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10 Surgical Intervention oftheMacular Hole
ab
Fig. 10.8 Challenges in depth perception during ILM peeling. (a) Insufcient depth: The tips of
the end-gripping forceps are positioned slightly above the ILM, resulting in an ‘‘empty’’ or failed
grasp. (b) Excessive depth: The forceps are positioned too deep, traumatizing the underlying neurosensory retina. Although the ILM is successfully engaged, iatrogenic hemorrhage occurs as a
result of mechanical injury
10.6.2 Flap Initiation Techniques
Flap initiation should avoid the nasal side of the macular hole to protect the papillomacular bundle, as injury to this area can lead to permanent central vision loss and
scotomata. The preferred sites are the superotemporal or inferotemporal regions,
approximately 1000–1500μm from the hole margin (roughly one optic disc diameter). Proximity to the hole increases the risk of foveal trauma, while initiation too
far into the periphery is hindered by the diminishing thickness of the ILM.
While various instruments are available, end-gripping forceps remain the most
widely utilized tool for ILM peeling in the era of minimally invasive vitrectomy.
The following section details the techniques for initiating and extending the ILM
ap using these specialized forceps.
End-gripping forceps feature sharp, near-right-angle tips. This ergonomic design
minimizes the contact area with the retinal surface during engagement, providing
sufcient sharp traction to tear the ILM while minimizing mechanical stress on the
underlying neurosensory retina.
1. Maintain a neutral, straight wrist and rest the ulnar side of the hand on the
patient’s forehead to ensure a stable fulcrum.
2. Adopt a ‘‘pen-grip’’ posture. As the forceps approach the macula, optimize
microscope magnication and center the macular hole in the eld of view to
ensure focused illumination.
3. Calibrate the endoilluminator. Intensity should typically be maintained at
30%–35%. Avoid placing the light tip too close to the macula to prevent ‘‘overexposure’’ (glare), which obscures textural details and induces surgeon eye fatigue.
10.6 Underlying Logic andPractical Skills ofInternal Limiting Membrane Peeling
225
4. Slightly open the forceps and gently engage the ILM with the tip. While apply-
ing a controlled squeeze through the nger joints, lift the forceps by slightly
extending the wrist. This ‘‘pinch-and-lift’’ motion creates a focal tear. The
maneuver must be subtle and precise—evoking the image of a ‘‘dragony skimming the water’’ (Fig.10.9).
5. After each pinch attempt, regardless of success, briey pause and retract the
forceps slightly to observe and assess the tissue response (Fig.10.10).
6. If an attempt fails or results in a focal hemorrhage, select an alternative safe site
to retry (Fig.10.11).
7. Upon conrmation of a successful ILM tear, proceed to expand the peel-
ing rhexis.
10.6.3 Extending theILM Flap
1. If a clear separation exists between the ILM ap and the underlying retina, conventional peeling techniques may be employed: securely grasp the edge of the
ap at its basal ‘‘platform’’ and steadily expand the peeling area (Fig.10.12).
2. If only a focal tear is visible without an identiable gap, continue applying the
‘‘pinch-and-lift’’ maneuver at the ILM margin. This subtle lifting action increases
the sub-ILM space, facilitating a safer transition to continuous peeling
(Fig.10.13).
3. Should both maneuvers fail to yield an adequate ap, re-initiate the process at an
alternative site. If necessary, re-apply vital dye to enhance contrast and ensure
precise identication of the ILM.
Fig. 10.9 Toothed
end-gripping forceps. The
right-angle tips at both
ends are used for ILM ap
initiation(photo courtesy
of Alcon)
226
Fig. 10.10 Following
‘‘Yin-Yang’’ staining of the
ILM with triamcinolone
acetonide (TA) and
indocyanine green (ICG), a
subtle ‘‘pinch-and-lift’’
maneuver—delicate as a
‘‘dragony skimming the
water’’—is performed to
initiate the ap at the
margin of the stained area.
The sharp tips of the
end-gripping forceps
engage the membrane with
minimal surface contact,
inducing a focal tear (red
arrow) in the taut ILM
Fig. 10.11 A focal
hemorrhage occurs at the
initial attempt site (white
arrow) due to mechanical
trauma during ILM
engagement. The site is
promptly abandoned, and
an alternative safe zone is
selected for re-initiation of
the ap
10 Surgical Intervention oftheMacular Hole
Extending the ILM peeling area typically requires a controlled maneuver analo-
gous to ‘‘continuous curvilinear capsulorhexis’’in cataract surgery. Utilizing internal or external wrist rotation helps maintain a steady, circular peeling motion.
Unlike ap initiation, if the membrane tears or breaks during this stage, it generally
does not signicantly increase the surgical complexity, as the established ap edge
can be readily re-engaged.
10.6 Underlying Logic andPractical Skills ofInternal Limiting Membrane Peeling
Fig. 10.12 This technique
is ideal when the ILMis
loosely adherent to the
underlying neurosensory
retina, providing a clear
sub-ILM surgical plane.
By gently grasping the
ap’s leading edge, the
surgeon can steadily
expand the peeling rhexis
with minimal traction on
the retinal architecture
Fig. 10.13 Controlled
‘‘pinch-and-lift’’ maneuver
to expand a focal ILM
lift’’ motion is applied at
the margin of the initial
ILM tear (blue area,
indicated by the red arrow)
to elevate the membrane
and develop a surgical
plane. This technique is
particularly effective when
the ILM is highly adherent
to the underlying
neurosensory retina,
lacking the spontaneous
separation required for
conventional grasping
227
tear.A subtle ‘‘pinch-and-
228
10 Surgical Intervention oftheMacular Hole
In patients with high myopia (particularly those with an axial length ≥30mm),
both ILM ap initiation and extension are exceptionally challenging. These difculties stem from: (1)Poor ILM staining contrast; (2)The presence of adherent macular retinoschisis or residual cortical vitreous;(3)Extreme axial length, which may
exceed the reach of standard intraocular instruments; (4) Posterior staphyloma,
which creates a steep, irregular contour that lacks a stable operating plane for the
temporal ILM.To manage these challenges, surgeons may consider switching from
a wide-angle viewing system to a corneal contact lens for higher magnication and
better depth perception. If standard forceps are too short, one may utilize specialized long-reach forceps or temporarily remove the trocar to extend the instrument’s
effective intraocular length. Throughout the procedure, maneuvers must be executed with extreme delicacy to prevent iatrogenic injury to the thinned, fragile neurosensory retina.
10.6.4 ILM Flap Techniques
Advanced ILM ap techniques, such as coverage and insertionmaneuvers, have
revolutionized the management of complex macular holes. Mastery of standard
ILM peeling remains a prerequisite for exploring these specialized approaches. For
large or chronic macular holes, these ap-based strategies signicantly improve
primary surgical success by providing a biological scaffold for anatomical repair
(Fig.10.14).
10.7 Complications
While complications for MH and ERM surgery are generally similar, MH procedures involve more intensive use of vital dyes, necessitating close monitoring for
dye-related retinal toxicity and visual eld loss. Precision during ILM peeling is
critical, as iatrogenic damage from forceps can lead to irreversible functional decits. For cases involving non-closure or recurrence, the decision to re-operate should
be based on a realistic evaluation of potential benets. Furthermore, specialized
macular hole tamponade or ‘massage’ maneuvers must be approached with caution
due to their potential for further retinal trauma.
ab
cd
10.8 Summary
Fig. 10.14 Combined application of ILM “Yin-Yang” staining and ap coverage technique. (a)
Preoperative minimum macular hole diameter: 425μm; corrected visual acuity: 0.15. Intraoperative
ILM “Yin-Yang” staining shows unstained ILM at and around the fovea (red circle). Flap initiation
starts from the stained inferotemporal area. (b) Intraoperative view shows the peeled ILM ap
covering the macular hole, with a small amount of ICG-stained ILM ap visible at the edge (white
arrow). (c) OCT at 10days postoperatively shows closed macular hole with the ILM ap still
overlying it; corrected visual acuity: 0.5. (d) Fundus photograph shows residual gas and no obvious abnormalities in the posterior pole retina
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10.8 Summary
As suggested in the ancient allegory, ‘‘Great oaks from little acorns grow,’’the ultimate success or failure of macular hole surgery often hinges upon the subtlest of
details. From the precision of the initial incision and the gentle calibration of intraocular illumination to the uid dynamics of a single-pass ILM peel, each minor
maneuver acts as a seed for the nal outcome.
For the retinasurgeon, there are no ‘small’ steps; a microscopic tremor or a
moment of misplaced traction can alter a patient’s visual prognosis entirely.
Therefore, meticulous attention to every procedural nuance is not merely a technical
requirement but a fundamental philosophy essential to achieving a consistently successful anatomical and functional result.
Prevention andManagement
ofProliferative Vitreoretinopathy
Proliferative vitreoretinopathy (PVR) is a complex intraocular condition character-
response following vitreoretinal injury. As a frequent complication of rhegmatogenous retinal detachment (RRD), ocular trauma, or previous vitreoretinal intervention, PVR markedly increases surgical complexity and remains the primary etiology
of anatomical failure in retinal detachment repair.
The incidence of PVR secondary to RRD is estimated at 5%–10%. Currently,
there are no clinically proven pharmacologic therapies for its prevention or treatment. Once PVR manifests, the majority of patients require salvage vitreoretinal
surgery. This chapter explores the underlying pathogenesis of PVR, with a primary
focus on the essential surgical principles and maneuvers required for successful
management.
11
ized by pathological cellular proliferation, resulting from an aberrant wound-healing
11.1 Etiology
11.1.1 Cell Composition ofProliferative Vitreoretinopathy
PVR membranes are heterogeneous, consisting of various cell types that contribute
to membrane formation and contraction, including:
• Retinal glial cells: Primarily Müller cells, microglia, and astrocytes.
• Epithelial cells: Retinal pigment epithelial (RPE) cells and ciliary epithelial cells.
• Vitreous cells: Primarily hyalocytes.
• Inammatory/immune Cells: Macrophages, lymphocytes, and neutrophils.
© 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_11
231
232
11 Prevention andManagement ofProliferative Vitreoretinopathy
mesenchymal transition (EMT) or transdifferentiation into contractile myobroblasts, which drive the mechanical shortening of the membrane and subsequent
retinal traction.
11.1.1.1 RPE Cells
The transformation of RPE cells through EMT drives the development of
PVR.While normally quiescent, RPE cells are activated by the disruption of the
blood-retinal barrier during RRD.Cytokine exposure causes these cells to shed their
epithelial characteristics—such as tissue polarity and tight junctions—and transdifferentiate into mesenchymal cells. These newly formed cells are highly migratory,
resistant to apoptosis, and serve as the primary source of extracellular matrix (ECM)
production within PVR membranes.
11.1.1.2 Glial Cells
PVR is essentially an exaggerated wound-healing response to retinal injury, with
Müller cells serving as central mediators. Müller cell activation begins within 24
hours of retinal detachment. By day 3, these cells migrate into the subretinal space,
collaborating with RPE cells and immune cells (microglia/macrophages) to form subretinal proliferative strands.
Pathological changes include the downregulation of inwardly rectifying potassium
channels, triggering a loss of cell polarity and subsequent proliferation. The resulting
glial-neuronal unit dysfunction and Müller cell depolarization lead to neuronal degeneration and characteristic retinal thinning. Furthermore, activated Müller cells secrete
pro-inammatory cytokines that sustain a feedback loop of cellular migration and
extracellular matrix deposition, ultimately forming contractile PVR membranes.
During the progression of PVR, these precursor cells undergo epithelial-
11.1.1.3 Macrophages
Disruption of the blood-retinal barrier allows systemic macrophages to enter the
vitreous and subretinal spaces, where they secrete pro-inammatory cytokines and
regulate photoreceptor cell death. Experimental induction of PVR via intravitreal
rich, with the cells exhibiting broblastic transdifferentiation. Consequently, macrophages are increasingly recognized as critical initiators of the PVR cascade.
11.1.2 Regulation ofCell Proliferation andMigration
Blood-retinal barrier disruption allows hematic components to enter the vitreous
and subretinal spaces, fueling PVR via several mechanisms:
• Thrombin induces glial proliferation and RPE-to-mesenchymal transdifferentiation (EMT).
• Fibronectin acts as a chemoattractant for glial cells and mediates ECM.
• Plasmin upregulates the production of platelet-derived growth factor (PDGF).
macrophage injection conrms their role: the membranes formed are macrophage-
11.2 Clinical Classication andStaging ofPVR
Beyond blood-derived regulators, activated RPE and glial cells secrete a diverse
array of cytokines that drive PVR progression. These include platelet-derived
growth factor (PDGF), vascular endothelial growth factor (VEGF), epidermal
growth factor (EGF), transforming growth factor (TGF), basic broblast growth
factor (bFGF), colony-stimulating factor (CSF), insulin-like growth factor (IGF),
and monocyte chemoattractant protein-1 (MCP-1).
233
11.1.3 Extracellular Matrix Remodeling
Composed of proteins like collagen and bronectin, the extracellular matrix (ECM)
serves as a dynamic scaffold that regulates cell behavior through continuous feedback loops. Cells both respond to and remodel the ECM via protein secretion. In
PVR, this process becomes dysregulated, leading to a progressive increase in ECM
deposition. The brous contraction and maladaptive remodeling of the ECM are the
terminal pathological events that drive retinal traction in PVR.
11.1.4 Susceptibility Genes
While PVR lacks a mendelian inheritance pattern, genetic associations have been
established through case-control studies. Identied risk-associated genes are predominantly involved in cytokine regulation, cell cycle control, and programmed cell
death, highlighting the role of individual genetic backgrounds in PVR development.
11.2 Clinical Classification andStaging ofPVR
11.2.1 Clinical Manifestations
11.2.1.1 Characteristic Retinal Changes
The hallmark manifestations of PVR include retinal shortening, reduced elasticity,
full-thickness fold formation, and the development of broproliferative membranes.
These pathological changes progressively restrict retinal mobility, eventually culminating in retinal detachment with a wide-funnel or closed-funnel conguration.
Severe preoperative PVR not only complicates the primary surgical repair but also
signicantly elevates the risk of postoperative recurrence. Preoperative PVR is an
established anatomical state that cannot be reversed prior to surgical intervention.
Consequently, the surgeon’s focus must be on maximizing intraoperative reattachment and implementing strategies to mitigate postoperative proliferative responses.
Direct consequences of postoperative PVR include the following:
1. Reopening of primary retinal breaks (Fig.11.1)
2. Formation of new retinal breaks
3. Preretinal proliferative membranes (Fig.11.2)
4. Subretinal proliferative membranes or strands (Fig.11.3)
5. Retinal stiffness and shortening
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Fig. 11.1 Recurrent PVR under silicone oil tamponade resulting in the reopening of inferior primary breaks. The peribasal retina is characterized by marked stiffness and longitudinal shortening,
representing one of the most challenging manifestations of postoperative PVR.Several high-risk
factors contributed to this outcome: (1) young age (20 years), (2) the presence of two large, inferiorly located breaks, and (3) signicant vascular permeability accompanied by localized
microhemorrhages
11 Prevention andManagement ofProliferative Vitreoretinopathy
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Fig. 11.2 Epiretinal proliferative membrane following vitrectomy and silicone oil tamponade. (a)
Intraoperative visualization: A dense epiretinal proliferative membrane is shown, exerting signicant traction and causing marked vascular distortion. (b) Following complete removalof the proliferative membrane, the underlying macular is fully exposed and the tractional distortion is
relieved