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Management of inflammatory glaucoma

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Mark Werner,  M.D.

 

Inflammatory glaucomas are relatively uncommon, but they present a very unique challenge and frustration for eye care professionals.  There are many causes of ocular inflammation, many of which have a unique clinical course.  Patients often are involved with multiple subspecialists.  Systemic conditions may have a direct role in the disease and its therapy.  Patients may endure relapses or even chronic, refractory inflammation and/or pressure elevation.  Other consequences of inflammation, including cystoid macular edema (CME) and cataract, may complicate clinical decisions.  The medical management of inflammatory glaucoma is challenging.  The relative contribution of steroid response and inflammatory blockage of trabecular outflow may be difficult to sort out.  Proper timing of and selection of surgical treatment is complex, and the approach should be tailored to the individual patient.
When confronted with a patient with inflammatory glaucoma, there are several questions which the clinician must answer, and this can be divided into the etiology of inflammation, the cause of the pressure rise, and the status of the optic nerve.  Based on the answers to these questions the clinician can begin to formulate a treatment plan.
               

In any patient with recurrent or bilateral uveitis, an attempt should be made to rule out specific underlying conditions, either ocular or systemic.  The ocular syndrome will dictate the workup and directed history.  Anterior uveitis is frequently idiopathic.  At minimum, an appropriate review of systems, focusing on arthritis, infections or exposures, mucosa or skin lesions, and cough should be conducted.  A complete blood count and syphilis serology may be appropriate for all patients, while specific tests such as angiotensin converting enzyme and chest x-ray may be advisable for patients of African descent.  Conditions such as scleritis, pars planitis, and posterior uveitis are all approached in a unique way. 
Many syndromes may have unique characteristic features, either in clinical presentation or examination findings.  History of laser capsulotomy shortly prior to presentation, with retained cortical material may suggest P.acnes infection.  Findings such as disciform keratitis or a characteristic distribution of skin lesions may implicate herpetic infection.  A rapid episodic rise in IOP with mnimal cellular reaction may suggest Posner-Schlossman syndrome.  A complete synopsis of all ocular findings in uveitic syndromes and their management implications is beyond the scope of this discussion.  The American Academy of Ophthalmology Basic and Clinical Science Course and other textbooks may provide a more detailed review.  Once the diagnosis is made, the patient should be referred as appropriate for specific systemic and ocular therapies as indicated.  Good communication on the part of the glaucoma specialist with the doctor managing the disease is important.

Systemic antiinflammatory treatment may be required in extreme cases.  This should be done with informed consent from the patient, and short-and long-term side effects discussed beforehand.  Administering of therapy should be done under supervision by a doctor who is experienced in dealing with these potent medications and can monitor the patient appropriately.  Often times regular blood tests are required, particularly for steroid-sparing agents.  Specific treatment for the underlying condition should of course be employed as well where appropriate. 
               

The ophthalmologist should then evaluate the timing and extent of the pressure rise.  If the pressure was elevated at the time of diagnosis, it is more likely that the inflammation is contributing to the pressure elevation.  In this case, the priority should be in escalating anti-inflammatory treatment until the inflammation has been controlled.  If topical eyedrops are unable to control inflammation, sub-Tenon’s steroids may help.    Often times the time course of pressure rise cannot be well established. 
A good general approach is to start with aggressive, high-potency topical steroids (such as prednisolone acetate drops hourly) and follow up the patient within a few days to establish the status of inflammation and the IOP.  If there is not a rapid response to medical treatment directed at the inflammation and IOP, surgery will most likely be required.  Chronic synechial angle closure may also be present, and may decrease the reserve of the outflow system and increase the chance that surgery will be necessary.  Aqueous suppressants are preferred initially.  Prostaglandins are to be avoided at first, as they may potentiate inflammation and are ineffective in the setting of active inflammation1.  However, in a quiet eye with continued pressure elevation, they may be of service2-4. 
If the pressure elevation began weeks after treatment, however, steroid response must be strongly considered.  Steroid responses can apparently occur after a single treatment, however.  The steroids should be suspended when possible.  The status of the optic nerve should be assessed with fundus examination and visual field testing.   Baseline stereo disc photographs are important to pick up change later on.  There have been some reports of effectiveness of laser trabeculoplasty in some steroid responders, though it may be difficult to separate the effect of removing the steroids5.  One general rule of thumb may be that the duration of steroid treatment should also be the duration required for withdrawal of steroid to allow the pressure to come down.  This is a very rough guideline, but may help the clinician in managing such cases.
               

Surgery may be required in several situations.  If the optic nerve is severely damaged, and the pressure is very high, a short course of medical treatment may be advised.  If the patient does not respond to treatment, however, surgery may be required relatively soon.  If the optic nerve is healthy the eye should be thoroughly quieted down, steroids weaned off as much as possible, and medical therapy maximized.  If the pressure is still high, the risk of future damage to the nerve must be considered and weighed against the risk of any intervention.  The condition of the fellow eye, the age of the patient, and treatment of any related systemic condition should also be taken into account.
               

Surgery for uveitic glaucoma may involve trabeculectomy or tube shunt placement.  Trabeculectomy may carry a risk of scarring and failure, even with mitomycin use, either in the short or long term (with chronic or repetitive episodes of inflammation), though some glaucomatologists advocate its use in this context and report similar results to non-uveitic patients6-8.  In terms of tube implants, nonvalved glaucoma drainage implants may carry a risk of hypotony, either in the short or long term, particularly in patients with active or recurrent inflammation.  In these patients, a valved implant such as the Ahmed may be preferred9-10.  However, in patients with only a remote history of inflammation, the larger surface area of a nonvalved impant such as the Baerveldt may offer better long term pressure control11-12.  Chronic hypotony may occasionally require removal of the implant or exchange for a smaller valved implant.  In children goniotomy may be successful in some patients, and should be considered given the high incidence of problems with tubes in this group, including tube rotation and exposure13.

References

  1. Saccà S, Pascotto A, Siniscalchi C, Rolando M.  Ocular complications of latanoprost in uveitic glaucoma: three case reports.  J Ocul Pharmacol Ther. 2001 Apr;17(2):107-13.
  2. Fortuna E, Cervantes-Castañeda RA, Bhat P, Doctor P, Foster CS.  Flare-up rates with bimatoprost therapy in uveitic glaucoma.  Am J Ophthalmol. 2008 Dec;146(6):876-82.
  3. Markomichelakis NN, Kostakou A, Halkiadakis I, Chalkidou S, Papakonstantinou D, Georgopoulos G.  Efficacy and safety of latanoprost in eyes with uveitic glaucoma.  Graefes Arch Clin Exp Ophthalmol. 2009 Jun;247(6):775-80. Epub 2009 Jan 28.
  4. Sallam A, Sheth HG, Habot-Wilner Z, Lightman S.  Outcome of raised intraocular pressure in uveitic eyes with and without a corticosteroid-induced hypertensive response.  Am J Ophthalmol. 2009 Aug;148(2):207-213.e1. Epub 2009 Apr 29.
  5. Rubin B, Taglienti A, Rothman RF, Marcus CH, Serle JB.  The effect of selective laser trabeculoplasty on intraocular pressure in patients with intravitreal steroid-induced elevated intraocular pressure.  J Glaucoma. 2008 Jun-Jul;17(4):287-92.
  6. Kaburaki T, Koshino T, Kawashima H, Numaga J, Tomidokoro A, Shirato S, Araie M.  Initial trabeculectomy with mitomycin C in eyes with uveitic glaucoma with inactive uveitis.  Eye (Lond). 2009 Jul;23(7):1509-17. Epub 2009 Jun 12.
  7. Noble J, Derzko-Dzulynsky L, Rabinovitch T, Birt C.  Outcome of trabeculectomy with intraoperative mitomycin C for uveitic glaucoma.  Can J Ophthalmol. 2007 Feb;42(1):89-94.
  8. Park UC, Ahn JK, Park KH, Yu HG.  Phacotrabeculectomy with mitomycin C in patients with uveitis.  Am J Ophthalmol. 2006 Dec;142(6):1005-12. Epub 2006 Aug 10.
  9. Rachmiel R, Trope GE, Buys YM, Flanagan JG, Chipman ML.  Ahmed glaucoma valve implantation in uveitic glaucoma versus open-angle glaucoma patients.  Can J Ophthalmol. 2008 Aug;43(4):462-7.
  10. Papadaki TG, Zacharopoulos IP, Pasquale LR, Christen WB, Netland PA, Foster CS.  Long-term results of Ahmed glaucoma valve implantation for uveitic glaucoma.  Am J Ophthalmol. 2007 Jul;144(1):62-69. Epub 2007 May 9.
  11. Ceballos EM, Parrish RK 2nd, Schiffman JC.  Outcome of Baerveldt glaucoma drainage implants for the treatment of uveitic glaucoma.  Ophthalmology. 2002 Dec;109(12):2256-60.
  12. Vuori ML.  Molteno aqueous shunt as a primary surgical intervention for uveitic glaucoma: long-term results.  Acta Ophthalmol. 2009 Nov 7. [Epub ahead of print]
  13. Freedman SF, Rodriguez-Rosa RE, Rojas MC, Enyedi LB.  Goniotomy for glaucoma secondary to chronic childhood uveitis.  Am J Ophthalmol. 2002 May;133(5):617-21.

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