The document provides an overview of retinopathy of prematurity (ROP), including:
- ROP is abnormal retinal blood vessel development in premature infants that can lead to blindness if left untreated.
- Risk factors include very preterm birth and low birth weight.
- International classification system grades ROP by zone, stage, extent, and presence of "plus disease".
- Timely screening by an ophthalmologist using binocular indirect ophthalmoscopy is key to diagnosis.
- Treatment such as laser photocoagulation or cryotherapy aims to destroy undeveloped retina and prevent further progression when ROP reaches threshold or pre-threshold levels.
ROP current understanding and managementFarhadul Alam
Retinopathy of prematurity (ROP) is a vascular disease of the eye unique to preterm infants characterized by failure of retinal blood vessels to grow and develop normally. It results in severe visual impairment and blindness in newborns.
Retinopathy of prematurity (ROP), initially described as retrolental fibroplasia one of the leading cause of blindness in children.
Despite advances in diagnosis and treatment, as medicine and technology advances and premature infants are surviving at earlier gestational ages, ROP continues to be a significant problem.
ROP results in disorganized growth of retinal blood vessels, which may lead to scarring and retinal detachment.
ROP current understanding and managementFarhadul Alam
Retinopathy of prematurity (ROP) is a vascular disease of the eye unique to preterm infants characterized by failure of retinal blood vessels to grow and develop normally. It results in severe visual impairment and blindness in newborns.
Retinopathy of prematurity (ROP), initially described as retrolental fibroplasia one of the leading cause of blindness in children.
Despite advances in diagnosis and treatment, as medicine and technology advances and premature infants are surviving at earlier gestational ages, ROP continues to be a significant problem.
ROP results in disorganized growth of retinal blood vessels, which may lead to scarring and retinal detachment.
To understand ROP is very important so the newborns can be managed according to the stage efficiently and better visual rehabilitation can be offered to the patients and adequate knowledge can be given to the parents with counseling.
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
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
To understand ROP is very important so the newborns can be managed according to the stage efficiently and better visual rehabilitation can be offered to the patients and adequate knowledge can be given to the parents with counseling.
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
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
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
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Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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.
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The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
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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.
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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
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Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
1. Welcome to Seminar
Dr. Anindita Bose, FCPS student
Dr. Farah Naz Dola, Resident, year 2
Department of Neonatology
BSMMU
2. Case scenario
• Fatema, diagnosed as a case of Preterm (30 weeks) VLBW
(1420 gm), AGA, PNA, HIE (stage 2), Late onset neonatal
sepsis(Acinetobacter growth positive in blood culture),
BPD, Laryngomalacia.
• During NICU course baby was treated with O2 inhalation,
CPAP care, Mechanical ventilation, several antibiotics,
Blood transfusion for several times
3. • At 21 days of post natal age, ROP screening
was done which revealed APROP.
Ophthalmologist had advised to do Laser
photocoagulation.
5. Overview of presentation
• Introduction
• Incidence and historical background
• Embryology of retinal vessels
• Pathogenesis of ROP
• Risk factors
• International classification of ROP
• Diagnosis and Screening of ROP
• Treatment and Complication of treatment
• Prevention
• Prognosis
6. Introduction
• Retinopathy of prematurity is defined as a disorder
of the developing retinal vasculature resulting from
interruption of normal progression of newly forming
retinal vessels.
• Premature birth may result in abnormal retinal blood
vessels development, ROP, which may progress to
blindness or severe visual impairment.
7. • The ‘window’ for treatment is narrow , 1-2 weeks in
some cases. Failure to diagnose and treat ROP at the
right time can lead to permanent, bilateral, complete
blindness.
• ROP is the leading cause of childhood blindness
worldwide.
8. • A baby developing blindness in early days of life, can
never regain vision and will have no perception of
light of this colourful world. Therefore he or she has
to bear this lifetime visual disability as a long lasting
scar of premature birth.
9. History of ROP
• ROP was first described in 1942 by Terry.
• Association with oxygen use in newborn was
described by Patz in 1984.
• There were two epidemic of blindness in last century.
• First was in 4th and 5th decades and was caused by
the use of unrestricted oxygen.
• 2nd ‘epidemic’ of ROP emerged during the late 1970s
because of improved survival of very-low-birth
weight infants.
10. Incidence
• Related to gestational age and birth weight
• ROP rare in birth weight > 2000 grams.
• 70% ROP in birth weight<1250g & 7% develop threshold
ROP.
• Threshold ROP very rare in bw > 1250gm
• 95% ROP begins at 32-34 weeks GA.
• Threshold disease at 36 weeks.
• Incidence of ROP in West ranges from 21 to 65.8%
Ref: Mayet & Cockinos et al.Eye(London).2006(23)322-327.
Fielder AR et al.Natural history of retinopathy of prematurity: A prospective study.
Eye 1992;6:233-42.
11. Incidence of ROP in Bangladesh
• In Bangladesh preterm infants of gestational age <33 weeks
between December 1998–July 2003 had an incidence of 5.5%
(five babies) in 114 babies, all presenting at various stages.
• Another study assessed the presence of ROP and potential
risk factors other than supplementary oxygen in premature
infants ≤34 wks and or ≤1500g, and detected ROP in 40% of
cases (23 out of 58).
Ahmed ASMA, Muslima H, Anwar KS, Khan NZ, Chowdhury MAKA,Saha SK, Darmstadt GL.
Retinopathy of Prematurity in Bangladeshi Neonates. Journal of Tropical Pediatrics, Volume
54, Issue 5, 1 October 2008, Pages 333–339
Akter S,Hossain MM, Shirin M, Anwar KS. Retinopathy of Prematurity -
Neonatologists’Experience. J Bangladesh Coll Phys Surg 2013; 31: 181-
188,nov.2014.ISSN1015-0870.
12. • Between January 2013 and March 2017 over 2000 preterm
infants were screened.
• About a third of these babies had different stages of ROP.
• 40% of the babies had birth weight between 1500- 2000g and
38% had BW < 1500g.
• The mean gestational age of babies with ROP was 31.09 ±
2.28 weeks (range: 26-36 weeks) and mean birth weight was
1354.13 ± 266.38g (range: 700 -1900g).
Nahar, Nazmun & Adolore Badmus, Sarat & Kumer Das, Sanjoy & Malek, Mohammad &
Rahman, Mostafizur & Abdul Mahid Khan, Mohammad. (2018). Retinopathy of prematurity
in Bangladesh: an overview. Community eye health. 31. S25-S26.
13.
14. Some Data of ROP in NICU, BSMMU
• From January 2017 to December 2017, total
142 newborns were screened; among them 31
infants had ROP
• From august 2018 to march 2019, 92
newborns were screened and 22 infants had
ROP
15. Embryology of retinal blood vessels
• Retinal vascularization begins at
15 to 18 weeks’ gestation.
• Retinal blood vessels extend out
from the optic disc and grow
peripherally.
• Vascularization in the nasal
retina is complete at
approximately 32 – 34 weeks
and temporal retina by 40
weeks.
• Insulin-like growth factor-1 (IGF-
1) supports normal retinal
vascular growth and interacts
with VEGF under influence of
hypoxic state in utero.
18. International Classification for
Retinopathy of Prematurity (ICROP)
4 components:
Zone (1-3)
Stage (1-5)
Extent: refers to the circumferential location of
disease; reported as clock hours in the appropriate
zone (30° clock hours in a total of 12 clock hours of
30° each)
Plus disease (Plus disease is a primary factor in
treatment decision)and Pre-plus disease
19. International classification of ROP
The classification system consists of four components.
1. According to zone:
The retina is divided into three concentric circles or zones.
a. Zone 1: consists of an imaginary circle with the optic
nerve at the centre and a radius of twice the distance from
the optic nerve to the macula.
b. Zone 2: extends from the edge of zone 1 to the ora
serrata on the nasal side of the eye and approximately half
the distance to the ora serrata on the temporal side.
c. Zone 3: consists of the outer crescent shaped area
extending from zone 2 out to the ora serrata temporally.
21. 2. According to severity:
A. Stage I:
Thin white demarcation
line between vascularized
area of the retina and
avascular zone.
Classification of ROP (cont..)
22. B. Stage II:
The line develops into a
ridge and protruding into
vitreous.
Classification of ROP (cont..)
23. C. Stage III:
Extraretinal fibrovascular
proliferation occurs with
the ridge. Neovascular
tufts may be found just
posterior to the ridge.
Classification of ROP (cont..)
24. D. Stage IV:
Fibrosis and scarring
occur as the neo-
vascularization extends
into the vitreous.
Traction occurs on the
retina causing partial
retinal detachment.
Classification of ROP (cont..)
27. E. Stage V:
Complete retinal
detachment occurs.
Retina assumes a funnel
shaped appearance and
is described as either
open or closed in the
anterior and posterior
regions
Classification of ROP (cont..)
29. F. Plus disease:
It is an additional designation that refers to the
presence of vascular dilatation and tortuosity of the
posterior retinal vessels in at least two quadrant. This
indicates a more severe degree of ROP and may also
be associated with iris vascular engorgement, pupillary
rigidity and vitreous haze.
G. Pre plus disease:
Vascular abnormalities of the posterior pole that are
present but are insufficient for the diagnosis of plus
disease.
Classification of ROP (cont..)
30. Composite Categories of ROP
A. Aggressive posterior ROP ( AP-ROP)
B. Pre-threshold ROP
C. Threshold ROP
31. A. Aggressive posterior ROP ( AP-ROP):
This is rapidly progressive severe form of ROP
primarily in zone I, if untreated progresses rapidly to
stage 5 ROP. The characteristics features of this type
of ROP includes it’s posterior location, prominence
of plus disease, and the ill-defined nature of the
retinopathy.
This requires immediate treatment
32. B. Pre-threshold ROP:
Type 1 Pre threshold ROP includes:
1.In Zone 1: Any stage of ROP and plus disease or
stage 3 with or without plus disease
2.In Zone 2: Stage 2 or 3 ROP with plus disease
treatment at this stage showed significant benefit
Type 2 Pre threshold ROP includes:
1.In Zone 1: Stage 1 or 2 ROP, without plus disease
2.In Zone 2: Stage 3 ROP, without plus disease
close observation;
Treatment is needed if progresses to type 1 or
threshold ROP
33. C. Threshold ROP
• Stage 3 ROP with 5 or more contiguous clock hours or
8 cumulative clock hours with plus disease in either
zone 1 or 2
• ROP with 50% likelihood of progression to retinal
detachment if left untreated
• Risk of blindness reduced to 25% after treatment
Ref:James D et al,Evidence based screening criteria for ROP:Natural history data from
CRYO-ROP and LIGHT-ROP studies:Arch Ophthalmol.2002;120(11):1470-1476
34. Rush disease
• Occurs at neonates whose birth weight less than
1200 gm and those born at 24-30 weeks gestational
age.
• It develops earlier.
• More aggressive.
• Need to screen these smaller babies at the earliest
(Not later than 3 weeks).
Ref: Jalali S et al,Programme Planning and Screening Strategy in Retinopathy of Prematurity
Indian J Ophthalmol 2003;51:89-99
35. Diagnosis
• Timely and regular retinal examination (ROP
screening) is the key to diagnosis.
• Ophthalmologic examination by an expert examiner
usually confirms the diagnosis.
• Binocular indirect ophthalmoscopy (BIO) is generally
used.
36. •Newer digital camera
technology demonstrated 100%
sensitivity in detecting ROP
requiring treatment. But it does
not permit adequate
assessment of retinal periphery.
RetCam
38. Equipments used in Indirect Ophthalmoscopy
Speculum
Hand-held
condenser lens
Binocular indirect
ophthalmoscope
39.
40. ROP screening
In BSMMU:
Candidate
• Birth weight <2000 gm and/or gestation <35 weeks
• Birth weight ≥ 2000 gm or gestation > 35 weeks are
screened if they had an unstable neonatal period.
Timing
• At 4 weeks of postnatal age for infants born>30
weeks of gestation or birth weight ≥1200 gm
• At 3 weeks of postnatal age for infants < 30 weeks of
gestation or birth weight <1200 gm.
41. Frequency of screening
Zone of retinal findings Stage of retinal findings Follow up interval
Zone 1 Immature vascularization 1- 2 weeks
Stage 1 or 2 1 week or less
Regressing ROP 1- 2 weeks
Zone 2 Immature vascularization 2- 3 weeks
Stage 1 2 weeks
Stage 2 1- 2 weeks
Stage 3 1 week or less
Regressing ROP 1- 2 weeks
Zone 3 Stage 1 or 2 2- 3 weeks
Regressing ROP 2- 3 weeks
Mannan, M., Moni, S., & Shahidullah, M. (2015). Retinopathy of Prematurity (ROP):
Current Understanding and Management. Bangladesh Journal of Child Health, 38(3),
142-150.
42. Termination of Screening:
Criteria to stop further examination:
• Full retinal vascularization; this usually occurs at
about 40th weeks of postmenstrual age and mostly
completed by the 45th weeks.
• Regression of ROP noted
Mannan, M., Moni, S., & Shahidullah, M. (2015). Retinopathy of Prematurity (ROP):
Current Understanding and Management. Bangladesh Journal of Child Health, 38(3),
142-150.
43. Criteria for ROP screening in different
countries
Countries Gestational age Birth weight
United States ≤30 weeks <1500 gm
Or >30 weeks and an
unstable clinical course.
United Kingdom ≤31 weeks ≤1500 gm
Canada ≤30 weeks ≤1250 gm
India < 34-35 weeks. < 1500 gm
•Exposed to oxygen for
more than 30 days
• < 37 weeks and/or <
2000gms with risk factors
•Ref: Elizabeth H M et al ,Mechanisms and management of ROP. N Engl J Med
2012;367:2515-26.
•Ref: Jalali S et al,Programme Planning and Screening Strategy in Retinopathy of
Prematurity.Indian J Ophthalmol 2003;51:89-99
44. AIMS Protocol 2014
Which infants should be screened?
• Babies with birth weight <1500 g
• Babies born at <32 weeks of gestation
• Selected preterm infants with a birth weight
between 1500 and 2000 g or gestation of more than
32 weeks with eventful neonatal period
45. Treatment
• Treatment of ROP consists of destroying the portion of the
retina that is nonvascularized in order to preserve the rest
of it.
• The rationale for why this works is thought to be that the
avascular retina is a source of growth factors (VEGF and
other growth factors) that promote abnormal
neovascularization. When the avascular retina is destroyed,
the release of growth factors ceases, and neovascularization
involutes and regresses.
• Timely recognition of the disease is important because of
the short window of opportunity during which treatment is
effective.
46. Treatment
Indications of treatment:
• ROP in zone 1 retina that has reached stage 3 with
or without plus disease or eyes with any stage of
ROP with plus disease
• ROP in zone 2 that has reached stage 2 or 3 and is
accompanied by plus disease.
When treatment should be started:
Once a treatment decision has been made,
treatment should be performed within 48-72 hours
Ref: WilliamV G et al,Early treatment for ROP:A Randomized trial;Trans Am
Ophthalmol Soc.2004;102:233-250
47. Treatment modalities
• Laser photocoagulation
• Circumferential cryopexy.
• Anti-VEGF therapy
• Gene therapy
• Supplemental oxygen for pre-threshold ROP.
• Dietary supplement of omega-3 polyunsaturated
fatty acid (PUFA).
• Retinal reattachment
o Vitrectomy with or without lensectomy
o membrane peeling, if necessary
48. Laser
• Preferred initial
treatment
• Successful in infants
with severe ROP
• Can be performed with
local anaesthesia and
sedation, thus avoiding
the possible adverse
effects of general
anaesthesia
Cryotherapy
• Necessary in special
cases, e.g. when there
is poor pupillary
dialation or vitreous
hemorrhage
• Usually done under
general anaesthesia
• Causes more
inflammation and
requires more analgesia
than Laser therapy
49. Anti-VEGF Therapy
Indications:
Zone 1 ROP
AP-ROP
Salvage treatment after Laser therapy
In conjunction with vitroretinal surgery
Agents used:
Avastin (bevacizumab)
Macugen (pegaptanib sodium)
Lucentis (ranibizumab)
Aflibercept (VEGF Trap)
Route of administration:
Intravitreal injection
•Less stressful
•Procedure time is
short
•Only requires topical
anaesthesia
•Less destruction of
retina compared to
laser or cryotherapy
•Long term adverse
effects are less
Benefits:
50. Comparison between Anti-VEGF agents & Laser
photocoagulation
• Both laser photocoagulation and IVB injection are
effective modalities for the treatment of eyes with
zone II ROP;
• However, re-treatment may be required in some
cases after IVB injection.
• Also, re-injection of IVB is effective for persistent or
recurrent cases with ROP in zone II.
Roohipoor R, Torabi H, Karkhaneh R, Riazi-Eafahani M. Comparison of intravitreal
bevacizumab injection and laser photocoagulation for type 1 zone II retinopathy of
prematurity. J Curr Ophthalmol. 2018;31(1):61-65. Published 2018 Nov 9.
doi:10.1016/j.joco.2018.10.008
51.
52.
53. Outcome of treatment
• Treatment of acute ROP generally results in normal
or near normal anatomy of macula and posterior
retina.
• Treatment fails in small proportion of cases and
retinal detachment ensues.
• Prompt vitreoretinal surgery may be needed to
preserve vision.
• Severe visual impairment continue to occur in some
infants.
56. Prevention of complications
Laser therapy
Drug:
• Steroid eye drop
• Pupil dilating eye drop
Duration:
Continue for 1 week after
LASER therapy.
Anti VEGF therapy
Drug:
• Antibiotics eye drop
Duration:
For 1 week after giving
intra -vitreal injection
57. Prevention of ROP
Currently no proven methods are available to prevent ROP.
Care in NICU:
• Maintain SpO2 88 – 93 %
• Avoid fluctuation of SpO2 while on O2 supplementation.
• Keep Hemoglobin level not less than 10 gm/dl
• Ensure adequate weight gain.
Prophylactic vitamin- E therapy, administration of D-
penicillamine, and limited exposure to bright light have been
evaluated in multiple large clinical trials to prevent ROP but
none of these have shown clear benefit.
58. Prognosis
Bad Prognostic Factors:
• Posterior location (zone 1 or posterior zone 2)
• Presence of ROP on the first properly timed
examination
• Increasing severity of stage
• Circumferential involvement
• Presence of plus disease
• Rapid progression of disease
• Involvement of macula
• Detachment of retina
59. Short Term Prognosis
Spontaneous regression
• Stage-I and stage-II: 90%.
• Stage III+ disease : 50%.
• Any Zone 3 disease : Excellent prognosis for complete
recovery
• Pre-threshold ROP type 2: 77%
• Pre-threshold ROP type 1 : 32%
Progression to severe ROP
15% type 2 ROP progress to type 1
60. Long Term Prognosis
Retinal Dragging
and Folds
Others:
Acute angle closure glaucoma
Late onset Retinal Detachment( 22%)
Significant myopia (80%)
Anisometropia
Amblyopia
Astigmatism
Strabismus
61. Take Home Message
• Retinopathy of prematurity has become a leading but
preventable cause of childhood blindness worldwide.
• It occurs primarily in infants of low birth weight and low
gestational age at birth.
• Other than blindness, infants with ROP have higher risk for
developing certain eye problems later in life e.g. myopia,
strabismus, amblyopia, glaucoma.
• Some ocular complications can arise after treatment also.
• Timely screening is the key to early diagnosis and treatment.
• Timely intervention can preserve eyesight of many affected
infants
• Safety and efficacy of different treatment modalities are
being studied
• No preventive therapy has been proven effective yet