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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_6023_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Foreword 1
- •Foreword 2
- •Preface
- •Contents
- •Abbreviations
- •1.1.1 Pre-Jules Gonin Era
- •1.1.2 Post-Jules Gonin Era
- •2.3 Poiseuille Equation
- •1.6 Summary
- •2.1 Bernoulli’s Principle
- •2.4.1 Surface Tension
- •2.4.2 Interfacial Tension
- •2.5 Boyle’s Law
- •2.6 Fick’s Diffusion Law
- •2.7 Other Physical Principles
- •2.8 Summary
- •3.2.1 Density
- •3.2.2 Buoyancy
- •3.2.3 Interfacial Tension
- •3.2.4 Viscosity
- •3.3 Gases
- •3.3.2 Pneumatic Retinopexy
- •3.3.4 Gas Injection Techniques
- •3.3.6 Precautions After Intravitreal Gas Injection
- •3.4 Silicone Oil
- •3.4.2 Silicone Oil Usage Rate
- •3.5 Heavy Liquid
- •3.6 Summary
- •4.1 Doctor-Patient Interaction
- •4.3.1 Local Anesthesia
- •4.3.2 General Anesthesia
- •4.4 Summary
- •5.1.1 Instrument Diameter
- •5.1.2 Trocar-Cannula System
- •5.1.3 Vitrectomy Machine
- •5.2 Basic Steps
- •5.3.3 Posterior Vitreous Detachment (PVD)
- •5.4 Summary
- •6.3.2 Lincoff’s Rules
- •6.5.2 Subretinal Fluid Drainage
- •6.5.3 Scleral Encircling
- •6.6.1 Persistent Subretinal Fluid
- •6.6.2 Recurrent Retinal Detachment
- •6.6.3 Elevated Intraocular Pressure
- •6.6.4 Anterior Segment Ischemia
- •6.6.6 Extraocular Muscle Dysfunction
- •6.6.7 Refractive Changes
- •6.7 Summary
- •7.3.1 Cutting Central Vitreous
- •7.3.2 Confirming or Creating Posterior Vitreous Detachment
- •7.3.5 Removing Peripheral Vitreous
- •7.3.7 Sealing Retinal Breaks
- •7.3.9 Adjusting Intraocular Pressure
- •7.6.1 Pathological Basis
- •7.6.2 Surgical Principles
- •7.6.3 Surgical Strategies
- •7.9.1 360° Laser Encircling
- •7.9.2 Scleral Buckling
- •7.11 Summary
- •8.1.1 Retinal Proliferative Changes
- •8.1.2 Vitreous Status
- •8.5.1 Segmentation Technique
- •8.5.2 Delamination Technique
- •8.5.3 En Bloc Technique
- •8.6.1 Staining Agents
- •8.6.2 Tamponades
- •8.7.1 Corneal Edema
- •8.7.2 Lens Opacity
- •8.7.3 Pupillary Constriction
- •8.7.4 Iatrogenic Retinal Tears
- •8.7.5 Intraoperative Bleeding
- •8.8.1 Elevated Intraocular Pressure
- •8.8.3 Lens Opacity
- •8.8.5 Anterior Hyaloidal Fibrovascular Proliferation
- •8.8.6 Intraocular Fibrin Syndrome
- •8.8.7 Vitreous Hemorrhage
- •8.9 Summary
- •9.1 Clinical Characteristics
- •9.4.1 Surgical Timing
- •9.4.2 Prognostic Factors
- •9.5 Standard Surgical Steps
- •9.6.1 Triamcinolone Acetonide (TA)
- •9.6.2 Indocyanine Green (ICG)
- •9.6.3 Brilliant Blue G (BBG)
- •9.7.1 Preparation
- •9.7.2 Flap Initiation Methods
- •9.8 Complications
- •9.8.1 Intraoperative Complications
- •9.8.2 Postoperative Complications
- •9.9 Summary
- •10.2.1 Classification
- •10.4 Routine Surgical Procedures
- •10.5.1 Commonly Used Dyes
- •11.1.1.2 Glial Cells
- •11.1.1.3 Macrophages
- •11.1.3 Extracellular Matrix Remodeling
- •11.1.4 Susceptibility Genes
- •11.2.1 Clinical Manifestations
- •11.2.1.1 Characteristic Retinal Changes
- •10.6.2 Flap Initiation Techniques
- •10.6.4 ILM Flap Techniques
- •10.7 Complications
- •10.8 Summary
- •11.1 Etiology
- •11.1.1.1 RPE Cells
- •11.2.1.2 Anterior Segment Manifestations
- •11.2.2 Grading
- •11.4.2.2 Retinotomy
- •11.4.2.3 Retinectomy
- •11.4.3 Radial Retinotomy
- •11.5 Summary
- •12.2.2 Anti-VEGF Intraocular Injection
- •12.2.3 Retinal Laser Photocoagulation
- •12.2.4 Vitreoretinal Surgery
- •12.3.1 Overview
- •12.5 Summary
- •13.8 Showcase Your Art Works
- •13.9 Summary
- •15: Combined Phaco/Vitrectomy
- •15.1 The Surgery
- •15.2 Main Surgical Steps
- •15.3.2 Phacoemulsification
- •15.3.10 Fluid Against Air Exchange
- •15.3.13 Tamponade
- •15.3.14.1 Postoperative Posture
- •15.3.14.2 Complications
- •15.3.14.5 Fractionized PFCL Injection
- •15.3.15 FAQ
- •16.1 Surgery
- •16.2 Main Surgical Steps
- •16.4 FAQ
- •17: Easy Diabetic Retinopathy
- •17.1 Introduction
- •17.3 Vitrectomy
- •17.3.1 The Surgery Step-by-Step
- •17.3.2 Complications
- •17.4 FAQ
- •19.1 Introduction
- •19.3 The Surgery Step-by-Step
- •19.4.1 Encircling Band (cerclage)
- •19.4.3 Pars Plana Vitrectomy
- •19.4.5 Vitreous Base Shaving
- •19.4.6 Membrane Dissection
- •19.4.9 Retinotomy
- •19.4.11 Laser Photocoagulation
- •19.4.13 Tamponade
- •20: Difficult Proliferative Diabetic Retinopathy
- •20.1 Introduction
- •20.2 General Introduction
- •20.3.5 Hemostasis
- •20.3.9 Intravitreal Avastin
- •20.3.10 Internal Postoperative Tamponade
- •20.4 Complications
- •20.5 FAQ
- •Bibliography

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9.6 Use of Vital Dyes
203
Fig. 9.5 Negative staining technique for ERM visualization. (a) Thin ERM with unclear contour
even after TA injection, making ap initiation difcult. (b) After ICG injection, the ILM outside
the ERM is stained, while the ERM itself is not—revealing the ERM edge (white arrows). (c)
Successful ap initiation at the junction of the ILM and ERM using ILM forceps, with complete
ERM peeling. (d) Reinjection of ICG after ERM peeling showing stained ILM around the fovea
9.6.2 Indocyanine Green (ICG)
ICG specically binds to theILMand has a negligible staining effect on the ERM
itself. In ERM surgery, ICG is utilized for “negative staining” (Fig.9.5): by staining
the surrounding ILM, the non-stained ERM becomes clearly demarcated, outlining
its borders for safer initiation of the peeling process.
In addition to TA, ICG is the most widely available vital dye in ophthalmic clinical practice. Its high afnity ILMhas made it a preferred tool for many vitreoretinal
surgeons. While a standard concentration of 5 mg/mL provides robust ILM staining,
its potential retinal toxicity remains a subject of ongoing clinical debate. Four primary hypotheses have been proposed regarding ICG toxicity:

204
1. Osmotic imbalance: ICG may alter intraocular osmotic pressure, leading to cel-
lular stress.
2. Phototoxicity: Intense light from the endoilluminator ber optic may exacerbate
the toxicity of the staining solution.
3. Direct retinal damage: High-concentration ICG may exert a direct toxic effect
upon contact with the neurosensory retina.
4. Degradation products: ICG decomposes when exposed to light; its degradation
byproducts are potentially toxic to the retina and RPE.
9 Surgical Management ofEpiretinal Membrane
9.6.3 Brilliant Blue G (BBG)
BBG exhibits high afnity for the ILM and is typically utilized at a concentration of
0.25 mg/mL.Research consistently indicates that BBG possesses a superior intraocular safety prole compared to other dyes, leading to its U.S.FDA approval for
intraocular use in December 2019.
In ERM surgery, vital dyes (other than TA) should be utilized judiciously and are
generally reserved for cases where membrane planes are difcult to identify. When
their use is necessary, surgeons must strictly manage both the concentration and the
duration of exposure. To minimize the risk of phototoxicity, the endoilluminator
should be directed away from the macula or temporarily withdrawn during the
staining process. Furthermore, repeated dye injections should be avoided to prevent
cumulative retinal toxicity.
9.7 Underlying Logic andPractical Skills
ofMembrane Peeling
While many professional textbooks detail ERM peeling, the majority emphasize the
initial ap formation—indoubtedly the most critical phase of the procedure.
However, for novice surgeons, pre-peeling preparation is equally vital.As previously noted, an epiretinal membrane is a structural abnormality with measurable
elevation. To successfully leverage this physical characteristic, the surgeon must
rst clearly delineate the ERM margins. Establishing a distinct visual boundary
signicantly bolsters surgical condence and enhances hand stability during these
delicate intraoperative maneuvers.
9.7.1 Preparation
Before initiating the ap, the following conditions must be optimized:
1. Adequate anesthesia: Retrobulbar anesthesia should follow standard protocols,
including sufcient orbital compression to ensure a complete block. This

9.7 Underlying Logic andPractical Skills ofMembrane Peeling
205
minimizes patient anxiety and involuntary ocular movements, providing the
stable environment necessary for delicate membrane peeling.
2. Optimal trocar placement: Strategic placement is critical for ergonomic stability.
Hand movements during peeling are categorized into four components (Fig.9.6):
(a) Grasping: Force is generated by the thumb-index nger adduction.
(b) Vertical Control: Controlled by wrist exion and extension.
(c) Horizontal control: Controlled by wrist abduction and adduction.
(d) Rotational movement: Controlled by internal and external wrist rotation to
expand the peeling range.
The surgeon’s hand should rest gently on the patient’s forehead as a fulcrum,
with joints above the wrist relaxed. Positioning the primary trocar at 10
o’clock (for right-handed surgeons) allows for a neutral, extended wrist.
Deviation from this position forces compensatory wrist adjustments, which
signicantly reduces tip stability and increases the risk of “empty” or inaccurate grasping.
3. Optimizing visualization: Minimize anterior segment interference. In pseudo-
phakic eyes with posterior capsule opacication (PCO), consider preoperative
laser capsulotomy or an intraoperative clear zone creation with the vitrectomy
cutter to clear the visual axis (Fig.9.7a).
Furthermore, remember that excessively high brightness does not necessarily
enhance detail. Maintain illumination at a moderate level (e.g., 35%) and
avoid placing the endoilluminator tip too close to the macula. This prevents
‘overexposure,’ which obscures membrane texture, induces surgeon eye
fatigue, and increases the risk of phototoxicity (Fig. 9.7b).
4. Ergonomic and psychological relaxation: Sympathetic activation due to ner-
vousness leads to muscle tension and tremors. Excessive effort to resolve macu-
lar details often leads to accommodative fatigue, shifting the focal plane
anteriorly and blurring the view. For less experienced surgeons, this loss of clar-
ity can cause undue stress and hinder the ow of the procedure.
If tension arises, surgeons should: (1) Pause the procedure briey to break the
stress cycle; (2) Regulate breathing with deep, slow respirations; (3) Relax
the posture by lowering the shoulders and momentarily looking away to ease
eye strain; (4) Communicate briey with the surgical team to help diffuse
situational stress.

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9 Surgical Management ofEpiretinal Membrane
ab
cd
Fig. 9.6 Schematic of hand kinematics and intraocular forceps manipulation. (a) Grasping mech-
anism: Adduction of the rst metacarpophalangeal (thumb-index) joint controls the opening and
closing of the forceps tips. (b) Vertical positioning: Flexion and extension of the wrist regulate the
vertical (anterior-posterior) depth of the forceps within the vitreous cavity. (c) Horizontal positioning: Abduction and adduction (radial and ulnar deviation) of the wrist control the horizontal (lateral) placement of the forceps. (d) Rotational control: Internal and external rotation (pronation and
supination) of the wrist enables rotational maneuvering of the forceps, typically utilized for continuous curvilinear membrane peeling

9.7 Underlying Logic andPractical Skills ofMembrane Peeling
207
a b
Fig. 9.7 Optimization of illumination and visualization for ERM peeling. (a) Clearing the visual
axis: Intraoperative creation of a central opening in an opacied posterior capsule using a vitrectomy cutter to ensure an unobstructed view of the posterior pole. (b) Suboptimal illumination: The
endoilluminator tip is positioned too close to the macula, resulting in “overexposure” (glare). This
obscures ne membrane architecture while increasing the risk of surgeon eye fatigue and retinal
phototoxicity
9.7.2 Flap Initiation Methods
The following techniques are essential for safe and effective ap initiation.
Regardless of the chosen method, novice surgeons must prioritize safety: it is far
better to “grasp thin air” (miss) than to “grasp incorrectly” (traumatize the retina).
1. Strict svoidance of high-risk zones: Flap initiation should always be performed
away from retinal blood vessels. Furthermore, avoid the papillomacular bundle
located between the fovea and the optic disc; injury to this area can lead to irre-
versible central vision loss.
2. Target the steepest margin: Selecting a “steep” or elevated ERM edge provides a
more accessible target for forceps. This elevation increases the safety margin
between the forceps tips and the underlying neurosensory retina (Fig. 9.8),
reducing the risk of accidental retinal engagement.
3. Recognizing and halting inadvertent retinal grasping: Inadvertent retinal grasp-
ing is a risk even for experienced surgeons. Identifying this error depends on
tactile feedback: the adhesion between an idiopathic ERM and the retina is typi-
cally much weaker than the attachment between the retina and the RPE.If the
forceps encounter a “stiff or resistant” sensation, the surgeon must immediately
release the grip to prevent a retinal tear.
4. Avoiding sites of high adhesion: In areas where the ERM is rmly incarcerated
into the retinal surface, forceful peeling can compromise retinal integrity.
Indicators of excessive traction include the presence of retinal fragments on the
peeled membrane or localized retinal whitening (pallor). If signicant resistance
is met, the surgeon should seek an alternative, less adherent initiation site.

208
ab
9 Surgical Management ofEpiretinal Membrane
c
d
Fig. 9.8 Preoperative planning and selection of safe sites for ERM ap initiation. (a) Photograph
suggesting a steep ERM edge approximately two-disc diameters temporal to the fovea (white
arrows). (b) Multicolor fundus imaging conrming this observation. (c) iOCT verifying the predicted edge as an ideal ap initiation site, showing a steep ERM edge. (d) Successful ERM grasping, with iOCT conrming no residual ERM

9.8 Complications
209
9.7.3 Expanding theFlap
Once a ap is successfully initiated, the expansion phase is generally straightforward and carries a lower risk of iatrogenic retinal damage. For novice surgeons, the
primary objective is to maintain continuous controlled movement, thereby minimizing the need for repeated re-grasping and additional ap initiations. During this
process, precise wrist kinematics remain critical.
Expanding the ap relies predominantly on wrist extension and rotation, complemented by subtle radial or ulnar deviation (abduction/adduction) to modulate the
trajectory. After engaging the ERM margin, the surgeon should translate the forceps
in a plane tangential to the retinal surface. By avoiding vertical traction, the force is
directed specically toward the ERM–retinal interface, effectively lysing adhesions
while minimizing mechanical stress on the underlying neurosensory retina.
9.7.4 Deciding Whether toPeel theILM
ILMpeeling is not always mandatory; often, portions of the ILM are sequestered
and removed concurrently during ERM peeling. Whether routine ILM peeling
should be performed remains a subject of ongoing clinical debate.
The potential benets of ILM peeling include the complete removal of the scaffold for myobroblast proliferation, which may reduce the rate of ERM recurrence.
Conversely, the potential drawbacks include mechanical trauma to the supercial
retinal nerve ber layer (RNFL) and structural disruption of the Müller cell
footplates.
Novice surgeons should not feel compelled to perform ILM peeling in every
case. The guiding principle is pragmatic: if a vital dye has been utilized and the
stained ILM is clearly visible, one may attempt to peel the identied areas. However,
if no stain was used and the clinical outcome appears satisfactory, it is wise to follow the adage, “If it isn’t broken, don’t x it.” Avoid performing additional, potentially redundant maneuvers that require extra staining and surgical time unless
clinically indicated.
9.8 Complications
9.8.1 Intraoperative Complications
(1) Hemorrhage
Unless major retinal vessels are compromised, intraoperative hemorrhage is typically punctate and self-limiting, requiring no specic intervention. Surgeons should
avoid direct manipulation of the bleeding site with a ute needle or vitrectomy cutter, as mechanical irritation can exacerbate the hemorrhage and expand the area of
involvement.

210
9 Surgical Management ofEpiretinal Membrane
In rare instances of deep retinal or vascular trauma leading to signicant vitreous
hemorrhage, the surgeon should allow the clot to partially consolidate before
attempting aspiration with a ute needle or vitrectomy cutter. Once the bleeding
point is localized, hemostasis should be achieved via endophotocoagulation or cautery. Excessive energy or conuent laser applications must be avoided to minimize
the risk of permanent visual eld defects.
(2) Iatrogenic Retinal Breaks
The incidence of iatrogenic retinal breaks during ERM surgery is low, with most
occurring during peripheral vitrectomy. These are manageable if identied early:
the break should be surrounded by laser photocoagulation, followed by a ltered air
or inert gas tamponade. Postoperative positioning should be dictated by the location
of the break to ensure adequate internal tamponade.
(3) Lens Injury
Iatrogenic lens trauma during PPV is a known risk during the learning curve. While
mild, peripheral lens touch may not impede the current procedure, severe injury
requires primary intervention.
For signicant lens damage, phacoemulsication is preferred over lensectomy to
preserve the capsular bag, which is essential for stable intraocular lens (IOL)
implantation. If secondary cataract surgery is deferred, the patient must be informed
that lens opacity will progress rapidly. Regular B-scan ultrasonography is mandatory to monitor the posterior segment until the cataract is removed.
During subsequent cataract surgery in vitrectomized eyes, surgeons must account
for reduced vitreous support. Maintaining anterior chamber stability and ensuring a
meticulous capsulorrhexis and gentle hydrodissection are critical. Should the lens
nucleus displace into the vitreous cavity, a repeat PPVis necessary for retrieval.
9.8.2 Postoperative Complications
(1) Cataract Progression
Cataract development is the most frequent postoperative complication of ERM surgery. Patients often report transient visual improvement followed by a gradual
decline in acuity. This is primarily due to nuclear sclerosis, which signicantly
impacts vision and necessitates subsequent cataract surgery. Consequently, combined phacovitrectomy (simultaneous lens extraction and vitrectomy) is increasingly performed. However, for novice surgeons, the added complexity of a combined
procedure increases intraoperative risk and is generally not recommended during
the learning curve.
(2) Retinal Detachment
Although rare, postoperative retinal detachment (RD) can progress rapidly and
cause severe visual loss; thus, meticulous prevention is paramount. The three primary etiologies include:

9.9 Summary
Fig. 9.9 Superior nasal
retinal dialysis (white
arrow) secondary to ERM
surgery
211
1. Entry-site related breaks: Iatrogenic tears may occur if instrument tips inadver-
tently traumatize the peripheral retina during insertion through the trocars.
2. Undetected peripheral pathology: Inadequate 360° scleral indentation may lead
to overlooked retinal breaks or pre-existing degenerative lesions.
3. Vitreous traction: Residual vitreous may become incarcerated in the scleral inci-
sions or undergo contraction, leading to secondary retinal breaks (Fig. 9.9).
Notably, the incidence of this complication has signicantly decreased with the
widespread adoption of small-gauge minimally invasive vitrectomy.
(3) ERM Recurrence
The long-term recurrence rate for epiretinal membrane is reported to be less than
20%. In most instances, recurrent ERM does not substantially impair visual acuity,
and surgical re-intervention is typically not indicated. However, in cases of secondary ERM, the risk of recurrence may rise signicantly if the underlying primary
pathology—such as intraocular inammation or vascular disease—remains poorly
controlled.
9.9 Summary
ERMsurgery is generally straightforward with a favorable prognosis, this high success rate often engenders elevated patient expectations—rendering surgical safety
the paramount priority. Novice surgeons should adopt a deliberate approach to clinical practice, meticulously rening their maneuvers to develop techniques tailored to
their individual skill sets. When encountering intraoperative challenges during
membrane peeling, it is vital to adhere to the principle advocated by Steve Charles:
“Be patient, be persistent, slow is better.” As the saying goes, “The shortest way is
often the most reliable one,”reminding us that precision should never be sacriced
for speed.

Surgical Intervention oftheMacular
Hole
A macular hole (MH) is a lamellar or full-thickness defect of the neurosensory retina at the fovea. It predominantly affects individuals over the age of 50, with a
higher prevalence in women and a bilateral incidence ranging from 20% to 30%.
The primary clinical manifestations include diminished visual acuity, metamorphopsia, and central scotomata. Optical coherence tomography (OCT) has become
the gold standard for diagnosing MH, providing precise imaging data essential for
understanding its pathogenesis and evaluating surgical prognosis.
While surgical intervention for MHhas existed for only three decades, high success rates have driven vitreoretinal surgeons to continuously rene techniques, signicantly advancing the surgical paradigm. Notably, MH surgery is unique among
vitreoretinal procedures as it is perhaps the only intervention capable of facilitating
the anatomical restoration of a neurosensory tissue defect. Consequently, surgical
management must prioritize the preservation of healthy retinal tissue. The ultimate
goal is to achieve closure with minimal trauma, ensuring the restored macula can
effectively perceive and transmit light—a fundamental principle for every vitreoretinal surgeon.
10
10.1 How Macular Hole Became aCurable Disease: Lessons
forSurgeons
In 1869, the German-American ophthalmologist Hermann Knapp rst reported a
case of traumatic MH.Notably, he also founded the journal in which this case was
published—Archives of Ophthalmology (now JAMA Ophthalmology)—that same
year. In 1871, Henry Noyes, a NewYork-based physician, provided the rst comprehensive clinical description of traumatic MH.The term “hole at the macula” was
later coined in 1900 by the British surgeon F.M.Ogilvie. While MH was initially
categorized as a degenerative condition, subsequent research identied vitreomacular traction as its primary etiologic factor. Donald Gass further advanced the eld
© 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_10
213
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