Glaucoma Grand Rounds Robert E. Prouty, O.D., F.A.A.O. Omni Eye Specialists Denver, Co RProuty@DrMyii.com Description: This course will be lectured in a grand rounds format presenting various interesting glaucoma cases encountered in optometric primary care. The course will present all cases in an interactive method with the audience and will highlight management dilemmas and controversies. Objectives: Review various glaucoma cases. Review various visual field testing techniques and strategies. Familiarize the primary care OD with glaucoma management dilemmas. Case I: Glaucoma Cases: What Was Done Wrong? Differential diagnosis: Acute angle closure glaucoma Angle recession glaucoma with sudden onset IOP increase Ciliochoroidal effusion induced angle closure Diagnosis and discussion: Ciliochoroidal effusion induced angle closure secondary to Topamax use o Topamax has been shown to induce ciliochoridal effusion causing forward displacement of the lens-iris diaphragm and anterior chamber shallowing. o This can induce myopia and angle closure. Treatment/management: Management differs from conventional acute angle closure glaucoma in that miotics are contraindicated Cycloplegics are suggested to decrease the lens-iris shallowing 1
Monitor migraine and Topamax patients for induced myopia and increase IOP Evaluation keys are shallowed anterior chamber and induced myopia Manage any IOP increases with cycloplegia and discontinue Topamax use Case II: Differential diagnosis: Chronic angle closure glaucoma Axenfeld s Syndrome with glaucoma ICE syndrome Diagnosis and discussion: Axenfeld s Syndrome o Axenfeld's anomaly is characterized by iris strands attaching to the posterior embryotoxon, which is a prominent, anteriorly displaced Schwalbe's line o Hypoplasia of the anterior iris stroma may be present, but more severe defects are not. o The disease is usually bilateral and transmitted as an autosomal dominant trait. o Axenfeld's syndrome includes glaucoma and occurs in 50% of patients with the anomaly. Treatment/management: Management over the next years included treatment with: Betoptic with the addition of Iopidine and Trusopt with tensions in the right eye remaining in the mid-teens and the left eye in the high teens to low 20 s. Visual Fields were relatively stable in both eyes but the OS became increasingly unreliable Surgical trabeculectomy with Mitomycin-C After years of management, family members were evaluated and her 3 of her 4 children were diagnosed with Axenfeld s Syndrome. Monitor IOP closely o Medical management is usually sufficient o Surgical trabeculectomy (with Mitomycin-C) is frequently required Establish family pedigree Always evaluate family members due to autosomal dominant inheritance 2
Case III: Angle closure Phacomorphic glaucoma Diagnosis and discussion: Phacomorphic Glaucoma o Swelling of the lens may convert an anterior chamber of medium depth into one that is markedly shallow and precipitate acute angle-closure. o Medical treatment may not adequately manage IOP and there may be paradoxical response to pilocarpine. o YAG peripheral iridotomy may help eliminate pupillary block o Definitive treatment is removal of the lens: o Medication agents causing lens swelling and reported with glaucoma: Aspirin: Sanford-Smith: Transient myopia after aspirin, Br J Ophthalmol, 1974. Diamox: Fan JT et. al.: Transient myopia, angle closure glaucoma, and choroidal detachment after oral acetazolamide, Am J Ophth, 1993. 3
Quinine: Segal A et. al.: Quinine, transient myopia and angle-closure glaucoma, Bull Soc Ophthalmol Fr; 83.Vagitrol: Maddalena MD: Transient myopia associated with acute glaucoma and retinal edema following vaginal administration of sulfanilamide, Arch Ophthalmol; 1968 Treatment/Management: Acute management of elevated IOP using: o Diamox 500mg stat (monitor blood glucose) o Alphagan q15 min (with punctal occlusion) till decrease in IOP o Timolol ½% q15 min (with punctal occlusion) till decrease in IOP o Once IOP reaches 30 or less release for the evening o Cataract extraction within 24-48 hours Degree of cataract formation MUST relate to degree of vision decrease Systemic consult is valuable on cases where etiology of decreased visual acuity remains unknown or undetermined Lens/cataract induced (Phacomorphic) narrowing of angular structures can reduce outflow facility both acutely and chronically Medication related effects are also possible in phacomorphic glaucoma Cataract extraction is curative. Case IV: Ocular hypertension secondary to increased CCT COAG Lid related VF defect Learning effect VF Treatment/management options: Serial follow-up SWAP visual fields Initiate treatment prophylactically Treat optic nerves and risk of progression NOT just IOP 4
Case V: Diagnosis: Pigment dispersion glaucoma (PDG) confused with uveitis. Treatment/management: Krukenberg Spindles, pigment in TM and iris transillumination defects are diagnostic for pigment dispersion syndrome (PDS). o Elevated IOP with VF and ONH changes converts diagnosis to PDG Monitor IOP carefully since stable IOP in PDG can easily rise despite treatment SLT/ALT have a mixed success in management/control particularly in younger patients There is evidence that YAG PI may reduce the incidence of reverse pupillary block PDS. Not all PDS/PDG patients show an improved iris concavity after PI Uveitis is rarely noted in glaucoma Management must vigilant since IOP can be stable for years and then increase Laser PI may assist in management Case VI: Bitemporal sphenoid wing meningioma Vascular anomaly Management options: MRI Refer for neuro workup after results of MRI Treatment: None needed Visual field/oct/gdx should add up If not, get an MRI 5
Case VII: COAG NTG/LTG BRVO Management options: MRI Refer for neuro workup after results of MRI Literature: NTG study Some untreated NTG pts. remained stable or showed slow progression; others showed rapid progression No reliable methods distinguished which patients would progress In the treated group (30% IOP reduction), some eyes had rapid progression with loss of fixation Distinction based on a highly variable and questionable parameter: IOP! POAG and NTG cannot be differentiated pathophysiologically. NTG study concludes that IOP is a causal factor in NTG. *********************************************************************** A link between corneal elasticity and glaucomatous damage The physiology of the cornea, not only its anatomy, appears to be strongly correlated with glaucomatous damage Nathan Congdon, MD, examined physiologic factors such as corneal bioelasticity (hysteresis) as predictors of glaucomatous damage. The study was not able to establish causality and was limited by the fact that much of the data were attained retrospectively. However, it is one of the first studies to suggest the link between corneal deformability and glaucoma damage. AJO Vol 141 #5 May 2006, Pgs 868-875 *********************************************************************** Treatment: Lowering IOP has shown to be of assistance yet many LTG/NTG case will continue to progress. LASIK/PRK can complicate glaucoma monitoring and management Monitor ONH hemes closely for possible NTG/LTG 6
Case VIII: Recurrent iritis Unknown corneal dystrophy with recurrent edema (Fuch s) Uveitic Glaucoma Glaucomatocyclitic crisis Management options: Systemic workup Uveitic serology: Negative!! (CBC, ESR, CXR, PPD, VDRL, FTA-ABS) Posner-Schlossman Syndrome (Glaucomatocyclitic Crisis): o Unilateral involvement o Recurrent attacks of mild cyclitis o Slight decrease in vision o Elevated IOP (40-60) (symptoms usually minimal) o Open angle o Crisis has a duration from a few hours to weeks and optic nerve and VF are usually normal. o IOP and exam are normal between attacks o Age group: 20-50 yo o Usually unilateral (bilateral cases reported) Etiology?? Treatment: Mydriatics and Cycloplegics: o Prevent or break posterior synechiae (PS) and help relieve pain of ciliary spasm. IOP Suppressants: B-Blockers: mainstay of Tx Adrenergics: i.e. Alphagan and Iopidine CAI: Topical or systemic Prostaglandins:??? Miotics: avoid! o may potentiate uveitis and also lead to Posterior Synechiae. Hyperosmotics: i.e. Glycerine or Mannitol may be indicated in the context of acute IOP rise (ACG) Depending on the iritis anti-inflammatories may or may not be used. Consider non-steroidals for possible steroid responders. No proof that interim treatment between attacks reduces risk of attacks. 7
Uveitis is rarely seen in glaucoma with only a few exceptions Angle closure Uveitic Glaucomatocyclitic Case IX: Large diurnal IOP flux COAG Chronic narrow angle glaucoma Non-compliance Diagnosis and discussion: Chronic narrow angle glaucoma Treatment/Management: ALWAYS accomplish gonioscopy! Laser PI Monitor IOP status after laser PI Standard COAG management Effective & thorough glaucoma evaluation is essential NEVER trust another doctor s gonioscopy 8