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Clinical science
Sympathetic ophthalmia following diode laser cyclophotocoagulation Abdullah Albahlal,1 Hassan Al Dhibi,1 Sami Al Shahwan,1 Rajiv Khandekar,1 Deepak P Edward1,2 1
King Khaled Eye Specialist Hospital, Riyadh, Kingdom of Saudi Arabia 2 Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA Correspondence to Dr Deepak P Edward, King Khaled Eye Specialist Hospital, Riyadh 11642, Kingdom of Saudi Arabia; [email protected] Received 29 August 2013 Revised 19 February 2014 Accepted 16 March 2014 Published Online First 7 April 2014
ABSTRACT Background Sympathetic ophthalmia is a rare form of bilateral uveitis that develops following an ocular penetrating injury to one eye. Several cases of sympathetic ophthalmia have been reported after nonpenetrating cyclodestructive procedures including Nd: YAG and diode laser cyclophotocoagulation (CPC) but information on inciting factors and outcome is limited. In this case series we investigated the inciting factors, clinical features, course and outcome of six patients who developed sympathetic ophthalmia after diode CPC. Methods Six patients who developed sympathetic ophthalmia after diode CPC were identified from the King Khaled Eye Specialist Hospital uveitis database between 2008 and 2013. The medical records of these patients were reviewed for demographic information, ocular history, diode laser parameters, clinical presentation, treatment and outcome. Results Six patients were diagnosed with sympathetic ophthalmia following treatment with diode laser CPC, an incidence of 0.001% during the study period. Two patients had a history of accidental trauma and all patients had undergone at least one ocular surgery that included a variety of procedures. At presentation, two patients had predominantly posterior segment findings in the sympathising eye, one patient had only anterior segment findings and the rest had panuveitis. All patients were treated with topical and systemic corticosteroids and/or immunosupressive therapy that resulted in complete resolution of inflammation and return to baseline vision in the sympathising eye within 2–48 months of treatment. Conclusions Sympathetic ophthalmia after diode CPC is rare and is seen in patients with a history of intraocular surgery with or without previous trauma. Early recognition of sympathetic ophthalmia and aggressive management with immunosuppressive therapy results in good outcomes for these patients.
INTRODUCTION
To cite: Albahlal A, Al Dhibi H, Al Shahwan S, et al. Br J Ophthalmol 2014;98:1101–1106.
Sympathetic ophthalmia is a rare bilateral granulomatous uveitis that develops after a variable latent period following an injury to one eye (the inciting eye) leading to devastating compromise of vision in both eyes.1 The injury could be from accidental trauma, ocular surgery or even a non-penetrating cyclodestructive procedure.2 Diode laser trans-scleral cyclophotocoagulation (CPC) has been known as a simple, safe and effective modality in the management of refractive glaucoma, neovascular glaucoma and glaucoma in a blind painful eye.3 4 A number of complications have been reported following diode cyclodestruction, including sympathetic ophthalmia.
In 2004, 2006 and 2009 four cases of sympathetic ophthalmia after diode laser trans-scleral CPC were reported.5–7 In this study, we report six additional cases of sympathetic ophthalmia diagnosed between 2008 and 2013. This report describes the spectrum of precipitating factors, clinical presentation and the outcome of these patients.
MATERIAL AND METHODS The authors reviewed medical records of six patients with sympathetic ophthalmia seen at the King Khaled Eye Specialist Hospital (KKESH) from 2008 to 2013. Data collected from the records of patients included the following factors and characteristics: age, sex, history of trauma, previous surgery, preoperative visual acuity, preoperative intraocular pressure (IOP), indication for the procedure, laser parameters used during diode laser CPC, interval between date of CPC procedure and the onset of uveitis, clinical features, treatment and outcome. In addition, the total number of diode CPC procedures between 2008 and 2013 was used to calculate the incidence of diode cyclophotcoagulation at the hospital.
RESULTS A total of 3840 diode CPCs were performed at KKESH during the study period, suggesting that the risk of sympathetic ophthalmia following treatment is 0.001% (4/3840). The findings at presentation and clinical course of the six cases are summarised in tables 1 and 2. The mean age of patients with sympathetic ophthalmia in this series was 46.5 years (range 24–56) and five of the affected individuals were women. A history of blunt and penetrating trauma was present in two patients which resulted in the development of glaucoma. All patients had additional procedures besides the CPC in the inciting eye before the onset of sympathetic ophthalmia. Three patients had a history of multiple ocular surgeries ( patients 3, 4 and 6; table 1). The remaining patients had undergone a single surgical procedure that included penetrating keratoplasty, trabeculectomy and cyclocryotherapy. The medical records did not indicate the presence of iris prolapse or incarceration into the surgical wound in any of the patients. The causes of glaucoma in patients treated with diode CPC included neovascular glaucoma (n=2); primary open angle glaucoma (n=1); ghost cell glaucoma (n=1); glaucoma following penetrating keratoplasty (n=1); and angle recession glaucoma (n=1). The parameters used for laser treatment ranged from 22 to 37 applications, with power ranging from 1000 to 2200 mW and application
Albahlal A, et al. Br J Ophthalmol 2014;98:1101–1106. doi:10.1136/bjophthalmol-2013-304257
1101
Clinical science
1102
Baseline information of patients with sympathetic ophthalmia Inciting eye
#
Age
Sex
History of trauma
Previous surgery
VA
IOP
1
53
M
Absent
PKP OU for keratoconus PKP OS ×2 for corneal ulcer
20/30 HM
17/32
Glaucoma filtering surgery OS
20/25 NLP
N/A
PPV for vitreous haemorrhage OD Lens aspiration+PC IOL OD Peripheral iridotomy OD Retinal detachment repair. OD
3/200 20/20
28/20
PPV for vitreous haemorrhage OD ECCE+PC IOL OD YAG capsulotomy OD Cyclocryotherapy OD Panretinal photocoagulation OU Cyclocryotherapy OS
20/300 NLP
14/39
N/A
N/A
2
3
Albahlal A, et al. Br J Ophthalmol 2014;98:1101–1106. doi:10.1136/bjophthalmol-2013-304257
4
5
52
24
55
39
F
F
F
F
Present
Present
Absent
Absent
Diagnosis
CPC OS
High IOP after failed graft
56
F
Absent
Trabeculectomy, mitomycin C OU ECCE+PC IOL OD PKP for PBK OD PPV OD Removal of dislocated IOL OD PPV for aqueous misdirection OD
HM 20/125
24 days 33 burns 2000–2200 mW
OS Angle recession glaucoma. (blind painful eye)
15 years Diode CPC done elsewhere. Laser parameters not available
OD Ghost cell glaucoma following blunt trauma
26 days 37 burns 1500 ms 1600–1700 mW 360°
OS Neovascular glaucoma OU Blind painful eye OS
31 days 22 burns 4000 ms 1100 mW 360°
OS Absolute neovascular glaucoma
6
51/16
37 days Diode CPC done elsewhere. Laser parameters not available
OD Refractory glaucoma
CPC-SO interval
1 year+16 days 24 burns 1500 ms 1000–1500 mW
CPC, cyclophotocoagulation; ECCE, extracapsular cataract extraction; F, female; HM, hand motion; IOL, intraocular lens; IOP, intraocular pressure; M, male; N/A, not available; NLP, no light perception; OD, right eye; OS, left eye; OU, both eyes; PBK, pseudophakic bullous keratopathy; PC, posterior chamber; PKP, penetrating keratoplasty; PPV, pars plana vitrectomy; SO, sympathetic ophthalmia; VA, visual acuity.
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Table 1
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Clinical science Table 2
Clinical features and course of patients in the study
#
Clinical features of sympathising eye
Treatment
Outcome
1
OD Loss of vision, painful eye movement, bifrontal headache VA: 5/200, IOP: 21 Cornea: clear graft A/C: deep, occasional cells, no flare Iris/pupil: RRR Lens: early cataract changes Vitreous: no cells, no haze Disc: swollen hyperaemic Retina: elevation around disc and macula FFA: pinpoint hyperfluorescent area around macula. No typical leak around disc B-scan: mild vitreous opacity, 360 shallow peripheral choroidal detachment. OCT: exudative RD, subretinal fluid OD Photophobia, blurry vision; temporal pain VA: 20/70, IOP: 11 Cornea: mutton fat KPs A/C: 3+ cells, 1+ flare Iris/pupil: Koeppe nodules, posterior, synechia Lens: clear Vitreous: 1+ cells Disc: hyperaemic Retina: multiple yellowish lesions at level of RPE at posterior pole FFA: hard disc, multiple pinpoint hyperfluorescent lesions in the posterior pole, late leakage OS Blurred vision VA: 20/30, IOP: 15 Cornea: clear A/C: deep, occasional cells Iris/ pupil: RRR Lens: clear Vitreous: no cells, no flare Retina: exudative RD at the macula Disc: C/D 0.5; no hyperaemia FFA: multiple points of early hypofluorescence with late leakage and pooling in the macular area OCT: neurosensory detachment OD Loss of vision VA: 20/300, IOP: 14 Cornea: diffuse mutton fat KPs A/C: deep, 1+ cells, no flare Iris/pupil: RRR, large PI Lens: aphakia Retina: flat Disc: no hyperaemia or elevation FFA: no disc leakage; multiple areas of retinal leakage due to tractional RD, microaneurysms OCT: no subretinal fluid OD Loss of vision, headache, tinnitus ×1 week VA: LP, IOP: 18.5 Cornea: fine KPs inferiorly Conjunctiva: slightly injected A/C: deep, +3 cells, no flare Iris/ pupil: RRR Lens: clear Vit.: 1+ cells, no haze Retina: bullous exudative RD involving the macula with multiple deep white lesions at the level of RPE Disc: 2+hyperaemic disc FFA: multiple diffuse areas of pinpoint hyperfluorescence with diffuse leakage under extensive detachment of neurosensory retina and leaking disc. OCT: huge subretinal fluid with neurosensory elevation at the macular area
Intravenous methylprednisolone 1 mg for 3 days Tapering dose of oral prednisone over 7 months Azathioprine 50 mg Pred Forte 1% oph solution
Complete resolution of inflammation after 1 week of treatment At last visit, 2 years later, VA: OD: 20/30, OS: HM, IOP: 22/14. Patient was on maintenance dose of prednisone 7.5 mg and azathioprine 50 mg
Intravenous methylprednisolone 1 g for 3 days Tapering dose of oral prednisone over 15 months Mycophenolate mofetil 1 g orally for 2 months Pred Forte 1% oph solution
Complete resolution of inflammation after 3 weeks At last visit, 15 months after treatment, VA: OD: 20/30, OS: NLP, IOP:15/06. Patient was on maintenance dose of prednisone 5 mg and mycophenolate mofetil 500 mg
Intravenous methylprednisolone 1 g for 3 days Tapering dose of oral prednisone over 18 months Pred Forte 1% oph solution
Complete resolution of inflammation after 1 week At last visit, 4 years later, VA: OD: 20/300, OS: 20/20, IOP: 18/20. Patient was on maintenance dose of prednisone 5 mg every other day
Pred Forte 1% oph solution
Complete resolution of inflammation at last visit, 9 weeks after treatment VA: OD: 20/300, OS: NLP, IOP: 13/20. Patient was on maintenance dose of Pred Forte once daily. Patient lost to follow-up following the 9-week visit
Intravenous methylprednisolone 1 g for 3 days Tapering dose of oral prednisone over 1 month Pred Forte 1% oph solution
At last visit, 1 month after treatment, patient showed no visible improvement except for the resolution of KPs. VA: OD:HM, OS: NLP, IOP:16/soft. After that, Pt as lost to follow-up
2
3
4
5
Continued
Albahlal A, et al. Br J Ophthalmol 2014;98:1101–1106. doi:10.1136/bjophthalmol-2013-304257
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Clinical science Table 2
Continued
#
Clinical features of sympathising eye
Treatment
Outcome
6
OS Blurry vision ×10 days Granulomatous panuveitis, low-grade inflammation VA: 20/200, IOP: 20 Cornea: KPs Sclera: ciliary injection A/C: deep, 2+ cells, 3+ flare Iris/pupil: peripheral anterior synechia, PI Lens: PC IOL Retina: flat, mild non-proliferative diabetic retinopathy Disc: C/D 0.8, hyperaemic disc with blurry margins FFA: hazy view, multiple points of hyperfluorescence with late leakage and hot leaking disc
Tapering dose of oral prednisone over 6 months Mycophenolate motefil 1 g orally Pred Forte 1% oph solution
Complete resolution of inflammation after 5 weeks At last visit, 10 months after treatment, VA: OD: HM, OS: 20/100, IOP: 23/13. Patient was on maintenance dose of prednisone 2.5 mg and mycophenolate mofetil 500 mg
A/C, anterior chamber; C/D, cup/disc ratio; FFA, fundus fluorescein angiography; HM, hand motion; IOL, intraocular lens; IOP, intraocular pressure; KP, keratic precipitate; LP, light perception; NLP, no light perception; OCT, optical coherence tomography; OD, right eye; OS, left eye; OU, both eyes; PC, posterior chamber; RD, retinal detachment; RPE, retinal pigment epithelium; RRR, round, regular and reactive; VA, visual acuity.
duration ranging from 1500 to 2000 ms; in one case the power was 1100 mW for 4000 ms. Symptoms developed in four patients within 45 days of CPC. In the remaining two patients, the symptoms developed within 1 year and 15 years after treatment with diode CPC. All patients presented with visual loss; three had associated ocular pain in the sympathising eye. The clinical presentation ranged from mild anterior uveitis to panuveitis. The patients with panuveitis had granulomatous uveitis in the anterior segment and posterior segment findings that ranged from focal macular findings to large exudative detachments (figure 1). A point of interest is that two patients presented with predominantly posterior pole signs that included serous detachment of the macula in the
sympathising eye (figures 1 and 2). None of the patients underwent enucleation of the inciting eye. Five patients responded very well to topical and oral steroid therapy. Three patients required additional immunosuppressive therapy. Complete resolution of inflammation occurred within 1 month of treatment in four patients and within 2 months in one patient. Patient five had poor vision in the sympathising eye at baseline without much improvement after treatment. However, there was improvement in the inflammation up until the last visit before the patient was lost to follow-up. Three patients maintained 20/30 or better visual acuity in the sympathising eye and the remaining three patients regained baseline vision.
Figure 1 Top left: fundus photograph of sympathising eye of patient 3 at initial presentation showing hypopigmented deep lesions with overlying serous retinal detachment. Top right: Fluorescein angiogram showing pin point hyperflurorescence with localised overlying serous detachment. Bottom: optical coherence tomography demonstrating serous retinal detachment. 1104
Albahlal A, et al. Br J Ophthalmol 2014;98:1101–1106. doi:10.1136/bjophthalmol-2013-304257
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Clinical science
Figure 2 Top left: fundus photograph of sympathising eye of patient 5 at initial presentation showing hyperaemic swollen optic disc. Top right: fluorescein angiogram showing pin point hyperfluorescence in the posterior pole and a localised exudative retinal detachment in the inferotemporal quadrant. Middle left: patient 5 at 10 days after treatment showed extensive exudative retinal detachment as a sign of unresponsiveness to treatment that was confirmed by B scan ultrasound (middle right) and also demonstrated by optical coherence tomography (bottom).
DISCUSSION Diode laser CPC has been shown to be effective in lowering IOP in end-stage glaucoma. Due to its more targeted destruction, it produces less inflammation6 and therefore fewer side effects than those produced by cyclocryotherapy and Nd:YAG CPC.4 Several cases of sympathetic ophthalmia have been reported after Nd:YAG CPC.2 8–13 However, all these cases had a history of multiple ocular surgeries which made investigators question the role of laser procedures as an inciting event and considered laser treatment as a triggering factor.12 Also, it is important to note that many eyes that undergo diode CPC with multiple procedures do not develop sympathetic ophthalmia, and that there is a variable period between a surgical procedure and the onset of sympathetic ophthalmia. Taking these observations into consideration and the low rate of sympathetic ophthalmia, the role of the diode laser as a trigger should be interpreted with caution. Lam and colleagues10 suggested that the incidence of sympathetic ophthalmia was 5.8% and 0.67% after non-contact and contact Nd:YAG cyclotherapy, respectively, which was considered high compared with the incidence of sympathetic ophthalmia after other ocular surgery, which is 0.007%.14 Based on the
number of cases of diode CPC done at our institution, the incidence of sympathetic ophthalmia after diode CPC was computed as 0.001%, which is quite low compared with that reported after ND:YAG laser related cyclodestruction. Sympathetic ophthalmia occurs after a widely variable period of time following the inciting injury. However, 85% of the reported cases had occurred within 6 months of the initial trauma.15 In the four previously reported cases of sympathetic ophthalmia following diode laser CPC, symptoms started 5– 8 months after treatment with CPC.5–7 Four of the cases in our study developed sympathetic ophthalmia 1 month after treatment with diode laser. The inciting eyes had a combination of previous trauma or surgical procedures that were events that preceded the development of sympathetic ophthalmia. In previous case reports in which sympathetic ophthalmia occurred after diode laser, the energy used during the diode laser ranged between 1800 and 2000 mW.2 3 In this series the treatment range was within normal limits, except for two cases in which the total energy delivered was higher than usual. It is difficult to make any definitive conclusions regarding the role played by increased laser energy in the development of sympathetic ophthalmia in these cases. However, we recommend that in eyes
Albahlal A, et al. Br J Ophthalmol 2014;98:1101–1106. doi:10.1136/bjophthalmol-2013-304257
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Clinical science that have predisposing risk factors for sympathetic ophthalmia, such as trauma and surgery, conservative diode energy levels should be considered while treating these eyes for elevated IOP. The clinical presentation of the cases presented here is similar to the classic description of sympathetic ophthalmia and also comparable to two of the cases reported following diode CPC in which deterioration of vision was accompanied by granulomatous uveitis and exudative retinal detachments.5 6 No description of the clinical presentation was found for the other two cases.7 An interesting observation in our study was the prominent posterior segment involvement in four cases, two of which had extremely mild anterior segment inflammation. Two of the cases presented with serous detachment of the macula, which is clearly demonstrated by optical coherence tomography and no cells were found in the vitreous. Serous detachment of the macula can be the earliest sign of inflammation and may produce significant visual loss.16 Based on this observation, we suggest that careful examination of the posterior pole is warranted if a patient presents with blurred vision after diode treatment in the contralateral eye. It was suggested in some studies that enucleation of the inciting eye within 2 weeks of the onset of sympathetic ophthalmia improves the visual outcome in the sympathising eye.15 In our series, none of the patients underwent enucleation of the inciting eye, although three eyes had no light perception. Most eyes responded rapidly to immunosuppressive therapy between 1 and 9 weeks of initiation. All patients were treated with topical and systemic corticosteroids with dosing based on the severity. Therapy was initiated with intravenous pulse steroid therapy followed by oral prednisolone tapered over an average of 11 months. When inflammation was inadequately controlled, immunosuppressive therapy was supplemented with azathioprine and mycophenolate mofetil, which helped to resolve the inflammation as previously reported.17 18 This management regimen resulted in complete resolution of signs of inflammation, minimised adverse sequelae and prevented severe visual loss. The outcome was similar to that described for two cases of sympathetic ophthalmia after diode laser treatment, which resulted in complete resolution of all findings within a few weeks of initiation of immunosuppressive therapy.5 6 It is also similar to the outcome of cases of sympathetic ophthalmia reported by Lam et al10 after Nd:YAG laser, with patients responding very well to topical and oral corticosteroids. Considering the complicated clinical presentation of some patients we were impressed with the overall final outcome. All patients maintained their premorbid visual acuity, which was 20/ 30 or better in three patients. Previously reported cases of sympathetic ophthalmia after diode laser also had good outcomes following treatment.5 6 In summary, sympathetic ophthalmia after diode laser CPC is uncommon. Most eyes that developed this condition had previous trauma or had undergone surgical procedures. The clinical
1106
course in the sympathising and inciting eye was fairly typical, with the exception of prominent posterior segment findings in two eyes. Adequate control of inflammation and good visual outcome was achieved by aggressive topical and systemic immunosuppression in all patients. Contributors AA-B: drafting the article or revising it critically for important intellectual content and final approval of the version to be published. HAD: revising the article critically for important intellectual content and final approval of the version to be published; data interpretation. SAS: data interpretation; revising the article critically for important intellectual content and final approval of the version to be published. RK: revising the article critically for important intellectual content and final approval of the version to be published. DPE: conception and design; interpretation of data; drafting the article or revising it critically for important intellectual content and final approval of the version to be published. Funding None. Competing interests None. Ethics approval King Khaled Eye Specialist Hospital IRB/Ethics Board. Provenance and peer review Not commissioned; externally peer reviewed.
REFERENCES 1 2 3 4 5
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Arevalo JF, Garcia RA, Al-Dhibi HA, et al. Update on sympathetic ophthalmia. Middle East Afr J Ophthalmol 2012;19:13–21. Bechrakis NE, Muller-Stolzenburg NW, Helbig H, et al. Sympathetic ophthalmia following laser cyclocoagulation. Arch Ophthalmol 1994;112:80–4. Martin KR, Broadway DC. Cyclodiode laser therapy for painful, blind glaucomatous eyes. Br J Ophthalmol 2001;85:474–6. Pastor SA, Singh K, Lee DA, et al. Cyclophotocoagulation: a report by the American Academy of Ophthalmology. Ophthalmology 2001;108:2130–8. Kumar N, Chang A, Beaumont P. Sympathetic ophthalmia following ciliary body laser cyclophotocoagulation for rubeotic glaucoma. Clin Experiment Ophthalmol 2004;32:196–8. Roberts MA, Rajkumar V, Morgan G, et al. Sympathetic ophthalmia secondary to cyclodiode laser in a 10-year-old boy. J AAPOS 2009;13:299–300. Su DH, Chee SP. Sympathetic ophthalmia in Singapore: new trends in an old disease. Graefe’s Arch Clin Exp Ophthalmol 2006;244:243–7. Pastor SA, Iwach A, Nozik RA, et al. Presumed sympathetic ophthalmia following Nd: YAG transscleral cyclophotocoagulation. J Glaucoma 1993;2:30–1. Edward DP, Brown SV, Higginbotham E, et al. Sympathetic ophthalmia following neodymium:YAG cyclotherapy. Ophthalmic Surg 1989;20:544–6. Lam S, Tessler HH, Lam BL, et al. High incidence of sympathetic ophthalmia after contact and noncontact neodymium:YAG cyclotherapy. Ophthalmology 1992;99:1818–22. Brown SV, Higginbotham E, Tessler H. Sympathetic ophthalmia following Nd:YAG cyclotherapy. Ophthalmic Surg 1990;21:736–7. Singh G. Sympathetic ophthalmia after Nd:YAG cyclotherapy. Ophthalmology 1993;100:798–9. Minckler DS. Does Nd:YAG cyclotherapy cause sympathetic ophthalmia? Ophthalmic Surg 1989;20:543. Liddy L, Stuart J. Sympathetic ophthalmia in Canada. Can J Ophthalmol 1972;7:157–9. Lubin JR, Albert DM, Weinstein M. Sixty-five years of sympathetic ophthalmia. A clinicopathologic review of 105 cases (1913–1978). Ophthalmology 1980;87:109–21. Gupta V, Gupta A, Dogra MR. Posterior sympathetic ophthalmia: a single centre long-term study of 40 patients from North India. Eye 2008;22:1459–64. Tessler HH, Jennings T. High-dose short-term chlorambucil for intractable sympathetic ophthalmia and Behcet’s disease. Br J Ophthalmol 1990;74:353–7. Lau CH, Comer M, Lightman S. Long-term efficacy of mycophenolate mofetil in the control of severe intraocular inflammation. Clin Experiment Ophthalmol 2003;31:487–91.
Albahlal A, et al. Br J Ophthalmol 2014;98:1101–1106. doi:10.1136/bjophthalmol-2013-304257
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Sympathetic ophthalmia following diode laser cyclophotocoagulation Abdullah Albahlal, Hassan Al Dhibi, Sami Al Shahwan, Rajiv Khandekar and Deepak P Edward Br J Ophthalmol 2014 98: 1101-1106 originally published online April 7, 2014
doi: 10.1136/bjophthalmol-2013-304257 Updated information and services can be found at: http://bjo.bmj.com/content/98/8/1101
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Clinical science
Sympathetic ophthalmia following diode laser cyclophotocoagulation Abdullah Albahlal,1 Hassan Al Dhibi,1 Sami Al Shahwan,1 Rajiv Khandekar,1 Deepak P Edward1,2 1
King Khaled Eye Specialist Hospital, Riyadh, Kingdom of Saudi Arabia 2 Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA Correspondence to Dr Deepak P Edward, King Khaled Eye Specialist Hospital, Riyadh 11642, Kingdom of Saudi Arabia; [email protected] Received 29 August 2013 Revised 19 February 2014 Accepted 16 March 2014 Published Online First 7 April 2014
ABSTRACT Background Sympathetic ophthalmia is a rare form of bilateral uveitis that develops following an ocular penetrating injury to one eye. Several cases of sympathetic ophthalmia have been reported after nonpenetrating cyclodestructive procedures including Nd: YAG and diode laser cyclophotocoagulation (CPC) but information on inciting factors and outcome is limited. In this case series we investigated the inciting factors, clinical features, course and outcome of six patients who developed sympathetic ophthalmia after diode CPC. Methods Six patients who developed sympathetic ophthalmia after diode CPC were identified from the King Khaled Eye Specialist Hospital uveitis database between 2008 and 2013. The medical records of these patients were reviewed for demographic information, ocular history, diode laser parameters, clinical presentation, treatment and outcome. Results Six patients were diagnosed with sympathetic ophthalmia following treatment with diode laser CPC, an incidence of 0.001% during the study period. Two patients had a history of accidental trauma and all patients had undergone at least one ocular surgery that included a variety of procedures. At presentation, two patients had predominantly posterior segment findings in the sympathising eye, one patient had only anterior segment findings and the rest had panuveitis. All patients were treated with topical and systemic corticosteroids and/or immunosupressive therapy that resulted in complete resolution of inflammation and return to baseline vision in the sympathising eye within 2–48 months of treatment. Conclusions Sympathetic ophthalmia after diode CPC is rare and is seen in patients with a history of intraocular surgery with or without previous trauma. Early recognition of sympathetic ophthalmia and aggressive management with immunosuppressive therapy results in good outcomes for these patients.
INTRODUCTION
To cite: Albahlal A, Al Dhibi H, Al Shahwan S, et al. Br J Ophthalmol 2014;98:1101–1106.
Sympathetic ophthalmia is a rare bilateral granulomatous uveitis that develops after a variable latent period following an injury to one eye (the inciting eye) leading to devastating compromise of vision in both eyes.1 The injury could be from accidental trauma, ocular surgery or even a non-penetrating cyclodestructive procedure.2 Diode laser trans-scleral cyclophotocoagulation (CPC) has been known as a simple, safe and effective modality in the management of refractive glaucoma, neovascular glaucoma and glaucoma in a blind painful eye.3 4 A number of complications have been reported following diode cyclodestruction, including sympathetic ophthalmia.
In 2004, 2006 and 2009 four cases of sympathetic ophthalmia after diode laser trans-scleral CPC were reported.5–7 In this study, we report six additional cases of sympathetic ophthalmia diagnosed between 2008 and 2013. This report describes the spectrum of precipitating factors, clinical presentation and the outcome of these patients.
MATERIAL AND METHODS The authors reviewed medical records of six patients with sympathetic ophthalmia seen at the King Khaled Eye Specialist Hospital (KKESH) from 2008 to 2013. Data collected from the records of patients included the following factors and characteristics: age, sex, history of trauma, previous surgery, preoperative visual acuity, preoperative intraocular pressure (IOP), indication for the procedure, laser parameters used during diode laser CPC, interval between date of CPC procedure and the onset of uveitis, clinical features, treatment and outcome. In addition, the total number of diode CPC procedures between 2008 and 2013 was used to calculate the incidence of diode cyclophotcoagulation at the hospital.
RESULTS A total of 3840 diode CPCs were performed at KKESH during the study period, suggesting that the risk of sympathetic ophthalmia following treatment is 0.001% (4/3840). The findings at presentation and clinical course of the six cases are summarised in tables 1 and 2. The mean age of patients with sympathetic ophthalmia in this series was 46.5 years (range 24–56) and five of the affected individuals were women. A history of blunt and penetrating trauma was present in two patients which resulted in the development of glaucoma. All patients had additional procedures besides the CPC in the inciting eye before the onset of sympathetic ophthalmia. Three patients had a history of multiple ocular surgeries ( patients 3, 4 and 6; table 1). The remaining patients had undergone a single surgical procedure that included penetrating keratoplasty, trabeculectomy and cyclocryotherapy. The medical records did not indicate the presence of iris prolapse or incarceration into the surgical wound in any of the patients. The causes of glaucoma in patients treated with diode CPC included neovascular glaucoma (n=2); primary open angle glaucoma (n=1); ghost cell glaucoma (n=1); glaucoma following penetrating keratoplasty (n=1); and angle recession glaucoma (n=1). The parameters used for laser treatment ranged from 22 to 37 applications, with power ranging from 1000 to 2200 mW and application
Albahlal A, et al. Br J Ophthalmol 2014;98:1101–1106. doi:10.1136/bjophthalmol-2013-304257
1101
Clinical science
1102
Baseline information of patients with sympathetic ophthalmia Inciting eye
#
Age
Sex
History of trauma
Previous surgery
VA
IOP
1
53
M
Absent
PKP OU for keratoconus PKP OS ×2 for corneal ulcer
20/30 HM
17/32
Glaucoma filtering surgery OS
20/25 NLP
N/A
PPV for vitreous haemorrhage OD Lens aspiration+PC IOL OD Peripheral iridotomy OD Retinal detachment repair. OD
3/200 20/20
28/20
PPV for vitreous haemorrhage OD ECCE+PC IOL OD YAG capsulotomy OD Cyclocryotherapy OD Panretinal photocoagulation OU Cyclocryotherapy OS
20/300 NLP
14/39
N/A
N/A
2
3
Albahlal A, et al. Br J Ophthalmol 2014;98:1101–1106. doi:10.1136/bjophthalmol-2013-304257
4
5
52
24
55
39
F
F
F
F
Present
Present
Absent
Absent
Diagnosis
CPC OS
High IOP after failed graft
56
F
Absent
Trabeculectomy, mitomycin C OU ECCE+PC IOL OD PKP for PBK OD PPV OD Removal of dislocated IOL OD PPV for aqueous misdirection OD
HM 20/125
24 days 33 burns 2000–2200 mW
OS Angle recession glaucoma. (blind painful eye)
15 years Diode CPC done elsewhere. Laser parameters not available
OD Ghost cell glaucoma following blunt trauma
26 days 37 burns 1500 ms 1600–1700 mW 360°
OS Neovascular glaucoma OU Blind painful eye OS
31 days 22 burns 4000 ms 1100 mW 360°
OS Absolute neovascular glaucoma
6
51/16
37 days Diode CPC done elsewhere. Laser parameters not available
OD Refractory glaucoma
CPC-SO interval
1 year+16 days 24 burns 1500 ms 1000–1500 mW
CPC, cyclophotocoagulation; ECCE, extracapsular cataract extraction; F, female; HM, hand motion; IOL, intraocular lens; IOP, intraocular pressure; M, male; N/A, not available; NLP, no light perception; OD, right eye; OS, left eye; OU, both eyes; PBK, pseudophakic bullous keratopathy; PC, posterior chamber; PKP, penetrating keratoplasty; PPV, pars plana vitrectomy; SO, sympathetic ophthalmia; VA, visual acuity.
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Table 1
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Clinical science Table 2
Clinical features and course of patients in the study
#
Clinical features of sympathising eye
Treatment
Outcome
1
OD Loss of vision, painful eye movement, bifrontal headache VA: 5/200, IOP: 21 Cornea: clear graft A/C: deep, occasional cells, no flare Iris/pupil: RRR Lens: early cataract changes Vitreous: no cells, no haze Disc: swollen hyperaemic Retina: elevation around disc and macula FFA: pinpoint hyperfluorescent area around macula. No typical leak around disc B-scan: mild vitreous opacity, 360 shallow peripheral choroidal detachment. OCT: exudative RD, subretinal fluid OD Photophobia, blurry vision; temporal pain VA: 20/70, IOP: 11 Cornea: mutton fat KPs A/C: 3+ cells, 1+ flare Iris/pupil: Koeppe nodules, posterior, synechia Lens: clear Vitreous: 1+ cells Disc: hyperaemic Retina: multiple yellowish lesions at level of RPE at posterior pole FFA: hard disc, multiple pinpoint hyperfluorescent lesions in the posterior pole, late leakage OS Blurred vision VA: 20/30, IOP: 15 Cornea: clear A/C: deep, occasional cells Iris/ pupil: RRR Lens: clear Vitreous: no cells, no flare Retina: exudative RD at the macula Disc: C/D 0.5; no hyperaemia FFA: multiple points of early hypofluorescence with late leakage and pooling in the macular area OCT: neurosensory detachment OD Loss of vision VA: 20/300, IOP: 14 Cornea: diffuse mutton fat KPs A/C: deep, 1+ cells, no flare Iris/pupil: RRR, large PI Lens: aphakia Retina: flat Disc: no hyperaemia or elevation FFA: no disc leakage; multiple areas of retinal leakage due to tractional RD, microaneurysms OCT: no subretinal fluid OD Loss of vision, headache, tinnitus ×1 week VA: LP, IOP: 18.5 Cornea: fine KPs inferiorly Conjunctiva: slightly injected A/C: deep, +3 cells, no flare Iris/ pupil: RRR Lens: clear Vit.: 1+ cells, no haze Retina: bullous exudative RD involving the macula with multiple deep white lesions at the level of RPE Disc: 2+hyperaemic disc FFA: multiple diffuse areas of pinpoint hyperfluorescence with diffuse leakage under extensive detachment of neurosensory retina and leaking disc. OCT: huge subretinal fluid with neurosensory elevation at the macular area
Intravenous methylprednisolone 1 mg for 3 days Tapering dose of oral prednisone over 7 months Azathioprine 50 mg Pred Forte 1% oph solution
Complete resolution of inflammation after 1 week of treatment At last visit, 2 years later, VA: OD: 20/30, OS: HM, IOP: 22/14. Patient was on maintenance dose of prednisone 7.5 mg and azathioprine 50 mg
Intravenous methylprednisolone 1 g for 3 days Tapering dose of oral prednisone over 15 months Mycophenolate mofetil 1 g orally for 2 months Pred Forte 1% oph solution
Complete resolution of inflammation after 3 weeks At last visit, 15 months after treatment, VA: OD: 20/30, OS: NLP, IOP:15/06. Patient was on maintenance dose of prednisone 5 mg and mycophenolate mofetil 500 mg
Intravenous methylprednisolone 1 g for 3 days Tapering dose of oral prednisone over 18 months Pred Forte 1% oph solution
Complete resolution of inflammation after 1 week At last visit, 4 years later, VA: OD: 20/300, OS: 20/20, IOP: 18/20. Patient was on maintenance dose of prednisone 5 mg every other day
Pred Forte 1% oph solution
Complete resolution of inflammation at last visit, 9 weeks after treatment VA: OD: 20/300, OS: NLP, IOP: 13/20. Patient was on maintenance dose of Pred Forte once daily. Patient lost to follow-up following the 9-week visit
Intravenous methylprednisolone 1 g for 3 days Tapering dose of oral prednisone over 1 month Pred Forte 1% oph solution
At last visit, 1 month after treatment, patient showed no visible improvement except for the resolution of KPs. VA: OD:HM, OS: NLP, IOP:16/soft. After that, Pt as lost to follow-up
2
3
4
5
Continued
Albahlal A, et al. Br J Ophthalmol 2014;98:1101–1106. doi:10.1136/bjophthalmol-2013-304257
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Clinical science Table 2
Continued
#
Clinical features of sympathising eye
Treatment
Outcome
6
OS Blurry vision ×10 days Granulomatous panuveitis, low-grade inflammation VA: 20/200, IOP: 20 Cornea: KPs Sclera: ciliary injection A/C: deep, 2+ cells, 3+ flare Iris/pupil: peripheral anterior synechia, PI Lens: PC IOL Retina: flat, mild non-proliferative diabetic retinopathy Disc: C/D 0.8, hyperaemic disc with blurry margins FFA: hazy view, multiple points of hyperfluorescence with late leakage and hot leaking disc
Tapering dose of oral prednisone over 6 months Mycophenolate motefil 1 g orally Pred Forte 1% oph solution
Complete resolution of inflammation after 5 weeks At last visit, 10 months after treatment, VA: OD: HM, OS: 20/100, IOP: 23/13. Patient was on maintenance dose of prednisone 2.5 mg and mycophenolate mofetil 500 mg
A/C, anterior chamber; C/D, cup/disc ratio; FFA, fundus fluorescein angiography; HM, hand motion; IOL, intraocular lens; IOP, intraocular pressure; KP, keratic precipitate; LP, light perception; NLP, no light perception; OCT, optical coherence tomography; OD, right eye; OS, left eye; OU, both eyes; PC, posterior chamber; RD, retinal detachment; RPE, retinal pigment epithelium; RRR, round, regular and reactive; VA, visual acuity.
duration ranging from 1500 to 2000 ms; in one case the power was 1100 mW for 4000 ms. Symptoms developed in four patients within 45 days of CPC. In the remaining two patients, the symptoms developed within 1 year and 15 years after treatment with diode CPC. All patients presented with visual loss; three had associated ocular pain in the sympathising eye. The clinical presentation ranged from mild anterior uveitis to panuveitis. The patients with panuveitis had granulomatous uveitis in the anterior segment and posterior segment findings that ranged from focal macular findings to large exudative detachments (figure 1). A point of interest is that two patients presented with predominantly posterior pole signs that included serous detachment of the macula in the
sympathising eye (figures 1 and 2). None of the patients underwent enucleation of the inciting eye. Five patients responded very well to topical and oral steroid therapy. Three patients required additional immunosuppressive therapy. Complete resolution of inflammation occurred within 1 month of treatment in four patients and within 2 months in one patient. Patient five had poor vision in the sympathising eye at baseline without much improvement after treatment. However, there was improvement in the inflammation up until the last visit before the patient was lost to follow-up. Three patients maintained 20/30 or better visual acuity in the sympathising eye and the remaining three patients regained baseline vision.
Figure 1 Top left: fundus photograph of sympathising eye of patient 3 at initial presentation showing hypopigmented deep lesions with overlying serous retinal detachment. Top right: Fluorescein angiogram showing pin point hyperflurorescence with localised overlying serous detachment. Bottom: optical coherence tomography demonstrating serous retinal detachment. 1104
Albahlal A, et al. Br J Ophthalmol 2014;98:1101–1106. doi:10.1136/bjophthalmol-2013-304257
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Clinical science
Figure 2 Top left: fundus photograph of sympathising eye of patient 5 at initial presentation showing hyperaemic swollen optic disc. Top right: fluorescein angiogram showing pin point hyperfluorescence in the posterior pole and a localised exudative retinal detachment in the inferotemporal quadrant. Middle left: patient 5 at 10 days after treatment showed extensive exudative retinal detachment as a sign of unresponsiveness to treatment that was confirmed by B scan ultrasound (middle right) and also demonstrated by optical coherence tomography (bottom).
DISCUSSION Diode laser CPC has been shown to be effective in lowering IOP in end-stage glaucoma. Due to its more targeted destruction, it produces less inflammation6 and therefore fewer side effects than those produced by cyclocryotherapy and Nd:YAG CPC.4 Several cases of sympathetic ophthalmia have been reported after Nd:YAG CPC.2 8–13 However, all these cases had a history of multiple ocular surgeries which made investigators question the role of laser procedures as an inciting event and considered laser treatment as a triggering factor.12 Also, it is important to note that many eyes that undergo diode CPC with multiple procedures do not develop sympathetic ophthalmia, and that there is a variable period between a surgical procedure and the onset of sympathetic ophthalmia. Taking these observations into consideration and the low rate of sympathetic ophthalmia, the role of the diode laser as a trigger should be interpreted with caution. Lam and colleagues10 suggested that the incidence of sympathetic ophthalmia was 5.8% and 0.67% after non-contact and contact Nd:YAG cyclotherapy, respectively, which was considered high compared with the incidence of sympathetic ophthalmia after other ocular surgery, which is 0.007%.14 Based on the
number of cases of diode CPC done at our institution, the incidence of sympathetic ophthalmia after diode CPC was computed as 0.001%, which is quite low compared with that reported after ND:YAG laser related cyclodestruction. Sympathetic ophthalmia occurs after a widely variable period of time following the inciting injury. However, 85% of the reported cases had occurred within 6 months of the initial trauma.15 In the four previously reported cases of sympathetic ophthalmia following diode laser CPC, symptoms started 5– 8 months after treatment with CPC.5–7 Four of the cases in our study developed sympathetic ophthalmia 1 month after treatment with diode laser. The inciting eyes had a combination of previous trauma or surgical procedures that were events that preceded the development of sympathetic ophthalmia. In previous case reports in which sympathetic ophthalmia occurred after diode laser, the energy used during the diode laser ranged between 1800 and 2000 mW.2 3 In this series the treatment range was within normal limits, except for two cases in which the total energy delivered was higher than usual. It is difficult to make any definitive conclusions regarding the role played by increased laser energy in the development of sympathetic ophthalmia in these cases. However, we recommend that in eyes
Albahlal A, et al. Br J Ophthalmol 2014;98:1101–1106. doi:10.1136/bjophthalmol-2013-304257
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Clinical science that have predisposing risk factors for sympathetic ophthalmia, such as trauma and surgery, conservative diode energy levels should be considered while treating these eyes for elevated IOP. The clinical presentation of the cases presented here is similar to the classic description of sympathetic ophthalmia and also comparable to two of the cases reported following diode CPC in which deterioration of vision was accompanied by granulomatous uveitis and exudative retinal detachments.5 6 No description of the clinical presentation was found for the other two cases.7 An interesting observation in our study was the prominent posterior segment involvement in four cases, two of which had extremely mild anterior segment inflammation. Two of the cases presented with serous detachment of the macula, which is clearly demonstrated by optical coherence tomography and no cells were found in the vitreous. Serous detachment of the macula can be the earliest sign of inflammation and may produce significant visual loss.16 Based on this observation, we suggest that careful examination of the posterior pole is warranted if a patient presents with blurred vision after diode treatment in the contralateral eye. It was suggested in some studies that enucleation of the inciting eye within 2 weeks of the onset of sympathetic ophthalmia improves the visual outcome in the sympathising eye.15 In our series, none of the patients underwent enucleation of the inciting eye, although three eyes had no light perception. Most eyes responded rapidly to immunosuppressive therapy between 1 and 9 weeks of initiation. All patients were treated with topical and systemic corticosteroids with dosing based on the severity. Therapy was initiated with intravenous pulse steroid therapy followed by oral prednisolone tapered over an average of 11 months. When inflammation was inadequately controlled, immunosuppressive therapy was supplemented with azathioprine and mycophenolate mofetil, which helped to resolve the inflammation as previously reported.17 18 This management regimen resulted in complete resolution of signs of inflammation, minimised adverse sequelae and prevented severe visual loss. The outcome was similar to that described for two cases of sympathetic ophthalmia after diode laser treatment, which resulted in complete resolution of all findings within a few weeks of initiation of immunosuppressive therapy.5 6 It is also similar to the outcome of cases of sympathetic ophthalmia reported by Lam et al10 after Nd:YAG laser, with patients responding very well to topical and oral corticosteroids. Considering the complicated clinical presentation of some patients we were impressed with the overall final outcome. All patients maintained their premorbid visual acuity, which was 20/ 30 or better in three patients. Previously reported cases of sympathetic ophthalmia after diode laser also had good outcomes following treatment.5 6 In summary, sympathetic ophthalmia after diode laser CPC is uncommon. Most eyes that developed this condition had previous trauma or had undergone surgical procedures. The clinical
1106
course in the sympathising and inciting eye was fairly typical, with the exception of prominent posterior segment findings in two eyes. Adequate control of inflammation and good visual outcome was achieved by aggressive topical and systemic immunosuppression in all patients. Contributors AA-B: drafting the article or revising it critically for important intellectual content and final approval of the version to be published. HAD: revising the article critically for important intellectual content and final approval of the version to be published; data interpretation. SAS: data interpretation; revising the article critically for important intellectual content and final approval of the version to be published. RK: revising the article critically for important intellectual content and final approval of the version to be published. DPE: conception and design; interpretation of data; drafting the article or revising it critically for important intellectual content and final approval of the version to be published. Funding None. Competing interests None. Ethics approval King Khaled Eye Specialist Hospital IRB/Ethics Board. Provenance and peer review Not commissioned; externally peer reviewed.
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Albahlal A, et al. Br J Ophthalmol 2014;98:1101–1106. doi:10.1136/bjophthalmol-2013-304257
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Sympathetic ophthalmia following diode laser cyclophotocoagulation Abdullah Albahlal, Hassan Al Dhibi, Sami Al Shahwan, Rajiv Khandekar and Deepak P Edward Br J Ophthalmol 2014 98: 1101-1106 originally published online April 7, 2014
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