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 Table of Contents  
CASE REPORT
Year : 2011  |  Volume : 1  |  Issue : 1  |  Page : 25-27

HSV-1 in a case of intractable glaucoma with rapid progress of cataract after transscleral cyclophotocoagulation


1 Department of Ophthalmology, Taipei City Hospital, Taipei, Taiwan
2 Department of Ophthalmology, Taipei City Hospital; Community Medicine Research Center and Institute of Public Health, National Yang-Ming University, Taipei, Taiwan
3 Department of Ophthalmology, Taipei City Hospital; Department of Ophthalmology, Taipei Medical University; Department of Ophthalmology, National University Hospital, Taipei, Taiwan
4 Department of Ophthalmology, Taipei City Hospital; Department of Ophthalmology, National University Hospital, Taipei, Taiwan

Date of Web Publication1-Dec-2011

Correspondence Address:
I-Lun Tsai
Department of Ophthalmology, Zhongxing Branch, Taipei City Hospital, No. 145, Zhengzhou Road, Datong District, Taipei City 10341
Taiwan
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Source of Support: None, Conflict of Interest: None


DOI: 10.1016/j.tjo.2011.09.002

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  Abstract 


A 22-year-old female patient received penetrating keratoplasty (PK) of her right eye for ocular rosacea complicated with corneal perforation. Intraocular pressure (IOP) fluctuated and could not be well controlled by full antiglaucomatous agents after surgery. Therefore transscleral diode laser cyclo-photocoagulation (TSCPC) was performed for the intractable glaucoma one year after PK. Unfortunately, acute cataract formation was noted 50 days after the laser treatment. Pigmented keratic precipitates (KPs) developed and IOP rose subsequently. Cataract extraction with intraocular lens implantation combined with trabeculectomy was performed 3 months later. Polymerase chain reaction (PCR) tests of the aqueous humor to detect cytomegalovirus (CMV) and herpes simplex virus (HSV) were negative. However, HSV type I DNA was detected in the lenticular material and excised trabecular tissue. Trabe-culitis caused by herpetic infection could be the reason of fluctuated and intractable IOP elevation. The virus hidden in the intraocular tissue could be reactivated by TSCPC and result in cataract formation. Therefore, performing TSCPC in a phakic eye with atypical IOP presentation should be undertaken with caution.

Keywords: herpes simplex virus (HSV), intractable glaucoma, polymerase chain reaction (PCR), rapid cataract formation, transscleral cyclophotocoagulation (TSCPC)


How to cite this article:
Chung HC, Tsai IL, Tsai CY, Liou SW, Woung LC. HSV-1 in a case of intractable glaucoma with rapid progress of cataract after transscleral cyclophotocoagulation. Taiwan J Ophthalmol 2011;1:25-7

How to cite this URL:
Chung HC, Tsai IL, Tsai CY, Liou SW, Woung LC. HSV-1 in a case of intractable glaucoma with rapid progress of cataract after transscleral cyclophotocoagulation. Taiwan J Ophthalmol [serial online] 2011 [cited 2021 Sep 21];1:25-7. Available from: https://www.e-tjo.org/text.asp?2011/1/1/25/203095




  1. Introduction Top


Glaucoma is one of the most serious complications of penetrating keratoplasty (PK) because of its high incidence, morbidity and difficulty of diagnosis and treatment. Transscleral diode laser cyclophotocoagulation (TSCPC) is a well-established, effective method of cyclodestruction in glaucoma therapy, especially for post-PK glaucoma.[1] Early complications, such as pain, iritis and conjunctival burns are common and transient, while severe complications, such as phthisis and bulbus hypotonia are rare.[2] However, cataract after TSCPC has not yet been reported. Here, we report on a rapid cataract formation which might be due to reactivation of herpes simplex virus type 1 (HSV-1) in the eye after TSCPC for an intractable glaucoma after PK. This case was conducted according to the Tenets of Helsinki, was approved by the hospital Institutional Review Board (IRB), and the patient provided written, informed consent to participate.


  2. Case presentation Top


A 22-year-old female received PK in her right eye for ocular rosacea with leucoma adherence in December 2007. Intraocular pressure (IOP) was elevated to 40 mmHg on Day 8 after surgery. Steroid-induced glaucoma was suspected. Hence, 0.1% dexameth-asone eye drop every 2 hours was changed to 0.1% fluorometholone acetate (Flarex, Alcon, Fort Worth, TX, USA) four times a day and combined with 2% Carteolol (Arteoptic, Otsuka, Japan) twice a day to treat her glaucoma. IOP decreased to 16 mmHg within one week. Preoperative best corrected visual acuity (BCVA) of 10/200 improved to 20/25 2 months after PK. Topical steroid was decreased to once a day 6 months after PK, and discontinued at one year. Clear graft with silent anterior chamber and a posterior synechiae on pupil margin in the 5 to 6 o’clock position were noted in June 2008 [Figure 1]. However, the patient’s IOP fluctuated between 12 and 40 mmHg during the follow-up period and could not be controlled with full antiglaucomatous agents starting in November 2008. The angle was generally wide except there are few peripheral anterior synechiae with moderate pigmentation on trabecular meshwork around the 6 o’clock position. Initially, the cup to disc ratio was about 20–30% of both eyes immediately after penetrating keratoplasty. However, it increased to 80% one year after the onset of glaucoma. Therefore, a TSCPC (810 nm diode laser, power: 1500 mW, duration: 2 seconds, 19 applications over inferior 180°) was performed on February 20, 2009. About 50 days after TSCPC, the patient complained of rapid decline of right eye vision for 2 weeks. Slit lamp examination disclosed a totally opacified lens [Figure 2] with a mild anterior chamber reaction. IOP of 14.6 mmHg rose to 30+ mmHg during subsequent visits. A few pigmented keratic precipitates (KPs) developed on both recipient and donor endothelia. Rejection with possible viral keratouveitis was suspected and the aqueous humor was aspirated for polymerase chain reaction (PCR) test to detect herpes simplex virus (HSV) types I and II and cytomegalovirus (CMV) DNA. For the nested PCR assay, we used an initial activation of 94°C for 1 minute, followed by35 cycles at 94° C for 30 seconds, 57° C for 30 seconds and 72° C for 40 seconds, with a final reaction at 72° C for 1 minute. Two microliters of the first amplified products were used for a second amplification as the same protocol. All results were negative. The corneal button excised from PK was also negative of these viral DNAs. The serum IgG titer of HSV-1 was 159.1 (+). Reviewing her past history, we found no major systemic diseases in the patient except for rosacea. After hourly topical 0.1% fluorometholone acetate instillation, the intraocular inflammation was gradually alleviated but the IOP was still above 25 mmHg under full medication. Because the vision was only counting fingers, a cataract extraction with intraocular lens implantation combined with a trabeculectomy was performed on May 29, 2009. Surprisingly, PCR showed a positive result of HSV-1 in the aspirated lenticular material and the excised trabecular tissue [Figure 3], but not in the aqueous humor. Acyclovir 400 mg twice a day was subsequently started and tapered gradually for 8 months. One month after the operation, BCVA improved to 20/30. The number of pigmented KPs decreased, and IOP remained around 10 mmHg without any anti-glaucomatous agents during one year of follow-up.
Figure 1: Clear graft with silent anterior chamber and a posterior synechiae on the pupil margin in the 5 to 6 o’clock position 6 months after penetrating keratoplasty.

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Figure 2: Totally opacified lens 2 months after transscleral diode laser cyclophotocoagulation. The pupil was dilated for fundus examination.

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Figure 3: Polymerase chain reaction result of herpes simplex virus 1 analysis. M = molecular marker; N = negative control; P = positive control; S = sample.

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  3. Discussion Top


TSCPC is a well-established and effective method of cyclo-destruction for glaucoma after PK.[1] Most common complications, including anterior chamber reaction, IOP spikes and conjunctival burns, are mild and transient and do not influence the success of the glaucoma treatment.[2] Hardman et al[3] observed cataract development after TSCPC in canines. They use higher total laser energies delivered to the eye than has been previously reported. It is possible that an increased level of uveitis occurred after diode laser TSCPC using a higher energy protocol, and the uveitis resulted in cataract formation. Lens metabolism may be altered by the change in aqueous humor composition after TSCPC. Cook et al[4] suggest that the lens opacities seen may be in part a sequela to the IOP elevation and/or its associated inflammation, rather than a direct laser effect. In our case, the total laser energy was within recommended ranges. This unusual complication was noted in the right eye 50 days after TSCPC. Accordingly, we strongly suspect this complication to be related to the laser surgery because cataracts developed shortly after this treatment.

Herpes simplex is a common latent infection in humans which spreads from sites of initial infection on skin or mucosal surfaces to neuronal cell bodies, forming a long-term relationship with their host.[5] Reactivation of latent HSV could result in such ocular complications as blepharitis, conjunctivitis, keratitis, iridocyclitis and retinitis. Herpes virus infection has been also known to cause cataract formation. In 1996, Bartz-Schmidt et al[6] reported a case of a 15-year-old female with recurrent herpes keratits, hypotonic iridocyclitis and acute cataract formation, which diagnosis was supported by aqueous humor immunological analysis. Biswas et al[7] presented the case of a 23-year-old male with acute retinal necrosis syndrome with complicated cataract in which HSV-1 was isolated from the vitreous humor and lens material. Therese et al[8] also reported a case of a 33-year-old male presenting with HSV-induced a posterior subcapsular cataract one year after an episode of acute retinal necrosis syndrome. The diagnosis of HSV infection was based on detection of HSV DNA in aqueous humor by PCR. Mitchell and Martin[9] used a mouse model to generate cataracts after corneal inoculation with HSV type 1 strain F. They found lens lesions appeared to be induced directly by viral replication within the lens. Raghu et al[10] presented four cases of congenital cataract associated with HSV-1 infection. In their report, three specimens from four lens aspirates collected at the time of cataract surgery demonstrated the existence of HSV-1 in tube culture, and all four lens aspirates were positive for HSV-1 DNA by PCR.

We did not have a result for viral culture but the PCR result did show the existence of HSV-1 in lens aspirates. Although, our patient developed a cataract shortly after TSCPC, we would like to believe that the rapid cataract formation was virus-related. We reason that TSCPC caused a reactivation of HSV-1, which then replicated in the lens and resulted in cataract formation.

Glaucoma after PK can occur as a result of angle compression, inflammation, progressive synechial closure, pupillary block or prolonged use of steroids. HSV-1 has also been implicated as an important cause of secondary glaucoma.[11] In our case, the angle of the right eye was generally wide, and no chronic inflammation of the anterior segment was noted. The HSV-1 DNA was detected in excised trabecular tissue indicating that HSV-1 might have been involved in the patient’s intractable glaucoma. Furthermore, the clinical response to anti-viral agents was promising to further support the association with HSV-1 infection in our case. Therefore, these pictures supported the association of HSV-1 with the formation of cataract and other clinical appearances.

In conclusion, a latent virus infection, such as HSV-1 in the intraocular tissue could be reactivated by either surgery or steroid usage, resulting in virus replication in the trabecular meshwork and leading to a subsequent refractory glaucoma which may be difficult to control with conventional anti-glaucomatous treatment. TSCPC could also induce reactivation of a latent HSV-1 in the lens and result in cataract formation. Therefore, we strongly suggest exercising caution when performing TSCPC in a phakic eye with atypical IOP presentation to avoid these complications.



 
  References Top

1.
Shah P, Lee GA, Kirwan JK, Bunce C, Bloom PA, Ficker LA, et al. Cyclodiode photocoagulation for refractory glaucoma after penetrating keratoplasty. Ophthalmology 2001;108:1986–91.  Back to cited text no. 1
    
2.
Schlote T, Derse M, Rassmann K, Nicaeus T, Dietz K, Thiel HJ. Efficacy and safety of contact transscleral diode laser cyclophotocoagulation for advanced glaucoma. J Glaucoma 2001;10:294–301.  Back to cited text no. 2
    
3.
Hardman C, Stanley RG. Diode laser transscleral cyclophotocoagulation for the treatment of primary glaucoma in 18 dogs: a retrospective study. Vet Oph-thalmol 2001;4:209–15.  Back to cited text no. 3
    
4.
Cook C, Davidson M, Brinkmann M, Priehs D, Abrams K, Nasisse M, et al. Diode laser transscleral cyclophotocoagulation for the treatment of glaucoma in dogs: results of six and twelve month follow-up. Vet Comp Ophthalmol 1997;7:148–54.  Back to cited text no. 4
    
5.
Pepose JS, Keadle TL, Morrison LA. Ocular herpes simplex: changing epidemiology, emerging disease patterns, and the potential of vaccine prevention and therapy. Am J Ophthalmol 2006;141:547–57.  Back to cited text no. 5
    
6.
Bartz-Schmidt KU, Hartmann C, Kirchhof B, Krieglstein GK. Pathogenesis of complicated cataract in herpetic kerato-uveitis. Klin Monatsbl Augenheilkd. 1996;209:228–31 [In German, English abstract].  Back to cited text no. 6
    
7.
Biswas J, Madhavan HN, Badrinath SS. Demonstration of herpes simplex virus from lens aspirate in healed acute retinal necrosis syndrome. Br JOphthalmol1997; 81:802–3.  Back to cited text no. 7
    
8.
Therese LK, Priya K, Rao SK, Biswas J, Madhavan HN. Herpes simplex virus DNA in the lens one year after an episode of retinitis. Indian JOphthalmol 2000;48:140–1.  Back to cited text no. 8
    
9.
Mitchell WJ, Martin JR. Herpes simplex virus type 1 replicates in the lens and induces cataract in mice. Lab Invest 1992;66:32–8.  Back to cited text no. 9
    
10.
Raghu H, Subhan S, Jose RJ, Gangopadhyay N, Bhende J, Sharma S. Herpes simplex virus-1 – associated congenital cataract. Am JOphthalmol 2004;138: 313–4.  Back to cited text no. 10
    
11.
Jones III R, Pasquale LR, Pavan-Langston D. Herpes simplex virus: an important etiology for secondary glaucoma. Int Ophthalmol Clin 2007;47:99–107.  Back to cited text no. 11
    


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1. Introduction
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3. Discussion
References
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