This document provides an overview of proliferative vitreoretinopathy (PVR). It defines PVR as a fibrotic wound healing response involving proliferation of cells that can cause retinal traction and detachment. The pathophysiology involves epithelial-mesenchymal transition of retinal pigment epithelium cells and proliferation of glial cells, which secrete extracellular matrix proteins. Growth factors and cytokines promote proliferation and contraction of fibrocellular membranes. Risk factors include retinal detachment, inflammation, and previous vitreoretinal surgery. Early diagnosis and timely surgery aiming to relieve traction and reattach the retina are important for treatment.
This lecture is part of the yearly Basic Course Lectures in Ophthalmology given by the Dept of Ophthalmology and Visual Sciences at the Philippine General Hospital.
Originally given by Dr Pearl Tamesis-Villalon, it is a 1:30:00 hour lecture on the pathologic lesions seen in the vitreous, retina and choroid. It is meant for the general physician and the beginning ophthalmology resident who is interested in the basics of retinal pathology.
It includes pathologic changes seen in hypertension, diabetes, vaso occlusive disease, vitreous, membranes, choroid, retinal pigment epithelium, retinal detachments, etc. Lesions such as hemorrhages, cotton wool spots, hard exudates and their location in the retinal layers are explained. Fluorescein angiogram and OCT images are also incorporated.
Some images were grabbed from the internet, apologies for not making the necessary acknowledgements.
This is a beginner's guide to retinoblastoma. I have briefly covered all the aspects of this most common intraocular tumor of childhood. Hope it will help the undergraduate medical students. Please check out our blog, http://pgblaster.wordpress.com for more presentations and useful stuffs like this one.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
2. WHAT IS PVR?
Definition:
The clinical syndrome associated with retinal traction and
detachment in which cells with proliferative potential multiply
and contract on retinal surfaces and in the vitreous
compartment.
3. • Vitreoretinal wound-healing response
• Nonangiogenic and fibrotic
• Seen in:
• Rhegmatogenous Retinal Detachment (RRD)
• Surgical intervention (most common scenario)
• Trauma
• Longstanding inflammation
4. • Incidence: 5-10% of all RRD
• Higher incidence, rapid and aggressive in children
• Most common cause of failure of RRD surgeries
5. PATHOPHYSIOLOGY
The prerequisites:
• Intravitreal dispersion of RPE cells or
• Breakdown of Blood-Retinal barrier (BRB)
Important factors:
• Size of breaks
• Extent of RD
• Preoperative inflammation or PVR
6. The sequence of overlapping phases (4-8 weeks)
1. Inflammation
2. Cellular proliferation
3. Extracellular matrix remodelling
7. Cellular basis of PVR:
Interplay between cytokines/growth factors, matrix proteins and different cell
types undesirable preretinal membranes
Composition of membranes:
• Retinal glial cells (Muller cells, microglia cells and astrocytes)
• RPE and Ciliary body epithelial cells
• Hyalocytes
• Blood borne immune cells
• Fibrocytes and myofibrocytes
8. THE CELL CYCLE
• G0 phase:
• Resting phase of the cell cycle
• Interphase:
• Gap1, Synthesis and Gap2
phases
• Cell prepares itself for the cell
division
• Mitosis
9. RPE Cells:
• Major cell type involved
• Epithelial Mesenchymal Transition (EMT): The RPE cells
transdifferentiate morphologically into mesenchymal cells and
fibroblast-like phenotypes.
10.
11. Pathogenetic steps:
EMT Proliferation and
directional migration
Fibrocellular membranes in
vitreous and both retinal
surfaces
12. RRD cause cytokines to leak in subretinal space
RPE cells stimulated, lose cell-cell adhesion
Undergo EMT
Proliferation and migration
(in the vitreous cavity and detached retina)
13. Glial Cells (Muller cells, microglia and fibrous astrocytes):
• Physiology
• Support neuronal activity
• Integrity of BRB
• Ionic and osmotic homeostasis
• Reactive gliosis: Cellular hypertrophy and upregulation of vimentin
filaments
• Begins within minutes of RD, proceeds as long as retina is detached.
• Muller cells proliferate, migrate out and be a part of fibroproliferative
membrane.
• Provide focal attachment between membrane and retina.
14. Reactive Gliosis
• Glial cells replace the dying neuronal and degenerated axons
with glial scars
• Mechanical obstruction for regenerative axon growth
Thus a limiting factor for vision recovery post surgery.
15. Proliferation of Muller cells
Downregulation of Potassium channels
• Depolarisation causes reentry into proliferation cycle
• Impairment of regular glial-neuronal interactions
16. Blood borne cells:
• Macrophages and circulating fibrocytes are precursors of
myofibroblasts
• Hyalocytes have a role in synthesis of ECM and modulation of
inflammation.
• Hyalocytes also have contractile properties
18. ECM Remodelling and Myofibroblasts:
• ECM – A dynamic, complex array of collagens, glycoproteins, GAGs
and proteoglycans
• Functions:
• Mechanical and structural support
• Interacts with cytokines and cytoskeleton – transmits biological signals.
• Re-modelling is a healing response detrimental to the retinal
function.
19. HOW REMODELLING HAPPENS
1. Structural proteins
2. Adhesive proteins
3. Antiadhesive proteins
Structural Proteins:
• Collagens of various types.
• Produced by RPE cells, glial cells and fibroblast-like cells
20. Adhesion protein:
• Fibronectin, expression is low in normal retina.
• Promotes adhesion amongst ECM cells.
• Also enhances EMT of RPE cells.
Antiadhesive protein:
• Thrombospondin functions contrary to Fibronectin
• Facilitate the detachment of activated RPE cells and migrate to wounded
areas.
21. The loss of Balance:
• Normally, MMPs and Tissue Inhibitor of MMP (TIMPs) function in
balance.
• In pathology, RPE cells, glial cells and fibroblasts overproduce
MMP-2 and MMP-9.
22. Myofibroblasts:
• Characterized by smooth-muscle actin and generate Tractional
force by contraction
• Transmembrane integrins at the myofibroblast surface link
actin microfilaments
• Cytokines, PDGF, IGF and TNF-B mediate the ECM contraction.
23. BIOMARKERS AND GENETIC PROFILING
• MMP concentration in vitreous is raised
• Chemokine CXCL-1 correlates with the grade of PVR
• Inflammation associated proteins:
• Alpha 1-Antitrypsin
• Apolipoprotein A-IV
• Transferrin
• Kininogen-1 – Serum biomarker of PVR
• Laser flare photometry – Risk estimation for PVR development.
• Genetic association – TNF locus and PVR
24. RISK FACTORS FOR PVR
• Trauma to the eye
• Vitreous Hemorrhage with retinal tears
• Previous eye surgery
• RD with more than two quadrants
• RD associated with Choroidal Detachment
26. PREDICTION OF PVR
• Asaria et al presented a formula based on risk factors
Preoperative Grade B PVR 1.85+
Preoperative Grade C PVR 2.88+
Aphakia 2.92+
Each quadrant of RD 1.23+
Anterior Uveitis 1.77+
Vitreous Haemorrhage 0.83+
Previous Cryotherapy 1.23+
Score of >6.33+ is a high risk for PDR
27. HOW TO DIAGNOSE PVR?
Early Signs:
• Very subtle
• Cellular dispersion in vitreous
and on retina
• Localised fibrocellular
membranes – White
opacification and small wrinkles
or folds
28. • Rolled posterior edges of
tears
• Extensive PVR:
• Fixed folds, mainly inferiorly.
• Fine membranes bridging the
valleys of detached retina
• Decreased motility
29. • Advanced PVR with PVD:
Funnel-shaped RD with
contracted equatorial
membrane.
• Anterior traction at vitreous
base: Draws retina towards
Ciliary body or detaches the
ora serrata.
30. • Preoperative identification of PVR may result in modification of
surgical techniques
• Recognition of PVR post-operatively:
• At 4-12 weeks after surgery
• Allows timely intervention and avoid substantial visual loss
31. CLASSIFICATION OF PVR
• Classifying PVR allows:
• Cross-comparison of severity of a disease
• Assessment of effects of various therapies in clinical trials
• No classification of PVR is without flaws
• Most commonly used classification system: Retina Society PVR
Classification – 1983 AD.
32. Retina Society PVR Classification:
Classifies on basis of:
• Clinical Signs
• Geographical Distributions
Grade
(stage)
Characteristics
A Vitreous haze, vitreous pigment clumps
B Wrinkling of the inner retinal surface,
rolled
edge of retinal break, retinal stiffness,
vessel
Tortuosity
C Full-thickness retinal folds in
C-1 One quadrant
C-2 Two quadrants
C-3 Three quadrants
D Fixed retinal folds in four quadrants
D-1 Wide funnel shape
D-2 Narrow funnel shape (anterior end of
funnel visible by indirect ophthalmoscopy
with 20 diopter lens)
D-3 Closed funnel (optic nerve not visible)
37. Drawbacks:
• Ignores antero-posterior epiretinal proliferation and hence
anterior traction.
• Ignores degree of cellular proliferative activity at the time of
grading.
• Inactive Grade D may have a better prognosis than a very active Grade C
PVR
38. Revised Classification of PVR
(1991)
• Includes location, extent and
severity of PVR
• More useful, mainly for
clinical trials
Grade Features
A Vitreous haze, vitreous pigment
clumps, pigment clusters on inferior
retina
B Wrinkling of the inner retinal surface,
retinal
stiffness, vessel tortuosity, rolled and
irregular edge of retinal break,
decreased mobility of vitreous
CP 1-12 Posterior to equator, focal, diffuse or
circumferential full-thickness folds,
subretinal Strands
CA 1-
12
Anterior to equator, focal, diffuse, or
circumferential full-thickness folds,
subretinal strands, anterior
displacement, condensed vitreous
39. Type Location (in
relation to
equator)
Features
Focal Posterior Star fold posterior to vitreous base
Diffuse Posterior Confluent star folds posterior to vitreous base; optic
disc may not be visible
Subretinal Posterior/Anteri
or
Proliferation under the retina; annular strand near
disc; linear strands; motheaten-appearing Sheets,
Napkin ring around disc
Circumferent
ial
Anterior Contraction along posterior edge of vitreous base
with central displacement of the retina; peripheral
retina stretched; posterior retina in radial folds
Anterior Anterior Vitreous base pulled anteriorly by proliferative tissue;
peripheral retinal trough; displacement ciliary
processes may be stretched, may be covered by
40. CAN PVR BE PREVENTED?
• Most eyes with PVR will have undergone some treatment for RD, 1-3 months ago
• PVR develops almost regardless of the technique of surgery used.
• Identify the eyes at risk and keep a close watch
• Intraoperative complications:
• Choroidal haemorrhage
• Retained vitreous haemorrhage
• Intense photocoagulation
• Heavy cryotherapy
Laser may be preferred over cryotherapy.
41. PVR in eyes with no intervention yet:
• At early subtle stages – Vitrectomy to prevent the progression
to the full syndrome
• Better to combine scleral buckling with vitrectomy rather than
treating with either of them.
• Longer acting vitreous substitutes should be preferred.
42. SURGERY FOR PVR
• Timely surgery is of utmost importance in cases with PVR
• Urgent if macula is attached and vision salvageable
• Aim of surgery:
• Close any open retinal breaks
• Permanently support the retina and relieve the tractions
• Should be achieved without causing prolonged inflammation or
cellular access to the retinal surface.
43. SCLERAL BUCKLING – FUNDAMENTAL
REQUIREMENT
• Inferior vitreous base
becomes fibrocellular
• Contracts even after a formal
vitrectomy
• Virtually impossible to
remove complete vitreous
base
44. HOW BUCKLE HELPS?
• Supports vitreous base against the traction
• Prevents leakage from new or small missed retinal breaks in
periphery
• Inactive PVR may not need a vitrectomy.
• For chorioretinal adhesion, laser is better but cannot be used in
a residual SRF.
45. VITRECTOMY
• Meticulous vitrectomy and Silicone oil (SO) tamponade has been reported
comparable to combined procedure
• Vitrectomy is essential for removal of cellular and inflammatory material and
fibroblastic membranes
• Efficiency in surgery due to advances in technology.
• Better view
• Faster core vitrectomy
• Safer cutting and aspiration near retinal surface
46.
47. • Use of Perfluorocarbon (PFCL) fluid:
• Displaces SRF anteriorly
• Flattens posterior retina
• Highlights membranes
• Stabilizes the retina
• Relaxing retinotomy may be resorted to if needed.
• Persistent retinal elevation after fluid-air exchange indicates presence of
traction.
48.
49.
50. Subretinal bands:
• Seen with longstanding PVR
• Cause tenting of retina
• Prevent retinal reattachment
• Removed through a
retinotomy.
51. Fluid-air exchange:
• Done to achieve totally flat
retina
• With or without the aid of PFCL
• Carefully aspirate the egressing
SRF
• Avoid spreading the mobilized
pigment cells on retinal surface
• Persistent retinal elevation
indicates traction
52. Role of Silicone Oil:
• Less postoperative inflammation
• Quicker rehabilitation
• Fewer reoperations
• Heavy SO gives better inferior tamponade
53. Silicone oil removal:
• Wound-healing sequence of PVR takes around 3 months, hence
SO should be kept in-situ for 3 months
• Delayed removal of up to 18 months – No improvement in
functional outcomes
54. COMPLICATIONS OF SURGERY
• Possibility of substantial vision loss despite anatomical success
• Intraoperative bleeding while dissecting membranes and retinotomy
• Regrowth of membranes (Perisilicone proliferation) and recurrent
detachment (33-50%).
• Commonest: Inferior RD with a new or reopened retinal break
• Reoperate: If fluid extends towards posterior pole and threatens
macula.
• Macular pucker (5-15%): Peeled if significant visual potential
55. • Retinotomy and retinectomy edges may fibrose and retract
back to posterior pole
56. • Hypotony due to interference with Ciliary body secretory
function
• Rubeosis iridis: Recurrent persisting RD with intraocular
inflammation
57. MEDICAL ADJUNCTIVE THERAPY
• Systemic Prednisolone, subtenon’s injection of Triamcinolone to
control inflammation
• Beneficial dose persists after intraoperative use of Triamcinolone
• Studies on PDGF and Connective Tissue Growth Factor (CTGF) are in
preliminary stages.
• Antineoplastic drugs:
• 5-FU and Daunorubicin have been studied, less success and fear of potential
toxicity to normal neuronal cells
58. RESULTS OF SURGERY
• Anatomical success: Retinal reattachment for at least 6 months.
• Earlier, Scleral buckling reattached 50% of milder cases
• With all the techniques at disposal, 90% cases are anatomically
reattached
• Many eyes need more than one surgery due to cellular
proliferation and retinal traction
• 360 degree extensive laser and long term SO may improve
success rates
59. • Functional success: Any improvement in vision.
• Macula detached for more than a few days: Unlikely to recover more than 10-20%
Stable visual results:
• Reattachment attained for 6 years after surgery
• Eyes who needed only one surgery
No significant difference was seen in reattachment rates and visual acuity gain with C3F8
and SO, at 6 years follow-up.
60. Dilemma of SO removal:
• Settled eyes were likely to gain >/= 3 lines with improvement
in quality of vision
• 19% eyes developed recurrent RD (twice that of eyes where SO
was not removed)
61. WHEN NOT TO OPERATE?
Second eye has good vision and no disease, and the affected eye has
• Chronic RD and no hope of macular redemption
• Extensive Intraretinal gliosis
• Inferior retinal shortening with posterior retinal breaks
• Failure after SO injection
If second eye is lost already and affected eye has poor prognosis,
surgery may still be attempted for ambulatory vision
62. Decision-making is still flexible and depends a lot on:
• Patients and relative having thorough understanding of
expectations and possible outcomes
• Prudence of the surgeon after considering factors involved for
each patient.