Atlas of RetinalDetachment

123

Diagnosis andDi� erential Diagnosis

Wenbin WeiEditor

Atlas of Retinal Detachment

Wenbin WeiEditor

Atlas of Retinal DetachmentDiagnosis and Differential Diagnosis

EditorWenbin WeiBeijing Tongren Eye CenterBeijing Tongren Hospital, Capital Medical UniversityBeijingChina

ISBN 978-981-10-8230-6 ISBN 978-981-10-8231-3 (eBook)https://doi.org/10.1007/978-981-10-8231-3

Library of Congress Control Number: 2018955196

© Springer Nature Singapore Pte Ltd. and Beijing Science and Technology Press 2018This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed.The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use.The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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We once heard retinal specialists, both clinicians and scientists, share a fascination with the retina, a unique tissue in our body. The retina forms the anatomic and physiologic basis for the gift of sight and accounts for over 35% of the neurons entering and exiting the human brain.

It is helpful to recall that although there had long been a fascination with the eye and sight, it was not until the nineteenth century that modern ophthalmology and the study of the retina truly began. Everyone in our field points with pride to the revolution brought about by von Helmholtz in 1850 with his introduction of his innovative ophthalmoscope in Berlin.

In recent years, great progress has been made in the treatment of retinal detachment, and we hope and expect this is a prelude to even greater progress in the near future. Despite these new treatments and the explosion of knowledge on the basic mechanisms of retinal biology, the detachment of the retina remains to date a major cause of blindness in all age groups.

In revising The Atlas of Retinal Detachment: Diagnosis and Differential Diagnosis edition, we begin with many pictures and imagings, where there is a veritable revolution underway. The human eye cannot resolve what advanced imaging technologies including ocular coher-ence tomography (OCT) can detect.

Human retina is a direct outgrowth of the forebrain and, therefore, is the most accessible part of the brain for neuroscience studies. Many of us consider the retina to be aesthetically the most beautiful tissue in nature. We hope the reader will enjoy and appreciate the major revi-sions to the figures and illustrations throughout the text.

The editors gratefully acknowledge the support of the contributing authors who, in addition to their large clinical load and scientific research efforts, found the time to make such a large contribution to the completion of this project.

Beijing, China Wenbin Wei November 2017

Preface

vii

Contents

1 Introduction of Retinal Detachment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1Kai Ma, Nan Zhou, and Wenbin Wei

2 Rhegmatogenous Retinal Detachment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13Ruilin Zhu, Nan Zhou, and Wenbin Wei

3 Special Types of Rhegmatogenous Retinal Detachment . . . . . . . . . . . . . . . . . . . . 33Kai Ma, Nan Zhou, and Wenbin Wei

4 Exudative Retinal Detachment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67Haiying Zhou, Nan Zhou, and Wenbin Wei

5 Congenital Abnormalities of the Fundus and Retinal Detachment . . . . . . . . . . . 117Yao Huang, Nan Zhou, and Wenbin Wei

6 Tractional Retinal Detachment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135Lei Shao, Nan Zhou, and Wenbin Wei

7 Traumatic Retinal Detachment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 165Jinqiong Zhou, Nan Zhou, and Wenbin Wei

8 Pathologic Myopia and Retinal Detachment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 177Liqin Gao, Nan Zhou, and Wenbin Wei

9 Infectious Uveitis and Retinal Detachment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 191Liqin Gao, Nan Zhou, and Wenbin Wei

10 Uveitis and Retinal Detachment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 205Yao Huang, Nan Zhou, and Wenbin Wei

11 Ocular Tumor and Retinal Detachment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 221Jinqiong Zhou, Nan Zhou, and Wenbin Wei

12 Surgical Techniques of Rhegmatogenous Retinal Detachment and Complications After Surgeries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 253Haicheng She, Nan Zhou, and Wenbin Wei

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Contributors

Haicheng She, M.D., Ph.D. Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China

Haiying Zhou, M.D., Ph.D. Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China

Jinqiong Zhou, M.D., Ph.D. Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China

Kai Ma, M.D., Ph.D. Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China

Lei  Shao, M.D., Ph.D. Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China

Liqin  Gao, M.D., Ph.D. Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China

Ruilin Zhu, M.D., Ph.D. Peking University First Hospital, Beijing, China

Yao  Huang, M.D., Ph.D. Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China

Editors

Wenbin Wei, M.D., Ph.D. Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China

Nan  Zhou, M.D., Ph.D. Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China

Yang Lihong, M.D. Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China

Shi  Xuehui, M.D., Ph.D. Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China

Contributors and Editors

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List of Editors

Editor-In-Chief

Wenbin Wei, M.D., Ph.D. Director, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China

Deputy Editor-In-Chief

Nan  Zhou, M.D., Ph.D. Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China

Haicheng She, M.D., Ph.D. Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China

Ruilin Zhu, M.D., Ph.D. Peking University First Hospital, Beijing, China

1© Springer Nature Singapore Pte Ltd. and Beijing Science and Technology Press 2018W. Wei (ed.), Atlas of Retinal Detachment, https://doi.org/10.1007/978-981-10-8231-3_1

Introduction of Retinal Detachment

Kai Ma, Nan Zhou, and Wenbin Wei

Abstract

Retinal detachment is a common disease; this chapter mainly introduces the anatomy, histology, and embryol-ogy of retinal detachment, classification of retinal detach-ment, and the development and natural history of rhegmatogenous retinal detachments.

1.1 Anatomy, Histology, and Embryology of Retinal Detachment

1.1.1 Embryology and Development of the Retina

The development of bulbus oculi involves the development of neuroectoderm, surface ectoderm, and mesoderm consti-tuting blood vessels. The primary optic vesicle forms the optic cup, whose outer wall develops into the cellular layer of retinal pigment epithelium. Apart from the metabolism of visual cells, monolayer cells also keep the retina pellucid, acting as an outer barrier of the retina. The inner wall of the optic cup is highly differentiated forming the sensory cell layer of retina, including the structure of tertiary neuron [1]. The potential space between retinal pigment epithelium and the neuroepithelial layer is a weak area, prone to separate to cause retinal detachment. According to histological changes, retinal detachment should be termed separation within the retina, instead of separation of the retina from the choroid. However, the term of “retinal detachment” is still being used (Figs. 1.1, 1.2, and 1.3).

K. Ma, M.D., Ph.D. · N. Zhou, M.D., Ph.D. · W. Wei, M.D., Ph.D. (*)Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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2

A

B

C

D

Fig. 1.2 Construct relationship between photoreceptor cells’ segments and retinal pigment epithelium revealed by electron microscope (×500). A, Photoreceptor cells’ segments. B, The potential space between the photoreceptor cells’ segments and retinal pigment epithelium. C, The nucleus of a retinal pigment epithelium. D, Bruch membrane Fig. 1.3 Detachment between neurosensory retina and retinal pigment

epithelium (×200). A, Interspace between detached neurosensory retina and retinal pigment epithelium. B, Ganglion cell layer

Fig. 1.1 Cross-sectional histologic preparations of the retina (×200)

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Fig. 1.4 A normal ocular fundus image by Optos Panoramic200 scan-ning laser ophthalmoscope

Fig. 1.5 Lattice degeneration and thin retina area in the right eye’s peripheral inferior temporal quadrant

Fig. 1.6 Cystoid degeneration in retinal plexiform layer

Fig. 1.7 Retinal detachment associated with retinal dialysis (×200). A, The large subretinal space. B, The filamentous connection between neurosensory retina and the ora serrata. C, The ciliary body

1.1.2 Blood Supply of the Retina

The central retinal artery supplies the five inner layers of the retina, while the uveal ciliary arteries supply the four outer layers of the neurosensory retina and the retinal pigment epi-

thelial layer. These two circulations are both terminal branches, which are ended at the outer plexiform layer and the ora serrata. Due to poor blood flow, these two areas are prone to degeneration and then lead to retinal detachment (Figs. 1.4, 1.5, 1.6, and 1.7).

1 Introduction of Retinal Detachment

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Fig. 1.9 B-scan ultrasounds showing posterior vitreous detachment

Fig. 1.10 Optical coherence tomography (OCT) showing vitreoretinal traction of the retina causing the macular hole

1.1.3 The Interrelation Between the Vitreous and Retina

The normal vitreous is transparent and gelatinous and pro-vides support for the eyeball. It adheres firmly to the retina at the vitreous base, optic nerve head, and macula. Aging and myopia or other diseases can cause the vitreous to degenerate and liquefy. After certain extent of liquefaction, the vitreous detaches, especially in the posterior and/or

superior quadrants (Figs. 1.8 and 1.9) [2]. Following acute vitreous detachment, vitreous traction can cause a retinal break due to retinal adhesion [3]. The retinal breaks are usually macular holes (Fig.  1.10) and horseshoe tears (Figs. 1.11 and 1.12), with flap adherent or signs of vitre-ous traction [4].

The liquid vitreous passes into the potential space between the neurosensory retina and retinal pigment epithelium through the retinal breaks and leads to retinal detachment.

Fig. 1.8 Posterior vitreous detachment. Annular opacity floater in the vitreous is observed before the optic nerve, the Weiss ring

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Fig. 1.11 Vitreoretinal traction of the retina causes the horseshoe tear, rolled edge of retinal break

Fig. 1.12 Rolled posterior edge of giant retina tear indicating vitreo-retinal traction

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1.2 Classification of Retinal Detachment

Retinal detachment is classified based on pathology, and different treatment strategies apply accordingly. Rhegmatogenous retinal detachment is caused by retinal breaks, while non-rhegmatogenous retinal detachment is caused by other ocular disease or systemic disease.

1.2.1 Rhegmatogenous Retinal Detachment

Rhegmatogenous retinal detachments are associated with congenital or acquired disease and the interaction of the vitreous and retina that led to retinal break and retinal detachment. It is sometimes referred to as primary or idio-pathic retinal detachment. The key to the successful treat-ment for this type of retinal detachment is to seal retinal breaks.

1.2.2 Non-rhegmatogenous Retinal Detachment

The two general categories of non-rhegmatogenous retinal detachments are termed tractional and exudative. Tractional retinal detachments are more common. It occurs due to the vitreoretinal adhesions or membranes that mechanically pull

the retina away after vitreoretinal hemorrhage of retinal vascular disease or trauma. Exudative detachments occur when ocular disease or systemic disease causes retinal ves-sels to leak and produce subretinal fluid.

1.2.2.1 Tractional Retinal DetachmentsThe causes of tractional retinal detachments include cellular proliferation resulting from retinal hemorrhage and vitreous hemorrhage of retinal vascular disease, cicatricial contraction in trauma, intraocular foreign body extraction, and incision of surgery [5]. Usually tractional retinal detachments are without retinal tears. However, in few cases, contraction may tear off the retina to cause secondary rhegmatogenous retinal detach-ments. The key to treatment is eliminating the vitreoretinal or epiretinal traction. For wide tractional retinal detachments, vitrectomy may be required (Figs. 1.13 and 1.14).

1.2.2.2 Exudative Retinal DetachmentsExudative retinal detachment is associated with systemic disease or ocular dysemia, such as nephropathy, pregnancy-induced hypertension, intraocular inflammation, tumor, Vogt-Koyanagi-Harada disease, sympathetic ophthalmia, Coats disease, bullous detachment of the retina, idiopathic central serous chorioretinopathy, uveal effusion syndrome, etc. The exudative subretinal fluid elevates the retina, which causes retinal detachment without retinal tears (Figs. 1.15, 1.16, 1.17, 1.18, 1.19, 1.20, and 1.21).

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Fig. 1.13 Tractional retinal detachments with intraocular foreign body Fig. 1.14 Proliferative diabetic retinopathy and tractional retinal detachment

Fig. 1.15 Secondary retinal detachment with nephropathy

a

b

Fig. 1.16 Secondary retinal detachment with Vogt-Koyanagi-Harada disease. (a) Secondary exudative retinal detachment with Vogt-Koyanagi- Harada disease. (b) Terminal stage of Vogt-Koyanagi-Harada disease, photograph shows sunset glow fundus

1 Introduction of Retinal Detachment

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Fig. 1.18 Idiopathic central serous chorioretinopathy

Fig. 1.17 Secondary retinal detachment with Coats disease

Fig. 1.19 Secondary retinal detachment with retinoblastoma

Fig. 1.20 Secondary retinal detachment with choroidal hemangioma

Fig. 1.21 Secondary retinal detachment with choroidal melanoma

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Fig. 1.22 Early retinal detachments

Fig. 1.23 A relatively early stage of retinal detachment

Fig. 1.24 A long-standing retinal detachment with subretinal strands

Fig. 1.25 Retinal detachment associated with inferior temporal retinal dialysis. As demonstrated, there are subretinal pigmented demarcation lines

1.3 The Development and Natural History of Rhegmatogenous Retinal Detachments

1.3.1 Early Retinal Detachments

The common symptoms of early rhegmatogenous retinal detachments are floaters (“bugs”), flashes of light, blurred vision, and vision field loss. The detachments are bulbiform or flat elevation of the retina, with certain mobility of vitre-ous and soft and moist appearance. After careful examina-tion of the entire retina, retinal breaks could be detected (Fig. 1.22).

1.3.2 Long-Standing Retinal Detachments

1. The retina is thinner and translucent in long-standing reti-nal detachments. Due to proliferation, the retina could be with wrinkling of inner retinal surface, retinal stiffness, and/or subretinal proliferation (Figs. 1.23 and 1.24).

2. In some cases, inferior detachments develop slowly. It could not be noticed until it affected central vision. Usually one to three curved demarcation lines in detach-ment area could be detected which are matched with the borders of retinal detachment, which mark the trail of detachment progress (Fig. 1.25).

3. Translucent and spherical intraretinal macrocysts may develop in long-standing retinal dialysis, due to degenera-tion of peripheral retina (Fig. 1.26).

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1.3.3 Appearance Following Reattachment of Retinal Detachments

After the seal of retinal tears and resorption of subretinal fluid (Figs. 1.27, 1.28, 1.29, and 1.30), the reattachment area is dark and gray due to alteration of pigment granules, which is distinctly different with the normal retina.

Fig. 1.27 After scleral buckling, the retina reattached on the posterior visible crest of the buckle

Fig. 1.28 An annular crest of the buckle. After scleral buckling, the retina reattached on the posterior visible crest of the buckle

Fig. 1.30 An annular crest of scleral buckling in B-scan ultrasounds

Fig. 1.29 An annular crest of scleral buckling in B-scan ultrasounds

Fig. 1.26 An intraretinal cystoid in detached retina with retinal breaks

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References

1. Graw J. Eye development. Curr Top Dev Biol. 2010;90:343–86. 2. Okun E. Histopathology of changes which precede retinal detach-

ment. Bibl Ophthalmol. 1966;70:76–97. 3. Machemer R.  The importance of fluid absorption, traction, intra-

ocular currents, and chorioretinal scars in the therapy of rhegmatog-

enous retinal detachments. XLI Edward Jackson memorial lecture. Am J Ophthalmol. 1984;98(6):681–93.

4. Foos RY.  Tears of the peripheral retina; pathogenesis, inci-dence and classification in autopsy eyes. Mod Probl Ophthalmol. 1975;15:68–81.

5. Machemer R, Aaberg TM, Freeman HM, et  al. An updated clas-sification of retinal detachment with proliferative vitreoretinopathy. Am J Ophthalmol. 1991;112(2):159–65.

1 Introduction of Retinal Detachment

13© Springer Nature Singapore Pte Ltd. and Beijing Science and Technology Press 2018W. Wei (ed.), Atlas of Retinal Detachment, https://doi.org/10.1007/978-981-10-8231-3_2

Rhegmatogenous Retinal Detachment

Ruilin Zhu, Nan Zhou, and Wenbin Wei

Abstract

Rhegmatogenous retinal detachment (RRD) is the most common type of retinal detachment. Different types of retinal degeneration may lead to retinal detachment. The shape and location of retinal breaks and detachment are various in different patients. In this chapter, we provide a large number of fundus photographs and diagrams of reti-nal degeneration, retinal breaks and detachment. With these pictures, the lesions are showed more clearly and distinctly.

2.1 Introduction

Retinal detachment (RD) is the separation of the neurosen-sory retina from the retinal pigment epithelium (RPE). Some detachments are secondary to ocular or systemic disease, while others do not have a distinct etiology. The most com-mon type of RD is primary RD, in which there is no obvious original disease. The retina detaches with a full-thickness retinal break and vitreous degeneration, so it is usually called as rhegmatogenous retinal detachment (RRD). Previous stud-ies have reported the incidence rate of RRD ranging from 9.7 to 20.7 per 100,000 persons per year [1–5]. The peak inci-dence is at 50–69  years of age, with a secondary peak at 20–29 years [3, 6]. Men are more likely to be affected [1–3]. Rates of bilateral RRD vary between 1% and 1.67%, increas-ing with study duration [4, 5, 7]. Risk factors for RRD include male gender, trauma, pseudophakic eye, and myopia [3, 8].

R. Zhu, M.D., Ph.D. Peking University First Hospital, Beijing, China

N. Zhou, M.D., Ph.D. · W. Wei, M.D., Ph.D. (*) Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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2.2 Retinal Degeneration Related to Retinal Detachment

Peripheral retinal degeneration includes lattice degeneration (Fig. 2.1), paving-stone degeneration, and retinal white with-out pressure (Fig. 2.2a, b). Lattice degeneration is the most significant peripheral retinal disorder predisposing to RD.

Lattice degeneration is present in 5.2%–12.2% of the healthy population [9–12], in 30% of RD patients [13], and in 12.2%–13.6% of high myopic patients [12, 14]; 61.3% of the lesions occur in both eyes [9]. The temporal quadrant is the most affected area, especially the lower temporal quad-rant, followed by the upper temporal quadrant, lower nasal quadrant, and upper nasal quadrant [15]. Lattice degenera-tion is most commonly located near the vertical meridian between 11 and 1 o’clock and between 5 and 7 o’clock [16], with its long axis parallel to the ora serrata. The width of the lesion has been reported to be 1/4 disc diameter (DD)–2/3 DD and the length to be 1/2 DD–12 DD [15]. The lesions are normally round-, oval-, or linear-shaped retinal thinning zone, with a distinct and slightly elevated border and rough surface. About 81.7%–92% of the degeneration shows pig-ment clumps underneath retinal blood vessels. White lines can be seen in 12% of the lesions [15], indicating the occlu-sion of blood vessels; these lines appear in the late stage of the disease, while in the early stage the vessels are con-

stricted (Fig. 2.3a, b). Vitreous degeneration associated with lattice degeneration includes vitreous liquefaction, changes in vitreous concentration, vitreous detachment, and vitreo-retinal traction. Atrophic holes within lattice lesions have been found in 18.2%–24.9% of eyes, and tractional retinal tears have been found in 1.5%–2.4% of them [15] (Fig. 2.4a, b).

Fig. 2.1 Lattice degeneration in inferior temporal quadrant of right eye. Multiple atrophic holes reside in the degenerated lesion. Pigment change and yellowish dots can be seen in the lesion. Blood vessels con-stricted and appear as white lines

a b

Fig. 2.2 (a, b) Retinal white without pressure

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a b

Fig. 2.3 (a, b) Lattice degeneration. Blood vessels constricted and appear as white lines. A horse-shoe shaped retinal tear can be seen near the lesion with retinal detachment

a b

Fig. 2.4 (a, b) Lattice degeneration. (a) A horse-shoe shaped retinal tear can be seen on the right side of the lesion with retinal detachment. Pigment change and yellowish dots can be seen in the lesion. Blood

vessels constricted and appear as white lines. (b) Multiple atrophic holes reside in the degenerated lesion

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2.3 Retinal Breaks

With improvements in clinical practice, the pathogenesis of RRD is now better understood. The key point in the treat-ment of RRD is to close the retinal breaks and then to perma-nently seal them with retinopexy.

2.3.1 Shapes of Retinal Breaks

2.3.1.1 Round HoleRegional retinal tissue degeneration and thinning lead to atrophic retinal holes. The holes are usually round or oval,

with a distinct margin. The RPE and the red background of the uvea can be seen through the holes. In some cases, the retinal tissue is tilted up at the edge of the hole, and in some cases the retinal tissue on the surface of the hole is detached. The size and shape of the operculum coincides with the hole. Retinal holes are usually less than 1/4 DD and are seldom larger than 1 DD.  The holes can be solidary, multiple, or clustered. It has been reported that in 85% of patients who had round holes the fellow eye was affected [17]. About 95.4% of the atrophic holes are associated with lattice degen-eration [18]. Round-hole retinal detachments accounted for 10% of primary retinal detachments [17, 19] (Figs. 2.5a–c and 2.6a–c).

a b

c

Fig. 2.5 (a–c) Round holes. (a) Idiopathic macular hole in left eye. (b) Round retinal hole at peripheral retina of right eye. (c) Round retinal hole with subretinal proliferation and retinal detachment

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2.3.1.2 Horseshoe TearTraction of a vitreoretinal adhesion leads to a retinal tear, with a horseshoe, crescent, or “U” shape. The shape of the tear is related to the magnitude and direction of the tractive force. Since the stress point resides at the peripheral retina, the basal part of a horseshoe tear always points toward the peripheral retina, and the acme points to the macula (Figs. 2.7a–c and 2.8a, b). Horseshoe tears account for 23.1% of the total number of breaks, and 60.2% of them are tears with attached flaps, while 39.8% are tears with free opercula [18]. The tears are usually larger than 1 DD, and are located at the equator or peripheral retina, near the junction of the diseased and healthy retina. Retinal horseshoe tears accounted for 70%–86.3% of the total number of RRDs [19, 20]. The retinal blood vessels can be involved and lead to vitreous hemorrhage (Fig. 2.9a–d). In cases of sudden vitre-ous hemorrhage in patients without hypertension, diabetes, or other ocular vessel disorders, one must investigate whether a retinal tear has caused the hemorrhage, and ultrasonogra-phy is recommended in such cases.

2.3.1.3 Retinal DialysisRetinal dialysis, also known as ora serrata dialysis, is the dis-insertion of the retina along the ora serrata. It has been reported that retinal dialysis was found in 5.9%–8.2% of RD cases [20–22]. Vitreous base backward traction results in retinal dialysis at the ora serrata. The anterior edge of the dialysis is at the ora serrata and is without a front edge, while the posterior edge is thickened and curved, and usually attached to the vitreous base. The extent of the dialysis varies from one quadrant up to 360° (Fig. 2.10a–c).

Dialysis at the ora serrata usually occurs after severe blunt contusion trauma to the globe. Most of the cases are unilat-eral, while bilateral cases have been reported accounting for 5%–10.3% of the patients [21, 23]. As the result of a blunt blow to the eyeball, the retina detaches from the ora serrata, and avulsion of the nonpigmented ciliary epithelium or vitre-ous occasionally occurs.

a b

c

Fig. 2.6 Multiple round retinal holes. (a) Multiple round retinal holes with retinal detachment. (b) Multiple round retinal holes. (c) Laser photo-coagulation was applied to seal the retinal holes

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Fig. 2.8 (a, b) Horseshoe shaped retinal tear treated by laser photocoagulation. Laser burns can be seen around the tear

a b

a b

c

Fig. 2.7 (a–c) Horseshoe shaped retinal tear with retinal detachment

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a b

c d

Fig. 2.9 (a–d) Retinal tear with retinal detachment. A blood vessel crosses over the edge of the retinal tear

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a b

c

Fig. 2.10 (a–c) Ora serrata dialysis with retinal detachment. The posterior edge is thickened and curved

2.3.2 Sizes of Retinal Breaks

Retinal breaks are of various sizes, from as small as a pin-hole to all around the retina. Atrophic holes are usually small and multiple, and tractional tears are usually large and soli-tary. A break that extends circumferentially around the retina

for 90° or more is also called a giant retinal tear, and is usu-ally located at the peripheral retina [24]. Giant retinal tears are usually caused by vitreous traction, and the posterior edge of the tears curl. Severe RD in the peripheral region often causes giant ora serrata dialysis. These two kinds of retinal breaks can both extend up to 360° (Fig. 2.11a–i).

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