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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_6023_Библиотеки_им_академика_М_И_Перельмана.pdf
Surgical Management ofEpiretinal
Membrane
Epiretinal membrane (ERM) is a common structural abnormality of the vitreomacular interface. It is characterized by the proliferation of collagen bers on the inner
retinal surface, resulting in varying degrees of brocellular tissue attachment to the
macula. Clinically, ERM primarily manifests as decreased visual acuity and metamorphopsia. Optical coherence tomography (OCT) has become an essential tool for
diagnosing ERM and provides critical evidence for determining surgical timing.
ERM is classied into two types: idiopathic and secondary. The former lacks a
denitive clinical cause and remains a diagnosis of exclusion. (Etymologically,
‘idiopathic’ combines the Greek idios, meaning ‘self’ or ‘private,’ with the sufx pathic, indicating a pathological condition). Secondary ERM, conversely, is directly
attributable to specic ocular pathologies. This chapter explores the pathogenesis of
ERM, with a focus on surgical management techniques and key clinical
considerations.
9
9.1 Clinical Characteristics
9.1.1 Classification andEtiology ofERM
Idiopathic ERM: No denitive cause is identiable, making it a diagnosis of
exclusion. Before conrming this diagnosis, a comprehensive fundus examination
and a thorough medical history review are mandatory.
Secondary ERM: This form is associated with various ocular pathologies, including retinal vein occlusion, diabetic retinopathy, uveitis, trauma, retinal detachment,
hamartomas, and retinal angiomas. While identifying the primary disease is often
straightforward, it is vital to meticulously examine the peripheral retina for breaks.
If indicated, uorescein angiography should be performed to assess vascular
exudation.
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2026
Z. Zhang, U. Spandau, Vitreoretinal Surgery,
https://doi.org/10.1007/978-3-032-25271-5_9
193
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9 Surgical Management ofEpiretinal Membrane
“Iatrogenic” ERM: Though technically a subset of secondary ERM, it is highlighted here to underscore that ocular intervention is a frequent trigger. This includes
ERM formation following retinal detachment repair, silicone oil tamponade, laser
photocoagulation, or cryotherapy—typically driven by postoperative inammatory
activation.
9.1.2 Staging ofIdiopathic Epiretinal Membrane
Idiopathic epiretinal membrane (iERM) peaks in incidence among individuals aged
60–70 years, with a slightly higher prevalence in women. According to the Gass
classication, it is divided into three clinical stages:
• Stage 0 (cellophane maculopathy): Characterized by a thin, transparent membrane that produces a shimmering, cellophane-like reex over the macula. At this
stage, the membrane does not distort the underlying retina. Patients are typically
asymptomatic, and the condition is often an incidental nding during routine
examination (Fig.9.1a). Because the risks of surgery signicantly outweigh the
potential benets, surgical intervention is not recommended, and observation is
the standard of care.
Because the risks of surgery signicantly outweigh the potential benets, sur-
gical intervention is not recommended, and observation is the standard of care.
• Stage 1 (Crinkled Cellophane Maculopathy): The membrane begins to contract,
causing ne wrinkles or striae in the inner retinal layers. If contraction involves
the fovea, patients may report mild decreased visual acuity or metamorphopsia.
These symptoms are often subtle and may only be noticed during monocular
testing—especially if the affected eye is non-dominant (Fig.9.1b).
For patients with stable, good visual acuity, surgeons should prioritize longterm monitoring over immediate surgery, tracking the progression of visual
distortion.
• Stage 2: Stage 2 (macular pucker): The membrane thickens and becomes increasingly opaque, appearing translucent or grayish-white. Signicant contraction
results in full-thickness retinal folds, vascular tortuosity, and potential displacement of the fovea. Secondary clinical signs such as small hemorrhages, exudates,
or cotton-wool spots may be present, and cystoid macular edema (CME) occurs
in approximately 20%–40% of cases (Fig.9.1c, d).
Clinical symptoms do not always correlate perfectly with imaging ndings in
these patients; approximately 80% report decreased visual acuity or metamorphopsia. Prior to recommending surgery, surgeons must thoroughly evaluate the
patient’s primary complaints. Given the typically elderly demographic, concurrent conditions such as cataracts or dry eye syndrome should be considered.
Surgical decisions must align with the patient’s functional goals; intervention is
rarely urgent if symptoms are mild or if the patient is hesitant.
Secondary and iatrogenic ERMs are not typically staged.
ab
cd
9.2 Etiology ofEpiretinal Membrane
195
Fig. 9.1 Fundus photographs of ERM at different clinical stages (a) Cellophane-like reection on
the macula (Stage 0). (b) Mild contraction and wrinkling of the ERM (Stage 1). (c) Vascular tortuosity near the macula (Stage 2). (d) Thickened ERM with small hemorrhages (Stage 2)
9.2 Etiology ofEpiretinal Membrane
While the precise initiating trigger for ERMremains elusive, the transdifferentiation of various precursor cells into myobroblasts is considered a critical step in
ERM formation. During this process, cells often lose their original markers, complicating denitive identication. However, immunohistochemical studies suggest that
retinal glial cells and retinal pigment epithelial (RPE) cells are the primary contributors.The mechanism by which these cells migrate to the inner retinal surface is still
debated, though three prominent theories have been proposed:
1. ILM dehiscence theory: Following a posterior vitreous detachment (PVD), minor
defects or “breaks” in the internal limiting membrane (ILM) may allow retinal glial
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9 Surgical Management ofEpiretinal Membrane
cells to migrate onto the inner retinal surface. However, because visible ILM damage is rarely observed in idiopathic cases, this theory is not universally accepted.
2. Vitreous remnant theory: Following PVD, residual vitreous cortical cells (hyalocytes) remain on the retinal surface, where they proliferate and undergo metaplasia. A limitation of this theory is its inability to account for ERM cases occurring
in the absence of a PVD.
3. Chronic traction theory: In eyes without PVD, chronic vitreomacular traction
(VMT) may stimulate Müller cells, triggering glial proliferation and vascular
leakage. Glial cells then migrate and proliferate along the posterior vitreous cortex, eventually forming the ERM.
Currently, no single theory comprehensively explains all clinical presentations of
ERM formation.
Histologically, an ERM typically consists of two distinct layers:
• The outer layer: This layer is in direct contact with the ILM and is composed of
an acellular extracellular matrix (ECM) secreted by the membrane’s cellular
components.
• The inner layer: This is the cellular component of the ERM, consisting of single
or multiple strata of glial cells, RPE cells, broblasts, and immune cells. The
specic cellular composition often reects the underlying etiology and chronicity. For instance, ERM secondary to proliferative vitreoretinopathy (PVR) is
typically RPE-dominant, whereas idiopathic ERM is primarily composed of
glial cells.
9.2.1 Cellular Components ofERM
(1) Glial Cells
Microglia, astrocytes, and Müller cells are all implicated in the pathogenesis of
ERM.The reactive proliferation of glial cells is a primary driver of both ERM and
proliferative vitreoretinopathy (PVR). Upon migrating to the retinal surface, these
cells proliferate to provide a scaffold for extracellular matrix (ECM) deposition.
Glial cells can also transdifferentiate into myobroblasts; furthermore, they secrete
transforming growth factor-beta (TGF-β), which acts as a potent paracrine signal
promoting the myobroblastic transformation of other cellular constituents within
the membrane.
(2) Hyalocytes
Hyalocytes are vitreous-resident mononuclear phagocytes primarily located within
the posterior vitreous cortex and vitreous base. Within the ERM, these cells are
characterized by long cytoplasmic processes and often cluster around broblasts.
Research indicates that hyalocytes exhibit a robust contractile response to TGF-β2.
Consequently, it is hypothesized that ERM may develop post-PVD due to the
9.3 Evaluation andDierential Diagnosis
197
proliferation of residual premacular hyalocytes. If the posterior vitreous detachment
occurs cleanly, completely separating the hyalocyte-containing layer from the macula, the likelihood of ERM formation may be reduced.
(3) Retinal Pigment Epithelial (RPE) Cells
RPE cells typically reach the inner retinal surface through retinal breaks, making
them a dominant cellular component in PVR and ERM secondary to rhegmatogenous retinal detachment. While they are not a hallmark of idiopathic ERM, RPE
cells on the retinal surface can differentiate into myobroblasts under the inuence
of TGF-β2. While their migration pathway in idiopathic cases remains debated, one
hypothesis suggests that other retinal cell types may undergo transdifferentiation
into RPE-like cells.
(4) Macrophages
Macrophages are frequently identied in ERM secondary to vitreous hemorrhage.
Although their exact role in membrane formation is not fully elucidated, they are
known to secrete a variety of cytokines and growth factors that likely modulate the
myobroblastic transformation of surrounding cells.
(5) Fibroblasts and Myofibroblasts
The contractile properties of broblasts and myobroblasts are responsible for the
mechanical distortion of the underlying retinal architecture. This traction results in
the formation of retinal folds, vascular tortuosity, and, in severe cases, the development of secondary macular holes.
9.3 Evaluation andDifferential Diagnosis
While diagnosing ERM is often straightforward, surgeons must avoid “diagnostic
monism.” Because ERM predominantly affects the elderly, concurrent ocular
pathologies are common. Misclassifying an ERM as idiopathic without a thorough
evaluation can lead to overlooked details and potential medical disputes.
A comprehensive fundus examination and medical history are essential to distin-
guish between idiopathic, secondary, and iatrogenic types. Identifying the underlying etiology is critical for:
1. Patient communication: Providing an accurate diagnosis manages patient expectations and fosters a realistic understanding of their condition.
2. Comprehensive care: Facilitating the detection of associated abnormalities, such
as peripheral vascular lesions or retinal breaks.
3. Optimizing outcomes: Identifying contraindications to surgery. For instance, in
ERM secondary to uveitis, surgery should be deferred until inammation is
controlled.
4. Prognostic accuracy: Enabling objective predictions of visual recovery and complications, which is vital for informed consent.
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9 Surgical Management ofEpiretinal Membrane
The differential diagnosis ofERM includes: (1)Vitreomacular traction (VMT):
High-resolution OCT easily distinguishes VMT from ERM by the presence of a
continuous posterior vitreous cortex band. If VMT and ERM coexist, surgeons must
exercise caution to avoid iatrogenic foveal traction; (2): Cystoid macular edema
(CME): Centered on the fovea, CME appears as cystic intraretinal spaces on OCT,
typically without vascular tortuosity. Fluorescein angiography (FA) may reveal
characteristic “petaloid” leakage in late phases. If ERM and CME coexist (e.g., in
retinal vein occlusion), surgeons should evaluate whether conservative treatments—
such as anti-VEGF or corticosteroid implants—are indicated before proceeding
with surgery.
9.4 Surgical Timing andPrognostic Factors
9.4.1 Surgical Timing
Historically, a best-corrected visual acuity (BCVA) of 20/100 (0.2) was the standard
threshold for intervention, with metamorphopsia considered a secondary factor.
However, the improved safety prole of minimally invasive vitrectomy (MIVS) and
the increasing visual demands of modern lifestyles—particularly mobile device
use—have made surgical indications more exible. For novice surgeons, the following principles should be strictly observed before considering a more relaxed criteria:
1. ERM Severity and Baseline Visual Acuity
Denser membranes are typically associated with lower BCVA.While thick membranes are often easier to grasp and peel—facilitating the creation of an initial ap
and a broader peeling range—they present unique challenges. If the ERM is highly
concentrated or tightly adherent at the fovea (Fig.9.2), the risk of mechanical retinal
trauma signicantly increases. In such cases, surgical intervention is not recommended for surgeons still in the early stages of their learning curve.
2. Patient Expectations
While ERM often causes moderate metamorphopsia, visual acuity frequently
remains above 20/200 (0.1) in the absence of signicant cataracts. Because pars
plana vitrectomy is a specialized and costly intervention, patients typically harbor
high expectations for functional recovery. If a patient’s expectations are unrealistic
or if they are intolerant of potential postoperative limitations, the surgeon must prioritize thorough communication. Avoiding overcondence and ensuring informed
consent are essential to prevent medical disputes—a common challenge when evaluating ERM patients in a clinical setting.
3. Primary Clinical Complaint
The patient’s motivation for seeking care is a critical, yet often overlooked, factor.
Patients may not notice metamorphopsia if the affected eye is non-dominant or if a
9.4 Surgical Timing andPrognostic Factors
199
a
b
c
Fig. 9.2 Centrally localized ERM with high foveal adherence, increasing the difculty of ap
initiation. (a) Multicolor fundus imaging: Clearly delineates a localized ERM concentrated at the
fovea with distinct, identiable margins (white arrows). (b) Standard fundus photograph: The
ERM boundaries are poorly visualized; the primary clinical sign is the loss of the foveal light
reex. (c) OCT: Conrms the localized nature of the ERM (demarcated by white arrows), showing
focal traction and the loss of the physiological foveal depression
dense cataract masks macular symptoms. Such cases are frequently referred by
cataract or general specialists after ERM is incidentally detected. In these scenarios,
a conservative approach is often warranted. Initial management may include treating ocular surface issues (e.g., dry eye or foreign body sensation). If cataracts are
signicant, performing cataract surgery rst may yield satisfactory visual improvement, potentially reducing the patient’s desire for further retinal intervention.
Generally, ERM surgery has a high safety prole and is considered a foundational procedure in many specialized training programs. However, given the risk of
irreversible macular damage during membrane peeling, it is traditionally performed
by experienced vitreoretinal surgeons. Novice surgeons should adopt a graduated
approach to training, prioritizing the principle of “Primum non nocere” (First, do no
harm) before transitioning to independent practice.
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9 Surgical Management ofEpiretinal Membrane
9.4.2 Prognostic Factors
Most patients do not experience immediate visual improvement following surgery. Signicant recovery typically occurs only after postoperative inammation
subsides and macular anatomy begins to stabilize. While approximately
60%–80% of patients eventually achieve improved visual acuity and reduced
metamorphopsia, phakic patients frequently face progressive cataract formation
(Fig.9.3). This decline in vision can lead to patient anxiety during the recovery
period. To mitigate this, surgeons must provide comprehensive preoperative
counseling and ongoing reassurance during follow-up visits. Furthermore, clinicians should be aware that lens opacity can be underestimated without pupillary
dilation; some patients may report transiently improved clarity once the pupil is
dilated, highlighting the need for thorough monitoring of lens changes.
Beyond lens opacity, preoperative BCVA is the primary determinant of postoperative vision. High-resolution OCT allows surgeons to objectively quantify retinal
involvement (Fig.9.4). Key indicators of a limited visual prognosis include chronic
duration, dense ERM, signicant tractional elevation, and structural damage such as
EZ disruption or inner plexiform layer thinning.
Fig. 9.3 Progression of
nuclear cataract 6 months
after ERM surgery. BCVA
decreased from 0.6
(1-month post-op) to 0.1
9.5 Standard Surgical Steps
Fig. 9.4 Multicolor fundus photograph (left) and OCT (right) of a thin ERM with minimal retinal
involvement and an intact ellipsoid zone. BCVA improved from 0.6 preoperatively to 0.9 following
surgical intervention
201
9.5 Standard Surgical Steps
Approximately 60% of ERMsare associated with some degree of PVDat the time
of diagnosis, which typically facilitates the surgical process. MIVSis currently the
standard approach, with the 25-gauge platform offering an optimal balance between
instrument rigidity, invasiveness, and surgical efciency. Following the general
principles of PPV, the procedure typically follows these steps:
1. Core vitrectomy: Resection of the central vitreous is performed, extending to
the mid-periphery to create sufcient space for posterior pole maneuvers and
PVD induction.
2. Conrm the presence of PVD: This step is essential for a thorough procedure.
The use of triamcinolone acetonide (TA) is recommended to conrm the presence of PVD and to assist in subsequent membrane visualization.
3. Staining: Staining may be bypassed if ERM boundaries are clearly visible,
allowing for direct peeling.
4. Initial ap formation: An initial ap is created at the edge of the ERM using
ILM forceps. This step is considered a critical technical skill in the training of
vitreoretinal surgeons.
5. Membrane peeling: The peeling is expanded with an emphasis on hand stability
and controlled movements to ensure a smooth transition across the macula.
6. ILMpeeling: The decision to remove the ILM remains a subject of clinical
debate. The approach may be adjusted based on intraoperative ndings, such as
the presence of spontaneous ILM aps.
7. Peripheral vitrectomy: Thorough shavingof the mid-peripheral vitreous is rec-
ommended to mitigate the risk of postoperative traction. Vitreous surrounding
the trocarshould be meticulously cleared to prevent vitreous incarceration at
the incision sites.
8. Peripheral retinal examination: A 360° scleral indentation is performed to
inspect the peripheral retina. Any identied retinal breaks or degenerative areas
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9 Surgical Management ofEpiretinal Membrane
should be addressed with surrounding vitreous removal and laser
photocoagulation.
9. Intraocular tamponade: Balanced salt solution (BSS) is the standard tampon-
ade; however, ltered air may be utilized based on surgeon preference. While
some suggest air tamponade may help maintain dry incisions, this remains a
theoretical benet.
10. Incision closure: The requirement for sutures is determined by the integrity and
seal of the scleral incisions. While beveled incisions are often self-sealing,
suturing may be performed to ensure postoperative wound stability.
9.6 Use ofVital Dyes
In ERM surgery, staining is not strictly mandatory, as the membrane’s morphology
often provides sufcient contrast for dissection. However, vital dyes are frequently
utilized to accentuate architectural details and ensure the safe identication of surgical planes.
Commonly used agents include triamcinolone acetonide (TA), indocyanine
green (ICG), and brilliant blue G (BBG). Less frequent options include trypan blue,
patent blue, and infracyanine green. It is important to note that the intraocular safety
prole of these agents is dose-dependent, and surgeons must remain cognizant of
potential retinal toxicity.
9.6.1 Triamcinolone Acetonide (TA)
TA suspension does not chemically stain the ERM.Instead, TA particles adhere to
residual vitreous cortex or the viscous surface of the ERM, providing a “coating”
effect that enhances textural details and contours.
Typically, 4mg (0.1 mL) of TA is sufcient to visualize the posterior vitreous
and membrane. A modied technique involves diluting 0.1 mL of the original sus-
dilution facilitates more rapid intraocular clearance during irrigation. TA is
considered highly safe for intraocular use, as it can be thoroughly aspirated during
the procedure, leaving minimal residue.
pension into 1.0 mL of balanced salt solution (BSS) prior to injection; this pre-