may respond to oral acetazolamide.
1. Dull Foveal reflex
Avoid epinephrine(Epitrate,Propine)& Prostaglandin
2. Macular thickening-is checked on fundus drops(e.g.Latanoprost)in postop patients particularly
biomicroscopy. Macular Edema however can be in aphakes.
confirmed on OCT. Normal thickness of macula is
<180µ. Thickening can be most objectively assessed Inflammatory ME may follow various retinal
and serially followed up by OCT. vasculitis(e.g.Eales,Behcet's,Sarcoidosis,ARN,etc)&
is treated according to the etiology.

S Etiology Pathophysiology Special Clinical& Course,Treatment& Comments
No. FFA features Prognosis

1. Post-cataract extraction (Irvine- Cause basically Typically starts at 4-8 weeks Most cases resolve Incidence of angiographic

Gass syndrome) unknown. Blood-retinal postop. spontaneously within 3-4 months. CME'is 20% in uneventful

barrier of Mild to moderate diffuse Chronicity in<1% ECCE&60%in ICCE.

Other Postop causes- perifoveal capillaries vitreous haze. especially, if disc leak is present on FFA. However 'visually significant

i) Any intraocular procedures is broken. Prevention is better as no drug is proven to CME'(VA<6/12)occurs only

e.g. PK, surgical capsulotomy, Much commoner in On FFA, unlike DME there is be effective. Preoperative in~2%

Trab., Antr Vit. ICCE&Complicated early peri-foveal symmetric NSAID drops may help in prevention. －Chronic CME is the one

ii) Non-incisional surgeries e.g. ECCE surgeries (PCR+/- leakage with late pooling & Treatments tried: persisting for>6months.o
Cryo, PHC,YAG procedures vit.loss) Hypotheses include associated optic nerve head i) Systc/Topical CSd －Most imp.D/D is Diabetic
iii) Extra-ocular surgeries e.g. staining is also common. ii) Systc/Topical NSAIDs macular edema. It is not
Scleral buckling.（Clinical i) AC inflamn causing PG iii) Oral acetazolamide, 500mg OD centered symmetrically
picture & Tr.are similar to liberation（topical NSAIDs iv) Hyperbaric 02 around
post cataract CME) block this). v) Vitrectomy in chronic CME for vitreous fovea&is also assd with hard
Pars Plana Vitrectomy generally ii) Foveo-macular traction incarceration with vitreo-macular traction. exudates or other DR
never results in CME syndrome （best picked upon Among drops 0.5% Ketorolac tromethamine changes.
OCT)either following vit.loss qid X 3months probably works the best.

or partial PVD Focal laser helps in these

iii) Photic-Normal blue & UV cases. However both may co-

filtering effect of crystalline exist. Do focal PHC if

lens is removed diabetic process is

dominating, otherwise

observe.

－Keep other D/Ds also in
mind e.g. Preexisting ARMD
with CNVM, Hypotonous
maculo-pathy, RD(always do
I/O),
Photic retinopathy before
labeling it a Postop CME
－Fellow eye is at higher risk
of developing CME
－DM&HT predispose to
CME

102

2. Diabetic macular Increased capillary ETDRS defined PHC of thickened areas by －Only thickening(as noted
edema(DME) permeability of CSME as focal(if focal leak),grid(for on
（Thickening perifoveal capillaries. i) Thickening within central diffuse leak)or modified grid fundus biomicroscopy or
Long-standing diffuse 500u （for multiple focal leaks OCT)is the sole criterion for
within 2 DD of DME results in cystoid ii) Hard exudate within 500u which may extend even Tt&NOT the visual acuity or
fovea) formation.Sometimes vitreo- with adjoining thickening beyond macula) fluorescein leakage.
－Focal or Diffuse macular traction may be iii) Thickening of IDD, part of Treatable lesions include- －Always first treat the
responsible (Best detected on which is within the central i) Focal leaks away from central 500u macular edema by
OCT) IDD of macula. Always check ii) Focal leaks in 300-500p provided rest of PHC&wait for 6-8 wks
thickening by fundus the perifoveal network is intact. before doing PRP provided
biomicroscopy e.g.+90D), iii) Previously untreated diffuse leakage or PRP is not required urgently
although OCT measures it avascular zones.For focal Tt-obtain definite in which case, first
most objectively. FFA is whitening of MA/leaking site sitting of PRP may be given
essential to study FAZ& nasally immediately or after
other avascular areas. －Early treatment of thickening has better 2
prognosis than delaying Tt. weeks).
－Focal (leaking micros or －Macular Grid-is 100u laser －Always warn the patient of
dilated capillaries) or diffuse spots applied in'C'fashion possible worsening of vision
(leakage from diffusely dilated with mild intensity(faintly （either qualitatively or
capillaries) leak is seen & is visible burns)&placed 11/2- quantitatively)after macular
usually not located 2 burns width apart. PHC.
symmetrically around fovea －Modified grid treatment is －Pts with assd.extensive
unlike postop CME burns applied on all
thickened areas&not in a classical'C'fashion foveal
－ME is best monitored by ischemia(FAZ
OCT(serial retinal thickness broken/enlarged)are poor
analysis)If no response in 6-8 candidates for PHC
wks either repeat PHC or give I-Vit －While Macular Grid laser
Triamcinolone(0.1ml works better for DDME,I-
i.e.4 mg of Tricort/Kenacort VitTriam.works better for
in mid-vitreous cavity by cystoid ME.
slow injn). Effect comes in －Pts.with assd.vitreo-
2-4 wks&lasts for avg.of~3 macular traction syndrome
months.BenzylOH don't
（preservative) free Triamcino. respond well to PHC&may
Is preferred.Subtenon's need VR surgery.
Triam is also effective.

3. BRVO Breakdown of Petalloid pattern. Usually Grid laser treatment to thickened areas if ME is the most common &
endothelium by involves only the affected VA is ＜6/12 & edema is persisting even most important cause of
4. CRVO increased hydrostatic sector after 3 months in absence of macular visual loss in BRVO
5. Uveitis especially Pars pressure. nonperfusion. PHC protocol is similar to
that of diabetic ME.
Planitis －Do-
CRVO study Although grid laser reduces
Edema primarily due to the ME but visual acuity is not improved
Inflammatory & not
of stasis &/or No role of NSAIDs (block COX pathway
ischemic origin only).
Periocular/ Systemic steroids （block both
COX&
Lipoxygenase pathways
indirectly)if V.A.is <6/12

No leak CME i.e. Pseudo-CME(intracellular edema retinopathy unlike postop CME presents in the first
within Muller cells)is caused by Nicotinic acid one or two days with para-central scotoma. Whitish
intake(used in lipid disorders)and X-linked parafoveal lesion is usually seen which stains on FFA.
retinoschisis.
Address for Correspondence :
All causes of CNVM(e.g.ARMD)may have assd. ME
which needs to be treated accordingly,These Pis Dr.Aakash Sharma
besides having fluid within NSR due to ME, presence Jr. Resident,
of CNVM in them causes thickening at RPE RIO, PGIMS,
level&shallow NSR detachment&sometimes also Rohtak-124001(Haryana)
subretinal lipids. Other causes of CME include an E-mail : [email protected]
epiretinal membrane, Intraocular tumors, isolated Mobile : 8318769375
autosomal dominant disorder, inferior RD, retinal
telangiectasias&Angiomatosis.

Always look for peripheral retinal Angioma(von-
Hippels) in a young patient with unexplained ME.Tt is
PHC or cryo of angiomas in multiple sessions. photic

103

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Printed & Published by : Prof. Dr. Manisha Nada on behalf of Haryana Ophthalmological Society, Published at Room No. 14, OPD 'B' Block, RIO, PGIMS, Rohtak-124001

Printed at : SP Enterprises, Rohtak-124001 (Haryana) India. M : 9253026152 Editor Prof. Dr. Manisha Nada