Posterior Segment Complications of Cataract Surgery [1st ed.] 9789811510175, 9789811510199

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Posterior Segment Complications of Cataract Surgery Meena Chakrabarti Arup Chakrabarti Editors

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Posterior Segment Complications of Cataract Surgery

Meena Chakrabarti  •  Arup Chakrabarti Editors

Posterior Segment Complications of Cataract Surgery

Editors Meena Chakrabarti Chakrabarti Eye Care Centre Trivandrum Kerala India

Arup Chakrabarti Chakrabarti Eye Care Centre Trivandrum Kerala India

ISBN 978-981-15-1017-5    ISBN 978-981-15-1019-9 (eBook) https://doi.org/10.1007/978-981-15-1019-9 © Springer Nature Singapore Pte Ltd. 2020 This 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, expressed 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. This Springer imprint is published by the registered company Springer Nature Singapore Pte Ltd. The registered company address is: 152 Beach Road, #21-01/04 Gateway East, Singapore 189721, Singapore

Introduction

This book deals with the recognition and management of all posterior segment complications associated with cataract surgery and will provide a comprehensive coverage of these sight-threatening complications. Written for the benefit of the novice as well as experienced surgeon, each chapter is structured to offer pertinent pearls in identifying patients at risk and will emphasise on surgical strategies to be adopted to minimise the occurrence of this complication as well as management options and long-term post-operative care of these compromised eyes. The authors who have contributed are experienced surgeons who have a long track record of successful management of these complications and are by themselves sought after teachers in this field.

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Contents

1 Risk Factors for Posterior Segment Complications of Cataract Surgery �������������������������������������������������������������������������������������� 1 Sabyasachi Sengupta, Rahul Mahajan, Rhuta Mahajan, and Arup Chakrabarti 2 Needle Stick Globe Injuries������������������������������������������������������������������������ 11 Atul Kumar, Prateek Kakkar, Divya Agarwal, and Aman Kumar 3 The Dropping and Dropped Nucleus �������������������������������������������������������� 17 Meena Chakrabarti and Arup Chakrabarti 4 Pseudophakic Retinal Detachment������������������������������������������������������������ 29 Amit B. Jain and Muna Bhende 5 Pseudophakic Cystoid Macular Oedema�������������������������������������������������� 39 Venkat Kotamarthi 6 Prophylaxis of Postoperative Endophthalmitis Following Cataract Surgery������������������������������������������������������������������������ 63 Steve A. Arshinoff and Milad Modabber 7 Postoperative Endophthalmitis������������������������������������������������������������������ 81 Deeksha Katoch and Mangat Ram Dogra 8 Toxic Anterior Segment Syndrome������������������������������������������������������������ 95 He Li, Konstantinos T. Tsaousis, Jun J. Guan, Nicolas Reiter, and Nick Mamalis 9 Expulsive Choroidal Hemorrhage������������������������������������������������������������ 107 Itika Garg, Pranita Sahay, Prafulla K. Maharana, and Namrata Sharma 10 Operating Microscope-Induced Phototoxic Maculopathy �������������������� 117 Nitin Nema, Siddharth Malaiya, and Prakhar Singhai 11 Progression of Retinal Diseases After Cataract Surgery������������������������ 125 David Liao and David Boyer 12 Dislocated Intraocular Lens���������������������������������������������������������������������� 139 Meena Chakrabarti and Arup Chakrabarti vii

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Risk Factors for Posterior Segment Complications of Cataract Surgery Sabyasachi Sengupta, Rahul Mahajan, Rhuta Mahajan, and Arup Chakrabarti

1.1

Introduction

Cataract surgery has evolved over the past few decades into a very safe and efficient procedure. Advances in intraocular lenses have complimented the technical surgical advances making cataract surgery a refractive procedure with excellent visual outcomes. Despite these advances in technology and techniques for safety, complications occur occasionally, even in the best of hands. Posterior segment complications of cataract surgery are rare and in a few instances they may be anticipated in view of risk factors that the eye may harbor. Awareness of these risk factors will enable the cataract surgeon to prepare well in advance and modulate a surgical strategy to prevent these complications. In this chapter, we discuss the risk factors for the following posterior segment complications of cataract surgery. 1. Needle stick injury 2. Dropped nucleus

S. Sengupta Future Vision Eye Care and Research Centre, Mumbai, India R. Mahajan EyeQ Superspecialty Hospital, Jalgaon, India R. Mahajan Subdistrict Hospital, Ponda, India A. Chakrabarti (*) Chakrabarti Eye Care Centre, Trivandrum, Kerala, India © Springer Nature Singapore Pte Ltd. 2020 M. Chakrabarti, A. Chakrabarti (eds.), Posterior Segment Complications of Cataract Surgery, https://doi.org/10.1007/978-981-15-1019-9_1

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3. Rhegmatogenous retinal detachment 4. Pseudophakic cystoid macular edema 5. Endophthalmitis 6. Toxic anterior segment syndrome 7. Suprachoroidal hemorrhage 8. Dislocated IOL 9. Progression of retinal disease after cataract surgery 10. Phototoxic retinopathy 1. Needle Stick Injury—This complication can occur if cataract surgery is planned under either peribulbar or retrobulbar anesthesia. As most cataract surgeries are currently being performed under topical anesthesia, the incidence of needle stick injury is negligible. Needle stick injury can lead to globe perforation if the sclera is injured, vascular insufficiency if the central retinal artery is damaged or toxic optic neuropathy and Purtscher’s like retinopathy if the optic nerve is injured during anesthesia. Risk for globe perforation is high in the following conditions: (a) High myopia: Incidence of scleral perforation is estimated to be 0.13% in eyes with high myopia (axial length > 26 mm) and higher in eyes with posterior staphyloma [1, 2]. (b) Retrobulbar block poses greater risk compared to peribulbar block [2, 3] (c) Deep socket eyes with difficult access to the orbit [2] (d) Uncooperative patient, mentally challenged, etc. (e) Faulty techniques: Most common site is the inferotemporal quadrant followed by the superonasal quadrant [3]. 2. Dropped Nucleus: Cataract surgery leading to posterior capsular rupture (PCR) prior to segment removal carries the risk of nuclear fragments sinking into the vitreous cavity. Risk factors for dropped nucleus can be classified as under: (a) Posterior polar cataract: Posterior polar cataracts are often associated with dehiscence of the central part of the posterior capsule. Forceful hydrodissection can lead to intraoperative “capsular block syndrome” with rupture of the dehiscent posterior capsule leading to drop of the entire nucleus [4, 5]. (b) Zonular instability: Zonular laxity or loss of zonules can be detected as phacodonesis during preoperative evaluation. This is best observed in an undilated pupil under slit lamp magnification by asking the patient to perform rapid horizontal saccades. Coexistent conditions such as pseudoexfoliation [6], blunt trauma or syndromic habitus such as Marfan’s and Ehler Danlos [7, 8] should alert the surgeon to look for subtle phacodonesis during preoperative evaluation. Ultrasound biomicroscopy (UBM) can be used to detect zonular integrity preoperatively in doubtful cases though careful clinical evaluation is the best indicator. Similarly, history of zonular prob-

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(c)

(d)

(e)

(f)

(g)

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lems during cataract surgery of the other eye should prompt the surgeon to anticipate the same in the eye to be operated. Poor mydriasis: Inadequate pupillary dilatation increases the risk of PCR and nucleus drop [9, 10]. A small pupil hampers adequate visualization leading to a small capsulorhexis and difficulty in nuclear disassembly. Traumatic maneuvers during phacoemulsification can lead to either zonular loss or posterior capsular rupture and resultant nucleus drop. Pupillary diameter can be assessed preoperatively using the slit lamp beam length and should be documented in the case files to alert the surgeon of this possibility. Cause of poor mydriasis such as pseudoexfoliation, floppy iris secondary to tamsulosin, age-related sclerosis of the sphincter, chronic pilocarpine use, etc. should also be determined. Cataract density: Very dense brunescent/ black cataracts and mature/hypermature cataracts significantly increase the risk for nucleus drop due to myriad reasons [5, 9]. Peripheral capsulorhexis extension, poor visualization of the posterior capsule, poor red glow, and inadvertent posterior capsular trauma due to the chopper and/or phaco probe all increase the likelihood of nucleus drop in dense/mature cataracts. Additionally, black cataracts and hypermature cataracts have preexisting zonular laxity in view of the sheer cataract mass being supported by the zonules. Capsulorhexis tear: Capsulorhexis tear due to any cause increases chances of PCR and nucleus drop [9, 10]. Capsulorhexis tear and peripheral extension is commonly seen with hypermature cataracts, eyes with angle closure glaucoma and when the intralenticular pressure is high. Surgeons in training also experience peripheral extension of the rhexis margin without any predisposing risk factors. Irrespective of the underlying cause, capsulorhexis tear and extension must alert the surgeon to possible extension to the posterior capsule and potentially high risk of PCR and nucleus drop during phacoemulsification maneuvers. Post PPV eyes: Eyes that have undergone previous vitreous surgery are always at a slightly greater risk of PCR and nucleus drop [5, 9]. A documented history of prior posterior capsular touch by vitreoretinal instruments almost always leads to posterior capsular instability and warrants careful surgical maneuvers. Post silicone oil removal, the posterior epinucleus becomes abnormally leathery and is difficult to crack or chop. Additionally, lack of vitreous support leads to unusual deepening of the anterior chamber during cataract surgery. The red fundal glow may also be altered due to previous retinal surgical maneuvers making surgery difficult and leading to PCR and nucleus drop. High myopia: Eyes with very high myopia have very deep anterior chamber and weak zonules making it difficult to reach the cataract surface and chop/emulsify it. Such eyes are prone to surge, alterations in intraocular pressure intraoperatively and are at an increased risk of PCR and nucleus drop [5, 9].

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(h) Positive pressure: Excessive amount of anesthetic injected into the retrobulbar space causes positive pressure and raised intraocular pressure. This leads to repeated shallowing of anterior chamber and thus increases chances of PCR and nucleus drop. (i) Poor patient cooperation: Especially while performing surgery under topical anesthesia can predispose to PCR and dislocation of nucleus. 3 . Rhegmatogenous Retinal Detachment: Cataract surgery especially complicated by PCR and vitreous loss increases the risk of retinal detachment [11]. The following risk factors should be kept in mind and the risk of retinal detachment assessed periodically after cataract surgery: (a) Posterior vitreous detachment: It is presumed that alterations in intraocular pressure during cataract surgery induce posterior vitreous detachment (PVD) [12–14]. As PVD progresses, regions of strong vitreoretinal adhesions are prone to develop retinal tears and subsequent retinal detachment. History of retinal detachment in the other eye should prompt the surgeon to examine the retinal periphery well and periodically monitor for retinal tears in the postoperative period as PVD progresses. (b) PCR with vitreous loss: Disruption of the anterior vitreous face and performance of anterior vitrectomy increases stress on the vitreous base, thus increasing traction and risk of retinal tears, giant retinal tears, and retinal detachment [12–14]. Use of automated vitrector with proper settings (high cut rate and low vacuum), bimanual vitrectomy (separating infusion and aspiration), and anterior vitrectomy in a closed chamber reduce the risk of retinal detachment. (c) Preexistent retinal degenerations: Preexistent lattice degeneration also increases the risk of retinal detachment, especially in eyes that are yet to develop a PVD [15]. (d) Posterior capsulotomy during and after cataract surgery: Especially in pediatric population, leads to vitreous disturbance and traction at the vitreous base and increases the risk of retinal detachment [16, 17]. (e) Traumatic maneuvers: Surgical maneuvers such as fishing the nucleus out from the mid-vitreous cavity increase the risk of giant retinal tears [18]. Posterior levitation via the pars plana has been described as an effective way to avoid sinking of the nucleus [19]. In this technique, a microvitreoretinal blade is inserted via the pars plana, and the nucleus is levitated into the anterior chamber and removed via a limbal approach. Such maneuvers also increase the risk of retinal detachment and are better avoided [20]. 4. Pseudophakic Cystoid Macular Edema (PCME): Usually, acute PCME occurs at about 3 months after cataract and can occur even after uncomplicated cataract surgery. However, the following situations increase the risk of PCME: (a) PCR with vitreous loss: This is also termed Irvine–Gass syndrome and is thought to be due to traction on the macula as a result of prior incomplete anterior vitrectomy [21, 22].

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(b) Diabetes: Individuals with diabetes, especially those with underlying diabetic retinopathy, are at an increased risk of PCME due to the compromised blood retinal barrier [22]. (c) Intraocular lens (IOL) positioning: Placement of the IOL other than “in the bag” increases the risk of PCME. IOL in sulcus, anterior chamber lens, papillary capture of IOL optic, iris claw lens, or sclera-fixated IOL all increase the risk of PCME.  Non-UV blocking IOLs are also known to increase the risk of PCME [22]. (d) Preexisting uveitis: Eyes with preexisting uveitis, especially anterior uveitis, are known to have a flare up after cataract surgery with resultant CME [22]. (e) Excessive tissue handling during surgery: Surgery performed by training ophthalmologists and involving maneuvers such as sphincterectomy and synechiae release lead to excessive postoperative inflammation and increase the risk of PCME [22]. (f) Others: Retinitis pigmentosa, retained cortical matter in the vitreous cavity, PCME in fellow eye, and the presence of epiretinal membrane also increase the risk of PCME [22]. Use of preoperative non-steroidal anti-inflammatory drugs has not been found to be effective in PCME prophylaxis by the American Board of Ophthalmology [20]. However, in the presence of the above risk factors, perioperative topical anti-­inflammatory drugs might be useful in PCME prophylaxis. 5. Endophthalmitis: Infective endophthalmitis is the most dreaded and visually threatening complication following cataract surgery. The incidence is low and ranges from 0.05 to 0.15%. Though endophthalmitis can occur after uneventful cataract surgery, its risk increases many-fold in the presence of the following risk factors: (a) PCR with/without vitreous loss: Increases the risk of endophthalmitis by breaching anatomical barriers and allowing organisms entry into the nutrient rich vitreous [23]. (b) Surgical tunnel complications: A leaking corneal tunnel with resultant hypotony increases the likelihood of organisms entering the eye [23, 24]. Wound burns after phacoemulsification, improper tunnel location, and depth are factors that predispose to wound leak and subsequent complications such as endophthalmitis. (c) Chronic dacryocystitis: Untreated chronic dacryocystitis is a source of continuous infection and increases the risk of endophthalmitis [24]. Preoperative syringing should be performed preferably in all patients and especially in those with history of persistent watering. (d) Poor lid hygiene, personal hygiene: These lead to alteration in the local flora in the conjunctiva and predispose to infections. It is recommended that blepharitis and other conditions of the lids be well controlled before taking up the patient for cataract surgery [24]. Additionally, proper draping keeping the eye lashes away from the surgical field also reduces the risk of infection.

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(e) Diabetes, chronic alcoholism, long-term use of systemic steroids, and other debilitating systemic diseases reduce immunity and predispose to endophthalmitis. (f) Contaminated eye drops: Contaminated Natamycin eye drops causing superimposed pseudomonas keratitis has been reported in the past [25]. Contaminated eye drops, irrigating solution, and viscoelastics can also potentially increase the risk of endophthalmitis. (g) Nocardia endophthalmitis: Very old and frail patients are at an increased risk for Nocardia endophthalmitis [26]. This infection is indolent, starts from the surgical tunnel, and gradually involves the vitreous cavity over weeks. (h) Chronic endophthalmitis caused by Propiniobacterium acne: Risk increases after Nd:YAG capsulotomy [27]. 6 . Toxic Anterior Segment Syndrome (TASS): Though TASS mainly involves the anterior segment, anterior vitreous involvement may occur in severe cases. TASS leads to severe anterior segment inflammation typically within 24 h of surgery. Risk factors for TASS include: (a) Alterations in pH, osmolality, and elevated endotoxin levels in ocular viscoelastic devices, balanced salt solution, IOLs, and ocular medications [28]. (b) Instruments with residual detergents and antiseptics lead to TASS outbreaks [29]. 7. Suprachoroidal Hemorrhage: Expulsive choroidal hemorrhage is a sudden catastrophic complication during cataract surgery. Torrential bleeding occurs in the suprachoroidal space leading to the development of hemorrhagic choroidal detachment and poor visual outcome. Risk factors for suprachoroidal hemorrhage are: (a) Uncontrolled blood pressure during surgery: Very high blood pressure leads to a high intravascular pressure in the choroidal circulation along with atherosclerotic changes [30, 31]. Sudden ocular hypotony leads to imbalance in the pressure gradient across the choroidal circulation and sudden explosive bleeding in the suprachoroidal space. (b) PCR with vitreous loss and excess vitrectomy: Vitreous loss followed by anterior vitrectomy leads to loss of the tamponading effect of the vitreous on the retinal and choroidal circulation [32, 33]. This can lead to sudden choroidal bleeding and progress to expulsive hemorrhage. (c) Sudden hypotony during surgery: Even without increased intravascular pressure, sudden severe hypotony during surgery can lead to pressure imbalances and expulsive choroidal hemorrhage [32, 33]. (d) Very high myopia: Eyes with degenerative myopia have choroidal sclerosis as a consequence of the myopia [34]. Even minimal hypotony during cataract surgery can cause choroidal bleeding in such eyes. Pressure fluctuations should be strictly avoided or minimized while operating on eyes with degenerative myopia. (e) Uncontrolled glaucoma: Very high intraocular pressure at the time of cataract surgery predisposes to expulsive choroidal hemorrhage [32].

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(f) Others: Advanced age, nanophthalmic eyes, Valsalva maneuver, use of systemic anticoagulants, and previous ocular trauma predispose to suprachoroidal hemorrhage [32]. 8 . Dislocated IOL: Risk factors for posterior dislocation of an IOL are similar to those for a dropped nucleus. The most common setting for a dislocated IOL is PCR with inadequate capsular support and zonular damage. (a) Surgical complication: Surgical complication such as PCR with vitreous loss leading to inadequate capsular support can lead to dislocation of the IOL into the vitreous cavity during surgery [35]. Improper placement of IOL in the ciliary sulcus or on an intact anterior vitreous face can lead to dislocation of the IOL in the early postoperative period. Use of single piece foldable IOL in eyes with PCR can also lead to instability and subluxation or dislocation of the IOL. (b) Zonular problems related to Marfan’s syndrome and pseudoexfoliation lead to subluxation and dislocation of the IOL in the early postoperative period as well as many years after cataract surgery [36, 37]. Zonular damage due to traumatic surgery, even if stabilized with capsular tension rings/segments, are at a greater risk of IOL dislocation in the early or late postoperative period. (c) High myopia: Eyes with degenerative myopia are more prone for “in-the-­ bag” IOL dislocation many years after uneventful cataract surgery [36]. 9. Progression of Retinal Disease After Cataract Surgery: Certain diseases progress rapidly after cataract surgery and can lead to vision-threatening consequences if not monitored. (a) Diabetic retinopathy: It is well known that diabetic retinopathy can progress much faster in pseudophakic eyes. PCR and vitreous loss are known risk factors for rapid progression of non-proliferative to proliferative retinopathy and early neovascular glaucoma [38, 39]. Similarly, poor glycemic control, very rapid preoperative control [38], coexistent hypertension, and long duration of diabetes also increase the risk of rapid progression in diabetic retinopathy status [40, 41]. (b) Glaucoma: Cataract surgery can cause spikes in intraocular pressure leading to progression of glaucomatous damage if IOP is not monitored closely and maintained under acceptable limits [42, 43]. Progression is seen in both open angle and angle closure glaucoma. (c) Phototoxic retinopathy: The occurrence of phototoxic injuries has been correlated with exposure to light of certain wavelengths, particularly blue light, and most significantly, the duration of surgery [44, 45]. Symptoms are decreased vision, metamorphopsia and scotoma. Retinal phototoxic lesions first appear a few days after exposure as a relatively normal looking macula to well-circumscribed outer retinal whitening with mild disturbances of the retinal pigment epithelium. Risk factors include 1. Emmetropic eyes 2. Patients with diabetic retinopathy 3. Strong illumination from operating microscope

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Conclusion

Posterior segment complications of cataract surgery are relatively rare. However, many of the complications described in this chapter have well-defined risk factors and can be predicted in most of the cases. Thorough preoperative assessment to identify these risk factors coupled with meticulous surgical planning to avoid complications can enhance surgical success and yield excellent results.

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19. Por YM, Chee S-P. Posterior-assisted levitation: outcomes in the retrieval of nuclear fragments and subluxated intraocular lenses. J Cataract Refract Surg. 2006;32(12):2060–3. 20. Schutz JS, Mavrakanas NA.  Posterior-assisted levitation in cataract surgery. Curr Opin Ophthalmol. 2010;21(1):50–4. 21. Henderson BA, Kim JY, Ament CS, Ferrufino-Ponce ZK, Grabowska A, Cremers SL. Clinical pseudophakic cystoid macular edema. Risk factors for development and duration after treatment. J Cataract Refract Surg. 2007;33(9):1550–8. 22. Grzybowski A, Sikorski BL, Ascaso FJ, Huerva V.  Pseudophakic cystoid macular edema: update 2016. Clin Interv Aging. 2016;11:1221–9. 23. Cao H, Zhang L, Li L, Lo S. Risk factors for acute endophthalmitis following cataract surgery: a systematic review and meta-analysis. PLoS One. 2013;8(8):e71731. 24. Li J, Morlet N, Ng JQ, Semmens JB, Knuiman MW. Significant nonsurgical risk factors for endophthalmitis after cataract surgery: EPSWA fourth report. Invest Ophthalmol Vis Sci. 2004;45(5):1321–8. 25. Krishnan T, Sengupta S, Reddy PR, Ravindran RD. Secondary pseudomonas infection of fungal keratitis following use of contaminated natamycin eye drops: a case series. Eye (Lond). 2009;23(2):477–9. 26. Lalitha P, Rajagopalan J, Prakash K, Ramasamy K, Prajna NV, Srinivasan M.  Postcataract endophthalmitis in South India incidence and outcome. Ophthalmology. 2005;112(11):1884–9. 27. Chaudhry M, Baisakhiya S, Bhatia MS. A rare complication of Nd-YAG capsulotomy: propionibacterium acnes endopthalmitis. Nepal J Ophthalmol. 2011;3(1):80–2. 28. Bodnar Z, Clouser S, Mamalis N. Toxic anterior segment syndrome: update on the most common causes. J Cataract Refract Surg. 2012;38(11):1902–10. 29. Leder HA, Goodkin M, Buchen SY, Calogero D, Hilmantel G, Hitchins VM, et al. An investigation of enzymatic detergents as a potential cause of toxic anterior segment syndrome. Ophthalmology. 2012;119(7):e30–5. 30. Srinivasan M. Expulsive choroidal haemorrhage. Indian J Ophthalmol. 1992;40(4):100. 31. Davison JA. Acute intraoperative suprachoroidal hemorrhage in extracapsular cataract surgery. J Cataract Refract Surg. 1986;12(6):606–22. 32. Ling R, Kamalarajah S, Cole M, James C, Shaw S.  Suprachoroidal haemorrhage complicating cataract surgery in the UK: a case control study of risk factors. Br J Ophthalmol. 2004;88(4):474–7. 33. Chu TG, Green RL. Suprachoroidal hemorrhage. Surv Ophthalmol. 1999;43(6):471–86. 34. Chak M, Williamson TH.  Spontaneous suprachoroidal haemorrhage associated with high myopia and aspirin. Eye. 2003;17(4):525–7. 35. Zheng D, Chen L, Sun Y, Shao Y, Liang J, Liu Y. Out-of-the-bag intraocular lens dislocation: outcomes of posterior chamber intraocular lens exchange, risk factors, and prevention. Chin Med J (Engl). 2010;123(18):2562–7. 36. Fernández-Buenaga R, Alio JL, Pérez-Ardoy AL, Larrosa-Quesada A, Pinilla-Cortés L, Barraquer R, et  al. Late in-the-bag intraocular lens dislocation requiring explantation: risk factors and outcomes. Eye. 2013;27(7):795–802. 37. Krėpštė L, Kuzmienė L, Miliauskas A, Janulevičienė I.  Possible predisposing factors for late intraocular lens dislocation after routine cataract surgery. Medicina (Kaunas). 2013;49(5):229–34. 38. Suto C, Hori S, Kato S, Muraoka K, Kitano S.  Effect of perioperative glycemic control in progression of diabetic retinopathy and maculopathy. Arch Ophthalmol. 2006;124(1):38–45. 39. Sadiq SA, Chatterjee A, Vernon SA. Progression of diabetic retinopathy and rubeotic glaucoma following cataract surgery. Eye. 1995;9(6):728–32. 40. Chung J, Kim M-Y, Kim H-S, Yoo J-S, Lee Y-C. Effect of cataract surgery on the progression of diabetic retinopathy. J Cataract Refract Surg. 2002;28(4):626–30.

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41. Menchini U, Cappelli S, Virgili G.  Cataract surgery and diabetic retinopathy. Semin Ophthalmol. 2003;18(3):103–8. 42. Kung JS, Choi DY, Cheema AS, Singh K. Cataract surgery in the Glaucoma patient. Middle East Afr J Ophthalmol. 2015;22(1):10–7. 43. Lee CK, Lee NE, Hong S, Kang E, Rho SS, Seong GJ, et  al. Risk factors of disease progression after cataract surgery in chronic angle-closure Glaucoma patients. J Glaucoma. 2016;25(4):e372–6. 44. Verma L, Venkatesh P, Tewari HK.  Phototoxic retinopathy. Ophthalmol Clin N Am. 2001;14(4):601–9. 45. Youssef PN, Sheibani N, Albert DM. Retinal light toxicity. Eye. 2011;25(1):1–14.

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Needle Stick Globe Injuries Atul Kumar, Prateek Kakkar, Divya Agarwal, and Aman Kumar

2.1

Introduction

Injury to the globe or its coats following the administration of medication either in the form of a peribulbar or retrobulbar anaesthesia or during the administration of a posterior subtenon medication is a well-known fact [1, 2]. Such a complication occurring as a result of the iatrogenic injury due to the needle is known as needle stick globe injury. It can result in mild laceration of the scleral coat or can lead to a perforating injury with serious effects on the vision.

2.2

Epidemiology and Risk Factors

Various authors have reported the occurrence of the globe perforations ranging from 0.024% for cataract patients to 0.1% [1]. The occurrence is more common in cases of retrobulbar anaesthesia, which involves the intraconal injection of the anaesthetic, compared with the technique of peribulbar anaesthesia, classically involving injections given outside the extraocular muscle cone [3]. The thickness of the needle used for drug delivery may vary from 22 to 26 G; thicker needles leading to more incidence of perforation. According to Duker et  al., 45% of globe perforations occurred in patients who had an axial length of ≥26 mm [2]. Cases of axial myopia have a 30 times greater risk of puncture of the globe compared to patients having normal axial

A. Kumar (*) · P. Kakkar · D. Agarwal Dr. Rajendra Prasad Centre for Ophthalmic Sciences, AIIMS, New Delhi, India A. Kumar Advanced Eye Centre, PGIMER, Chandigarh, India © Springer Nature Singapore Pte Ltd. 2020 M. Chakrabarti, A. Chakrabarti (eds.), Posterior Segment Complications of Cataract Surgery, https://doi.org/10.1007/978-981-15-1019-9_2

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length during intraconal injections. Some studies have estimated the risk rate of one in every 140 peribulbar blocks in eyes with axial length greater than or equal to 26 mm. Posterior staphyloma is the posterior outpouching of the globe resulting from pathological thinning of retina, choroid, and sclera and is associated with myopia. The frequency is seen more with high myopia, i.e. axial length greater than or equal to 26.5  mm. A review of 50,000 patients who received needle block revealed seven cases of perforation of the globe. All the cases had posterior staphyloma preoperatively [3]. It is also observed that with increasing axial length, the shape of the globe changes from globular to ellipsoid [4]. The usual location of posterior staphyloma is inferior to the posterior pole. The most common site of globe perforations observed in such eyes is in the inferotemporal quadrant. Other important risk factors include a repeated number of injections, uncooperative patient, enophthalmos, history of previous scleral buckling, the bevel of the needle facing away from the globe and block attempted by inexperienced surgeons lacking knowledge about technique or orbital anatomy.

2.3

Mechanism of Injury

Injury to the globe can be divided into a laceration, penetration, and perforation injury. The type of injury shall be responsible for the extent of ocular damage and the immediate signs that help us recognize them. Lacerations are usually superficial injury, involving only the scleral coat. Such an injury is usually not significant and may be left unattended. In cases of perforating injury, injection of anaesthetic agent will be limited to extraocular space contributing to limited ocular damage. The patient’s eye may become hypotonous, especially after the block. In cases of penetrating injury, intraocular injection of anaesthetic will be detectable immediately due to a significant rise of intraocular pressure. The patient may complain of sudden pain associated with vision loss. Therefore, type of break and its problems depend largely on the type of injury and the presence of anaesthetic injection in the globe. Another factor important is the size of the needle used. Larger needles tend to cause a larger break. Direction of needle injection into the peribulbar space or posterior segment is also important, especially in eyes predisposed to injury. The breaks caused by needle stick perforation are multiple sewing machine-type of breaks that are closely located. The breaks are usually large and oblong. Two widely separated oval-shaped breaks can be created if the needle pierces globe at an acute angle causing both entry and exit wound. The posterior break is usually located around the posterior pole or upper nasal quadrant. The perforations caused by peribulbar anaesthesia are usually larger in size compared to subconjuctival/ subtenon’s injection as smaller needles are used in the latter.

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Signs and Symptoms

It is prudent that the globe perforation is diagnosed at the earliest because of the nature of its severity. Therefore, its signs and symptoms must be carefully sought for, especially in cases where risk factors exist. Patient shall develop sudden-onset of severe ocular pain, associated with sudden-onset vision loss and change of intraocular pressure. In perforating injuries, the globe tends to become hypotonus, while in penetrating injuries the eye may become harder, especially if the anaesthetic drug is injected into the globe. Patient may have no symptoms immediately. Nearly half of the patients experience no immediate symptoms or signs of globe perforation [2]. In penetrating injuries, sudden give way of resistance after forceful insertion of needle tip may be a useful indicator of the globe being perforated. In such cases, the globe moves along with movement of the needle. Insertion of the drug in cases with penetrating globe injuries is difficult considering the resistance generated from the expansion of the globe. It is important to evaluate such a patient at the earliest. The surgeon should postpone the intended surgery and seek help from vitreoretinal specialist in cases of globe perforation. The operating surgeon should be consulted immediately in cases of suspected globe perforation. Detailed fundus evaluation should be done for better assessment of extent of damage. Most of the patients present initially with vitreous haemorrhage, which is fresh in nature. Such cases must be further evaluated using ultrasonography to rule out retinal detachment or choroidal detachment. If retinal detachment is noted, the elective case must be cancelled immediately. Patient should be immediately referred to a vitreoretinal specialist for further management. In untreated cases or cases which are not initially evaluated due to non-­recognition of the condition, a patient may present with retinal detachment and loss of vision, usually within 1 year after the surgery. Such cases usually present with proliferative vitreoretinopathy (PVR) which may even obscure the recognition of actual site of the retinal break. Globe penetration can also lead to globe rupture or ocular explosion [5]. It can result from accidental injection of local anaesthetic agent into the globe which can occur even after 2 ml volume of injection. Visual prognosis is poor in such cases [6, 7].

2.5

Management

Once the diagnosis of the globe perforation is certain, the elective case must be called off and the management of perforation must be given the highest priority. The management and the prognosis is different for cases presenting with retinal detachment than those eyes presenting with only vitreous haemorrhage. In cases with only vitreous haemorrhage without retinal detachment, the surgeon may initially observe the patient for the resolution of vitreous haemorrhage for the first week. If the vitreous haemorrhage clears within 7–10 days of the injury, the retinal breaks are clearly recognized and photocoagulation/cryopexy is done to

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prevent any retinal detachment. If the vitreous haemorrhage does not resolve within 7–10 days, early vitreoretinal surgery is advocated [8]. Certain patients who are left untreated, very frequently present with retinal detachment. Various factors may contribute to retinal detachment like myopia, vitreous haemorrhage, vitreous traction due to trauma, and untreated retinal breaks. Patients who are diagnosed later due to the event of perforation going unnoticed have PVR changes. PVR changes are usually severe. Each case is a surgical challenge to the retinal surgeon as the configuration of the retinal detachment is an admixture of vitreous traction syndrome and retinal holes, each unique to the case. Inferotemporal breaks are most commonly found in such cases. The rest of the breaks can be usually located along a line extending from inferotemporal break to upper nasal quadrant. Surgical treatment includes vitreoretinal surgery involving core and peripheral vitrectomy with shave excision of vitreous base, peeling of any membranes, followed by laser photocoagulation or transscleral cryopexy of the retinal breaks. Such patients require the insertion of silicon oil for adequate tamponade. It is not uncommon to observe recurrence of the retinal detachment. Most patients may require two to three retinal surgeries for stabilization of retinal detachment. Scleral buckling has been attempted but usually with poor results and follow-up need for vitreoretinal surgery. Submacular haemorrhage can be managed using recombinant tissue plasminogen activator.

2.6

Prognosis

Long-term visual acuity is usually poor especially in cases presenting with retinal detachment. Morris et al. showed that only one-fourth of patients with a globe perforation reach visual acuity >20/60 [9]. Hay et al. reported visual acuity of 6/120 in some cases in a series of retinal detachment with globe perforation [10].

2.7

Prevention

Prevention is better than cure. A B-scan echography of patients with pathological myopia must be practised as a norm to evaluate the exact site of staphyloma and plan the anaesthesia accordingly. Avoid inferotemporal route in such patients. A single needle prick for peribulbar injection is recommended for anaesthesia. Safer alternatives like topical, subconjuctival, or subtenon’s anaesthesia can be deployed to avoid needle-related complications. Choice of the needle to be used for prevention of globe perforations has been debated for long. Sharp needles cause less pain, less patient discomfort, and less

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ocular damage on accidental globe perforation [6]. Chances of globe perforation are less with use of blunt needles as increased resistance is felt on encountering the globe leading to early recognition. However, they lead to more ocular damage as compared to sharp needles in cases of perforation [11]. Therefore, the use of sharp needle is advocated for giving blocks especially in the hands of an experienced ophthalmologist. While for parabulbar approach, or with an inexperienced ophthalmologist, a blunt tipped needle may serve equally well. One should always try to minimize the number of injections given to the patient. Some precautions can be taken prior to injecting anaesthetic agent after initial prick like sideways movement of needle to see if it has not pierced the globe or asking the patient to move his/her eyes. The patient should be made to look straight with the help of fixation target. Injection should be avoided in cases of aspiration of blood or vitreous. Block should be discontinued if one sees corneal oedema or feels resistance while injecting. Eye should be checked once for intraocular pressure changes before applying Honan’s device [6, 7]. A few thoughtful steps could go a long way in preventing a long-term complication of a somewhat harmless procedure.

References 1. Rubin AP. In: Wildsmith JAW, Armitage EN, McLure JH, editors. Eye blocks in principles and practice of regional anaesthesia. 3rd ed. Churchill Livingston: London; 2003. p. 241–50. 2. Duker JS, Belmont JB, Benson WE, Brooks HL Jr, Brown GC, Federman JL, et  al. Inadvertent globe perforation during retrobulbar and peribulbar anesthesia. Ophthalmology. 1991;98:519–26. 3. Edge R, Navon S. Scleral perforation during retrobulbar and peribulbar anesthesia: risk factors and outcomes in 50,000 consecutive injections. J Cataract Refract Surg. 1999;25:1237–44. 4. Vohra SB, Good PA. Altered globe dimensions of axial myopia as risk factors for penetrating ocular injury during peribulbar anaesthesia. Br J Anaesth. 2000;85(2):242–5. 5. Bullock JD, Warwar RE, Green WR. Ocular explosion from periocular anesthesia injections. Ophthalmology. 1999;106:2341–53. 6. Hamilton RC, Gimbel HV, Strunin L. Regional anaesthesia for 12,000 cataract extraction and intraocular lens implantation procedures. Can J Anaesth. 1988;35:615–23. 7. Magnante DO, Bullock JD, Green RW.  Ocular explosion after peribulbar anesthesia. Ophthalmology. 1997;104:608–15. 8. Gopal L, Badrinath SS, Parikh S, Chawla G. Retinal detachment secondary to ocular perforation during retrobulbar anaesthesia. Indian J Ophthalmol. 1995;43:13–5. 9. Morris A, Elder MJ.  Warfarin therapy for cataract surgery. Clin Exp Ophthalmol. 2000;28:419–22. 10. Hay A, Flynn HW, Hoffmann JI, et al. Needle penetration of the globe during retrobulbar and peribulbar injections. Ophthalmology. 1991;98:1017–24. 11. Hamilton RC. A discourse on the complications of retrobulbar and peribulbar blockade. Can J Ophthalmol. 2000;35:363–72.

3

The Dropping and Dropped Nucleus Meena Chakrabarti and Arup Chakrabarti

3.1

Introduction

Phacoemulsification with posterior chamber intraocular lens implantation within the capsular bag, the gold standard for managing cataracts, requires preservation of the posterior capsular support for successful lens removal and intraocular lens placement. The most common intraoperative complication associated with this procedure is disruption of posterior capsule, resulting in vitreous loss [1]. The proportion of patients who have a posterior capsular rupture vary from 0.45% in the hands of a very experienced surgeon to 14.7% for residents in training [2]. The incidence of complications associated with this surgical procedure has significantly decreased with advances in technological, improved surgical techniques, and availability of structured residency programmes globally. The reported incidence of nuclear fragments in vitreous cavity following a PCR is 0.3% (2–3/1000 operations/year) [3, 4] to 1.1% [5]. PCRs during phacoemulsification are more central than in ECCE and posterior migration of the nuclear fragments are seen more commonly [6]. The complications of a dropped nucleus may include elevated intraocular pressure, uveitis, corneal edema, cystoid macular edema, and retinal detachment. Hence proper management of vitreous loss and retained lens fragments is the most important factor influencing the final visual outcome. von Lany et al. [7] in 2009 in the report of the British Ophthalmological Surveillance Unit (BOSU) and also various other authors in several retrospective case series [8–10] have reported a final corrected visual acuity ≥6/12.

M. Chakrabarti (*) · A. Chakrabarti Chakrabarti Eye Care Centre, Trivandrum, Kerala, India © Springer Nature Singapore Pte Ltd. 2020 M. Chakrabarti, A. Chakrabarti (eds.), Posterior Segment Complications of Cataract Surgery, https://doi.org/10.1007/978-981-15-1019-9_3

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M. Chakrabarti and A. Chakrabarti

Intraoperative Management by the Cataract Surgeon

When a PCR occurs, the primary goal of the cataract surgeon is to remove as much of the remaining nucleus as possible if it is visible and in an accessible position in the anterior vitreous. A dispersive ophthalmic viscosurgical device (OVD) can be injected into the anterior chamber to tamponade the vitreous and to support the nuclear fragment [11]. This maneuver ensures safe withdrawal of the phaco needle without aggravating further vitreous prolapse. The surgical procedure is thus “frozen-­in-time,” allowing the surgeon adequate time to think and plan his immediate surgical strategy. There are certain intraoperative maneuvers which aggravate the risk of vitreous traction and should be avoided. 1. PAL (posterior assisted levitation) popularized by Packard and Kinnear [12] in 1991 to raise the dropped nucleus into the anterior chamber for safe removal is associated with the risk of aggravating vitreous traction. It is technically difficult to cause a purely axial displacement of the lens fragment by injecting OVD behind the dislocating lens fragment. And in many cases the OVD may push the nuclear fragment peripherally under the iris and out of the surgeon’s view. 2. Inserting a spatula through the pars plana creates unpredictable vitreous traction which also predispose to the development of a suprachoroidal hemorrhage in a soft eye [13]. 3. Use of irrigation into the vitreous to “flush” the nucleus up into the pupillary space is associated with an increased risk of creating retinal tears and is not advisable [14]. There are several reports documenting the dangers of fishing for lens fragments [15–18]. 4. In the presence of vitreous, it is not advisable to continue use of phacoemulsification to remove nuclear fragments. The phaco tip cannot cut vitreous gel and will instead aspirate the vitreous leading to significant vitreoretinal traction and a high risk of developing a retinal tear [19]. The fluid flow into the vitreous through the capsular rent, if phacoemulsification is continued, will hydrate the vitreous, thereby increasing the vitreous volume and aggravate vitreous prolapse and further enlargement of the PCR. If the nucleus has drifted out of reach, no attempt should be made to retrieve it via the anterior route. So also if the nucleus drops into the vitreous cavity, unless optimal three port pars plana vitrectomy capability is immediately accessible, the cataract surgeon should focus on minimizing collateral damage by safe management of anterior vitreous (by adequate bimanual anterior vitrectomy), cortical cleanup, a stable IOL implantation wherever possible and assured incisional integrity [20]. An adequate bimanual anterior vitrectomy should be performed through the two paracentesis. Avoid use of the main incision. Using a low bottle height, high cut rate, and low suction, the anterior chamber should be cleared of vitreous [21]. Triamcinolone acetonide usage for visualization [22] ensures an adequate anterior vitreous removal and may be helpful in decreasing postoperative inflammation. The cutter is first passed through the rent in the posterior capsule (with the cutting port

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facing the rent in the posterior capsule) to remove an adequate amount of anterior vitreous [23]. This will ensure removal of all the prolapsed vitreous in the anterior chamber and prevent further vitreous prolapse and enlargement of the PCR. This technique ensures that the prolapsed vitreous is brought back home into the vitreous cavity before removal. The anterior vitrectomy can also be performed through the pars plana either directly through a sclerotomy (using an MVR knife) or by placement of a valved trocar 3 mm posterior to the limbus using MIVS [24, 25]. If the PCR is small and there is only a small amount of vitreous prolapse into the anterior chamber, a “dry” anterior vitrectomy can be performed taking care to maintain the anterior chamber by injecting OVD. Residual soft cortical lens matter in the anterior vitreous can also be removed using the vitreous cutter. After performing an adequate bimanual anterior vitrectomy, the location and status of residual lens matter should be reassessed, and an attempt is made to prevent it from dislocating into the posterior segment. Remaining lens matter can be maneuvered mechanically with the use of OVD and brought to the pupillary area, from where, it can be removed by resuming phacoemulsification over a temporary scaffold (Sheet’s glide [26] or Agarwal [27] three-piece IOL scaffold technique) or by converting to a large incision manual ECCE or manual small incision cataract surgery.

3.3

IOL Implantation Options for the Cataract Surgeon

The decision to implant an IOL during the primary surgery is usually made by the cataract surgeon taking into account the following factors: 1 . Visibility to assess capsular support and zonular integrity 2. Degree of hardness and size of the retained lens fragment. 3. Size and location of the posterior capsular rent. In a given case, if the surgery required excessive intraoperative manipulations and was prolonged, due to the presence of corneal edema or poor pupillary mydriasis, the visibility to assess the capsulozonular integrity is usually compromised. In this situation, it is not advisable to implant an IOL in the same sitting. The surgeon should also not attempt to implant an IOL in the same sitting if the retained lens fragment is very hard nuclear cataract (black or brown) since excessive ultrasound energy will be required to emulsify it, and if phacofragmentation is not feasible, the dislocated nucleus will have to be brought to the pupillary area using perflurocarbon liquid and removed through the limbal incision or scleral tunnel. However, if the dislocated lens matter is only soft cortex or soft nuclear matter, primary IOL implantation can be considered when adequate capsulo zonular support is present. In eyes with good visibility and a small central PCR, in general, a silicone IOL should be avoided, particularly in eyes with high risk of developing retinal

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detachment and possible need for silicone oil tamponade. This is because s­ ilicone oil–silicone IOL [28] interaction causes visual aberration for both patient and the operating retinal surgeon. Medical management of retained lens material in the interim period before the definitive surgery is aimed at treating its secondary complications including intraocular inflammation and glaucoma. Topical steroids and nonsteroidal anti-­ inflammatory drugs (NSAIDS) are used to control inflammation along with cycloplegic agents. Topical anti-glaucoma medications and oral carbonic anhydrase inhibitors may be necessary to bring the IOP under control.

3.4

Definitive Surgery

Timing of definitive surgery to retrieve the dropped nucleus is determined on an individual case basis [29–32]. Delayed vitrectomy can result in the development of glaucoma and corneal edema. Blodi et al. [33] reported glaucoma (elevated IOP) in 60% of eyes undergoing vitrectomy for removal of retained lens matter after 3 weeks. Margherio et  al. [13] found an increased incidence of retinal detachment associated with delayed vitrectomy due to persistent vitreous traction aggravated by prolonged inflammation. The eye can tolerate small amounts of soft cortical matter, and hence, these patients can be safely observed with a vigilant watch for the development of raised IOP or evidence of intraocular inflammation. In all other situations, the chance of chronic intraocular inflammation and raised IOP is very high. A vitreoretinal specialist’s availability to team up with the anterior segment surgeon at the same surgery or on the same day is ideal both emotionally for the patient and structurally for the eye. For the patient it avoids going through two postoperative periods for achieving the final best visual result. However, if vitreoretinal facility is not immediately available, an honest communication with the patient, good counselling, and appropriate referral to a vitreoretinal facility will almost always ensure a happy patient outcome. Vitrectomy for the removal of dislocated nuclear fragments can be delayed up to 3  weeks without significant difference in the visual and functional results. However, delaying vitrectomy for the removal of dislocated nuclear fragments will indefinitely almost always result in limited visual recovery and a higher incidence of recalcitrant glaucoma and retinal detachment. Some cases may have to be delayed to permit clearing of corneal edema for adequate visualization for vitrectomy. However, in cases with markedly elevated IOP refractory to medical management, urgent surgical intervention is necessary. The following information should be included while referring the patient for vitreoretinal intervention. • • • •

Amount/type/hardness of retained lens material. Presence/absence of IOL implant. Assessment of capsular support. Calculated IOL power

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The vitreoretinal surgeon should assess the patient thoroughly prior to taking up the case and make his own judgments about the amount and hardness of the nucleus fragment and the urgency with which the intervention should be performed. The following factors should also be assessed: (a) Integrity of cataract wound should be verified. (b) Slit lamp evaluation to assess corneal clarity, grade the degree of anterior chamber inflammation, and check the applanation IOP. (c) Indirect ophthalmoscopy should be performed to assess the nuclear fragment as well as to exclude peripheral retinal tears, retinal detachment, or choroidal detachment. (d) In eyes where presence of media haze (corneal edema, anterior soft cortical matter in pupillary area, or associated vitreous hemorrhage) precludes fundus visualization, a B-scan ultrasonography should be performed to evaluate the integrity of the posterior segment and to rule out the presence of retinal detachment or choroidal detachment. The dislocated lens fragment may appear hyperechoic and show acoustic shadowing. Surgical Procedure: A three-port pars plana vitrectomy is the procedure of choice and is today the standard of care for patients with posterior dislocated lens fragments. Hybrid or mixed gauge vitrectomy is performed with the active 20 G port for the introduction of the larger bore fragmatome [28–30]. A fragmatome is similar to a phaco probe without an infusion sleeve, and it cannot cut the vitreous. Hence, a complete vitrectomy should be performed before using the fragmatome for nucleus removal. This can be aided by the use of triamcinolone acetonide to delineate the posterior hyaloid face and for the induction of a posterior vitreous detachment (PVD) [31–33]. Soft nuclear or fluffy cortical fragments can be cut and aspirated with the vitreous cutter. The endoilluminator can be used to crush the fragments against the cutter and feed them into the cutting port [34–36]. For harder nuclear material, the fragmatome is used. Prior to phacofragmentation, majority of surgeons will introduce a small amount of perfluorocarbon liquid (PFCL) into the vitreous cavity to cover the macula and float the fragments away from the retinal surface [37]. This helps to protect the macula from fragments that tend to fall back during phacofragmentation. The settings for the fragmatome include a pulse mode with 10–20 pulses/min, 20–50% power depending on hardness of the nucleus, and a vacuum of 150–200 mmHg, as well as a high bottle height to prevent hypotony as higher flow rates are necessary to meet the demands of aspiration through the wider bore fragmatome. Small fragments stuck to the retinal surface or entrapped in the vitreous base should be removed (Fig.  3.1a–m). Any residual vitreous at the vitreous base should be excised to eliminate traction, and the retinal periphery should be scrutinized in detail for any retinal tears or detachment. In cases with dislocated black cataract where a prolonged and difficult phacofragmentation is anticipated or when visualization is impaired by corneal edema,

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a

b

c

d

e

f

g

h

i

j

k

l

m

Fig. 3.1 (a) A 78-year-old male patient who developed an intraoperative posterior capsular rent with retained lens matter in the vitreous cavity. This is an intraoperative still photography before (cortex aspiration, anterior as well as pars plana vitrectomy, phacofragmentation) secondary ciliary sulcus implantation of a three-piece hydrophobic acrylic IOL (Sensar) was performed. (b) Preservative-free triamcinolone acetonide is used to stain the vitreous which has prolapsed into the anterior chamber through the PCR. (c and d) Cortex admixed with vitreous is cut and aspirated. Note that the capsulorhexis margin is intact. (e–g) The limbal tunnel is opened up and the 2° IOL is introduced into the anterior chamber and placed with the haptics resting on the iris surface. (h–i) The haptics are compressed against the optic and placed in the ciliary sulcus. (j) Optic capture through the rhexis margin is performed. (k) Residual viscoelastic material is aspirated. (l) Phacofragmentation is performed after PVD induction and a thorough vitrectomy, followed by injection of a small amount of PFCL into the vitreous cavity. (m) Well-centered PCIOL with its haptics positioned in the ciliary sulcus and the optic captured behind the rhexis margin

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the nucleus can be floated up to the pupillary space using PFCL and delivered out through the enlarged phaco incision [37]. At the end of the procedure, the PFCL introduced into the vitreous cavity should be aspirated, and laser retinopexy should be performed to any retinal tears detected intraoperatively.

3.5

Management of Associated Complications

(a) Intraocular inflammation: The lens protein causes severe intraocular reaction when exposed to the ocular environment as it is an immunologically protected protein, meant to be confined within the lens capsule. The severity of the reaction is usually directly proportional to the volume of lens matter retained in the vitreous cavity, the extent of intraoperative manipulations and also on the individuals’ inflammatory response [38]. Topical steroids and NSAIDs are used to combat inflammation along with cycloplegics. (b) Glaucoma: Nearly 50% of patients undergoing pars planavitrectomy for retained lens matter have elevated IOP [33]. Patients in whom vitrectomy for the removal of retained nuclear fragments was delayed for more than 3 weeks for various reasons have shown a higher incidence of elevated IOP on long-term follow-up. The presumed mechanism for the development of elevated IOP in eyes undergoing delayed vitrectomy could be due to clogging of trabecular meshwork with lens protein, macrophages, and other inflammatory cells. Even though removal of retained lens material will control IOP in majority of cases, it is not uncommon that some eyes will require longer term glaucoma medications and/or glaucoma procedures. It is noteworthy that elevated IOP occurs despite attempted prophylaxis with slow release acetazolamide. Other factors contributing to elevated IOP are retained OVD and increased release of inflammatory mediators due to extra surgical manipulations [39]. There have been reports of recalcitrant secondary glaucoma due to retained OVD in vitreous after its usage to tamponade posterior capsular rupture [40]. Hence, it is important to ensure that as much of the residual viscoelastic and soft lens matter is cleared from the anterior chamber during the primary surgery. The importance of reviewing patients with PCR on postoperative day 1 and anticipating IOP rise is highlighted by these reports. Other causes of ocular hypertension after cataract surgery include pigment dispersion secondary to sulcus placement of the IOL, particularly if a single-­ piece acrylic lens is used, and also steroid responders who develop raised IOP secondary to postoperative steroid eye drops. The rise in IOP in the steroid responders will settle after discontinuation of topical steroids, but those in the former group will often require anti-glaucoma medication or even surgery in more extreme cases. (c) Corneal edema: It is seen in almost 33–85% of patients with retained nuclear fragments [33, 41–44]. Increased intraoperative manipulation, postoperative intraocular inflammation, and elevated IOP are the three important factors

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contributing to the development of corneal edema. With appropriate management of the postoperative inflammation and measures to control the elevated IOP, the corneal edema usually clears. Retinal Tears and Retinal Detachment (RD): The incidence of RD increases from ≤1% in uncomplicated cataract surgery to 6.8–8% after a complicated cataract surgery with PCR [45]. The incidence of RD associated with retained nuclear fragments is even higher and has been reported to vary from 4 to 16% [45–47]. RD can develop intraoperatively at the time of cataract surgery or in the early postoperative period. It can also develop after pars plana vitrectomy to remove dislocated nuclear fragments. In a series which reported the highest rates of RD (16%), 40% of the RD were seen during vitrectomy and 60% after pars plana vitrectomy [48]. Attempts to retrieve the dropping nuclear fragment using lens loop or trying to flush it out by irrigating into the vitreous cavity can cause traction on the vitreous base and development of retinal tears at the periphery or a Giant Retinal Tear intraoperatively [41, 43]. In a series published by Margheiro et al. 43% of the detachments occurred after vitrectomy among which 75% were diagnosed within 1 month after surgery and 50% were diagnosed after 3 months [41]. After a thorough pars plana vitrectomy with excision of vitreous base, PFCL is injected to float up the dislocated nuclear fragments and flatten the retina mechanically. The dislocated nuclear fragments can be removed using phacofragmentation in the anterior vitreous. The responsible retinal tear is lasered and a PFCL—air exchange with non expansile mixture of air—C3F8 tamponade or PFCL-SO exchange is performed. Vitreous Hemorrhage: It has been reported with attempts to flush out the dislocated nuclear fragments by posterior irrigation into the vitreous cavity [49]. Cystoid Macular Edema: It has been reported to occur in 7–41% of patients with retained nuclear fragments [44, 50]. Dislocated IOL with Retained Lens Material: Posteriorly dislocated IOL along with retained nuclear material can occur if the surgeon fails to recognize the presence of a rent in the posterior capsule or if the PC IOL is incorrectly positioned. The IOL removal or repositioning is performed after fragmentation and removal of the dislocated nuclear fragments. A three-piece IOL can be grasped with the vitreous forceps and manipulated into the ciliary sulcus, if adequate capsular support is present. In the absence of adequate capsular support, the haptics can be exteriorized and placed in a scleral tunnel in the bed of a partial thickness scleral flap to achieve sutureless scleral fixation. Prior dissection of the scleral flaps is necessary for this procedure. Single-piece IOLs or IOLs with broken haptics and plate haptic IOLs are generally explanted and replaced with an appropriate IOL as previously described.

Visual Outcomes: In eyes with retained lens fragments, a final visual acuity of 20/40 or better is achieved in 56–72% and is increased to 80% when pre-existing vision limiting ocular pathology is excluded [45, 51]. Eyes with softer non-nuclear retained lens fragments have better outcomes than eyes with harder retained nuclear

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fragments. Vanner et al. [52] have reported that 78% of eyes with non-nuclear fragments obtain 20/40 or better vision, compared to only 39% of eyes with retained nuclear fragments.Several studies have shown that the final visual acuity result in eyes with PCR is very gratifying, with 95% of cases achieving a best corrected visual acuity of 6/12 or better [39, 53–56]. The risk factors for poor visual outcome included older age, presence of coexisting ocular pathology, ACIOL implantation, and vitreous loss requiring anterior vitrectomy. The visual outcome in eyes with PCR, when eyes with comorbidities were included, was ≥6/12 in 88% of cases [56] implying that gratifying visual outcomes are possible in properly managed cases.

References 1. Stein JD.  Serious adverse events after cataract surgery. Curr Opin Ophthalmol. 2012;23(3):219–25. 2. Howcroft MJ, Warren K, Arbissar L, et al. Focal points module: anterior vitrectomy for the anterior segment surgeon. 2009;XXXVII(2):Module 2 of 3. 3. Mahamood B, vonLany H, Cole MD, et al. Displacement of nuclear fragments into the vitreous complicating phacoemulsification surgery in the UK: incidence and risk factors. Br J Ophthalmol. 2008;92(4):488–92. 4. Leaming DV.  Practice style and preferences of ASCRS members: 1994 survey. J Cataract Refract Surg. 1995;21:378–85. 5. Pande N, Dabba TR. The incidence of lens matter dislocation during phacoemulsification. J Cataract Refract Surg. 1996;22:737–42. 6. Harry W Flynn MD, Jr, Scott I. Perspective of lens and IOL surgery: management of dropped nucleus by a cataract surgeon. 7. von Lany H, Mahamood H, James CR, et al. Displacement of nuclear fragments into vitreous cavity complicating phacoemulsification surgery in UK: clinical features, outcomes. Br J Ophthalmol. 2008;92(4):493–5. 8. Kim JE, Flynn HW Jr, Smiddy WE, et al. Retained lens fragments after phacoemulsification. Ophthalmology. 1994;101:1827–32. 9. Vilar NF, Flynn HW Jr, Smiddy WE, et al. Removal of retained lens fragments after phacoemulsification reverses secondary glaucoma and restores visual acuity. Ophthalmology. 1997;104:787–92. 10. Borne MJ, Tasman W, Regillo C, et al. Outcomes of vitrectomy for retained lens fragments. Ophthalmology. 1996;103:971–6. 11. Chang DF, Packard RB. Posterior assisted levitation for nucleus retrival using Viscoat after posterior capsule rupture. J Cataract Refract Surg. 2003;29:1860–5. 12. Packard RBS, Kinnear FC.  Manual of cataract and intraocular lens surgery. Edinburg: Churchill Livingstone; 1991. p. 47. 13. Margherio RR, Margherio AR, Pendergast SP, et al. Vitrectomy for retained lens fragments after phacoemulsification. Ophthalmology. 1997;104:1426. 14. Aaberg TM Jr, Rubsamen PE, Flynn HW Jr, et  al. Giant retinal tears as a complication of attempted removal of intravitreal fragments during cataract surgery. Am J Ophthalmol. 1997;124:222–6. 15. Chang DF.  Chapter 6. Managing the broken posterior capsule. In: Colvard DM (editor). Achieving excellence in cataract surgery. A step-by-step approach, pp. 53–58. 16. Chang DF. Conquering capsule complications: a video primer. AAO-APAO Course 56; 2006. 17. Chang DF. Managing residual lens material after posterior capsular rupture. Tech Ophthalmol. 2003;1(4):201–6.

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18. Prasad S, Chang DF, Agarwal A, Tija K. Dropping or dropped nucleus. When and how to rescue threatened nuclear drop, when to refer and what happens after referral. ASCRS 2013, San Francisco, Course 22–206. 19. Ruiz-Moreno JM, Barile S, Montero JA. Phacoemulsification in the vitreous cavity for retained nuclear lens fragments. Eur J Ophthalmol. 2006;16:40–5. 20. Michelson MA. Chapter 18. The torn posterior capsule. In: Fishkind W (editor). Complications in phacoemulsification, pp. 123–132. 21. Arbisser LB, Charles S, Howcroft M, et al. Management of vitreous loss and dropped nucleus during cataract surgery. Ophthalmol Clin North Am. 2006;19:495–506. 22. Peyman GA, Cheema R, Conway MD, Fang T. Triamcinolone acetonide as a aid to visualising the vitreous and the posterior hyaloid during parsplanavitrectomy. Retina. 2000;20:554–5. 23. Kasbekar S, Prasad S, Kumar BV. Clinical outcomes of triamcinolone assisted anterior vitrectomy after phacoemulsification complicated by posterior capsular rupture. J Cataract Refract Surg. 2013;39:414–8. 24. Chalam KV, Shah VA.  Successful management of cataract surgery associated vitreous loss with sutureless small gauge pars planavitrectomy. Am J Ophthalmol. 2004;138:79–84. 25. Chalam KV, Gupta SK, Vinjamaran S, Shah VA.  Small gauge sutureless pars planavitrectomy to manage the vitreous loss during phacoemulsification. J Cataract Refract Surg. 2003;29:1482–6. 26. Michelson MA.  Use of a sheets’ glide as a pseudoposterior capsule in phacoemulsification complicated by posterior capsular rupture. Eur J Implant Refract Surg. 1993;5:70–2. 27. Kumar DA, Agarwal A, Prakash G, Jacob S, Agarwal A, Sivagnanam S. IOL scaffold technique for posterior capsular rupture. J Refract Surg. 2012;28(5):314–5. 28. Yaman A, Saatci AO, Sarioğlu S, et al. Interaction with intraocular lens materials: does heavy silicone oil act like silicone oil. J Cataract Refract Surg. 2007;33:127–9. 29. Colyer MH, Berinstein DM, et al. Same day verses delayed vitrectomy with lensectomy for the management of retained lens fragments. Retina. 2011;31:1534–40. 30. Vanner EA, Stewart MW, Liesegang IJ, et al. A retrospective cohort study of clinical outcomes for intra vitreal retained crystalline lens fragments after age related cataract surgery: a comparison of same day verses delayed vitrectomy. Clin Ophthalmol. 2012;6:1135–48. 31. Salehi A, Razmju H, Beni AN, et  al. Visual outcome of early and late pars planavitrectomy in patients with dropped nucleus during phacoemulsification. J Res Med Sci. 2011;16:1422–9. 32. Vanner EA, Stewart MW.  Vitrectomy timing for retained lens fragments after surgery for age related cataracts—a systematic review and meta analysis. Am J Ophthalmol. 2011;152:345–57. 33. Blodi BA, Flynn HW Jr, Blodi CF, et al. Retained nuclei after cataract surgery. Ophthalmology. 1992;99:41. 34. Kiss S, Vavvas D. 25 gauge transconjunctival sutureless pars planavitrectomy for removal of retained lens matter and intraocular foreign bodies. Retina. 2008;28:1346–51. 35. Ho LW, Walsh MK, Hassan TS. 25 gauge pars planavitrectomy for retained lens fragments. Retina. 2010;30:843–9. 36. Cho M, Chan RP, et al. 23 gauge pars planavitrectomy for posteriorly dislocated crystalline lens. Clin Ophthalmol. 2011;5:1737–43. 37. Miller ER, Steel DH. Small gauge transconjunctival vitrectomy with phacoemulsification in the pupillary plane of dense retained lens matter on perflurocarbon liquid after complicated cataract surgery. Graefes Arch Clin Exp Ophthalmol. 2013;251:1757–62. 38. Lai TY, Kwok AK, et al. Immediate pars planavitrectomy for dislocated intravitreal lens fragments during cataract surgery. Eye. 2005;19(11):1157–62. 39. Ang GS, Whyte JF, et al. Effect and outcomes of posterior capsular rupture in a district general hospital setting. J Cataract Refract Surg. 2006;32:623–7. 40. Sihota R, Saxena R, et al. Intravitreal sodium hyalorunate and secondary glaucoma after complicated phacoemulsification. J Cataract Refract Surg. 2003;29:1226–7.

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41. Margherio RR, Margherio AR, Pendergast SP, et al. Vitrectomy for retained lens fragments after phacoemulsification. Ophthalmology. 1997;104:1426. 42. Kim JE, Flynn HW, Smiddy WE, et  al. Retained lens fragments after phacoemulsification. Ophthalmology. 1994;101:1827. 43. Gilliland GD, Hutton WH, Fuller DG. Retained intra vitreal lens fragments after cataract surgery. Ophthalmology. 1992;99:1263. 44. Tommila P, Immonen I.  Dislocated nuclear fragments after cataract surgery. Eye. 1995;9:437. 45. Scott IU, Flynn HW Jr, Smiddy WE, et al. Clinical features and outcome of pars planavitrectomy in patients with retained lens fragments. Ophthalmology. 2003;110:1567–72. 46. Merani R, Hunyor AP, Playfair TJ, et al. Pars planavitrectomy for the management of retained lens material after cataract surgery. Am J Ophthalmol. 2007;114:364–70. 47. Smiddy WE, Guerrero JL, Pinto R, et al. Retinal detachment rate after vitrectomy for retained lens material after phacoemulsification. Am J Ophthalmol. 2003;135:183–7. 48. Ho LY, Doft BH, Wang L, et al. Clinical predictors and outcomes of pars planavitrectomy for retained lens material after cataract extraction. Am J Ophthalmol. 2009;147(4):587–94. 49. Fastenberg DM, Schwartz PL, Shakin JL, et al. Management of dislocated nuclear fragments after phacoemulsification. Am J Ophthalmol. 1991;112:535. 50. Miller ER, Allen D, et al. Effect of anterior capsulorrhexis optic capture of a sulcus fixated IOL on refractive outcomes. J Cataract Refract Surg. 2013;39:841–4. 51. Garg SJ, Lane RG. Parsplana torsional phacoemulsification for removal of retained lens fragments during parsplanavitrectomy. Ophthalmology. 2003;110:1567–72. 52. Vanner EA, Stewart MW, et  al. Vitrectomy timing for retained lens fragments after surgery for age related cataracts: a systematic review and meta-analysis. Am J Ophthalmol. 2011;152:345–57. 53. Tan JYH, Karwatowski WSS, et al. Phacoemulsification cataract surgery and unplanned anterior vitrectomy: is it bad news? Eye. 2002;16:117–20. 54. Yap EY, Heng WJ, et al. Visual outcome and complications after posterior capsular rupture in phacoemulsification surgery. Int Opthalmol. 2000;23:57–60. 55. Ionides A, Minassian D, et  al. Visual outcome following posterior capsular rupture during cataract surgery. Br J Ophthalmol. 2001;85:222–4. 56. Tabandeh H, Smeets B, et  al. Learning phacoemulsification: The surgeon-in-training. Eye. 1994;8:475–7.

4

Pseudophakic Retinal Detachment Amit B. Jain and Muna Bhende

Retinal detachment (RD) after cataract surgery remains one of the more serious vision-threatening events, with approximately half the patients not recovering better than 20/40 acuity [1]. Around 30–40% of patients undergoing retinal reattachment surgery have had prior cataract surgery [1, 2]. Although an uncommon complication, the absolute number of RDs is substantial because of the large number of cataract extractions currently performed [2, 3].

4.1

Epidemiology

The incidence of retinal detachment post cataract surgery varies with the type of procedure, use of intraocular lens (IOLs), position/type of IOLs, and need for Nd: YAG capsulotomy and type of refractive error. At 10 years, the risk of RD ranged from 4 to 7.5 times higher in post cataract surgery patients than in those who did not have this surgical procedure [4, 5]. Up to 94% of RD occurring within the first year were attributable to cataract surgery [6]. While the risk of RD with intracapsular cataract extraction (ICCE) was earlier noted to be around 6%, the risk has reduced with the newer extracapsular technique of cataract surgery—extracapsular cataract extraction (ECCE) and phacoemulsification (PE) to around 0.7% [7–9].With the advent of newer technology, the risk of pseudophakic retinal detachment (PRD) has reduced with time [10, 11]. A large case series showed that the risk of RD was highest with anterior chamber IOLs (ACIOLs) (10%) in comparison to 0.1% with posterior

A. B. Jain · M. Bhende (*) Shri Bhagwan Mahavir VR Services, Sankara Nethralaya, Chennai, India e-mail: [email protected] © Springer Nature Singapore Pte Ltd. 2020 M. Chakrabarti, A. Chakrabarti (eds.), Posterior Segment Complications of Cataract Surgery, https://doi.org/10.1007/978-981-15-1019-9_4

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chamber IOLs (PCIOL) [12]. The 4-year cumulative risk of RD was 3.2% (cases without IOL), and 0.9% (with IOL) in comparison to 0.1% in the unoperated group [5]. Posterior lens capsule opacification (PCO) is the most common complication of cataract surgery occurring in almost 15–50% [3, 13–15] cases after extracapsular cataract extraction with most eyes needing clearance of visual axis with Nd YAG-­ assisted capsulotomy. The risk of retinal break or RD among patients that had undergone YAG capsulotomy has ranged from 3.2 to 3.9 times more in comparison to cases with an intact posterior capsule [16, 17]. Clear lens extraction for myopic patients as a refractive procedure is also associated with increased risk of RD [18, 19].

4.2

Risk Factors

The risk factors can be divided as those present before the surgery (preoperative), those occurring during surgery (intraoperative), and those that occur after cataract surgery (postoperative) [3].

4.2.1 Preoperative Age: Younger patients are known to have higher incidence of RD following cataract surgery [20–22]. Reduction in the relative risk of PRD was noted by 6% for every 1  year increase in age [22]. Various proposed reasons to explain this difference include the absence of PVD in younger patients, anomalous PVD and formed vitreous causing more tractional forces [23–25]. Gender: Increased rates of posterior capsule rupture and PRDs have been noted in men [4, 5, 21, 25–28]. Possible explanations of difference in gender can be increased incidence of ocular trauma after cataract surgery in males [29], use of α-antagonists (e.g., Tamsulosin), which can increase the surgical difficulty by causing intraoperative floppy iris syndrome [30]. High myopia: Myopia is associated with increased risk of PRD [17, 20, 22, 31–34]. The relative risk of PRD in patients with axial length ≥25 mm has been reported to be approximately six times higher than that in patients with shorter axial length [20, 33]. Increase in axial length of 1 mm increases the relative risk of RD by 30% [22]. Lattice degeneration is also known to be associated with an increased risk of PRD [29, 32, 35]. The occurrence of RD in the fellow eye increases the risk of RD in the eye undergoing cataract surgery [17, 29]. Another factor that probably plays a role in the development of retinal detachment after cataract surgery is the status of PVD prior to cataract surgery. Presence of PVD before cataract surgery results in reduced tractional forces on the retina produced during and after cataract surgery [11].

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4.2.2 Intraoperative Vitreous loss: Vitreous loss increases the incidence of RD following cataract surgery [17, 36]. The incidence of RD after PE is 4–5 times higher in those cases complicated with vitreous loss or those that required anterior vitrectomy [36]. Accidental or planned posterior capsulectomy: Posterior capsule disruption during cataract surgery appears to increase the risk of PRD by 10–20 times compared to cataract surgery with an intact capsule [27, 29, 37]. Planned posterior capsule discission in ECCE also increases the frequency of RD by 2–2.5 times [17]. Erie et al. found that approximately 66% of cases of cataract surgery with a posterior capsular tear had an RD within 1 year of surgery [25]. Nuclear fragment manipulation with a posterior capsular rent and vitreous admixed can worsen traction and cause RD. Zonular dehiscence was also associated with increased risk of PRD [27].

4.2.3 Postoperative Vitreous changes following cataract surgery are probably responsible for the increased incidence of RD in pseudophakic eyes [38]. PVD is more common in those individuals in whom the crystalline lens has been removed [38, 39]. When PVD occurs, 10–15% of eyes are expected to develop retinal tears, which could lead to the development of RD [39]. Various causes of increased incidence of PVD have been postulated. The anterior movement of the vitreous after removal of crystalline lens could play a role in the development of PVD and producing dynamic traction at the posterior border of the vitreous base increasing the risk of retinal tear formation [17, 39–41]. The protuberance of the posterior surface of the crystalline lens could be an important factor reducing vitreous traction upon the peripheral retina during the ocular saccades with a subsequent loss of this protective factor after cataract surgery [40, 41]. Biochemical studies show consistently lower concentrations of hyaluronic acid in the vitreous in eyes that have undergone ICCE compared to those after ECCE with intact capsule thus suggesting role of the posterior capsule in maintaining the colloidal structure of the vitreous. The loss of hyaluronic acid could produce vitreous instability and an increased tendency for PVD [42–47].

4.3

After Nd:YAG Posterior Capsulotomy

Nd:YAG Posterior Capsulotomy: Nd:YAG posterior capsulotomy is reported to be associated with an almost four-fold increased risk of RD after cataract surgery [29]. An opening in the posterior capsule may lead to anterior displacement of the vitreous and in some cases, herniation of the vitreous in the anterior chamber with a subsequent PVD and development of peripheral retinal tears. Rupture of the anterior vitreous face at the time of Nd YAG can also lead to increased risk of retinal traction at ora serrata and retinal tears [48]. However, few studies did not find any

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increased risk of Nd YAG laser for PRD. Most of the tears that develop are located in the extreme periphery and not in the posterior pole which would be expected in case of Nd YAG laser. The mechanism proposed for Nd YAG-induced PRD is that the laser burst produces a short shock wave, known as an “acoustic transient,” and scattering of high velocity particles into and through the vitreous base leading to alteration in the chemical composition and physical properties of vitreous base [49]. A decrease in the viscosity of the vitreous by increased liquefaction could help in increasing the traction and subsequent retinal break formation [50].

4.4

Clinical Findings

Most cases of PRD occur within the first year of cataract surgery [17, 51] or the first 6  months after Nd YAG capsulotomy [52, 53]. The frequent symptoms include flashes of light, floaters, decreased visual acuity, or visual field defects [54]. Not infrequently, the patient may be asymptomatic and RD is diagnosed only on routine ophthalmological examination. Signs include Schaffer’s sign (tobacco dusting), grey reflex on distant direct ophthalmoscopy, reduced IOP or sometimes even increased IOP (Schwartz sign). PRDs are typically more extensive RDs, with increased frequency of associated macular detachment [55]. Retinal breaks are found less frequently with predominance of small horse shoe tears located mostly near the ora serrata, usually in the superotemporal quadrant or at 12 o’clock [55–57]. Fundus examination is often difficult in PRD due to smaller pupils, anterior and posterior capsular fibrosis, presence of cortical remnants, vitreous opacities, and optical aberrations related to the IOL [53, 56].

4.5

Management

The treatment of PRD was first described in 1966 by Tassman and Annesley using scleral buckling techniques [58]. Subsequently, other surgical techniques such as pneumatic retinopexy, pars plana vitrectomy (PPV) with or without scleral buckling (SB) have been used to successfully repair pseudophakic retinal detachments [3, 59–66]. However, the surgical method of choice for PRDs remains controversial. Characteristic break location, multiple small breaks, morphology of the RD, and poor view of peripheral fundus because of small pupil, posterior capsule fibrosis, and optical aberrations of IOL make preoperative decision-making sometimes difficult for the vitreoretinal surgeon [67, 68]. Individualized treatment is needed depending on factors like number, size and location of breaks, macular status, PVR, amount of subretinal fluid, and any associated medical or ocular comorbidity [69]. SB has been a time tested treatment modality for PRDs with good anatomical outcomes. Various studies have reported around 60–90% of anatomical success rates in retinal detachment repair after SB alone, and the final anatomic success rates have ranged between 82 and 99% for pseudophakic repair after additional

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procedures [51, 59–62, 70]. With proper selection of cases, SB gives very good results with reduced risk of endophthalmitis and complications related to tamponade. However, SB alone may be associated with a myopic shift with an encircling element, complications associated with external drainage like choroidal effusion, subretinal hemorrhage, hyphema, and missed breaks due to difficulty visualizing the peripheral retina through the peripheral capsule/posterior chamber implant edge. Other known complications of scleral buckling include PVR, macular pucker, bullous keratopathy, glaucoma, cystoid macular edema, dislocation of IOL, etc. [51, 59, 60, 69, 71] Pneumatic retinopexy is a treatment modality whereby an intravitreal gas bubble is injected for internal tamponade with laser photocoagulation around the break or transconjunctival cryopexy, followed by appropriate head positioning [72]. Pneumatic retinopexy is recommended in cases with a single small superior break or breaks within 1 o’clock hour in the absence of PVR > grade B [60]. As most of the PRD are associated with multiple small breaks, there are higher chances of failure compared to phakic RDs [73, 74]. However, being a less invasive procedure, a trial of pneumatic retinopexy can be done in selected cases. Complications include new retinal break formation, delayed subretinal fluid absorption, chronic macular detachment, PVR, macular pucker, subretinal gas and endophthalmitis etc. [60, 73, 75] Recently, the trend has shifted towards pars plana vitrectomy with/without encirclage and tamponade. Newer vitrectomy machines with high cutting rates, improved fluidics, well lighted endolaser probes, chandelier system for bimanual surgeries, wide angle visualization systems allowing excellent visualization up to the ora serrata, and newer instruments have resulted in safer surgeries with reduced risk of complications [76, 77]. The scleral buckling versus primary vitrectomy in rhegmatogenous retinal detachment study (SPR study) [67], a prospective randomized trial comparing primary vitrectomy and scleral buckling surgery for rhegmatogenous retinal detachment showed that the primary anatomical success rate was significantly higher in the PPV group. Similarly, a meta-analysis comparing vitrectomy with scleral buckling for PRD repair found higher single surgery anatomical success and favorable visual outcomes with vitrectomy than with scleral buckling [78]. Advantages of PPV over other treatment modalities include the benefits of direct removal of all traction on retinal tears, removal of vitreous membranes or hemorrhage, simultaneous treatment of any PVR component/epiretinal membrane, better visualization, and treatment of peripheral retinal pathologies and performing a posterior capsulectomy to clear the visual axis [79]. PPV with encirclage seemed to be the best treatment option for many years. The advantage of an encircling band is in relieving anterior traction by supporting the vitreous base at the ora, as there may be difficulty in performing adequate peripheral vitrectomy in these eyes due to poor view. Disadvantages of encirclage include a longer duration of surgery and anesthesia, risk of postoperative diplopia, buckle extrusion, or infection [80]. Recent studies comparing small gauge PPV alone with tamponade and PPV with encirclage and tamponade showed comparable results in terms of anatomical

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success thus questioning the use of encirclage element. However with most of them being retrospective series, bias in case selection with use of encirclage element in severe RD cases could not be ruled out [80–82]. The technological evolution of smaller gauge vitrectomy offers distinct advantages, such as improved fluidics, smaller cutter diameters and faster cut rates, faster wound healing, diminished conjunctival scarring, and improved patient comfort [69, 80, 83]. A potential disadvantage of wound leak resulting in poor gas or oil tamponade fill and lower anatomical success after first surgery exist [80, 83] and authors generally recommend closure of even small gauge wounds in PRDs.

4.6

Prognostic Factors

Poor prognostic factors include PVR, poor presenting vision, longer duration of symptoms, preoperative choroidal detachment, preoperative vitreous hemorrhage, large retinal breaks [71, 84].

4.7

Conclusion

PRD has been a known complication of cataract surgery and despite technological advances of cataract surgery, with an exponential rise in number of cataract surgeries performed, PRDs are on the rise. Thorough fundus examination should be done during preoperative assessment and any peripheral treatable lesions (including asymptomatic breaks) can be considered for prophylactic laser before performing cataract surgery. Patient education about RD and its symptoms is particularly important in eyes with high myopia, following complicated cataract surgery with vitreous loss, and those undergoing Nd:YAG posterior capsulotomy. Treatment of PRD has good outcomes, provided early treatment is undertaken. Selection of cases based on clinical findings and surgeon competence is the most important factor guiding the choice of treatment modality.

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7. Hyams SW, Bialik M, Neumann E. Myopia-aphakia I. Prevalence of retinal detachment. Br J Ophthalmol. 1975;59:480–2. 8. Jaffe NS, Clayman HM, Jaffe MS. Retinal detachment in myopic eyes after intracapsular and extracapsular cataract extraction. Am J Ophthalmol. 1984;97:48–52. 9. Powe NR, Schein OD, Gieser SC, et al. Synthesis of the literature on visual acuity and complications following cataract extraction with intraocular lens implantation. Cataract Patient Outcome Research Team. Arch Ophthalmol. 1994;112:239–52. 10. Quek DT, Lee SY, Htoon HM, Ang CL. Pseudophakic rhegmatogenous retinal detachment in a large Asian tertiary eye centre: a cohort study. Clin Exp Ophthalmol. 2012;40(1):e1–7. 11. Haug SJ, Bhisitkul RB. Risk factors for retinal detachment following cataract surgery. Curr Opin Ophthalmol. 2012;23:7–11. 12. Chambless WS. Incidence of anterior and posterior segment complications in over 3,000 cases of extracapsular cataract extractions: intact and open capsules. J Am Intraocul Implant Soc. 1985;11:146–8. 13. Lindstrom RL, Harris WS. Management of the posterior capsule following posterior chamber lens implantation. J Am Intraocul Implant Soc. 1980;6:255–8. 14. Seward HC, Doran RM. Posterior capsulotomy and retinal detachment following extracapsular lens surgery. Br J Ophthalmol. 1984;68:379–82. 15. Olsen G, Olson RJ.  Update on a long-term, prospective study of capsulotomy and retinal detachment rates after cataract surgery. J Cataract Refract Surg. 2000;26:1017–21. 16. Javitt JC, Tielsch JM, Canner JK, et al. National outcomes of cataract extraction. Increased risk of retinal complications associated with Nd:YAG laser capsulotomy. The Cataract Patient Outcomes Research Team. Ophthalmology. 1992;99:1487–97, discussion 1497–8. 17. Coonan P, Fung WE, Webster RG Jr, et  al. The incidence of retinal detachment following extracapsular cataract extraction. A ten-year study. Ophthalmology. 1985;92:1096–101. 18. Lyle WA, Jin GJ.  Phacoemulsification with intraocular lens implantation in high myopia. J Cataract Refract Surg. 1996;22:238–42. 19. Pucci V, Morselli S, Romanelli F, et al. Clear lens phacoemulsification for correction of high myopia. J Cataract Refract Surg. 2001;27:896–900. 20. Davison JA.  Retinal tears and detachments after extracapsular cataract surgery. J Cataract Refract Surg. 1988;14:624–32. 21. Javitt JC, Street DA, Tielsch JM, et  al. National outcomes of cataract extraction. Retinal detachment and endophthalmitis after outpatient cataract surgery. Cataract Patient Outcomes Research Team. Ophthalmology. 1994;101:100–5, discussion 106. 22. Ninn-Pedersen K, Bauer B. Cataract patients in a defined Swedish population, 1986 to 1990, V. postoperative retinal detachments. Arch Ophthalmol. 1996;114:382–6. 23. Yonemoto J, Ideta H, Sasaki K, et  al. The age of onset of posterior vitreous detachment. Graefes Arch Clin Exp Ophthalmol. 1994;232:67–70. 24. Neal RE, Bettelheim FA, Lin C, et al. Alterations in human vitreous humor following cataract extraction. Exp Eye Res. 2005;80:337–47. 25. Erie JC, Raecker MA, Baratz KH, Schleck CD, Burke JP, Robertson DM.  Risk of retinal detachment after cataract extraction, 1980–2004. A population-based study. Ophthalmology. 2006;113:2026–32. 26. Narendran N, Jaycock P, Johnston RL, et al. The cataract national dataset electronic multicentre audit of 55 567 operations: risk stratification for posterior capsule rupture and vitreous loss. Eye (Lond). 2009;23:31–7. 27. Tuft SJ, Minassian D, Sullivan P. Risk factors for retinal detachment after cataract surgery: a case-control study. Ophthalmology. 2006;113:650–6. 28. Stein JD.  Serious adverse events after cataract surgery. Curr Opin Ophthalmol. 2012; 23:219–25. 29. Tielsch JM, Legro MW, Cassard SD, et al. Risk factors for retinal detachment after cataract surgery. A population-based case–control study. Ophthalmology. 1996;103:1537–45. 30. Bell CM, Hatch WV, Fischer HD, et al. Association between tamsulosin and serious ophthalmic adverse events in older men following cataract surgery. JAMA. 2009;301:1991–6.

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31. Koch DD, Liu JF, Gill EP, Parke DW 2nd. Axial myopia increases the risk of retinal complications after neodymium- YAG laser posterior capsulotomy. Arch Ophthalmol. 1989;107:986–90. 32. Bhagwandien AC, Cheng YY, Wolfs RC, et al. Relationship between retinal detachment and biometry in 4262 cataractous eyes. Ophthalmology. 2006;113:643–9. 33. Clayman HM, Jaffe NS, Light DS, et al. Intraocular lenses, axial length, and retinal detachment. Am J Ophthalmol. 1981;92:778–80. 34. Colin J, Robinet A, Cochener B. Retinal detachment after clear lens extraction for high myopia: seven-year follow-up. Ophthalmology. 1999;106:2281–4. 35. Khan MA, Skidmore K, Ho AC. Perioperative retina evaluation of the cataract surgery patient. Curr Opin Ophthalmol. 2015;26:39–44. 36. Javitt JC, Vitale S, Canner JK, et al. National outcomes of cataract extraction, I. Retinal detachment after inpatient surgery. Ophthalmology. 1991;98:895–902. 37. Jakobsson G, Montan P, Zetterberg M, et al. Capsule complication during cataract surgery: retinal detachment after cataract surgery with capsule complication. Swedish Capsule Rupture Study Group report 4. J Cataract Refract Surg. 2009;35:1699–705. 38. Heller MD, Straatsma BR, Foos RY. Detachment of the posterior vitreous in phakic and aphakic eyes. Mod Probl Ophthalmol. 1972;10:23–36. 39. Jaffe NS, Light DS. Vitreous changes produced by cataract surgery. A study of 1,058 aphakic eyes. Arch Ophthalmol. 1966;76:541–53. 40. Hilding AC. Normal vitreous, its attachments and dynamics during ocular movement. Arch Ophthalmol. 1954;52:497–514. 41. Irvine AR. The pathogenesis of aphakic retinal detachment. Ophthalmic Surg. 1985;16:101–7. 42. Osterlin S.  On the molecular biology of the vitreous in the aphakic eye. Acta Ophthalmol. 1977;55:353–61. 43. Osterlin S. Vitreous changes after cataract extraction. In: Freeman HM, Hirose T, Schepens CL, editors. Vitreous surgery and advances in fundus diagnosis and treatment. New  York: Appleton-Century-Crifts; 1977. p. 15–21. 44. Harlan JB, Green RW. Vitreous degeneration, retinal tears, and retinal detachment after cataract extraction with and without capsulotomy. In: Stirpe M, editor. Acta of the fifth international congress on vitreoretinal surgery; 24–27 September 1987; Rome, Italy. New York: Ophthalmic Communications Society; 1998. pp. 78–84. 45. Osterlin S. Macromolecular composition of the vitrous in the aphakic owl monkey eye. Exp Eye Res. 1978;26:77–84. 46. Kawano SI, Honda Y, Negi A. Effects of biological stimuli on the viscosity of the vitreous. Acta Ophthalmol. 1982;60:977–91. 47. Coppé AM, Lapucci G. Posterior vitreous detachment and retinal detachment following cataract extraction. Curr Opin Ophthalmol. 2000;19:239–42. 48. Ficker LA, Steele AD.  Complications of Nd:YAG laser posterior capsulotomy. Trans Ophthalmol Soc U K. 1985;104:529–32. 49. Vogel A, Hentschel W, Holzfuss J, Lauterborn W. Cavitation bubble dynamics and acoustic transient generation in ocular surgery with pulsed neodymium:YAG lasers. Ophthalmology. 1986;93:1259–69. 50. Lerman S, Thrasher B, Moran M. Vitreous changes after neodymium-YAG laser irradiation of the posterior lens capsule or mid-vitreous. Am J Ophthalmol. 1984;97:470–5. 51. Ramsay RC, Cantrill HL, Knobloch WH. Pseudophakic retinal detachment. Can J Ophthalmol. 1983;18:262–5. 52. Ficker LA, Vickers S, Capon MR, et al. Retinal detachment following Nd:YAG posterior capsulotomy. Eye. 1987;1:86–9. 53. Yoshida A, Ogasawara H, Jalkh AE, et  al. Retinal detachment after cataract surgery. Predisposing factors. Ophthalmology. 1992;99:453–9. 54. Speicher MA, Fu AD, Martin JP, von Fricken MA.  Primary vitrectomy alone for repair of retinal detachments following cataract surgery. Retina. 2000;20:459–64. 55. Christensen U, Villumsen J. Prognosis of pseudophakic retinal detachment. J Cataract Refract Surg. 2005;31:354–8.

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5 6. Hagler WS. Pseudophakic retinal detachment. Trans Am Ophthalmol Soc. 1982;80:45–63. 57. Jungschaffer OH.  Retinal detachments and intraocular lenses. Int Ophthalmol Clin. 1979;19:125–37. 58. Tassman W, Annesley WH Jr. Retinal detachment in prosthetophakia. Arch Ophthalmol. 1966;75:179–88. 59. Ho PC, Tolentino FI.  Pseudophakic retinal detachment. Surgical success rate with various types of IOLs. Ophthalmology. 1984;91:847–52. 60. Tornambe PE, Hilton GF. Pneumatic retinopexy. A multicenter randomized controlled clinical trial comparing pneumatic retinopexy with scleral buckling. The Retinal Detachment Study Group. Ophthalmology. 1989;96:772–83, discussion 784. 61. Greven CM, Sanders RJ, Brown GC, et al. Pseudophakic retinal detachments. Anatomic and visual results. Ophthalmology. 1992;99:257–62. 62. Hassan TS, Sarrafizadeh R, Ruby AJ, et  al. The effect of duration of macular detach ment on results after the scleral buckle repair of primary, macula-off retinal detachments. Ophthalmology. 2002;109:146–52. 63. Heimann H, Bornfeld N, Friedrichs W, et  al. Primary vitrectomy without scleral buckling for rhegmatogenous retinal detachment. Graefes Arch Clin Exp Ophthalmol. 1996; 234:561–8. 64. Oshima Y, Yamanishi S, Sawa M, et  al. Two-year follow-up study comparing primary vitrectomy with scleral buckling for macula-off rhegmatogenous retinal detachment. Jpn J Ophthalmol. 2000;44:538–49. 65. Ranta P, Kivela T. Functional and anatomic outcome of retinal detachment surgery in pseudophakic eyes. Ophthalmology. 2002;109:1432–40. 66. Stangos AN, Petropoulos IK, Brozou CG, et  al. Pars-plana vitrectomy alone vs vitrectomy with scleral buckling for primary rhegmatogenous pseudophakic retinal detachment. Am J Ophthalmol. 2004;138:952–8. 67. Heimann H, Bartz-Schmidt KU, Bornfeld N, Weiss C, Hilgers RD, Foerster MH. Scleral buckling versus primary vitrectomy in rhegmatogenous retinal detachment: a prospective randomized multicenter clinical study. Ophthalmology. 2007;114:2142–54. 68. Romano MR, Angi M, Valldeperas X, Costagliola C, Vinciguerra P. Twenty-three–gauge pars plana vitrectomy, densiron-68, and 360° endolaser versus combined 20- gauge pars plana vitrectomy, scleral buckle, and SF6 for pseudophakic retinal detachment with inferior retinal breaks. Retina. 2011;31:686–91. 69. Miller DM, Riemann CD, Foster RE, Apetersen MR. Primary repair of retinal detachment with 25-gauge pars plana vitrectomy. Retina. 2008;28:931–6. 70. Schwartz SG, Kuhl DP, McPherson AR, et  al. Twenty-year follow-up for scleral buckling. Arch Ophthalmol. 2002;120:325–9. 71. Yoshida A, Ogasawara H, Jalkh AE, et al. Retinal detachment after cataract surgery. Surgical results. Ophthalmology. 1992;99:460–5. 72. Hilton GF, Grizzard WS. Pneumatic retinopexy. A two-step outpatient operation without conjunctival incision. Ophthalmology. 1986;93:626–41. 73. Chen JC, Robertson JE, Coonan P, et al. Results and complications of pneumatic retinopexy. Ophthalmology. 1988;95:601–6. 74. Han DP, Mohsin NC, Guse CE, et al. Comparison of pneumatic retinopexy and scleral buckling in the management of primary rhegmatogenous retinal detachment. Southern Wisconsin Pneumatic Retinopexy Study Group. Am J Ophthalmol. 1998;126:658–68. 75. Hilton GF, Kelly NE, Salzano TC, et al. Pneumatic retinopexy. A collaborative report of the first 100 cases. Ophthalmology. 1987;94:307–14. 76. Lesnoni G, Billi B, Rossi T, Stirpe M. The use of panoramic viewing system in relaxing retinotomy and retinectomy. Retina. 1997;17:186–90. 77. Rosen PH, Wong HC, McLeod D.  Indentation microsurgery: internal searching for retinal breaks. Eye. 1989;3:277–81. 78. Arya AV, Emerson JW, Engelbert M, et  al. Surgical management of pseudophakic retinal detachments. Ophthalmology. 2006;113:1724–33.

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79. Weichel ED, Martidis A, Fineman MS, et  al. Pars plana vitrectomy versus combined pars plana vitrectomy-scleral buckle for primary repair of pseudophakic retinal detachment. Ophthalmology. 2006;113:2033–40. 80. Orlin A, Hewing NJ, Nissen M, et al. Pars plana vitrectomy compared with pars plana vitrectomy combined with scleral buckle in the primary management of noncomplex rhegmatogenous retinal detachment. Retina. 2014;34(6):1069–75. 81. Kinori M, Moisseiev E, Shoshany N, et  al. Comparison of pars plana vitrectomy with and without scleral buckle for the repair of primary rhegmatogenous retinal detachment. Am J Ophthalmol. 2011;152:291–297.e2. 82. Mokete B, Williamson TH. Scleral buckling combined with vitrectomy for the management of rhegmatogenous retinal detachment associated with inferior retinal breaks. Eye (Lond). 2009;23:1233; author reply 1233–1234. 83. Misra A, Ho-Yen G, Burton RL. 23-gauge sutureless vitrectomy and 20 gauge vitrectomy: a case series comparison. Eye (Lond). 2009;23:1187–91. 84. Girard P, Karpouzas I. Pseudophakic retinal detachment: anatomic and visual results. Graefes Arch Clin Exp Ophthalmol. 1995;233:324–30.

5

Pseudophakic Cystoid Macular Oedema Venkat Kotamarthi

5.1

Introduction

The techniques of cataract surgery has evolved through several stages and the modern cataract surgery of phacoemulsification is by far the safest with good outcomes. Despite this, cystoid macular oedema can still be a compromising factor in the visual outcome, though the incidence of clinically significant cystoid macular oedema is less compared to intracapsular cataract extraction and conventional extracapsular cataract extraction. Cystoid macular oedema can occur following complicated cataract surgery or even after an uncomplicated cataract surgery. With the advent of optical coherence tomography (OCT), non-invasive cross-sectional imaging of the retina to detect sub-clinical CMO has possibly increased the prevalence of CMO and therefore early detection, monitoring and treatment in appropriate cases is possible with good outcomes [1].

5.2

Definition

Pseudophakic cystoid macular oedema is a condition which results in built of fluid in the extracellular space in the outer synaptic layer or plexiform layer and inner granular layer or nuclear layer of the retina in the central macular area. On slitlamp biomicroscopy either using a non-contact lens or a contact lens, it appears as a perifoveal multiple cystoid-like spaces due to scattering of the light as the separation of the retinal cells results in the formation of septae and multiple interfaces. As a consequence of this, there is loss of normal translucency of the retina with the loss of details of retinal pigment epithelium and underlying choroidal

V. Kotamarthi (*) Mid Cheshire Hospital NHS Foundation Trust Hospital, Crewe, Cheshire, UK © Springer Nature Singapore Pte Ltd. 2020 M. Chakrabarti, A. Chakrabarti (eds.), Posterior Segment Complications of Cataract Surgery, https://doi.org/10.1007/978-981-15-1019-9_5

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vasculature. When it results following a cataract surgery, the symptoms are painless blurring of central vision with visual disturbances like metamorphopsia (distortion of the central vision). Less common symptoms include micropsia (a type of metamorphopsia), scotomata and photophobia.

5.3

History

Roy Irvine in 1953 reported a case of loss of vision following intracapsular cataract extraction which was uncomplicated. This was attributed to changes in the macula and associated prolapse of the vitreous [2]. In 1966, Gass and Norton reported cystoid changes in the macula following intracapsular cataract extraction demonstrating it with the help of fluorescein angiogram showing petalloid appearance in the macular region and staining of the optic nerve head [3]. Thereafter the syndrome of cystoid macular oedema following cataract surgery was termed Irvine–Gass syndrome. Don Gass followed it up further stating that post-operative CMO has a peak incidence at 6 weeks after surgery and can be of two types, clinically significant and clinically not significant.

5.4

Incidence

The incidence of angiographic CMO [4] after intracapsular cataract extraction is as high as 60% [5]. The incidence of angiographic CMO after extracapsular cataract extraction is between 15 and 30% [5]. The incidence of clinical CMO after small incision phacoemulsification is between 0.1 and 2.35% [4, 6]. The OCT evidence of CMO after small incision phacoemulsification is 4–11% [7, 8] but could be as high as 41% [9] as reported. Most patients who have angiographic evidence of CMO will not have any visual symptoms. Most of the patients who have clinically manifest CMO will show spontaneous improvement in about 3–12 months [9]. A study by Hunter et al. in 2014 revealed the incidence of pseudophakic CMO to be 1.5% at an academic centre, in patients undergoing routine cataract extraction. The outcome was that 27% had less than 20/20 as best corrected visual acuity even after the condition of pseudophakic CMO showed complete resolution [10]. Approximately 20% of the patients who undergo uncomplicated phacoemulsification or extracapsular extraction develop angiographically proven CMO [11]. A clinically significant decrease in visual acuity is seen only in about 1% of these eyes [12]. However, in the event of a posterior capsule rupture with vitreous loss or with on-going vitreous traction at the wound or in case of severe trauma to the iris, the incidence of clinically apparent CMO would have significantly increased up to 20% and is independent of the presence of an anterior chamber IOL [13]. Normally the time taken to develop clinically significant CMO after an operation could be 3–12  weeks but in some cases there could be a late onset after several months or even after many years following surgery.

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In 80% of cases, the pseudophakic CMO shows spontaneous resolution within a period of 3–12 months [14]. It is interesting to note that in diabetic patients the incidence of pseudophakic CMO is pretty much the same irrespective of the type of cataract extraction that was undertaken, when phacoemulsification was compared with the conventional cataract extraction. So early intervention is the key factor rather than the technique of the cataract extraction [15].

5.5

Aetiopathogenesis

When cystoid macular oedema develops following recent cataract surgery, most often it is related to the operative procedure, and it is termed as Irvine–Gass syndrome or pseudophakic CMO. This was more common in the days of intracapsular cataract extraction and conventional extracapsular cataract extraction, but it is still seen even in the era of phacoemulsification with modern intraocular lens implants, in both complicated and uncomplicated cataract procedure. There is a multifactorial element in the pathogenesis of pseudophakic CMO and the possible aetiologic factors include inflammation with traction caused by vitreous and hypotony [16–18]. The main contributory factors include the release of endogenous inflammatory mediators due to surgically induced inflammation in the anterior segment. The inflammatory mediators like cytokines, prostaglandins and other vasopermeability factors which are released due to breakdown of blood–aqueous barriers during intraocular surgery secondary to trauma to the iris, ciliary body and epithelium of the lens capsule reach the perifoveal capillaries from aqueous through the vitreous and can cause disruption of the perifoveal capillary integrity which in turn can result in the accumulation of the fluid causing cystoid type of macular oedema [19, 20]. The degree of macular oedema is proportional to the amount of chemical mediators present in the aqueous and vitreous. In the inflammatory pathway, the arachidonic acid is released by the action of enzyme phospholipase. In the subsequent steps the arachidonic acid is converted to prostaglandins by cyclooxygenase. The prostaglandins have the propensity to cause a breakdown of the blood–retinal barrier resulting in vasodilation, along with an increased permeability from the tight endothelial junctions of the retinal capillaries along with an added insufficient removal of fluid by the retinal pigment epithelium. The formation of prostaglandins and their subsequent effects could be blocked by steroids which could inhibit the enzyme phospholipase. In comparison to this, aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) specifically target the cyclooxygenase pathway (see Fig. 5.1). Enzyme lipoxygenase is a product of arachidonic acid, which converts arachidonic acid to a chemotactic agent called leucotriene, the role of which in CMO is not very clear. At present there aren’t any lipoxygenase-specific blocking agents that have been approved for use in the treatment of pseudophakic CMO.

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em bra ne ph os ph olip id

Surgical Trauma

PLA2 Activation

Corticosteroids

Ce ll m

PLA2 − A key enzyme involved in the release of Arachdonic acid from the cell membrane

Lipoxygenase

Arachdonic acid

Leukotrienes

NSAIDS COX-2 (Inducible)

COX-1 Constitutive

Prostaglandins

Prostaglandins

Thromboxanes

Platelet aggregation

Inflammation Pain, Fever

Fig. 5.1  The inflammatory pathway

5.6

Histopathology

CMO after cataract extraction shows dilatation of the retinal capillaries. There is a collection of fluid in the outer plexiform and outer nuclear layers with infiltration of iris, ciliary body and the blood vessels around them [21]. In severe and long-­standing cases, there can be displacement of the photoreceptor nuclei and receptor axons associated with intracytoplasmic oedema of the Muller cells which results in perifoveal cysts or lamellar holes. The origin and location of the cystoid changes is attributed to the intracellular fluid accumulation which is seen as intracytoplasmic oedema of Muller cells histologically [22, 23] (see Figs. 5.2 and 5.3). There can be swollen mitochondria in prelaminar ganglion cell axons, astrocyte degeneration and occlusion of laminar blood vessels [24].

5.7

Classification of Pseudophakic CMO

Pseudophakic CMO has been classified as the following: 1. Angiographic CMO: This was originally described by Gass and Norton. It is the presence of detectable fluorescein leakage from the perifoveal capillaries on fluorescein angiography and also from the optic nerve. The angiographic evidence of leakage may go hand in hand with the slit lamp biomicroscopic changes, but there may not be any concomitant decrease in the visual acuity clinically. According to Wright et  al., this angiographic form may be present in up to

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Fig. 5.2  Histopathology of fovea in cystoid macular oedema, haematoxylin and eosin staining. Large cystoid cavities with exudates in the outer plexiform and outer nuclear layers. There is disorganization of the photoreceptors sub-foveally and disruption of the retinal pigment epithelium. (Image courtesy Ralph C Eagle Jr. MD, Director, Pathology department, Wills Eye Hospital)

Fig. 5.3  Histopathology of cystoid macular oedema showing cystoid spaces in the outer plexiform and in the inner nuclear layers of the retina. (Image courtesy John Harry, Gary P. Misson from Clinical Ophthalmic Pathology)

20–30% of patients following extracapsular cataract surgery [25]. Most often the angiographic CMO is self-limiting and in only in a minority of cases, it could cause significant visual loss. 2. Clinically significant CMO: It is defined as a reduction in the visual acuity with associated macular changes on clinical examination, on OCT and angiographic evidence of CMO.  According to Spaide et  al., clinically significant macular oedema is associated with complicated cataract surgery and would have had vitreous loss or anterior–chamber intraocular lens (IOL) implantation [26]. 3. OCT detectable pseudophakic CMO: With the advent of OCT, even subtle changes in the macular thickness can be detected. McColgin et al. reported that 12% of patients had increased retinal thickness following uncomplicated cataract surgery. Most of them with pseudophakic CMO do not have any significant reduction in the visual acuity quantitatively, but do show a qualitative change in the form of persistently reduced contrast sensitivity and colour desaturation, even though the visual acuity recorded on Snellen’s chart is normal [27].

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Classification Based on the Time of Onset [28]

Acute CMO: When CMO occurs within 4  months of a surgical procedure, it is termed as acute CMO. Late onset CMO: If the CMO set in more than 4 months after the surgical procedure, it is termed as late onset CMO.Chronic CMO: It is termed as chronic CMO, if it persists for more than 6 months.

5.9

Risk Factors for Pseudophakic CMO

1. Type of cataract surgery One of the risk factors that has been identified as cause for the pseudophakic CMO is the type of cataract surgery. With the evolution in the technique of cataract surgery, from intracapsular cataract extraction through conventional extracapsular extraction with a large incision with IOL implant to small incision phacoemulsification with IOL, the incidence of CMO has decreased considerably [29–31]. 2. Light In the past, phototoxicity (the source of light from the microscope) was implicated as a risk factor for pseudophakic CMO; however, a prospective randomized study did not show any evidence of this finding. There was no statistically significant difference in the incidence of angiographic CMO by using a pupillary light occluder [32]. However, studies have shown that by using IOLs that filter UV light, there is a reduction in the incidence of angiographic pseudophakic CMO [33]. 3. Age Due consideration has to been given to the age of the patient as factor responsible for pseudophakic CMO. Some studies have indicated that there is an increased incidence of pseudophakic CMO in older patients [29, 34]. 4. Changes that take place in the vitreous body during surgery It is a well-known fact that pseudophakic CMO can occur after an uneventful surgery. However, surgical complications associated with posterior capsule rupture during cataract surgery or secondary capsulotomy following Nd:YAG laser capsulotomy are associated with an increased incidence of pseudophakic CMO [35]. Vitreous loss during complicated cataract surgery increases the prevalence of CMO by 10–20% [5, 29, 36]. Several studies have clearly shown that the rate of clinically significant CMO is higher when there is vitreous loss compared to an uncomplicated conventional extracapsular cataract extraction or phacoemulsification [34, 36, 37]. The incidence of pseudophakic CMO is less when there is vitreous loss during complicated phacoemulsification, and this is attributed to the greater stability due to small and self-sealing incision [38–40]. When there is vitreous, going up to the incision, causing traction on the retina, there is corresponding prolongation of the duration of CMO, and this could lead to permanent structural damage resulting in poor prognosis for vision [5].

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5. Retained lens fragments Retained lens fragments in the vitreous cavity or in the anterior chamber can cause severe inflammation and CMO, even after their removal can cause persistent CMO. These cases are usually associated with longer duration of the surgery and with sulcus fixated or anterior chamber IOL [41–44]. 6. Diabetes mellitus There is an increased risk of developing post-operative CMO in diabetic patients, all the more if there is a pre-existing diabetic retinopathy [45]. The incidence of CMO in diabetic patients is higher compared to a normal person [46]. With the technique of phacoemulsification, the incidence is less, but it is still a significant risk of decreased vision in the post-operative period [47]. The sub-optimal visual acuity following cataract surgery in such patients could be due to a combination of diabetic macular oedema and Irvine–Gass syndrome [45, 48, 49]. When they co-exist, it may be difficult to differentiate, but some authors have suggested that if there is an associated hyperfluorescence of the optic disc in the angiograms along with CMO in a post-operative patient, it is most probably due to pseudophakic CMO (Irvine–Gass syndrome), and there is a likelihood of spontaneous resolution [50]. If there is a pre-existing diabetic macular oedema, this should be treated before undertaking the cataract surgery as the cataract surgery can make it worse with worsening of the vision. In case if it is not possible to treat the diabetic macular oedema prior to the cataract surgery, it can be combined with an intravitreal injection of a steroid or anti-VEGF. 7. Uveitis The most common cause of poor vision following cataract extraction in patients with uveitis is post-operative CMO [51]. There is a 50% incidence of post-cataract extraction CMO in patients with juvenile rheumatoid arthritis or pars planitis [52]. In a retrospective study with uveitic patients, Foster et  al. reported similar incidences [53]. A lower incidence was reported in few other studies. There is a wide variation in the postoperative CMO following cataract surgery, and the factors on which it is dependent are the severity of uveitis at the time of the cataract operation, the pre-existing macular oedema, and the intensity of treatment with steroids in the immediate post-operative period with gradual tapering of steroids over an extended period of time. It is imperative to commence on topical steroids 2 weeks before the cataract operation on an eye which had been quiet for at least 3 months. 8. Retinal vein occlusion There is an increased risk of developing postoperative cystoid macular oedema following cataract surgery in a patient who had retinal vein occlusion in the same eye. The cause for the cataract could be the use of steroids in any form, topical, periocular, intravitreal or oral. In one large study by Henderson et al. which was conducted between 2001 and 2006, it showed that the risk of postsurgical CMO in an uneventful cataract surgery was 30 times higher in an eye which had a pre-existing retinal vein occlusion [54]. The percentage of risk was the same even in eyes which did not have pre-existing macular oedema following retinal vein occlusion in the past.

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9. Epimacular membrane There is an increased incidence of pseudophakic CMO in patients with epimacular membrane because of a combination of factors of antero-posterior traction of vitreous following the removal of the cataract and liquefaction of vitreous [54]. 10. Topical prostaglandin analogues There are many reports about the association of pseudophakic CMO with the use of topical anti-glaucoma medications which are prostaglandin analogues, like latanoprost, travoprost, bimatoprost and tafluprost [55–59]. The cause for the increased incidence of CMO associated with the prostaglandin analogues is due to breakdown of blood–aqueous barrier causing inflammation. There are many reports which showed rapid resolution of pseudophakic CMO after stopping the topical prostaglandin analogue therapy, especially in combination with concomitant use of topical NSAIDS and steroids [58, 60, 61]. As there is a possibility of this happening, it is recommended to avoid the use of prostaglandin analogues before surgery or during peri-operative period and to substitute with another type of anti-glaucoma medication. However, there is no high-grade clinical evidence supporting this view.

5.10 Diagnosis, Symptoms and Signs Prior to the management of pseudophakic CMO, it is imperative to take a careful history which includes duration of the symptoms, past ocular history and any co-­existing comorbidities like diabetes mellitus and the medications that can cause CMO. In case of pseudophakic CMO, the most common finding is a reduced visual acuity following cataract surgery. The symptoms may range from reduced contrast to central scotoma, including metamorphopsia. It can happen typically between 4 and 12 weeks after surgery reaching a peak at 4–6 weeks following the surgery. Clinical examination of the anterior segment is mandatory with careful attention for the presence of anterior vitreous prolapse, vitreous strands up to the corneal section or sideport. Look for the shape of the pupil if there is any peaking, as this is the sign of adherence of the vitreous to anterior structures causing traction on the retina. Look for any retained lens matter in the anterior chamber and for uveitis. Clinical examination should include examination of the vitreous and peripheral retina with indentation, for vitritis, retained lens matter in the vitreous cavity and parsplanitis. Clinical examination of the fundus in general shows loss of the foveal depression and retinal thickening. Intraretinal parafoveal cystoid spaces may be observed, occasionally with splinter retinal haemorrhages. To identify the intraretinal cystoid changes, fundus contact lens or a narrow-slit beam with slit-lamp biomicroscopy may be helpful. A shallow sensory retinal detachment can develop as a result of diffusion of excess transudate extending underneath the photoreceptors. The subretinal fluid can stimulate the retinal pigment epithelium with hypotrophic or hypertrophic pigmentary changes and rarely can result in the formation of a disciform scar [62]. In up to 10% of the eyes that have developed pseudophakic CMO, the macular examination may show glistening reflexes after varying lengths of time due to the development of an epiretinal

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membrane [63, 64]. The fundus examination should include to look for any evidence of vitreomacular traction or diabetic maculopathy. In addition to this, many eyes with CMO may have a coexistent circumcorneal flush, mild iritis, vitritis, and a low-grade papillitis and even sometimes associated with peripapillary haemorrhages.

5.11 Diagnostic Tests Diagnostic testing, in particular OCT and fluorescein angiography (Figs. 5.4 and 5.5), should be performed to confirm the diagnosis and to exclude any other macular pathology that is missed during clinical evaluation like vitreomacular traction or any other associated macular pathology.

Fig. 5.4  OCT may show retinal thickening with loss of foveal contour, intraretinal fluid with cystoids changes and subretinal fluid

Fig. 5.5  The fluorescein angiogram shows perifoveal leakage from dilated capillaries in the early phase, and in the late phase, hyperfluorescent spots are seen in a petalloid fashion. Optic nerve staining is seen and is a distinguishing feature of pseudophakic CMO and is not seen in CMO due to other causes

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5.12 Management 5.12.1 Medical Treatment Conservative Management Angiographic CMO following cataract surgery is not associated with poor visual acuity at presentation and usually resolves spontaneously with good outcomes. Usually it resolves spontaneously (Fig. 5.6a–c). In about 1–3% of cases, it may persist and may cause visual symptoms leading to a clinical CMO with persistent symptoms. The principle of conservative management is also applied to the pseudophakic patients who are asymptomatic and have OCT detectable mild macular thickness.

a

b

c Fig. 5.6 (a) Cystoid macular oedema with subretinal fluid 4  weeks following uncomplicated phacoemulsification. (b) CMO with leakage from the optic disc. (c) Conservative treatment resolved the macular oedema in 8 weeks

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NSAIDS Nonsteroidal anti-inflammatory drugs (NSAIDS) are known to inhibit cyclo-­ oxygenase enzyme and therefore the production of prostaglandins. The two isoenzyme forms of cyclo-oxygenase enzyme are COX-1 and COX-2, of which the COX-1 is the produced form and COX-2 is the inducible form. COX-2 is induced by surgical trauma and is the most predominant isoform in the retinal pigment epithelium.COX-2 is the predominant isoform of the two in the retinal pigment epithelium [65]. Several studies have shown that the newer available NSAIDS are effective in reducing the incidence of CMO as they are potent COX-2 inhibitors. The role of cyclooxygenase is to catalyse the conversion of arachdonic acid to prostaglandins by acting on the cell membrane phospholipids. Several studies have shown that the NSAIDS could be used as prophylactic medications in preventing pseudophakic CMO. A meta-­analysis by Luca Rosetti, MD, and colleagues in 1998 concluded that the incidence was low for both clinical and sub-clinical (angiographically detected) CMO when topical NSAID was administered [66]. A randomized controlled trial enrolling 189 eyes showed that when topical indomethacin was used as a prophylaxis pre-­operatively for pseudophakic CMO, the incidence was zero percent, the incidence was 15% when it was used post-operatively, and the incidence in the controls was 33%. A large multicentre randomized controlled trial using 0.5% ketorolac tromethamine (Acular) showed improvement when used for the treatment of chronic aphakic or pseudophakic CMO [67]. McColgin and Raizman showed that the incidence of post-operative CMO was significantly reduced when topical NSAID was used in combination with a topical corticosteroids [27]. Wittpenn et al. demonstrated that when ketorolac was used in combination with a topical corticosteroid, there is reduction in the incidence of retinal thickness [68]. In a study on steroid responders, the topical NSAID on its own as a monotherapy was effective in reducing the retinal thickness and improving the visual acuity in patients who had pseudophakic CMO [67]. It appears that the currently available NSAIDs are effective in both prophylaxis and treatment of CMO (Fig. 5.7). There is only limited data on the long-term side effects of NSAIDs in case if they are used for more than 1 year in pseudophakic CMO. Topical NSAIDs do have side effects that should be taken into consideration especially when used for an indication like pseudophakic CMO. Common side effects include irritation, conjunctival hyperaemia and allergy. NSAIDs can cause corneal changes which can range from punctate epithelial erosions to corneal infiltrates or even melt. Delayed corneal epithelial wound healing has also been reported. Steroids Steroids were shown to be effective when they are used for post-operative anterior segment inflammation or chronic CMO following posterior capsule rupture during cataract surgery. A stepwise plan may be undertaken starting with topical administration, followed by local injection (sub-tenons preferred compared to deep orbital injection because of the risk of globe penetration and perforation) (Fig.  5.8a, b), reserving intravitreous administration for severe refractory cases (Fig. 5.9a–c). This

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Fig. 5.7  Right eye Pseudophakic CMO following Posterior Capsule rupture during phacoemulsification. Visual acuity 6/18 (has asteroid hyalosis as well). Complete resolution in 7 weeks with topical NSAIDS

a

b

Fig. 5.8 (a) Left eye pseudophalic CMO with EMM. (b) Not responded to topical NSAIDS and steroids but responded to sub-tenons injection of Triamcinolone with the restoration of the foveal contour

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a

b

c

Fig. 5.9 (a) Pseudophakic CMO recalcitrant type. (b) FFA showing CMO. (c) Pseudophakic CMO did not respond to topical NSAIDS or steroids and did not respond to sub-tenons injection of triamcinolone but showed a partial response to intravitreal triamcinolone

can result in the resolution of macular oedema that has recurred following successful treatment or was resistant and persisted despite treatment with NSAIDs or topical and or local injections of steroids [69, 70]. Pseudophakic CMO can recur even after successful treatment with intravitreal triamcinolone acetonide needing to repeat the procedure, sometimes even several times.

 ombination of Topical NSAIDS and Steroids C When used as a combination, the NSAIDs and steroids are synergistic. Thus pseudophakic CMO is a multifactorial disease and is best treated using a

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combination of different modalities of treatment. Most often the treatment is initiated using a combination of topical NSAIDs and corticosteroids (Fig. 5.10). This signifies the rationale that these different medications work synergistically as they affect the different aspects of the inflammatory cascade [69, 71]. In a small randomized double-blind prospective treatment trial, in 2000, it was reported that compared to a monotherapy using NSAIDs or steroids, a combination therapy for pseudophakic CMO showed significant improvement. In this small randomized controlled trial, the medications topical ketorolac on its own and topical prednisolone on its own were compared to a combination therapy of both in the treatment of pseudophakic CMO [71]. Over a period of 3  months, the average improvement in Snellen’s visual acuity was 1.6 lines in the ketorolac group compared to 1.1 lines in the prednisolone group and 3.8 lines in the combination group (MCHFT) (Fig. 5.11).

 arbonic Anhydrase Inhibitor (Acetazolamide) C The carbonic anhydrase inhibitors may help to reduce the macular oedema by several mechanisms like they may stimulate the RPE to pump out excess fluid

Fig. 5.10  Pseudophakic cystoid macular oedema responded to combination of topical NSAIDS and steroids, visual acuity improved from 6/12 to 6/6 in 4 weeks

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Fig. 5.11  Pseudophakic CMO in a previous retinal vein occlusion patient following cataract extraction. Responded well to a combination of topical NSAIDs and steroids. It shows that the CMO was not a recurrence secondary to the retinal vein occlusion in the past

from the macular area or by acidification of the sub-retinal space which in turn can increase the resorption of the fluid from the retina through the RPE into the choroid [70]. There are some reports showing the role of acetazolamide in the treatment of pseudophakic CMO, but on the whole their efficacy is unknown in the treatment of pseudophakic CMO [72]. They may be effective in the treatment of macular oedema secondary to retinitis pigmentosa and aphakia, but their efficacy is doubtful in pseudophakic CMO.

Anti-VEGF Therapy On reviewing the literature, anti-VEGFs have only a modest effect on pseudophakic CMO, they are more effective in reducing neovascularization. Further studies with these agents is needed to see whether they have any role, and if they do, where do they fit in the hierarchy of the agents that can be used to treat pseudophakic CMO. Bevacizumab, which is a pan anti-VEGF against all the available isoforms of VEGF, when used in case of pseudophakic CMO was found to

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Fig. 5.12  This patient was treated with a single injection anti-VEGF, ranibizumab as mistakenly it was thought it was neovascular AMD following cataract extraction because of the presence of a small RPED and the response was good

be ineffective [73]. Intravitreal anti-VEGF therapy can be useful in post-operative pseudophakic CMO associated with diabetic macular oedema or retinal vein occlusion. There are trials taking place to see whether a combination of corticosteroids and NSAIDS along with intravitreal anti-VEGF are effective in unresponsive cases (MCHFT) (Fig. 5.12).

5.12.2 Surgical 1. Laser surgery: YAG laser vitreolysis is obviously applicable only to a selected group of patients with CMO who have some vitreous adhesions to the anterior segment structures or to the main incision or sideports [12]. Vitreolysis of any incarcerated vitreous in the incisions for cataract surgery using Nd:YAG laser has shown good results in resolving the pseudophakic CMO [74] (Fig. 5.13a–e).

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2. Parsplana vitrectomy: Vitrectomy is indicated for patients with (a) In cases of obvious vitreous prolapse causing macular traction. (b) In certain refractory cases, associated with a decentred IOL, removal of the IOL could be beneficial. (c) In cases of pseudophakic CMO associated with epimacular membrane. (d) In cases of pseudophakic CMO associated with vitreomacular traction. (e) Vitrectomy is effective in pseudophakic CMO which is refractory to conservative management.

a

Vitreous strand going up to the limbal section

b

Vitreous strand going up to the limbal section

Fig. 5.13 (a–e) Surgical aphakia in a 90-year-old patient having vitreous strands going up to the limbal section and also the anterior vitreous broke causing prolapse of the vitreous into the anterior chamber causing vitreous traction and CMO. Anterior vitrectomy with insertion of anterior chamber IOL was done. (d) Showing CMO on FFA due to vitreous traction. (e) Showing resolution of CMO after anterior vitrectomy to remove the traction and insertion of an AC IOL

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c

d

e Fig. 5.13 (continued)

According to Peyman, in cases of chronic recalcitrant pseudophakic CMO, vitrectomy can be helpful [75]. The principle behind this is to relieve any mechanical traction which in turn has caused a release of inflammatory mediators into the vitreous cavity. A vitrectomy in such cases would remove the triggering factor and would restore a normal retinal architecture. In 1985, in a multicentre, randomized controlled trial, the cause for the chronic aphakic CMO was attributed to the vitreous adherence to the wound [76].

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5.12.3 Other Therapies In refractory cases, there have been case reports in small pilot series of sucessfully “treating” pseudophakic CMO using infliximab (Remicade, Centocor Ortho Biotech) [77], intravitreal diclofenac 500 μm/0.1 mL [78] and subcutaneous interferon alpha (Imgenex) [79].

5.13 Prophylactic Treatment At present there are no standardized protocols for prophylaxis against pseudophakic CMO as there aren’t any large prospective randomized controlled trials. Based on the proposed pathogenesis of inflammation, oedema and vitreous traction, therapeutic interventions have been suggested. The current guidelines suggest that the prevention of inflammation should be the main goal, with correct eye and patient preparation, intra-operative care to prevent any iris trauma, to treat more frequently with topical steroids in case a pupil expander or iris hooks are used, treating presurgical macular oedema in case of diabetic macular oedema or uveitic macular oedema, as these could get worse and cause chronic pseudophakic CMO. In patients with past history of diabetic macular oedema and uveitic macular oedema, per-operative intravitreal preservative free triamcinolone acetonide (4 mg) can be helpful. In these patients, it is recommended to first treat the macular oedema and only perform the surgery afterwards. In these cases, the use of intravitreal triamcinolone acetonide (4 mg), injected at the end of the cataract surgery is recommended. In uveitis patients, treatment should be given until the eye is quiet for at least 3 months without any signs of recurrence. Two weeks prior to the cataract surgery, prophylactic treatment with steroid drops at four times a day should be commenced. Post-operatively steroid drops are instilled more frequently and should be closely monitored with gradual tapering.According to Wittpenn et al., pseudophakic CMO developed only in five patients out of 278 when they received perioperative prednisolone and in 0 out of the 268 eyes who also received ketorolac tromethamine [68]. Similarly Yavas et al. showed that in an unmasked randomized controlled trial involving 189 patients, there was 0% of pseudophakic CMO when the subjects received pre-operative and post-operative topical indomethacin [80].

5.14 Nepafenac 1 mg in 1 mL in Adults, Including the Elderly Nepafenac can be used to prevent pain and inflammation, it is used at a tds dose 1 day prior to the cataract surgery and is continued on the day of the surgery and post-operatively for the first 2–3 weeks.

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In case of diabetic patients, with a history of diabetic maculopathy, nepafenac can be used to reduce the risk of post-operative macular oedema. It is used at a tds dose beginning 1 day prior to the cataract surgery, continued on the day of the surgery and up to 60 days of the post-operative period.

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44. Cohen SM, Davis A, Cukrowski C.  Cystoid macular edema and pars plana vitrectomy for retained lens fragments. J Cataract Refract Surg. 2006;32:1521–6. 45. Pollack A, Leiba H, Bukelman A, Oliver M. Cystoid macular edema following cataract extraction in patients with diabetes. Br J Ophthalmol. 1992;76:221–4. 46. Schmier JK, Halpern MT, Covert DW, et  al. Evaluation of cost for cystoid macular edema among patients after cataract surgery. Retina. 2007;27:621–8. 47. Henricsson M, Heijl A, Janzon L. Diabetic retinopathy before and after cataract surgery. Br J Ophthalmol. 1996;80:789–93. 48. Dowler JGF, Hykin PG, Lightman SL, et  al. Visual acuity following extracapsular cataract extraction in diabetes: a meta-analysis. Eye. 1995;9:313–7. 49. Schatz H, Atienza D, McDonald HR, et al. Severe diabetic retinopathy after cataract surgery. Am J Ophthalmol. 1994;117:314–21. 50. Dowler JGF, Sehmi KS, Hykin PG, et al. The natural history of macular edema after cataract surgery in diabetes. Ophthalmology. 1999;106:663–8. 51. Okhravi N, Lightman SL, Towler HM. Assessment of visual outcome after cataractsurgery in patients with uveitis. Ophthalmology. 1999;106:710–22. 52. Hooper PL, Rao NA, Smith RE.  Cataract extraction in uveitis patients. Surv Ophthalmol. 1990;35:120–44. 53. Foster RE, Lowder CY, Meisler OM, Zakov ZN. Extracapsular cataract extraction and posterior chamber intraocular lens implantation in uveitis patients. Ophthalmology. 1992;99:1234–41. 54. Henderson BA, Kim JY, Ament CS, Ferrufino-Ponce ZK, Grabowska A, Cremers SL. Clinical pseudophakic cystoid macular edema. Risk factors for development and duration after treatment. J Cataract Refract Surg. 2007;33:1550–8. 55. Callanan D, Fellman RL, Savage JA. Latanoprost- associated cystoid macular edema. Am J Ophthalmol. 1998;126:134–5. 56. Miyake K, Ota I, Maekubo K, et al. Latanoprost accelerates disruption of the bloodaqueous barrier and the incidence of angiographic cystoid macular edema in early postoperative pseudophakias. Arch Ophthalmol. 1999;117:34–40. 57. Moroi SE, Gottfredsdottir MS, Schteingart MT, et  al. Cystoid macular edema associated with latanoprost therapy in a case series of patients with glaucoma and ocular hypertension. Ophthalmology. 1999;106:1024–9. 58. Ayyala RS, Cruz DA, Margo CE, et al. Cystoid macular edema associated with latanoprost in aphakic and pseudophakic eyes. Am J Ophthalmol. 1998;126:602–4. 59. Wand M, Gaudio AR. Cystoid macular edema associated with ocular hypotensive lipids. Am J Ophthalmol. 2002;133:403–5. 60. Yeh P, Ramanathan S.  Latanoprost and clinically significant cystoid macular edema after uneventful phacoemulsification with intraocular lens implantation. J Cataract Refract Surg. 2002;28(10):1814–8. 61. Schumer RA, Camras CB, Mandahl AK. Latanoprost and cystoid macular edema: is there a causal relation? Curr Opin Ophthalmol. 2000;11:94–100. 62. Milch FA, Yannuzzi LA. Medical and surgical treatment of aphakic cystoid macular oedema. Int Ophthalmol Clin. 1987;27:205–17. 63. Gass JDM. Lamellar macular holes: a complication of cystoid macular edema after cataract extraction. Arch Ophthalmol. 1976;94:793–800. 64. Gass JDM. Lamellar holes: a complication of cystoid macular edema after cataract extraction. A clinicopathologic case report. Trans Am Ophthalmol Soc. 1975;73:231–50. 65. Chin MS, Nagineni CN, Hooper LC, Detrick B, Hooks JJ. Cyclooxygenase-2 gene expression and regulation in human retinal pigment epithelial cells. Invest Ophthalmol Vis Sci. 2001;42:2338–46. 66. Rosetti L, Chaudwi H, Dickersin K.  Medical prophylaxis and treatment of cystoid macular edema after cataract surgery: the results of a meta-analysis. Ophthalmology. 1998; 105:397–405. 67. Warren KA, Fox JE. Topical Nepafenac as an alternate treatment for cystoid macular edema in steroid responsive patients. Retina. 2008;28:1427–34.

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68. Wittpenn JR, Silverstein S, Heier J, et  al. A randomized masked comparison of topical ketorolac 0.4 percent plus steroid vs steroid alone in low-risk cataract surgery patients. Am J Ophthalmol. 2008;146:554–60. 69. Flach AJ. Nonsteroidal anti-inflammatorydrugs. In: Tasman W, editor. Duane’s foundations of clinical ophthalmology. Philadelphia: Lippincott; 1994. p. 1–32. 70. Tranos PG, Wickremasinghe SS, Stangos NT, et  al. Macular edema. Surv Ophthalmol. 2004;5:470–90. 71. Heier JS, Topping TM, Baumann W, et al. Ketorolac versus prednisolone versus combination therapy in treatment of acute pseudophakic cystoid macular edema. Am Acad Ophthalmol. 2000;107:2034–8. 72. Catier A, Tadayoni R, Massin P, et  al. Advantages of acetazolamide associated with antiinflammatory medications in postoperative treatment of macular edema. J Fr Ophtalmol. 2005;28(10):1027–31. (in French). 73. Spitzer MS, Ziemssen F, Yoeruek E, et  al. Efficacy of intravitreal bevacizumab in treating postoperative pseudophakic cystoidmacular edema. J Cataract Refract Surg. 2008;34:70–5. 74. Steinert RF, Wasson PI. Neodymium: YAG laser anterior vitreolysis for Irvine-Gass cystoid macular edema. J Cataract Refract Surg. 1989;15:304–7. 75. Peyman GA, Canakis C, Livir-Rallatos C, et al. The effect of internal limiting membrane peeling on chronic recalcitrant pseudophakic cystoid macular edema: a report of two cases. Am J Ophthalmol. 2002;133:571–2. 76. Fung WE, Vitrectomy-ACME Study Group. Vitrectomy for chronic aphakic cystoid macular edema. Results of a national, collaborative, prospective, randomized investigation. Ophthalmology. 1985;92:1102–11. 77. Wu L, Arevalo JF, Hernandez-Bogantes E, Roca JA. Intravitreal infliximab for refractory pseudophakic cystoid macular edema: results of the pan-american collaborative retina study group. Int Ophthalmol. 2012;32:235–43. 78. Soheilian M, Karimi S, Ramezani A, Peyman GA. Pilot study of intraviteal injection of diclofenac for treatment of macular edema of various etiologies. Retina. 2010;30:509–15. 79. Deuter CM, Gelisken F, Stubiger N, et al. Successful treatment of chronic pseudophakic macular edema (Irvine-Gass syndrome) with interferon alpha: a report of three cases. Ocul Immunol Inflamm. 2011;19:216–8. 80. Yavas GF, Ozturk F, Kusbeci T. Preoperative topical indomethacin to prevent pseudophakic cystoid macular edema. J Cataract Refract Surg. 2007;33:804–7. 81. Balent A, Civerchia LL, Mohamadi P. Visual outcomes of cataract extraction and lens implantation complicated by vitreous loss. J Cataract Refract Surg. 1988;14:158–60. 82. Flach AJ, Jampol LM, Weinberg D, et al. Improvement in visual acuity in chronic aphakic and pseudophakic cystoid macular edema after treatment with topical 0.5% ketorolac tromethamine. Am J Ophthalmol. 1991;112:514–9. 83. Jonas JB, Kreissing I, Segenring RF.  Intravitreal triamcinolone acetonide for pseudophakic cystoid macular edema. Am J Ophthalmol. 2003;136:384–6. 84. Boscia F, Furino C, Dammaco R, et  al. Intravitreal triamcinolone acetonide in refractorypseudophakic cystoid macular edema: functional and anatomic results. Eur J Ophthalmol. 2005;15:89–95. 85. Conway MD, Canakis C, Livir-Rallatos C, et al. Intravitreal triancinolone acetonide for refractory chronic pseudophakic cystoid macular edema. J Cataract Refract Surg. 2003;29:27–33. 86. Shepard DD. The fate of eyes from which intraocular lenses have been removed. Ophthalmic Surg. 1979;10:58–60.

6

Prophylaxis of Postoperative Endophthalmitis Following Cataract Surgery Steve A. Arshinoff and Milad Modabber

6.1

Introduction

Cataract surgery is one of the most common elective surgeries performed in the developed world. Postoperative endophthalmitis (POE) following cataract surgery represents an uncommon yet potentially devastating complication that can lead to permanent severe vision loss. In a recent Cochrane review of perioperative antibiotic prophylaxis in cataract surgery to reduce the risk of postoperative endophthalmitis, Gower et  al. estimated that the current global incidence of POE is approximately 1:1000 cases [1]. Given that approximately 30 million cataract procedures per year are performed worldwide, at the time of Gower’s publication (2013), this translates to 30,000 POE cases annually, of which approximately 10,000 eyes will become blind, making POE a significant public health problem [1]. The incidence of post-cataract surgery endophthalmitis varies considerably, ranging from a high of one case of POE per 315–368 surgeries in Africa and South America to a low of one case per 1418 surgeries in Europe [2, 3], and an even lower incidence of 0.006% (1:16,890) in patients receiving intracameral antibiotic prophylaxis in the recent study of bilateral cataract surgery, of Arshinoff and Bastianelli, among surgeons in the International Society of Bilateral Cataract Surgeons [4]. Pooled international data of over three million cataract extractions over a 40 y­ ear period (1963–2003) estimated a combined POE incidence rate of 0.128% (1:781) [5]. Reviews in the

S. A. Arshinoff (*) York Finch Eye Associates, Humber River Hospital, Toronto, ON, Canada Department of Ophthalmology and Vision Sciences, University of Toronto, Toronto, ON, Canada M. Modabber Department of Ophthalmology and Vision Sciences, University of California, Davis Eye Center, Sacramento, CA, USA © Springer Nature Singapore Pte Ltd. 2020 M. Chakrabarti, A. Chakrabarti (eds.), Posterior Segment Complications of Cataract Surgery, https://doi.org/10.1007/978-981-15-1019-9_6

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1990s arrived at the incidence of endophthalmitis after extracapsular cataract extraction and phacoemulsification to be 0.07% (1:1429) to 0.13% (1:770) [6–10]. More recently, with the use of intracameral antibiotics, infection rates are decreasing globally, and 1:5000 appears to be the current reasonable target. Although a broad spectrum of organisms have been implicated to cause POE, it has been repeatedly demonstrated that 95%, or more, of cases are caused by Gram-­positive bacteria, introduced perioperatively from colonization of lid and ocular surface flora [11, 12]. POE organisms include coagulase negative Staphylococcus aureus, Streptococcus spp., Enterococcus faecalis, and Gramnegative rods (Haemophilus influenzae and Pseudomonas aeruginosa) [2, 3, 13–15]. Propionibacterium acnes are often noted in more indolent cases [15]. However, in up to half of clinically diagnosed endophthalmitis cases, no causative micro-­organism is identified [2]. A variety of risk factors for POE have been identified. Patient factors such as increasing age [16–20] and systemic immunosuppression [18], surgical factors such as surgeon inexperience [21], intraocular lens (IOL) implant material [22], and method of IOL insertion [23, 24], clear corneal incisions [13, 20], wound leakage and dehiscence [25, 26], and posterior capsule rupture [3, 13, 27] have been implicated. Over the past few decades, the incidence of endophthalmitis has decreased with improving surgical techniques including extracapsular cataract extraction (ECCE), phacoemulsification and smaller-incision surgeries enabled by foldable intraocular lenses [16, 19, 28], although not always [29]. Advancements in aseptic techniques such as preoperative conjunctival sac disinfection [22] and the perioperative use of antibiotics have reduced the incidence of POE considerably. Important contributions to the prevention of postoperative endophthalmitis therefore include the position and type of incision, surgical technique, tight incisions, preventive antiseptic regimen, and the perioperative role of antibiotics. This chapter deals mostly with the last two of these.

6.2

Perioperative Nonantibiotic Prophylactic Measures

6.2.1 Povidone-Iodine (PVP-I) Historically, Povidone-iodine perioperative preparation of the eye and periocular skin was the mainstay of POE prophylaxis protocol. There is level 2 evidence that PVP-I 5–10% reduces postoperative infection by decreasing the bacterial load on the ocular surface at the time of surgery [30–33]. Speaker et al. demonstrated that PVP-I prophylaxis resulted in a threefold decrease in the incidence of POE (0.06% [1:1667]) compared with when it was not used (0.18% [1:555]) [34]. Almost the entire world uses PVP-I for surgical prophylaxis, except Sweden, where low-­ concentration 0.05% eye wash and 0.5% facial prep chlorhexidine have been used traditionally and continued (Hibitane for skin cleansing is 4 or 5% and unsafe for ocular use). Microbiological examinations have shown that the rate of contamination of the surgical fluids remains as high as 50% of cases in spite of preoperative

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preparation of the conjunctiva with povidone-iodine [35]. Compared to PVP-I, there is only level 3 evidence for other preoperative measures such as eyelash trimming, intraoperative heparin, and older antibiotic regimens (topical, subconjunctival injection, added to irrigating fluid, and systemic administration).

6.2.2 Incision Construction A watertight incision is very important for preventing POE [36]. Wound leak or dehiscence can provide a direct portal of entry for bacteria, increasing the risk of intraoperative infection. Clear corneal incisions in avascular zones have shown delayed wound healing and higher incidence of endophthalmitis compared with scleral tunnel incisions in the vascular limbal region [37–39]. However, a special white paper report of the American Society of Cataract and Refractive Surgery, in 2006, concluded that it may be poor construction of clear corneal incisions that leads to infection, and not the incision location, as many experienced surgeons using clear corneal incisions noted no increase in infection rates [40].

6.3

The Role of Antibiotics

Perioperative antibacterials have been a mainstay of POE prophylaxis for the cataract surgeon for decades. Multiple studies suggest that the route of antibiotic delivery may be among the most important considerations. There is a wide variability in the choice and delivery method of antibiotic prophylaxis, with the most common being topical administration, subconjunctival and intracameral injections. For prophylaxis of post-cataract surgery endophthalmitis, an ideal antibiotic should be potent, broad spectrum, of sufficient duration of effect, well tolerated with strong safety profile, low allergic risk, easy to prepare and not promoting resistance.

6.3.1 Preoperative Topical Antibiotics ASCRS and ESCRS surveys indicate that nearly all surgeons prescribe topical antibiotics after cataract surgery for prophylaxis of postoperative endophthalmitis, although there are regional differences in practice patterns [41]. Topical antibiotics are intended to reduce the bacterial load of the ocular flora, thus lowering the risk of potential intraocular contamination—intraoperatively or through a postoperative wound leak. Studies have shown that 3 days of preoperative topical antibiotic regimen reduces the count of positive conjunctival samples by approximately 50%, but still maintaining a significant bacterial burden despite antibiotic usage [42, 43]. The practice of administering topical antibiotics for a few days preoperatively for cataract patients became common after the publication of Katz, Masket et al., which showed that the level of topical moxifloxacin achieved in the anterior chamber was 30 times higher than the median MIC of common pathogens [44]. However, a study

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which appeared shortly thereafter, by Ong-Tone demonstrated that aqueous levels really only achieved bactericidal levels when the eye drops were given frequently within 1 h preoperatively, and the preceding 3 days of treatment made little difference [45]. Furthermore, it is an accepted principle in microbiology that the administration of an antibiotic to a specific space depletes populations of sensitive organisms but encourages the growth of resistant strains, as nutrients cease to be consumed by the killed antibiotic sensitive strains. It is the basis of techniques used to isolate specific bacterial strains in cultures and undoubtedly encourages growth of strains resistant to the treating agent when applied for a few days preoperatively topically to the conjunctiva, whereas application of the antibiotic repeatedly within an hour of surgery depletes the sensitive strains but does not allow the resistant ones sufficient time to reproduce and populate the space, thus making immediately preop application without preceding dosing a much better microbiologic strategy. The landmark European Society of Cataract and Refractive Surgeons (ESCRS) study did not find a significant difference in the rate of endophthalmitis in patients treated preoperatively with topical levofloxacin 0.5% QID versus those who did not receive it. A subsequent meta-analysis did not find evidence that pre- or postoperative topical antibiotics prevent endophthalmitis [2]. In Sweden, where topical antibiotic treatment is not routinely used, the rates of endophthalmitis are among the lowest reported worldwide. There, the rate of postoperative endophthalmitis was 0.7 per 1000 patients during the period when topical chloramphenicol was used versus 0.5 per 1000 patients after topical antibiotic use was discontinued and replaced with topical chlorhexidine and the implementation of universal intracameral antibiotic administration.

6.3.2 Antibiotics in the Irrigating Solution The use of vancomycin in the irrigating solution, first proposed by Gills to be the safest and most effective operative antibacterial prophylaxis of drug methods and agents available at the time [46], was adopted widely in the 1990s, but has been recently criticized, as studies failed to detect a statistically significant bactericidal effect [47, 48]. However, vancomycin does not cover Gram negatives, which make up 5% of postoperative endophthalmitis cases (usually the most severe cases), and has generally been reserved as an “agent of last resort,” along with its very low efficacy when added to the irrigating solution, has led the US Center for Disease Control and Prevention (CDC) and the American Academy of Ophthalmology (AAO) to issue guidelines against the routine use of intraoperative vancomycin in the irrigation bottle [49, 50]. The practice has largely been abandoned.

6.3.3 Intracameral Antibiotics The first use of routine intracameral antibiotic prophylaxis was by Gimbel in 1990 [51]. Beginning in about 1994 significant numbers of cataract surgeons were using

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the Gimbel formulation of intracameral vancomycin prophylaxis to prevent endophthalmitis. In 1996, Montan et al. introduced intracameral cefuroxime, 1 mg, for intracameral prophylaxis in Sweden, but it was not adopted widely [52, 53]. In 2006, the European Society of Cataract and Refractive Surgeons (ESCRS) conducted a large prospective randomized placebo-controlled trial to evaluate the prophylactic effect of intracameral cefuroxime using Montan’s formula (1  mg in 0.1 mL normal saline) and/or perioperative topical levofloxacin 0.5% on the incidence of postoperative endophthalmitis after cataract surgery [54, 55]. It was observed that the risk of endophthalmitis in patients receiving direct intracameral injection of cefuroxime at the conclusion of cataract surgery was fivefold lower (0.34% vs 0.07%; RR 0.21; 95% CI: 0.08–0.55) and that of culture-proven endophthalmitis was sixfold lower (RR 0.17; 95% CI 0.05–0.58) than those not receiving intracameral cefuroxime. The treatment effects were so marked that the Data Monitoring Committee (DMC) advised early termination of the study, believing it would be unethical to withhold the use of prophylactic intracameral cefuroxime in groups not receiving it. Perioperative topical levofloxacin 0.5% was not found to significantly reduce the risk for endophthalmitis (see topical section above). The finding of this landmark RCT was reaffirmed by several subsequent studies [56–59], although not globally [60]. Kessel et al. conducted a meta-analysis of 17 randomized and non-randomized studies describing the rate of endophthalmitis before and after implementing prophylactic intracameral antibiotics that included 1,192,330 cataract surgeries and 719 cases of endophthalmitis [2]. The risk of endophthalmitis was found to be significantly lower in patients treated with intracameral cefuroxime (RR 0.09; 95% CI: 0.05–0.15), cefazolin (RR 0.10; 95% CI: 0.06–0.17), and moxifloxacin (RR 0.22; 95% CI: 0.10–0.50). No significant effect was found for intracameral vancomycin (RR 0.30; 95% CI: 0.02–3.90). Overall, POE occurred on average in 1:2855 surgical cases when intracameral antibiotics were used compared to 1:485 surgeries when no intracameral antibiotic was used (RR 0.12; 95% CI: 0.08–0.18; p