GLAUCOMA SURGERY UPDATE
From the 2007 Annual Meeting, New Dimensions in Ophthalmology, presented by the Washington Academy of Eye
Physicians and Surgeons, Seattle, WA
Paul F. Palmberg, MD, PhD, Professor of Ophthalmology, Bascom Palmer Eye Institute, University of Miami,
Miller School of Medicine
| WHAT CLINICAL TRIALS TELL US ABOUT GLAUCOMA MANAGEMENT
|
| Intraocular pressure (IOP): epidemiologic studies suggest excessive IOP accounts for only ≈33% of glaucoma-
related damage; 1966 study of 4000 patients \>40 yr of age in United Kingdom found average IOP of 15 mm Hg in
general population and 23 mm Hg in patients with glaucoma; large overlap in pressure ranges between groups, and
presence of high IOP without concomitant glaucoma contributed to low estimate of effect of IOP; however, only
one patient with glaucoma had IOP <15 mm Hg (ie, low IOP possibly protective); Baltimore Eye Survey found
prevalence of glaucoma increased 50% with each 3-mm Hg increase in IOP; glaucoma almost never occurs when
IOP <12 mm Hg; decreasing IOP to pressure near episcleral venous pressure may improve blood flow to optic
nerve (exact mechanism unclear)
|
| Risk stratification: in 1959, Paul Chandler published suggestions for managing glaucoma based on initial IOP and
extent of disease (eg, damage to optic disc); suggested patients with more advanced disease benefit from lower
IOPs; findings from case-control series (1980) supported Chandler’s suggestions (target pressures decreased with
increasing stage of disease)
|
| Controversy over IOP: clinicians disagree about target IOP; researchers at Washington University found progression
(over 10 yr) of glaucoma in 73% of patients with IOPs of 18 mm Hg and assessed as “doing well”; 25% lost
half of remaining visual field; some clinicians view IOP as inconsequential; meta-analysis of clinical trials shows
association between IOP and risk for progression after filtering surgery
|
| Topical steroids: first drug therapy shown (in randomized trial) to inhibit scarring from glaucoma surgery, to decrease
IOP (≈5 mm Hg), and to slow loss of visual field
|
| Advanced Glaucoma Intervention Study (AGIS): 800 eyes with advanced disease followed for 10 to 13 yr;
average initial IOP, 25 mm Hg; IOPs measured every 6 mo; 20% to 30% of patients progressed; unpublished data
reveal no progression in patients with IOPs consistently <15 mm Hg; published analysis, based on proportion of
time during which patient had IOP ≥18 mm Hg, shows least progression in patients whose IOPs <18 mm Hg at every
visit; increasing frequency of elevated IOP associated with increased risk for progression; risk factors for
progression—fluctuation in IOP; age
|
| Mean IOP vs fluctuations: speaker suggests high IOPs (whether consistently elevated or widely fluctuating with
high peaks) cause damage; differences in philosophical and experimental approaches lead to different interpretations
of data
|
| Consequences of Surgical Intervention (CSI)-Miami: patients with advanced disease (mean deviation, -14
dB; average IOP, 26 mm Hg) underwent glaucoma filtering surgery with antimetabolites (5-fluorouracil [5-FU] or
mitomycin C [MMC]); mean IOP reduced to 11 mm Hg; patients received additional interventions, as necessary, to
maintain IOP; no progression of visual field loss occurred during follow-up (≈7.6 yr)
|
| Baseline measurements of visual field: important to establish accurate baseline visual field; otherwise, assessment
of improvement or progression difficult; ≥3 measurements recommended during first year
|
| Mean IOP vs maximum IOP: CSI-Miami showed mean IOP correlated with disease progression, but maximum
IOP had even greater correlation (no progression in patients with maximum IOP of 13 mm Hg)
|
| Normal-tension glaucoma: less responsive to lowering IOP; 20% of patients who decrease mean IOP from 16
mm Hg to 11 mm Hg still progress (vs 60% who would progress if IOP not lowered)
|
| Collaborative Initial Glaucoma Treatment Study (CIGTS): patients with mild disease (average loss in visual
field, 5 dB); strict adherence to target pressures required; patients in medical treatment arm reduced average
IOPs from 27 mm Hg to 17.5 mm Hg (35% reduction in IOP) and had no net loss of visual field over 5 yr; patients
in surgical treatment group had average IOP of 14 mm Hg, but had similar outcomes and decreased quality of life
(eg, irritative blebs, cataracts); however, surgery and reduced IOPs beneficial for patients with greater loss of visual
field (-10 dB) at baseline
|
| Early Manifest Glaucoma Trial: researchers denied importance of IOP (considered epiphenomenon); patients
with mild disease randomized to medical therapy or control; although treatment group had better outcomes, on average,
than control group, more patients progressed due to absence of target pressure
|
| Conclusions: ≥85% of damage from primary open-angle glaucoma preventable; lowering IOP by ≥35% in patients
with mild initial damage prevents 5-yr progression in ≥90% of patients; controlling IOP in patients with normal-
tension glaucoma reduces risk for progression by ≈66%
|
| SAFE PROTOCOLS FOR ANTIMETABOLITES IN GLAUCOMA SURGERY
|
| Treatment goals: clinical trials have demonstrated importance of lowering IOP; lowering IOP by 35% or to 12 mm
Hg ideal, but other factors may influence target pressure
|
| Medical therapy: prostaglandins and β-blockers foundation of treatment, but when used alone, result in large fluctuations
in IOP; success—single medication reduces IOP sufficiently in 80% to 90% of patients at risk of developing
glaucoma (data from Ocular Hypertension Treatment Study); need for additional therapies increases with severity of
disease (eg, initial therapy [ie, single drop per day] sufficient in 50%-65% of patients with moderate disease and in
only 10%-20% of patients with advanced disease); patient education—important to discuss possibility of adding
medications or other therapies as necessary to control IOP
|
| Target pressure as guideline: achieving target pressure predicts positive outcome, but long-term observation of individual
patient provides important information about disease progression and may affect treatment decisions (eg, patient
with stable IOP of 18 mm Hg who has no progression over 10 yr may not require intervention); to meet target
pressure, medical and laser therapies should be considered before surgical intervention; surgical intervention—in patients
with advanced disease, benefits of surgery generally outweigh risks, but clinical judgment important
|
| Antimetabolites: 5-FU and MMC; use improves outcome of surgery; 98% of glaucoma specialists surveyed recommend
use in all surgical cases; adverse effects—hypotony; bleb infections; certain precautions significantly reduce
risks
|
| Surgical strategies: resistance of scleral flap affects final IOP; use of antimetabolite prevents additional resistance;
if resistance increases postoperatively, compensatory adjustments (eg, lasering stitches) may be performed;
speaker aims to achieve IOP of 10 mm Hg (with goal of IOP <15 mm Hg in all patients with advanced damage)
and cautions about reducing IOP too much
|
 | Notes on technique: make very small scleral flap or tunnel; using Kelly Descemet’s membrane punch, make canal
in tunnel, stopping 0.5 mm short of mouth of tunnel; inject fluid by paracentesis until equilibrium reached (≈5 mm
Hg); place adjustable sutures; adjust sutures until IOP reaches 10 mm Hg (use portable tonometer [eg, TonoPen]
with sterilized tips to measure IOP); wound construction—achieving IOP of 5 mm Hg near wound construction
prevents late hypotony that may occur when nylon sutures melt; creating safety-valve incision avoids need for
iridectomy, reduces risk of bleeding, and prevents flattening of chamber and late hypotony
|
| Results and follow-up: ≈80% of patients require additional adjustments (eg, lasering sutures or internal ostium,
placing barbell implant, adding medications) to maintain mean IOP at 10 to 11 mm Hg; complications—12% of
patients had leaks; 3.8% developed blebitis; 2.8% developed endophthalmitis; 3 patients underwent vitrectomies;
2 patients (per 200 eyes) lost substantial vision
|
| Preventing complications: create fornix-based conjunctival flap and apply antimetabolite with thin sponges over
wider area; this spreads drainage over wider area and reduces risk for serious complications from 5% to 0.5%;
technique—cut thin pieces of sponge from side of Wexell sponge; apply MMC (0.4 mg/mL) for 2 min in primary
cases and for 5 min in combined surgeries or reoperations
|
| Wound closure: conjunctiva tears easily; mattress sutures using 10-0 nylon good option; square-wave bites going
half-way into sclera create water-tight closure; skimming bites (shallow entry and exit) may claw through and result
in leakage at corneal limbus; bite in conjunctiva should equal size of bite in sclera (compresses tissue without
tearing); alternative—make half-thickness grooves at junction of cornea and sclera; anchor 4 scleral sutures (10-0
nylon) in grooves and tie tightly (pulls knots into groove); progress laterally, adjusting tension evenly over 4 sutures;
tie knots along cornea, slipping knot underneath conjunctiva (upper knots eventually descend into bleb); inflate
eye to check; horizontal scleral-flap compression sutures—do not produce astigmatism; useful for repairing
hypotony
|
| Choice of antimetabolite: patients typically prefer MMC over 5-FU; MMC application—2 min in primary cases;
3 min in young black Caribbean patients; 5 min in repeat or combined surgery
|
| MANAGEMENT OF THE PAINFUL BLEB
|
| High-domed bleb causing dellen: exposed focal bleb interferes with secretions of meibomian glands, resulting
in dryness, thinning cornea, and pain; corrective bleb-compression sutures—anchor 9-0 nylon sutures in peripheral
cornea; pass suture over bleb, anchor deep in Tenon’s capsule (not sclera), then pass back over bleb to corneal
limbus; tie knot tightly, cut short, and rotate knot into cornea; preparation—anesthetize with proparacaine and
vasoconstrict with apraclonidine (Iopidine) to reduce postoperative reaction; medications—prednisolone (eg, Pred
Forte) and fluoroquinolone agent, both qid; results—immediate reduction of pain; formation of collagen “suspenders”;
reshaped bleb maintains integrity after suture removed
|
| Bleb dysesthesia with bubble: motion of upper eyelid over bleb captures air and tears, forming bubble; patient
experiences pain with blinking; correction—anchored bleb-compression sutures flatten bleb; preparation—
proparacaine; povidone iodine (eg, Betadine); apraclonidine; 2% lidocaine jelly; results—corrective in 83% of
patients
|
| Overhanging bleb: bleb hangs onto cornea, causing astigmatism and discomfort; correction—numb and sterilize
ocular surface; undermine bleb with Kimura spatula and amputate (under slit lamp); results—amputation does not
cause leakage (blebs not “balloons,” but “hydrated sponges”); epithelium heals quickly; astigmatism and visual acuity
improve; IOP remains stable; pain resolves; disfigurement improves
|
| Circumferential bleb: focal bleb spreads around corneal limbus, interfering with flow of tears; patients have wet
eyes and poor vision; correction—anesthetize eye; puncture unneeded portion of bleb with hot cautery (avoid contacting
sclera); roll cotton swab over bleb to force fluid through hole and flatten bleb; results—most patients had
good results; some needed second or third procedure; success rate ≈66%
|
| Prevention of bleb complications: MMC applied with thin wide sponges creates diffuse bleb, reducing risk for
painful blebs (circumferential blebs may occur occasionally)
|
| Leaks: peripheral holes caused by, eg, traumatic puncture, may be walled off with compression mattress sutures, anchored
in front and back; leaks that occur in center of ischemic blebs corrected using compression suture (9-0 Vicryl
monofilament on blood-vessel needle) anchored in sclera adjacent to hole; conjunctiva may be manipulated
using cotton swab; bow-tie knot (only one throw) compresses conjunctiva without clawing through (eventually descends
into bleb); results—central leaks more difficult to correct (Seidel-negative in 5 of 9 patients)
|
| Hypotony and hypotony maculopathy: simple hypotony—corrected by repairing resistance of scleral flap; hypotony
maculopathy—hypotony (after filtering surgery or traumatic cyclodialysis) causes elastic sclera to contract,
resulting in formation of chorioretinal folds; risk factors include young age and myopia; correction—use 2
sets of horizontal scleral-flap compression stitches; set scleral flap to achieve IOP of 10 mm Hg with first set; use
second set to temporarily increase IOP to 20 mm Hg (to stretch out collagen); loosen or laser second set of stitches
after retina flattens; use portable tonometer to confirm IOP; note—have extra sclera on hand (autologous or donor);
graft if scleral flap melted; when using MMC, make short thick flaps to prevent disintegration; if hole forms,
repair with autologous scleral patch (one-third thickness); results—when technique performed ≤6 mo after onset of
hypotony, 39 of 40 cases improved; visual acuity improved from 20/100 to 20/25; IOP increased from 2 mm Hg to
14 mm Hg; 2 blebs lost (healed); 4 patients required additional medical therapy; metamorphopsia resolved in all
but 2 patients; brief period of mildly elevated IOP did not result in loss of fixation or notable loss of visual field;
follow-up—critical to assess IOP on postoperative day 1 (especially as anesthetic wears off); timing of surgery—
patients who underwent surgery \>6 mo after onset of hypotony had poorer outcomes and some permanent damage
|
Suggested Reading
AGIS investigators: The Advanced Glaucoma Interventions Study (AGIS):7. The relationship between control of
intraocular pressure control and visual field deterioration. Am J Ophthalmol 130:429, 2000; Anis S et al: Sutureless
revision of overhanging filtering blebs. Arch Ophthalmol 124:1317, 2006; Anis S et al: Surgical reduction of symptomatic,
circumferential, filtering blebs. Arch Ophthalmol 124:890, 2006; Aykan U et al: Laser suture lysis or releasable
sutures after trabeculectomy. J Glaucoma 16:240, 2007; Bengtsson B et al: Fluctuation of intraocular
pressure and glaucoma progression in the Early Manifest Glaucoma Trial. Ophthalomology 114:205, 2007; Chandler
PA: Long-term results of glaucoma therapy. Am J Ophthalmol 49:221, 1960; Denis P et al: A meta-analysis
of topical prostaglandin analogues intraocular pressure lowering in glaucoma therapy. Curr Med Res Opin 23:601,
2007; Jampel HD et al: Perioperative complications of trabeculectomy in the Collaborative Initial Glaucoma
Treatment Study (CIGTS). Am J Ophthalmol 140:16, 2005; Mansberger SL et al: Comparison of initial intraocular
pressure response with topical beta-adrenergic antagonists and prostaglandin analogues in African American and
white individuals in the Ocular Hypertension Treatment Study. Arch Ophthalmol 125:454, 2007; Mietz H, Krieglstein
GK: Postoperative application of mitomycin C improves the complete success rate of primary trabeculectomy:
a prospective, randomized trial. Graefes Arch Clin Exp Ophthalmol 244:1429, 2006; Nicolela MT et al: Relationship
between central corneal thickness and hypotony maculopathy after trabeculectomy. Ophthalmology 2007 [epub
ahead of print]; Palmberg P: What is it about pressure that really matters in glaucoma? Ophthlamology 114:203,
2007; Reinthal EK et al: Dose, timing and frequency of subconjunctival 5-fluorouracil injections after glaucoma
filtering surgery. Graefes Arch Clin Exp Ophthalmol 245:369, 2007; Singh M et al: Imaging of trabeculectomy
blebs using anterior segment optical coherence tomography. Ophthalmology 114:47, 2007; Sisto D et al: The role
of antimetabolites in filtration surgery for neovascular glaucoma: intermediate-term follow-up. Acta Ophthalmol
Scand 85:267, 2007.
Educational Objectives
| The goal of this program is to improve the management of intraocular hypertension and glaucoma. After hearing and
assimilating this program, the clinician will be better able to:
|
| 1. Apply the findings of large clinical trials to the management of ocular hypertension and glaucoma.
|
| 2. Discuss the concept of target intraocular pressure and describe its impact on disease progression.
|
| 3. Describe the benefits and potential adverse effects of using antimetabolites during glaucoma filtering surgery.
|
| 4. Prevent adverse effects associated with glaucoma filtering surgery.
|
| 5. Correct painful bleb complications without sacrificing a functional filtering bleb.
|
Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty members to disclose
relevant financial relationships within the past 12 months that might create any personal conflicts of interest. Any
identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary
business or commercial interest. For this program, the faculty reported nothing to disclose.
Acknowledgements
Dr. Palmberg was recorded in Seattle, WA, at 2007 Annual Meeting, New Dimensions in Ophthalmology, presented
by the Washington Academy of Eye Physicians and Surgeons, and held March 29-30, 2007. The Audio-Digest Foundation
thanks Dr. Palmberg and the Washington Academy of Eye Physicians and Surgeons for their cooperation in
the production of this program.
|
