Retinopathy of Prematurity: Current Diagnosis and Management

157 Pages·2017·4.465 MB·English

by  Andrés Kychenthal B., Paola Dorta S. (eds.)

Andrés Kychenthal B.
Paola Dorta S. Editors
Retinopathy
of Prematurity
Current Diagnosis
and Management
123
Retinopathy of Prematurity
Andrés Kychenthal B. Paola Dorta S.
(cid:129)
Editors
Retinopathy
of Prematurity
Current Diagnosis and Management
123
Editors
Andrés KychenthalB., MD PaolaDorta S.,MD, MHA
KYDOFT KYDOFT
Santiago Santiago
Chile Chile
ISBN978-3-319-52188-6 ISBN978-3-319-52190-9 (eBook)
DOI 10.1007/978-3-319-52190-9
LibraryofCongressControlNumber:2017934304
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Contents
1 Pathophysiology of ROP. . . . . . . . . . . . . . . . . . . . . . . . . . . 1
Mary Elizabeth Hartnett
2 Classification of ROP. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13
Thomas Lee
3 Retinopathy of Prematurity Screening—Current
and Future Considerations. . . . . . . . . . . . . . . . . . . . . . . . . 19
Clare M. Wilson, Anna L. Ells and Alistair R. Fielder
4 Optical Coherence Tomography and Wide-Field
Fluorescein Angiography in Retinopathy of Prematurity . . . 29
AdamL.Rothman,RamiroS.Maldonado,LejlaVajzovicand
Cynthia A. Toth
5 Remote Imaging and Smart Software
for ROP Screening. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43
Eric Nudleman and Michael T. Trese
6 Aggressive Posterior Retinopathy
of Prematurity (APROP) . . . . . . . . . . . . . . . . . . . . . . . . . . 49
Michael J. Shapiro, Michael P. Blair and
Jose Maria Garcia Gonzalez
7 Photocoagulation for Retinopathy of Prematurity . . . . . . . . 71
Paola Dorta S. and Andrés Kychenthal B.
8 Pharmacomodulation in the Treatment of Retinopathy
of Prematurity. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79
Khaled Tawansy, Anand Muthiah and Anika Muthiah
9 Management of Stage 4 ROP . . . . . . . . . . . . . . . . . . . . . . . 95
Andrés Kychenthal B. and Paola Dorta S.
10 Stage 5 Retinopathy of Prematurity . . . . . . . . . . . . . . . . . . 107
Eric Nudleman and Antonio Capone Jr
v
vi Contents
11 Complications of Retinopathy
of Prematurity Treatment. . . . . . . . . . . . . . . . . . . . . . . . . . 119
Wei-Chi Wu and Jane Z. Kuo
12 Differential Diagnosis of ROP. . . . . . . . . . . . . . . . . . . . . . . 129
George Caputo
13 Anesthesia for Preterms with Retinopathy
of Prematurity. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135
María Eliana Eberhard and Patricio A. Leyton
14 Neonatologist Perspectives on ROP. . . . . . . . . . . . . . . . . . . 139
Monica Morgues
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151
Contributors
Michael P. Blair MD Retina Consultants, LTD, Des Plaines, IL, USA
AntonioCapone,Jr.MDDepartmentofOpthalmology,AssociatedRetinal
Consultants, William Beaumont School of Medicine, Oakland University,
Royal Oak, MI, USA
George Caputo MD Department of Pediatric Ophthalmology, Rothschild
Ophthalmological Foundation, Paris, France
Paola Dorta S. MD, MHA Ophthalmology, KYDOFT Foundation, Santi-
ago, Chile
Anna L. Ells MD, FRSCS (C) Department of Surgery, University of Cal-
gary, Calgary, AB, Canada
María Eliana Eberhard MD Anesthesia and Pain Unit, Universidad Del
Desarollo, Clinica Alemana de Santiago, Santiago, Region Metropolitana,
Chile
Alistair R. Fielder FRCP, FRCOphth Optometry & Visual Science, City
University London, London, UK
Jose Maria Garcia Gonzalez MD Retina Consultants, LTD, Des Plaines,
IL, USA
Mary Elizabeth Hartnett MD Ophthalmology and Visual Sciences,
University of Utah/John A. Moran Eye Center, Salt Lake City, UT, USA
JaneZ.KuoMD,PhDDepartmentofOphthalmology,ShileyEyeInstitute,
University of California, San Diego, La Jolla, CA, USA
Andrés Kychenthal B. MD Ophthalmology, KYDOFT Foundation, Santi-
ago, Chile
Thomas Lee MD Ophthalmology Department, The Vision Center, Chil-
dren’s Hospital Los Angeles, Los Angeles, CA, USA
Patricio A. Leyton MD Anestesiología, Clínica Alemana de Santiago,
Santiago, Región Metropolitana, Chile
RamiroS.MaldonadoMDOphthalmology,DukeUniversity,Durham,NC,
USA
vii
viii Contributors
Monica Morgues Neonatologist Pediatric Department, Campus North,
Universidad de Chile/San José Hospital, Santiago, Chile
Anand Muthiah MBBS, MBA, MPH Claremont, CA, USA
Anika Muthiah MBBS Claremont, CA, USA
Eric Nudleman MD, PhD Department of Ophthalmology, Shiley Eye
Institute, University of California, San Diego, La Jolla, CA, USA
Adam L. Rothman BS Ophthalmology, Duke University, Durham, NC,
USA
Michael J. Shapiro MD Retina Consultants, LTD, Des Plaines, IL, USA
Khaled Tawansy MD Children’s Retina Institute, Pasadena, CA, USA
Cynthia A. Toth MD Ophthalmology and Biomedical Engineering, Duke
University, Durham, NC, USA
Michael T. Trese MD Eye Research Institute, Oakland University
Associated Retinal Consultants, Royal Oak, MI, USA
Lejla Vajzovic MD Ophthalmology, Duke University, Durham, NC, USA
Clare M. Wilson PhD, FRCOphth Ophthalmology, Chelsea and West-
minster, London, UK
Wei-Chi Wu MD, PhD Ophthalmology, Chang Gung Memorial Hospital,
Kweishan, Taoyuan, Taiwan
1
Pathophysiology of ROP
Mary Elizabeth Hartnett
Keywords
(cid:1) (cid:1) (cid:1)
Preterm Angiogenesis Retinopathy of prematurity (ROP) Vasopro-
(cid:1)
liferation Vascular endothelial growth factor (VEGF)
through angiogenesis from existing angioblasts
Retinal Vascular Development
or endothelial cells, based on animal models
[3, 4]. In addition, Müller cells [5, 6] and other
It is difficult to study human retinal vascular
neurons, such as ganglion cells [7] are also
development because vascularization occurs
important in retinal vascular development.
before term birth, and it is difficult to obtain
In human preterm birth, retinal vascular
quality human fetal tissue. Therefore, most
developmentisincomplete.Additionalaspectsof
studies of retinal vascular development are from
premature birth and the stresses surrounding it
newborn animals that vascularize their retinas
and the neonatal period, cause abnormal retinal
after term birth. However, there are differences
vasculardevelopment,manifestedfirstasdelayed
between species, and therefore it is important to
physiologic retinal vascular development, and
review studies that have been done in human
later with aberrant vasoproliferation into the vit-
eyes [1, 2].
reous instead of into the retina. These are the
Studiesinfetalhumantissueprovideevidence
refined phases of human ROP (Fig. 1.1) [8].
that the initial vasculature of the retina develops
in the posterior pole covering at least the region
of zone I through the process of vasculogenesis,
Term Versus Preterm Birth
or development of vessels from de novo pre-
cursors. The precursors migrate from the deep,
Tounderstandwhatgoeswronginretinopathyof
neuroblastic layers of the retina to the inner
prematurity (ROP), it is helpful to review some
surface and become angioblasts. The process
of the relevant and known events that occur in
begins at about 15-week gestation [2] and con-
normal versus preterm birth, including the roles
tinues until at least 22-week gestation, after
of oxygen and oxidative stress, and nutritional
which insufficient human data are available.
deficiencies, which have been linked to ROP.
After 22-week gestation, it is assumed that the
inner and deep retinal vascular plexi develop
Oxygen
M.E.Hartnett(&) Inutero,ithasbeenestimatedthatoxygentothe
OphthalmologyandVisualSciences,University developing fetus is about 30–40 mm Hg, so the
ofUtah/JohnA.MoranEyeCenter,65Mario
ambient environment after birth is relatively
CapecchiDr,SaltLakeCity,UT84132,USA
e-mail:[email protected] hyperoxic, particularly when supplemental
©SpringerInternationalPublishingAG2017 1
AndrésKychenthalB.andPaolaDortaS.(eds.),RetinopathyofPrematurity,
DOI10.1007/978-3-319-52190-9_1
2 M.E.Hartnett
Fig.1.1 Phasesofhuman
ROP.DrawingbyJames
Gilman,CRA,FOPS.From
ophthalmology,2015
Jan;122(1):200–10,
HartnettME,
pathophysiologyand
mechanismsofsevere
retinopathyofprematurity
oxygenisusedforresuscitation[9].Highoxygen human and not animal models associated with
atbirthhasbeenshowntocausevasoattenuation retinal detachment [13]. When oxygen level was
anddeathtonewlyformedendothelialcells,[10] reduced, RLF virtually disappeared [11], but at
creating areas of retina devoid of capillary sup- toolowanoxygenleveltherewasincreasedrisk
port. Human preterm infants in the US exposed of cerebral palsy and death [14]. Now, countries
to 100% oxygen prior to the technologic advan- thatlack resourcesfor prenatal andperioperative
ces for monitoring and regulating oxygen, care and oxygen regulation report ROP and
developed retrolental fibroplasia (RLF), now hyperoxia-induced vasoattenuation, documented
believed to be stage 5, the worst form of ROP by fluorescein angiography, in large and older
[11].Theappearanceofawhitepupilrepresented gestational aged infants than those in the US
a retrolental fibrovascular scar with an underly- [15].Advancementsinneonatalcareandoxygen
ingretinaldetachment.Whatactuallyoccurredin regulationandmonitoringhavepermittedinfants
thepreterminfantretinapriortothedevelopment of lower birth weights and younger gestational
of RLF was limited because the Schepens/ ages to survive. In countries implementing these
Pomerantzeff binocular indirect ophthalmoscope changes,ROPisseenininfantsofextremelylow
and other methods to observe the peripheral birthweight(<1000 g)andgestationalages(<28
retina had not been widely adopted [12]. There- wks), and the two-phase description of ROP has
fore, experimental approaches using newborn been refined to be delayed physiologic retinal
animals exposed to conditions similar to what vasculardevelopmentwithsomevasoattenuation
preterm infants then experienced were analyzed. in phase 1 and vasoproliferation in phase 2.
Fromearlyexperiments,itwashypothesizedthat
highoxygen-inducedcapillarylossandavascular
retina, and that removal from supplemental Oxygen Stresses and Oxidation
oxygen to ambient air, caused the avascular
retina tobecomehypoxicandrelease angiogenic The mechanisms whereby high oxygen affects
factors that led to aberrant angiogenesis and newlydevelopedcapillariesandendothelialcells
scarring [10]. These experiments also led to a are not completely understood. Although the
phased approach description of ROP: phase 1, sensitivityofendothelialcellsforoxygenlessens
representing vasoobliteration, phase 2, vasopro- with development, hyperoxia-induced endothe-
liferation and phase 3, a fibrovascular phase in lial cell damage has still been reported in adult