Glaucoma Surgery
Atlas of
Glaucoma Surgery
Editors
Tarek Shaarawy MD
Consultant and Head, Glaucoma Sector
Department of Ophthalmology
Geneva University Hospitals
University of Geneva
Geneva, Switzerland
Andr Mermoud MD
Professor and Head
Glaucoma Unit
Department of Ophthalmology
Jules Gonin Eye Hospital
University of Lausanne
Lausanne, Switzerland
Foreword
Peter G Watson
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Atlas of Glaucoma Surgery
2006, Tarek Shaarawy, Andr Mermoud
All rights reserved. No part of this publication and Photo CD ROM should be reproduced, stored in a retrieval system,
or transmitted in any form or by any means: electronic, mechanical, photocopying, recording, or otherwise, without
the prior written permission of the editors and the publisher.
This book has been published in good faith that the material provided by contributors is original. Every effort is
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First Edition : 2006
ISBN 81-8061-651-7
Typeset at JPBMP typesetting unit
Printed at Replika Press Pvt. Ltd.
To
Mohamed Abd El-Samad Nada, Pierre Mermoud,
Mounir Shaarawy, Alex Mermoud,
and Hussein Shaarawy.
(A grand father, two fathers, and two sons)
Acknowledging that from the more distinguished gentlemen
we have learned that real excellence and
humility are not incompatible.
We in turn will always strive to pass this
on to the two young gentlemen.
Contributors
viii
Josef Flammer MD
Professor and Head
University Eye Clinic, Basel, Switzerland
Juan Jose Perez-Santonja MD PhD FEBO
Glaucoma and Refractive Surgery Department
Instituto Oftalmolgico de Alicante, Spain
Juan Roberto Sampaolesi MD
Department of Ophthalmology
School of Medicine, University of Beuenos Aires
Argentina
Kaweh Mansouri MD
Glaucoma Fellow
University Eye Clinic
Basel, Switzerland
Madhu Nagar MS Ophth FRCS Ophth
Consultant Ophthalmologist
Clayton Eye Centre
Wakefield, West Yorkshire, UK
Oscar Albis-Donado MD
Glaucoma Specialist from the Association Para Evitar
la Ceguera en Mxico
Assistant Professor, Universidad Del Norte
Chief, Glaucoma Service
Unidad Lser del Atlntico, Barranquilla, Colombia
Hospital Universidad del Norte, Barranquilla
Colombia
Pivi Puska MD
Docent of Ophthalmology, University of Helsinki
Head, Glaucoma Service
Helsinki University Eye Hospital
Helsinki, Finland
Paul J Foster PhD FRCS (Ed)
Clinical Senior Lecturer
Department of Epidemiology
Institute of Ophthalmology
University College London
and Honorary Consultant
Moonfields Eye Hospital, London
Foreword
Glaucoma does not constitute a disease entirely but embraces congeries of pathological conditions which have the
common feature that their clinical manifestations are to a greater or lesser extent dominated by an increase in intraocular pressure.1
The concept of angle closure dates back to 1876 when two investigators, Max Knies2 and Adolf Weber,3 working
independently noted the obstruction of the angle of the anterior chamber. Priestly Smith4 used this information to
develop the theory of peripheral angle closure and changed the emphasis from over-production of aqueous to a
failure of outflow from the eye as the cause of the raised pressure. He also noted that the change in size of the lens
with age contributed to acute glaucoma. It remained then, for Otto Barkan5 in the late 1903s to further define the
diseases of the angle and to reclassify the glaucomas into open and closed angles. It was then that Currans6
suggestion of the mechanism of angle closure through pupil block became accepted and formed the basis of
modern approaches to treating acute angle closure which are almost universally successful.
Von Graefes7 amaurosis with excavation of the disc without inflammation (what was subsequently called simple
glaucoma) is far from simple. The cause and effect of primary open angle glaucoma have been the subject of
circular arguments for several decades which are still not close to resolution. So far the only intervention known to
reduce the chances of progression of this condition is the reduction of intraocular pressure. Almost every
pharmacological mechanism known to be involved in the circulation of aqueous by either the conventional trabecular
or uveo-scleral pathways has been manipulated to provide drugs to maintain a low intraocular pressure with
minimal side effects. In this medical therapy has been largely successful but the pressure of advertising has, perhaps
deliberately, obscured the value of early surgical intervention in chronic open angle glaucoma. There are some
patients, particularly those who present with advanced disease and/or high initial intraocular pressures, who all
agree require early surgery but many have developed advanced visual field loss through procrastination and
reluctance to undertake the necessary surgery. One of the worst phrases ever coined was maximum tolerated
medical therapy which implies that surgery is a course of last resort rather than a highly successful sight saving
procedure performed early in the disease. Having to use these criteria certainly biased the results of the Advanced
Glaucoma Intervention Study.8
Surgery had, and to an extent still has, a degree of morbidity which, to those used to the almost complication-free
operation of cataract, is unacceptable. An eye left inadequately treated results in eventual blindness. This means that
a certain degree of risk must be accepted. McKenzie9 rightly associated the high intraocular pressure with the march to
blindness but thought that this pressure was caused by liquid vitreous and therefore advocated the broad iris knife be
driven into the vitreous and rotated to release the fluid! It is not surprising to us now that this did not work for long and
was associated with many problems. In 1857 Critchett,10 incorporated an iris wick into the wound so first establishing
the filtering cicatrix, a term coined by de Wecker.11 This is still the principle of all successful modern surgical, and some
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
laser, therapies. Since the 1860s history has repeated itself. The wheel has continued to turn with different groups
developing different ways of either retracting the iris root to allow more fluid to flow through or making a hole large
enough in the eye for the fluid to drain from it. This must be achieved without permitting too much fluid to escape
under the conjunctiva so that it becomes so thin that it is liable to infection. That so many have tried to achieve this
goal means that none has entirely filled the requirements of a completely satisfactory operation. In the last 50 years
we have had anterior lip sclerectomy12, 13 iridencleisis of Holth,14 Elliott trephination,15 and Scheies operation,16 Stallards
single pillar iris inclusion,17 trabeculotomy,18 trabeculectomy19, 20 and multiple laser procedures. Many attempts were
made during the 1960s by Remond Smith.21
Cairns22 and others to isolate Schlemms canal, allowing fluid to drain through the trabecular meshwork without
opening the eye. None of these was successful over the long-term and modern attempts to do the same thing seem
to have a poor record so far. So it is that one of the many modifications of trabeculectomy remains the current
preferred option because so far this is the only procedure in which the flow of fluid from the eye can move into the
sub-Tenons space at a slow enough pace. The underlying reason for this is that the sclera heals slowly if at all. The
layer of excised sclera is covered by a second scleral flap which is capable of moving slightly in the early postoperative stages. This not only allows the aqueous to flow through the operated region into the subepiscleral and
subconjunctival space, but also responds to the pressure variations which occur postoperatively. The aqueous itself
partly controls the healing reaction of the episclera and conjunctiva.
When normal, and not affected by either long-term topical medicaments or locally applied anti-metabolites,
the conjunctiva and episclera will allow diffusion of aqueous through them. Furthermore the aqueous itself inhibits
the scarring process so that a cavity is formed in which there is an equilibrium between the intraocular pressure, the
subepiscleral tissue pressure or the episcleral venous pressure if the aqueous drains into these vessels.
Surgery and laser therapy have been accepted completely for the treatment of angle closure glaucoma and it
still remains true that early aggressive treatment of chronic open angle glaucoma in an otherwise normal eye has
the greatest possibility of success. Unfortunately if fewer and fewer surgical procedures are being undertaken the
experience and confidence of the surgeon must diminish. This makes it essential that a text such as this is available
for all to refresh their memories and to ensure that the techniques of the masters of the subject can be followed
completely.
Even though we still do not fully understand the mechanisms and genetic background to the conditions known
as glaucoma, we are able to offer palliative and sometimes curable therapies. This will continue until we can target
each individual type of the multitude of conditions which we now call glaucoma.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
Herbert H. Subconjuncival fistula formation in the treatment of primary chronic glaucoma. Trans Ophthalmol Soc UK 1903;23: 324.
La Grange F. Production of a cicatrix in chronic glaucoma. Ophthalmoscope 1907;5: 467.
Holth S. Iridencleisis cum iridotomia meridionali. Arch Ophthalmol 1930;4: 803.
Elliot RH. A preliminary note on a new operative procedure for the establishment of a filtering cicatrix in the treatment of glaucoma. Ophthalmoscope 1909;7: 804.
Scheie HG. Peripheral iridectomy with scleral cautery for glaucoma. Arch Ophthalmol 1959;61: 291.
Stallard HB.Anterior flap sclerectomy with basal iridencleisis. Eye Surgery John Wright, Bristol 4th Edition., 1965;53-665.
Burian HM, Allen L. Trabeculotomy ab externo, a new glaucoma operation Am J Ophthalmol 1962;53: 19.
Cairns JE. Trabeculectomy. Preliminary report of a new method. Am J Ophthalmol 1968;66: 673.
Watson PG. Effectiveness of trabeculectomy in glaucoma. 1975;79, 5, 831-845.
Smith R. A new technique for opening the canal of Schlemm. Preliminary report. Br J Ophthalmol 1960;44: 370.
Cairns JE. Goniospasis. Eine Methode, die zur Entlastung der Kanalblockade bei Primarem Weitwinkelglaukom Entwickelt Wurde, Klin.Monatsbl. Augenheilkd. 1974;165: 549.
Acknowledgements
We would like to express our utmost appreciation to our co-authors who showed a sincere willingness to contribute
to this scientific endeavor. Sincere thanks are also due to Mr PG Watson for accepting to write the Foreword.
Our heartfelt gratitude to Professor AB Safran, Head, Department of Ophthalmology, University of Geneva
and Professor L Zografos, Head, Department of Ophthalmology, University of Lausanne, for their continued
support of our clinical and academic activities.
We would like to graciously acknowledge Dr K Mansouri for his efforts in the coordination of this extensive
undertaking. We also find it important to mention that were it not for the patience and understanding of our
Publisher Mr JP Vij, CMD of M/s Jaypee Brothers Medical Publishers, this piece of work would not have come to
see the light. Last but not least we would like to offer our sincere thanks to Mrs G Ibrahim for her meticulous
revision of the manuscript and for offering valuable suggestions and criticism.
Tarek Shaarawy
Andr Mermoud
MD
MD
Contents
xiv
INTRODUCTION
Glaucoma is a progressive optic neuropathy involving
characteristic structural-pathological changes in the optic
nerve head. 1-3 Estimate of the number of patients
bilaterally blind because of glaucoma ranges between 7
and 8 million people.4-6 Glaucoma is an increasingly
important public health concern due to our aging
population demographics, and has been identified as
the second leading cause of blindness world-wide and
the first cause of irreversible blindness.
It is irreversible because it results from the
degeneration of retinal ganglion cells, and to date there
is no cure for neuronal central nervous system
degeneration, or means of regenerating lost neurons.
After more than a century of active research in the
management of glaucoma, the Holy Grail of glaucoma
treatment is still elusive and we have to be pragmatically
content with our attempts to prevent further progression
of glaucomatous damage, rather than curing the disease.
Glaucoma progression is strongly associated with a
number of risk factors.7-14 Some of these factors are
unmanageable like ethnicity and age, while others can
be manipulated, with varying degrees of success, in an
attempt to slow or arrest progression, like IOP and
possibly vascular dysregulation.
Reducing IOP is presently the evidence based, most
accepted, and most practised therapeutical approach of
glaucoma patients. 12,15 Currently topical ocular
hypotensive medications, with its different classes, as well
as filtering surgery (trabeculectomy and non-penetrating
surgery) are in the forefront of therapeutic modalities to
reduce IOP.15, 16-22
This review article looks at the potential advantages
and disadvantages of topical medications versus filtering
Table 1.1: Ocular hypotensive medications and their potential systemic side effects
Medication
B Blockers
Carbonic anhydrase
inhibitors (oral and
topical)
Alpha agonists
Parasympathomimetics
Prostaglandin
analogues
Side effects
Dyspnea, bradycardia,
impotence, confusion,
depression, hypotension,
worsening of peripheral
vascular disease
Parasthesiae (systemic)
Renal stones (systemic)
Blood dyscrasias
(systemic and ? topical)
Rashes (either)
Hypokalemia (systemic)
Polyuria (systemic)
Metallic taste (topical
and systemic)
Dry mouth
GI upset
palpitations fatigue
decreased libido,
hypotension
respiratory arrest
in infants
Nausea
Vomiting
Headache
Confusion
Minimal systemic
side effects caution in
asthma?
contraindicated
in pregnancy
CONCLUSIONS
In essence, surgery has over drugs the potential to fulfill
many features of an ideal approach to reduce IOP. It
can lower IOP to low teens, achieve long-term IOP
reduction, minimize IOP fluctuations, lower cost, and
minimal systemic side effects. The major drawback
though, is the potentially devastating, but rare, ocular
side effects.
Although surgery is usually the first line treatment in
developing countries, it is still resorted to as a final attempt
REFERENCES
1. Anderson DR. Glaucoma: the damage caused by pressure. XLVI
Edward Jackson memorial lecture. Am J Ophthalmol 1989;108:48595.
2. Bathija R, Gupta N, Zangwill L, Weinreb RN. Changing definition
of glaucoma. J Glaucoma. 1998;7:165-9.
3. Foster PJ, Buhrmann R, Quigley HA, Johnson GJ. The definition
and classification of glaucoma in prevalence surveys. Br J Ophthalmol
2002;86:238-42.
4. Munoz B, West SK, Rubin GS, Schein OD, Quigley HA, Bressler SB,
et al. Causes of blindness and visual impairment in a population of
older Americans: The Salisbury Eye Evaluation Study. Arch
Ophthalmol 2000;118:819-25.
5. Quigley HA, Vitale S. Models of open-angle glaucoma prevalence
and incidence in the United States. Invest Ophthalmol Vis Sci
1997;38:83-91.
6. Quigley HA. Proportion of those with open-angle glaucoma who
become blind. Ophthalmology 1999;106:2039-41.
7. Buckley C, Hadoke PW, Henry E, OBrien C. Systemic vascular
endothelial cell dysfunction in normal pressure glaucoma. Br J
Ophthalmol 2002;86:227-32.
8. Gasser P. Why study vascular factors in glaucoma? Int Ophthalmol
1998;22:221-5.
9. Haefliger IO, Dettmann E, Liu R, Meyer P, Prunte C, Messerli J, et al.
Potential role of nitric oxide and endothelin in the pathogenesis of
glaucoma. Surv Ophthalmol 1999;43 Suppl 1:S51-S58.
10. Leske MC, Heijl A, Hussein M, Bengtsson B, Hyman L, Komaroff E.
Factors for glaucoma progression and the effect of treatment: the
early manifest glaucoma trial. Arch Ophthalmol 2003;121:48-56.
11. Osborne NN, Chidlow G, Nash MS, Wood JP. The potential of
neuroprotection in glaucoma treatment. Curr Opin Ophthalmol
1999;10:82-92.
12. Palmberg P. Risk factors for glaucoma progression: where does
intraocular pressure fit in? Arch Ophthalmol 2001;119:897-8.
13. Ritch R. Exfoliation syndrome. Curr Opin Ophthalmol 2001;12:12430.
14. Soltau JB, Zimmerman TJ. Changing paradigms in the medical
treatment of glaucoma. Surv Ophthalmol 2002;47 (Suppl) 1:S2-S5.
15. Heijl A, Leske MC, Bengtsson B, Hyman L, Bengtsson B, Hussein M.
Reduction of intraocular pressure and glaucoma progression: results
from the Early Manifest Glaucoma Trial. Arch Ophthalmol. 2002
Oct; 120 (10): 1268-79.
16. Collaborative Normal-Tension Glaucoma Study Group. The
effectiveness of intraocular pressure reduction in the treatment of
normal-tension glaucoma. Am J Ophthalmol 1998;126:498-505.
17. Bron A. Treatment of glaucomas. Rev Prat 2001;51:2198-2201.
18. Hedman K, Watson PG, Alm A. The effect of latanoprost on
intraocular pressure during 2 years of treatment. Surv Ophthalmol
2002;47 Suppl 1:S65-S76.
19. Rothman RF, Liebmann JM, Ritch R. Low-dose 5-fluorouracil
trabeculectomy as initial surgery in uncomplicated glaucoma: longterm follow-up. Ophthalmology. 2000 Jun;107(6): 1184-90.
20. Uchida S, Suzuki Y, Araie M, Shigeeda T, Hara T, Shirato S. Longterm follow-up of initial 5-fluorouracil trabeculectomy in primary
open-angle glaucoma in Japanese patients. J Glaucoma. 2001
Dec;10(6):458-65.
21. Wilensky JT. The role of medical therapy in the rank order of
glaucoma treatment. Curr Opin Ophthalmol 1999;10:109-11.
22. Shaarawy T. Surgery for glaucoma in the 21st century. Br J
Ophthalmol 2003;87:250.
23. Janz NK, Wren PA, Lichter PR, Musch DC, Gillespie BW, Guire KE,
et al. The Collaborative Initial Glaucoma Treatment Study: interim
quality of life findings after initial medical or surgical treatment of
glaucoma. Ophthalmology 2001;108:1954-65.
10
90.
91.
92.
93.
94.
95.
96.
97.
98.
99.
2 Trabeculectomy
INTRODUCTION
This chapter addresses the current techniques used in
glaucoma filtration surgery, in particular a guarded
sclerostomy procedure best known as trabeculectomy.
The decision to perform glaucoma surgery represents a
key point in the long-term management of the patients
disease, and should only be made after detailed
consultation with the patient. The timing of surgery and
selection of appropriate procedure need careful
consideration and consultation. It is important to
remember that the preoperative and postoperative
management are critical determinants of the outcome
of glaucoma surgery.
The field of glaucoma surgery is undergoing a period
of revolution with many new approaches to the traditional
methods of surgery. Like all surgery, it is essential that
surgeons have a sound understanding of the principles
involved in the modern range of surgical procedures,
and keep up to date with new procedures so that
technique can be varied depending on the surgical
circumstances. An example of new techniques that have
revolutionized glaucoma surgery and are still changing
is the use of adjuvant therapies to modify postoperative
wound healing. The identification of relative risk factors
for failure of glaucoma surgery enables the surgeon to
vary the adjuvant therapy as appropriate while
minimizing the risk.
Glaucoma filtration surgery was previously performed
when patients had uncontrolled intraocular pressures on
maximally tolerated medical treatment, or after failed
laser trabeculoplasty. The main reasons for delaying
surgery were the risk of postoperative complications
associated with standard trabeculectomy procedures and
ANESTHESIA
The various operations described in this chapter can be
carried out under local or general anesthetics. The
methods of anesthesia are covered in another chapter
in this book. However, there are specific points in terms
of anesthesia in glaucoma.
General Anesthesia
The lowering of intraocular pressure with anesthesia can
be used to advantage by the ophthalmic surgeon if
intraoperative pressure lowering is required. Blood
pressure and to some extent choroidal volume can be
reduced, if necessary, by varying the anesthetic in patients
at risk of choroidal hemorrhage.
12
Local Anesthesia
When performing glaucoma surgery under local
anesthesia it is important to try and avoid unnecessary
elevation of IOP. It is advisable to use a technique that
paralyzes orbicularis oculi to prevent eyelid squeezing
and increased pressure on the globe. Patients with preexisting glaucoma may have a marked elevation in their
IOP during peribulbar or retrobulbar anesthesia. This
may be particularly important in patients who have
advanced visual field loss. Reduced volumes of local
anesthetic agents with hyaluronidase should be used in
these patients if necessary, and orbital compressive
devices (e.g. mercury balloons) should be avoided, if
possible. Buphthalmic or myopic eyes often have
extremely long axial lengths and may have large posterior
staphylomas with the attendant risks of inadvertent ocular
perforation during retrobulbar or peribulbar anesthesia.
Patients occasionally notice an enlargement of their
scotoma as a retrobulbar anesthetic takes effect, this is
reversible but patients need to be warned of this. In an
only eye, this may render the patient effectively blind
for many hours. General anesthesia may be preferable
in these patients as it avoids this problem and allows
increased control of the operative conditions. Filtration
surgery can also be carried out using only
subconjunctival anesthesia. However, the patient may
experience pain when the iris is handled particularly when
an iridotomy is performed. Intracameral anesthetic may
potentially be useful in this context.
FILTRATION SURGERY
PREOPERATIVE DETAILS
The risks of any form of surgery should be explained to
the patient in advance. In particular it is vital to explain
that surgery for glaucoma is usually done to preserve
vision not to improve it. Patients should be warned that
their vision may well be blurred in the weeks after surgery
before approaching preoperative levels. Several studies
have demonstrated a loss of best-corrected visual acuity
(of about 1 line) in postoperative patients, and it is
essential that patients are aware of this. Patients with
advanced field loss should be told of the risks of loss of
their remaining field, the so called wipe out event,
Sympathetic Agonists
Topical adrenaline can be used at the beginning of the
operation. Solutions of 0.01 percent or 0.1 percent can
be dropped on the field of surgery. This produces
conjunctival vasoconstriction and a reduction in bleeding
during the course of the procedure. Blood contains many
growth factors that promote wound healing and increase
the chance of filtration surgery failure. The disadvantage
of using adrenaline, is that it does cause some pupillary
dilatation. However, this is not usually a problem,
particularly if the operation is carried out relatively rapidly.
Povidone-iodine
It has a broad spectrum of antimicrobial action. It can
be used to prepare the skin, and drops can be applied
to the superior and inferior fornices, to kill any bacteria.
This is particularly important if the patient has pre-existing
conjunctival or lid disease, which predisposes them to
bacterial colonization.
Steroids
It has been shown that chronic preoperative topical
treatment jeopardizes filtration surgery by increasing the
number of fibroblasts and inflammatory cells in the
conjunctiva. This is particularly marked in association with
the long-term use of adrenergic agents such as adrenaline
and dipivefrin. Topical steroids such as fluoromethalone
Trabeculectomy
reverse the histological change in the conjunctiva,
although whether this conclusively increases the success
rate has not been proven.
13
Hypotensive Agents
If possible aqueous suppressants particularly those that
have long-acting effects such as beta-blockers should be
stopped several days in advance with outpatient
monitoring. This will optimize aqueous flow
postoperatively, encouraging aqueous flow through the
new channel and help to prevent hypotony.
Traction Suture
Superior rectus traction sutures are still commonly used.
However, the use of a corneal traction suture is becoming
Conjunctival Incision
The conjunctiva can be incised at the limbus (fornixbased flap) or deep in the fornix (limbus-based flap).
The advantages and disadvantages of either approach
are summarized in Table 2.1. The conjunctiva should be
handled very gently to avoid buttonholing, particularly
if antimetabolites are used. If a limbus-based flap is used,
the incision should be made far into the fornix. The
conjunctiva and Tenons should be entered in separate
layers to minimize the chance of damaging the superior
rectus muscle. An incision length of at least 10 mm is
usually necessary to provide adequate exposure. For a
fornix-based flap an incision of about 5 to 10 mm is
necessary. A relieving incision is used by many surgeons
but is not necessary and increases the trauma and risk of
wound leakage.
14
Length of operation
More diffuse
(esp with MMC)
Technically easier
Limbus
Scleral Flap
Trabeculectomy
15
16
Possible modulations
Activated conjunctiva
pre-activated cells
Conjunctival/episcleral/scleral
incisions. Damage to
connective tissue
Release of plasma proteins
and blood cells
Activation of clotting and
complement. Fibrin/
fibronectin/blood cell clot
Release of growth factors
from blood
Wound contraction
Fibroblast synthesis of
tropocollagen
glycosaminoglycans and
fibronectin
Collagen cross-linking
and modification
Blood vessel endothelial
migration and proliferation
Resolution of healing,
apoptosis
Disappearance of fibroblasts
Fibrous subconjunctival scar
Risk 1- 3+ Comments
+++
+ + (+)
++
+ + (+)
+ + (+)
+++
++
++
++
Uncertain
Depends on type of
surgery
+ (+)
+++
+ (+)
+ (+)
Particularly if they
cause a red eye
+
+ + (+)
+
++
+ + (+)
+
+
(+)
(+)
Fig. 2.6: Showing diffuse bleb in patients right eye using large
area of treatment vs a smaller area of treatment with mitomycin-C
17
Trabeculectomy
Table 2.5: Moorfields Eye Hospital (More flow) intraoperative
single dose antiscarring regimen v2004 (Continuously
evolving). Lower target pressures would suggest a stronger
agent was required
5FU
50 or
25 mg/ml
beta-radiation
1000 cGy
MMC
0.2-0.5 mg/ml
Delivery
2-5 minutes
2-5 min
Cost
UK1.50
10 ml vial
Availability
Good
20 sec-3 min
depending on
output rate
Approx
UK3000
for probe but
lasts 10+ years
Special
ordering and
licensing
required
Lead shielded
area
Storage
Room
temperature
ready
constituted
Duration effect Several weeks Several weeks
on fibroblast Clinical effects
proliferation several years
Primary effect Growth
arrest
Control over Moderate
area treated
Growth arrest
Precise
Conjunctival Clamp
We use a special conjunctival T clamp designed
(Duckworth-and-Kent.com No 2-686) to hold back the
18
Type of Sponge
We use circular medical grade polyvinyl alcohol sponges
used for LASIK corneal shields rather than other sponges.
The sponges are cut in half and folded like a foldable
lens (Fig. 2.8) and they fit through the entrance to the
pocket without touching the sides (approximately 5 mm
3 and insert about 6 of these) (Fig. 2.9). We attempt
to treat as large an area as possible, including under the
scleral flap. The polyvinyl alcohol sponges maintain their
integrity and do not fragment. In contrast, methycellulose
sponges fragment relatively easily, with an increased
chance of leaving small pieces of sponge behind in the
wound. The large area of treatment results in more
diffuse non-cystic blebs clinically. Increasing the surface
area of treatment results in a much more diffuse noncystic
area clinically. A large area prevents the development of
a ring of scar tissue (the ring of steel) which restricts
flow and promotes the development of a raised cystic
avascular bleb.
Infusion
We use an anterior segment infusion (Lewicky, Visitec)
on a three-way tap through the paracentesis (Fig. 2.11).
This maintains the pressure and rigidity of the globe
Trabeculectomy
19
20
Peripheral Iridectomy
shallowing.
is used.
Trabeculectomy
21
Conjunctival Closure
The conjunctiva can be closed with a variety of sutures.
For a fornix-based flap the conjunctiva can either be
closed just with one or two sutures at either end of the
relieving incision, or more thorough closure can be
performed with interrupted mattress sutures or a
continuous suture with or without corneal grooves. We
make a series of corneal grooves (Groove closure) and
do all our closure sutures through these burying the knots
in the cornea so there is no discomfort from the nylon
sutures (Figs 2.16 to 2.19). This new technique has
virtually eliminated central conjunctival retraction, leaks
and suture discomfort.
22
Postoperative Medications
At the end of surgery a subconjunctival injection of steroid
and antibiotic should be given 180 degrees away from
the trabeculectomy site. Care should be taken to ensure
this does not directly enter the eye through the
sclerostomy. Mydriatics such as atropine are used by
many ophthalmologists. Advantages include a relaxation
of the ciliary muscle and pain relief, possible reduction
of anterior chamber shallowing and malignant glaucoma,
possible stabilization of the blood aqueous barrier
(Atropine mainly) and prevention of central posterior
synechiae. Disadvantages include a dilated pupil which
may increase the chance of lens-corneal touch if the
anterior chamber is shallow, and loss of accommodation
with blurred vision. With the use of the infusion and
tight control of postoperative flow we no longer use
mydriatics routinely.
Figs 2.17 to 2.19: Lateral purse string. Entry via corneal groove,
purse string then exit via corneal grove and tie in groove.
Repeated procedure except for the conjunctival purse string
for the 3 middle sutures
Trabeculectomy
Indications
1. As part of a planned regimen in a patient with a
significant risk of scarring or requiring a low
postoperative intraocular pressure.
2. In a patient showing signs of scarring and imminent
failure of the bleb.
3. Following a needling or rexploration procedure.
4. To prevent failure of an existing bleb after a healing
stimulus, e.g. cataract extraction surgery.
5. Injections may be given up to several months after
surgery if there is a persistent healing response and
the intraocular pressure is rising.
Technique
1. The eye is anesthetized with several drops of topical
amethocaine. It may also be useful to blanch the
conjunctiva with a drop of adrenaline 0.01 percent
or phenylephrine 2.5 percent if there is no
contraindication, as this may reduce the incidence of
postinjection subconjunctival hemorrhage.
2. Quantity and concentration. The original regime
involved injections of 5 mg of 5FU diluted with 0.5
ml of saline. 5FU is now generally given in a
concentration directly from the bottle, which is either
0.1 ml of a 50 mg/ml solution or 0.2 ml of a 25 mg/
ml solution (i.e. injection dose = 5 mg).
3. A thin needle is advantageous as it reduces the reflux
of 5FU into the tear film. For convenience we use a
presterilized insulin syringe with an integral 27-gauge
needle.
4. A lid speculum is inserted to improve access.
5. Site of injection. 5FU was originally given 180 degrees
from the bleb to minimize the risk of intraocular entry
of the 5FU solution which has an alkaline pH. We
now give the injection about 90 degrees from the
bleb to maximize the effect. Occasionally the injection
can be given deep in the upper fornix away from the
drainage bleb if there is very good exposure. The
conjunctiva is gently lifted with a non-toothed forceps
and the needle inserted subconjunctivally. If the
needle is too deep there is a danger of scleral bleeding
and direct tracking into the eye. The bleb resulting
from the injection is slowly raised and watched as it
advances towards the drainage bleb area, and
23
24
Trabeculectomy
Conjunctival, Scleral and iris Bleeding
Prevention
i. Bleeding can be avoided by appropriate use of
cautery. Close attention to hemostasis including clot
removal is important, because blood is a very potent
stimulus for fibrosis.
ii. Installation of G adrenaline 0.01 percent at the start
of surgery help reduce bleeding in the area.
iii. Stop aspirin and anticoagulants preoperatively, if
possible.
Management
i. If there is bleeding following the peripheral
iridectomy, it is best to wait, leaving the flap slightly
open, to allow the blood to exit the eye, rather than
collecting in the anterior chamber. In the vast
majority of cases, the bleeding stops within a minute
or two. The clot can then be irrigated out, and the
operation completed.
ii. If the bleeding continues the intraocular pressure in
the eye should be raised, with an anterior chamber
infusion if necessary.
Suprachoroidal Hemorrhage
Fortunately, this is very rare intraoperatively. The
intraocular contents will come forward and the pressure
will rise acutely.
Prevention
i. Caution in advising surgery in high risk eyes (e.g.
other eye expulsive hemorrhage).
ii. Avoid operating on inflamed eyes until quieter or
eyes with high pressures.
iii. Maintain intraoperative pressure (preplace sutures,
use an anterior chamber infusion throughout
procedure).
iv. Maintain postoperative intraocular pressure (e.g.
viscoelastic, C3F8 gas in aphakic eyes).
v. Stop aspirin and anticoagulants if possible and avoid
Valsalva maneuvres postoperatively.
vi. In nanophthalmic eyes, scleral decompression may
be required before entry into the eye. The diagnosis
will be missed unless it is looked for clinically (small
eyes) and with ultrasound (short eye and thick
ocular coat).
25
Management
i. Close all wounds rapidly.
ii. When eye is secured, assess posterior segment and
confirm diagnosis and presence of choroidal
hemorrhage. If they are peripheral and not
impinging on central vision consider leaving. If
hemorrhage is extensive then consider drainage
through one or two sclerostomies. Drainage must
be performed before the blood clots to be effective
at the time of surgery.
Vitreous Loss
Fortunately, this very rarely occurs.
Prevention
i. Keep sclerostomy as anterior as possible.
ii. Note any iridodonesis and subluxed lenses preoperativelyconsider tube surgery or filtration with
MMC if lensectomy and anterior vitrectomy
inevitable.
Management
i. Anterior vitrectomy
ii. Postoperative 5FU will be required as there is an
increased chance of filtration failure.
Wound Leak
Prevention
i. Use round vascular needle (e.g. BV needle) which
reduces conjunctival leakage and buttonholing.
ii. Place incision in limbal based flap as far away from
limbus as possible, deep in the fornix.
iii. Use extramattress suture(s) to close fornix based
conjunctival flaps.
iv. Protect cut edge of conjunctiva from drug (e.g.
special conjunctival clamp).
v. Avoid conjunctival dissection in scarred areasif
posssibleconjunctival buttonholing is more likely
in these areas due to multiple adhesions.
Management
i. Small leaks often settle spontaneously with
observation. If leaks persist then treatment options
include use of a pressure dressing, bandage contact
lens, Simmonds shell or suppression of aqueous
production with acetazolamide.
26
Postoperative Complications
(Glaucoma Filtration Surgery)
Wipe out of Remaining Field/Vision
This is a very rare but important complication of filtration
surgery. It is thought to occur more commonly if there is
advanced field loss, particularly if the field loss is within
10 degrees of fixation, although this has not been
conclusively proven.
Prevention
i. Check intraocular pressure in the first few hours
after surgery to detect and treat any pressure spike.
ii. Take precautions to avoid peri- and postoperative
hypotony as well as acute disk swelling may also
compromise a very damaged nerve.
iii. Avoid episodes of perioperative systemic
hypotension.
Choroidal Effusion
Choroidal effusions are common in eyes that are
hypotonous following filtration surgery. The collection
of fluid (high protein content) in the suprachoroidal space
is produced by transudation from leaky capillaries in the
choriocapillaris.
Prevention
i. Take measures to prevent hypotony (see above).
Management
i. Cycloplegicmydriatic agents and frequent topical
steroids.
ii. Surgical intervention is rarely required, but signs
that drainage of the effusions may be is needed
include: evidence of lens-corneal touch with corneal
edema, bleb failure with increasing IOP, marked
anterior segment inflammation and apposition of
the effusions (kissing choroidals).
iii. If the IOP is normal then other causes of choroidal
effusion should be considered including scleritis, and
low serum protein levels and nanophthalmos.
Trabeculectomy
Raised Intraocular Pressure
A high IOP after filtration surgery is one of the most
common complications of filtration surgery. It is almost
always due to inadequate aqueous outflow. Treatment
depends on the site of obstruction. Sometimes
obstruction can occur in several sites at once. The sites
of obstruction are as follows.
Posterior diversion of aqueous (Malignant glaucoma)
In malignant glaucoma the aqueous is misdirected
backwards into the vitreous cavity and is prevented from
flowing anteriorly by the anterior vitreous face. The
patient usually presents with a shallow anterior chamber,
and an elevated intraocular pressure several days after
surgery. Ultrasound reveals hypoechogenic areas on
ultrasound. It has been observed that ciliary processes
are rotated anteriorly in malignant glaucoma such that
they press against the lens equator and prevent anterior
flow of aqueous. It has also been noted that the anterior
vitreous hyaloid is abnormally positioned plugging spaces
between ciliary processes. An acute pupil block or
choroidal hemorrhage can sometimes give a similar
picture but is easily excluded clinically. The eye may have
a predisposing risk factors such as hypermetropia, and
angle closure glaucoma.
i. Prevention
Identify high-risk eyes preoperatively (Ultrasonic
measurement of axial length if necessary). It is
important to identify nanophthalmic eyes, as
prophylactic sclerotomies may be required.
Ensure that there is a relatively high resistance at
the level of the scleral flap by tight closure. If
necessary manage raised intraocular pressure
medically in the early postoperative period,
releasing sutures later. Overdrainage of aqueous
in the early postoperative period must be avoided
in high risk eyes.
Use of cycloplegics especially G. atropine or
homatropine is useful.
In high risk eyes if some cataract is present a
combined procedure may debulk lens volume. A
rigid one piece implant may help prevent a flat
anterior chamber. The capsulorrhexis should be
kept relatively small to prevent lens implant/pupil
capture occurring if the anterior chamber
27
28
Trabeculectomy
29
i. Prevention
Avoid unguarded sclerostomies. Full thickness
sclerostomies are much more likely to result in
thin cystic blebs, even without antimetabolite use.
Avoid excessive use of antimetabolites.
ii. Management
The decision to treat depends on several factors
including; patient factors (including symptoms),
the size of the leak, bleb morphology, risk factors
for infection, and the presence of hypotony and
complications of hypotony such as macular
edema. Small leaks may settle spontaneously. The
range of treatment options include:
Large diameter contact lenses.
Bleb compression sutures. 9/0 nylon sutures are
sewn across the bleb compressing it around the
leak site. This can be combined with blood
injection. While the sutures stay in situ the patient
should continue on prophylactic antibiotics (see
Fig. 2.13).
Laser treatment to the deep scleral flap.
Trichloracetic acid painted on bleb.
30
Trabeculectomy
i. Prevention
Take precautions to avoid postoperative hypotony
and flat anterior chambers
Avoid direct lens traumause of an oblique
paracentesis parallel to the limbus minimizes the
possibility of any lens trauma lowers the chance
of damage when reforming the anterior chamber
and or testing the resistance of the scleral flap
Consider combined cataract and filtration surgery
in primary glaucoma if there is significant lens
opacity.
Ptosis and strabismus
i. Prevention
Use a corneal traction suture rather than a superior
rectus suture
Avoid excessive traction on the eye which stretches
levator aponeurosis
Avoid rectus muscle traction sutures when placing
tube implants where possible
31
32
INTRODUCTION
Since its introduction by Cairns, trabeculectomy has
become the most commonly performed approach for
surgical reduction of interocular pressure.1-3 There are,
however, two major problems in daily practice with this
surgical approach. Very often, the success in lowering
intraocular pressure is limited in time. Attempts to
overcome this limitation have included the use of
antimetabolites such as mitomycin-C. The use of this
type of antimetabolites has dramatically increased the
incidents of postsurgical ocular hypotonicity. Many
technical modifications have been developed, whether
a modified trabeculectomy using releasable sutures or
scleral tunnel techniques similar to that used in phako
emulsification; or guarded procedures with
nonpenetrating deep sclerectomy. The success rate with
these various techniques has not been able to convince
glaucoma surgeons to abandon classical trabeculectomy.
Furthermore, although trabeculectomy with the primary
use of intraoperative mitomycin-C has been reported to
be a relatively safe procedure,4-5 many surgeons still fear
potential complications due to postoperative ocular
hypotonicity. In the following, we present a surgical
approach that attempts to take advantage of the longterm benefits of mitomycin-C by applying it routinely
while avoiding the early complications often observed
with such a drug by using a scleral-tunnel technique
combined with a tight scleral wound closure using
dissolvable sutures.
SURGICAL MODIFICATIONS
We describe a modified technique that has all the
advantages of scleral tunnel architecture, concomitant
33
34
35
36
Age
Preoperative Months
Postoperative IOP <
Hy %
IOP (mm Hg) follow-up IOP (mm Hg) 20 mm Hg
2.1%
11.1%
REFERENCES
1. Cairns JE. Trabeculectomy: preliminary report of a new method.
Am J Ophthalmol 1968;66:673-81.
2. Drance SM, Vargas E. Trabeculectomy and thermosclerostomy: a
comparison of two procedures. Can J Ophthalmol 1973;8:413-5.
3. Watson P. Trabeculectomy. A modified ab externo technique. Ann
Ophthalmol Glaucoma 1970;2:199-205.
4. Nuijts RA, Vernimmen RCJ, Webers CA. Mitomycin C primary
trabeculectomy in primary glaucoma of white patients. J Glaucoma
1997;6:293-7.
5. Scott I, Greenfield D, Schiffman J, et al. Outcomes of primary
trabeculectomy with use of adjunctive mitomycin. Arch Ophthalmol
1998;116:286-91.
6. Agarwal H, Sood N, Sihota R, Saga L, Honavar S. Mitomycin-C in
congenital glaucoma. Ophthalm Surg Lasers 1997;28:818-22.
7. Maumenee AE. External filtering operations for glaucoma: the
mechanism of function and failure. Trans Am Ophthalmol Soc
1960;58:219-28.
4 Cyclodestruction in Glaucoma
INTRODUCTION
When all medical and surgical therapies fail to control
intraocular pressure (IOP), it may be necessary to ablate
a par t of the ciliary body. Cyclodiathermy and
cyclocryocoagulation belong to the past because of the
severe side effects such as intense postoperative pain,
abrupt rise of intraocular pressure (IOP), intraocular
hemorrhage and phthisis. The side effects of Nd:YAG
laser cyclophotocoagulation are similar but milder.
These methods are being replaced by contact
transscleral infrared 810 nm diode laser, red 647 nm
krypton or 670 nm diode laser cyclophotocoagulation.
The energy of these wave lengths is excellently absorbed
by melanin pigment of the ciliary epithelium. In order to
produce similar coagulation effect in the rabbit ciliary
body only a half as much energy is required with the
647 nm krypton laser as compared to the 1064 nm
Nd:YAG laser. The red lasers do not impair the sensitivity
of the cornea, they do not injure corneal subbasal nerves
and they do not change tear secretion. Postoperative
pain is minimal, if any. Diode laser equipment is not
costly, it is mostly portable and easy to use. Transscleral
diode laser cyclophotocoagulation is performed on an
outpatient basis. An operation room is not needed. The
procedure is simple, safe, and easy to learn (Figs 4.1
and 4.2).
EARLY CYCLODESTRUCTIVE
PROCEDURES
Cyclodiathermy
In 1925 Curran1 cauterized the sclera over the ciliary
body using a red-hot galvanocautery loop. His aim was
to lower IOP by creating an artificial staphyloma to
38
Cyclocryocoagulation
Freezing of the ciliary body to lower IOP was suggested
by Bietti5 in 1950. However, it took about 15 years before
it was accepted that this method was useful in treating
patients with advanced treatment-resistant glaucoma.
Specific indications were neovascular, inflammatory and
aphakic glaucomas. 6 Favorable results have been
reported in neovascular glaucoma.7,8 Although visual
outcome may be poor, pain relief in 90 percent of the
patients has been the main benefit.9,10 Good results have
been also obtained in the treatment of aphakic openangle glaucoma11 as well as in glaucoma after penetrating
keratoplasty.12,13
The most frequent complications of cyclocryocoagulation are postoperative, intense pain, which may
last for several days, transient elevations of IOP, hyphema
and chronic secondary uveitis. Postoperative pain may
be reduced by performing the operation after conjunctival peritomy. Still strong analgesics are often needed.
In one study14 it was reported that IOP rose to 60 to 80
mm Hg during the freezing phase, but decreased to
baseline during thawing. Postoperatively IOP rose again
to 60 mm Hg and peaked for 6 hours after the operation.
Phthisis has been described in consecutive patients in 12
percent.15 Of eyes with neovascular glaucoma 22 percent
ended up with this extreme complication.
After the advent of ingenious new methods of
cyclodestruction, mainly transscleral contact
cyclophotocoagulation, cyclocryotherapy is not preferred
any more.
CURRENT CYCLODESTRUCTIVE
PROCEDURES
Although the intraocular pressure-lowering effects may
be similar with different cyclodestructive procedures such
as cyclocryocoagulation or Nd:YAG cyclophotocoagulation, the present trend is for various transscleral contact
diode laser techniques. The risk of transient postoperative
IOP rise, pain, conjunctival injection and iritis is
considerably less. Even repeated operations are well
accepted by the patients. Of great significance is also the
low incidence of visual loss (Figs 4.3 to 4.6).
Cyclodestruction in Glaucoma
Fig. 4.4: Before starting the operation the power through the
fiberoptic probe is checked using Power Max Laser Fiber Power
Meter
39
Fig. 4.5: After insertion of the lid speculum the site of pars
plicata is identified by transscleral illumination. Its distance
from the limbus is measured
40
held perpendicular and pressed against the sclera. Malalignment will markedly lessen the effect.
In treating various type of refractory glaucoma, about
70 percent achieved a final IOP of 21 mm Hg or less.28-32
The number of medications could be decreased and loss
of visual acuity was not a problem. Very favorable results
were obtained also in treating glaucomas associated with
chronic uveitis.33 After 12 months IOP was controlled in
77 percent of eyes. Repeat of the treatment was needed
in 64 percent. Reactivation of uveitis, persistent hypotonyt
and phthisis did not occur. Meta-analysis suggested that
higher total energy was associated with a higher percentage
Cyclodestruction in Glaucoma
41
42
MECHANISM OF INTRAOCULAR
PRESSURE REDUCTION
The mechanism of IOP reduction after cyclophotocoagulation is very much debated. The accepted
mechanism is ablation of the ciliary epithelium to
minimize aqueous production.43,46-48 Alternative theories
include damage of the ciliary vascular supply, 47
postoperative uveitis with reduced aqueous production,48
an increase of uveoscleral outflow44-46 and increased
uvescleral outflow from ciliary epithelial damage.44,46,48
An eye with treatment-resistant chamber angle recession
glaucoma was successfully treated with transscleral contact
krypton cyclophotocoagulation.50 When the eye was
examined at autopsy ten months later it was found that
effective ablation of the ciliary processes had been
achieved. Only a slight inflammatory reaction was
REFERENCES
1. Curran EJ. Subconjunctival cauterisation of sclera over ciliary body
for glaucoma. Arch Ophthalmol 1925; 54:321-2.
2. Weve HJM. Die Zyklodiathermie des Corpus Ciliare beim Glaukom.
Zentralbl Ophthalmol 1933; 29:256.
3. Vogt A. Versuche zur intraokularen Druckherabsetzung mittels
Diathermieschadigung des Corpus Ciliare (Zyklodiatermiestichelung). Klin Monatsbl Augenheilkd 1936; 97:467-78.
4. Walton DS, Grant WM. Penetrating cyclodiathermy for filtration.
Arch Ophthalmol 1970; 83:47-8.
5. Bietti G. Surgical intervention on the ciliary body: New trends for
relief of glaucoma. J Am Med Assoc 1950; 142:889-97.
6. Spaeth GL. Ophthalmic Surgery: Principles and practice. WB
Saunders: Philadelphia; 1990.
7. Feibel RM, Bigger JF. Rubeosis irides and neovascular glaucoma:
evaluation of cyclocryotherapy. Arch Ophthalmol 1972; 47:862-7.
8. Klein J, Kchle HJ. Cryotherapy of ciliary body in cases of secondary
glaucoma with poor prognosis. Klin Monatsbl Augenheilkd 1981;
179:470-6.
Cyclodestruction in Glaucoma
9. Krupin T, Mitchell KB, Becker B. Cyclocryotherapy in neovascular
glaucoma. Am J Ophthalmol 1978; 86:24-6.
10. Caprioli J, Strang SL, Spaeth GL, et al. Cyclocryotherapy in the
treatment of advanced glaucoma. Ophthalmology 1985; 92:947-2.
11. Bellows MT, Grant WM. Cyclocryotherapy in chronic open-angle
glaucoma in aphakic eyes. Am J Ophthalmol 1978;85:615-21.
12. West CE, Wood TO, Kaufman HE. Cyclocryotherapy for glaucoma
pre- and post-penetrating keratoplasty. Am J Ophthalmol 1973;
76:485-9.
13. Binder PS, Abel R Jr, Kaufman HE. Cyclocryotherapy for glaucoma
after penetrating keratoplasty. Am J Ophthalmol 1975;79:489-92.
14. Caprioli J, Sears M. Regulation of intraocular pressure during
cyclocryotherapy for advanced glaucoma. Am J Ophthalmol 1986;
101:542-5.
15. Brindley G, Shields MB. Value and limitations of cyclocryotherapy.
Graefes Arch Clin Exp Ophthalmol 1986; 224:545-9.
16. Weekers R, Lavergne G, Watillon M, et al. Effects of photocoagulation
of the ciliary body upon ocular tension. Am J Ophthalmol 1961;
52:156-63.
17. Smith RS, Stein MN. Ocular hazards of transscleral laser radiation.II.
Intraocular injury produced by ruby and neodymium lasers. Am J
Ophthalmol 1969; 67:100-9.
18. Beckman H, Sugar HS. Neodymium laser cyclophotocoagulation.
Arch Ophthalmol 1973; 90:27-8.
19. Brancato R, Giovanni L, Trabucchi G, et al. Contact transscleral
cyclophotocoagulation with Nd:YAG laser in uncontrolled glaucoma.
Ophthalmic Surg 1989; 20:547-51.
20. Schuman JS, Pulificato CA, Allingham RC, et al. Contact transscleral
continuous wave neodymium:YAG laser cyclophotocoagulation.
Ophthalmology 1990;97:571-80.
21. Schuman JS, Pulificato CA. Laser cyclophotocoagulation. Int
Ophthalmol Clin 1990;30:111-9.
22. Jennings BJ, Mathews DE. Complications of neodymium:YAG
cyclophotocoagulation in the treatment of open-angle glaucoma.
Optom Vis Sci 1999; 76:686-91.
23. Pastor SA, Iwach A, Nozik RA, et al. Presumed sympathetic
ophthalmia following Nd:YAG transscleral cyclophotocoagulation.
J Glaucoma 1993;2:30-1.
24. Bechrakis NE, Mller-Stolzenburg NW, Helbig H, et al. Sympathetic
ophthalmia following laser cyclogoagulation. Arch Ophthalmol 1994;
112:80-4.
25. Minckler DS. Does Nd:YAG cyclotherapy cause sympathetic
ophthalmia? (editorial). Ophthalmic Surg 1989;20:543.
26. Schuman JS, Jacobson JJ, Pulificato C, et al. Experimental use of
semiconductor diode laser in transscleral contact cyclophotocoagulation in rabbits. Arch Ophthalmol 1990; 108:1152-57.
27. Hennis HL, Assia E, Stewaret WC, et al. Transscleral
cyclophotocoagulation using a semiconductor diode laser in cadaver
eyes. Ophthalmic Surg 1991; 21:274-9.
28. Schlote T, Derse M, Rassmann K, et al. Efficacy and safety of contact
transscleral diode laser cyclophotocoagulation for advanced
glaucoma. J Glaucoma 2001; 10:294-301.
29. Mistlberger A, Liebmann JM, Tshciderer H, et al. Diode laser
cyclophotocoagulation for refractory glaucoma. J Glaucoma
2001;10:288-93.
30. Pucci V, Marcini G,Pedrotti E, et al. Transscleral diode laser
photocoagulation for refractory glaucoma. Ophthalmologica 2001;
215:263-6.
31. Threlked AB, Johnson MH. Contact transscleral diode laser
cyclophotocoagulation for refractory glaucoma. J Glaucoma 1999;
8:3-7.
43
44
56. Murphy CC, Burnett CAM Spry PGD, et al. A two-centre study of
the dose-response relation of transscleral diode laser
cyclophotocoagulation in refractory glaucoma. Br J Ophthalmol
2003;87:1252-7.
57. Walland MJ Diode laser cyclophotocoagulation: dose-standardized
therapy in end-stage glaucoma. Austr and New Zealand J Ophthalmol
1998;26:135-9.
58. Pastor SA, Singh K, Lee DA, et al. Cyclophotocoagulation: a report
by the American Academy of Ophthalmology. Ophthalmology
2001;108:2130-8.
59. Freigassner P, Eckhardt M. Transscleral cyclophotocoagulation versus
cyclocryotherapy in treatment of neovascular glaucoma: a
retrospective analysis. Acta Ophthalmol Scand 2003;81:674-5.
60. Delgado MF, Dickens CJ, Iwach AG, et al. Long-term results of
noncontact neodymium:yttrium-aluminium-garnet cyclophotocoagulation in neovascular glaucoma. Ophthalmology
2003;110:895-9.
INTRODUCTION
The desired goal of glaucoma filtering surgery is to
maintain indefinitely the patency of an artificially created
fistula between the inside of the eye and the extraocular
space. The key to successful management of the patient
undergoing surgery is anticipation of potential
postoperative problems, early detection and timely,
appropriate intervention to enhance filtration. Following
a patient after filtering surgery is like playing chessone
has to think several moves ahead and act, not necessarily
on what the findings are on a particular visit, but what
these findings suggest may be likely to occur at a
subsequent visit. In this chapter, we discuss the clinical
appearance and management of failing blebs following
filtering surgery.
46
47
C
Figs 5.6A to C: Successful bleb formation is characterized by
decreasing injection, elevation, and the presence of
conjunctival microcysts. A: 10 days. B: 1 month. C: 3 months
after surgery
48
C
Figs 5.7A to C: A bleb that developed progressive loculation,
hyperemia, and flattening. A: 3 days. B: 3 weeks. C: 6 weeks
after surgery
49
Bleb Encapsulation
Bleb encapsulation (Tenon cyst) develops in
approximately 10 to 28 percent of eyes following filtering
surgery,5,36-41 typically during the first 8 postoperative
weeks. Richter et al42 reported an incidence of 13.7
percent in over 400 consecutive surgeries. The incidence
was higher following filtering surgery for congenital (33%)
and juvenile glaucoma (44%). Signs of bleb
encapsulation developed a mean of 20 days following
filtration. Reported risk factors for encapsulation include
male gender,41,43 prior argon laser trabeculoplasty,36,43,44
anterior uveitis,45 prolonged preoperative topical blocker,36,44 and parasympathomimetic use,36 history of
encapsulated bleb, 36 surgical glove powder, 46 and
preoperative steroid injection over the fistula.47 The use
of adjunctive 5FU injections did not reduce the incidence
of bleb encapsulation in two prospective series.48,49
The encapsulation process consists of fibroblastic
overgrowth that results in a tense, opalescent bleb with
a thick wall in direct communication with the anterior
chamber (Fig. 5.8).39,50 Histopathology reveals dense
subconjunctival connective tissue, few cells and no cellular
lining.50,51 Bleb encapsulation may be accompanied by
progressive conjunctival hyperemia. One typically finds
loculation, thickening of the subconjunctival connective
tissue, and elevated IOP. The spectrum of appearance
ranges from incomplete loculation and mild hyperemia
to complete encapsulation. The dome-like region is firm,
although the overlying conjunctiva may be mobile, and
is in direct communication with the anterior chamber.
Complications of bleb encapsulation include uncontrolled
IOP, corneal dellen, and occasional discomfort.
The key to successful management is patience. In
most cases, the pressure will decrease within 2 to 4
months with the use of aqueous suppressants. It is
believed that the decrease in aqueous production and
IOP associated with medical therapy allows for
remodeling of the cyst wall and eventually improved
aqueous flow across it. The connective tissue remnant
remains within the subconjunctival space, but aqueous
50
Laser Suturelysis
Historical Aspects
Lieberman64 initially reported on the procedure in 1983,
obtaining good success using the triangular space
between two mirrors of a four-mirror Ziess lens. Hoskins
and Migalizzo65,66 designed a special lens for the procedure.
More recently, Ritch67,68 has designed a lens that provides
excellent compression of the conjunctva, an improved
view of scleral flap sutures, and effortless retraction of
the upper lid.
Indications
Laser suturelysis is indicated when inadequate filtration
from tight closure of the scleral flap is suspected. Timing
of the procedure is of crucial importance. It is safer to
delay it until the 2nd or the 3rd postoperative day to
minimize hypotony and flat anterior chambers. The
greatest effect in lowering IOP is achieved if suturelysis is
done in the first two postoperative weeks and rarely after
four weeks unless antimetabolites are used in conjunction
with glaucoma filtering surgery.69
Technique
Digital Compression
51
Complications
B
Figs 5.9A and B: A: Ritch laser suturelysis lens.
B: Magnified view of the suture
52
Bleb Needling
Revision of trabeculectomy through a small conjunctival
incision for filtration failure was described in 1941.78
Discission with a needle-knife was first described in
1962.79 Bleb needling, as currently performed, was
described by Pederson and Smith,39 and is capable of
restoring function to clinically failed blebs which would
otherwise require reoperation.19,80-82 This procedure
allows the surgeon to create an opening(s) in the wall of
an encapsulated bleb or raise a flattened bleb at the slitlamp or in the operating room via subconjunctival
manipulation with a small gauge needle. The technique
involves elevation of the conjunctiva off the surface of
the globe with balanced salt solution or anesthetic with a
small gauge needle. The underlying episcleral/Tenons
capsule scarring is then incised with the needle. If this
does not succeed in restoring filtration, the edge of the
scleral flap may be elevated. A Hoskins lens may be used
to enhance visibility of the needle tip during the
procedure.83
Using this technique, Pederson and Smith39 achieved
successful control of IOP in 96 percent of cases with or
without more complete surgical revision. Shin et al82
reported restoration of bleb function in 80 percent of
eyes with flat, failed blebs undergoing needle revision
with supplemental 5FU. Ewing and Stamper55 reported
successful outcome in 11/12 patients without significant
surgical complications. Common complications include
conjunctival hemorrhage and transient wound leak.
Ocular hypotony may occur, and although rare,
choroidal effusion has been reported. 56 Aqueous
misdirection has been also reported following needling
of trabeculectomy bleb.84,85 Aqueous may occasionally
leak from the needle entry site for several days, but does
not usually require any intervention. The main
advantages of the procedure include its ease, minimal
anesthesia, and few complications. Reoperation, however
may often be required.39,86 potential risk factors for failure
include pre-needling IOP over 30 mm Hg, lack of
mitomycin-C use during the previous filtering surgery,
and IOP over 10 mm Hg immediately after needling.87
Adjunctive 5FU decreases the propensity towards scarring
and increases the success rate. 88-93 Fornix-based
trabeculectomies may be more likely to fail the needle
Trephination
Earlier attempts at ab interno filtration included
goniopuncture, 101 electrocautery puncture, 102 and
goniodiathermy.103 For various reasons, these procedures
were never widely adopted. A true ab interno sclerostomy
technique producing excision of trabecular tissue was
first devised by Brown and coworkers using an
automated trephine.104,105
More recently, laser procedures have been described
to re-establish filtration when the blockage is internal to
the bleb, including external argon,32 Nd:YAG,26 internal
argon,30 mode-locked Nd:YAG,31,106-108 and Q-switched
Nd:YAG. Success with these modalities has been limited
by the excess fibrosis associated with thermal injury.
Nevertheless, ab interno trephination was largely
abandoned. In the mid-1990s, we revived the procedure
as a tool for bleb revision in selected, mature blebs with
failure at the level of the scleral flap (Fig. 5.11). We
retrospectively evaluated the effectiveness of this
procedure and found it to be a useful effective technique
for re-establishing flow through mature filtering blebs.
In 2004, at the ARVO meeting, we presented data on
ab interno trephinations performed on 40 failing blebs
of 38 patients who were followed for a mean period of
32.3 months (range 3 to 96) between 1995 and 2003.24
We defined success as IOP 21 mm Hg and at least 20
percent reduction from baseline on the same or fewer
number of pretrephination medications, 30/40 eyes
(75%) fit the criteria for success over the course of followup. Among all 40 eyes with 3 months of follow-up
there was a significant drop in IOP from pretrephination
to 3 months. The percentage of patients requiring 2
medications declined from 90 percent at pretrephination
to 21 percent at 3 months and was stable thereafter.
Some patients were able to eliminate all medications.
53
Technique
54
Bleb Reconstruction
When attempts at salvaging a failing bleb are ineffective,
bleb reconstruction at the same site can be performed.
Advancement of the conjunctiva with excision of the preexisting bleb may be successful.111,112 Failed blebs may
be reconstructed with free conjunctival autografts.113-115
Amniotic membrane transplantation has also been
described.116
B
Figs 5.13A and B: A: Pre-laser cautery of bleb vessels. B:
Post laser cautery of bleb vessels
REFERENCES
1. Cairns JE. Trabeculectomypreliminary report of a new method.
Am J Ophthalmol 1968; 66: 673-9.
2. Picht G, Grehn F. Classification of filtering blebs in trabeculectomy:
biomicroscopy and functionality. Curr Opin Ophthalmol 1998; 9:
2-8.
3. Cantor LB, Mantravadi A, WuDunn D, Swamynathan K, Cortes A.
Morphological classification of filtering blebs after glaucoma filtration
surgery: the Indiana Bleb Appearance Grading Scale. J Glaucoma
2003; 12: 266-71.
4. Kanski JJ. The Glaucomas. In. Clinical Ophthalmology: A systemic
approach. (4th edition). Woburn: Butterworth Heinmann, 1999:
183-261.
5. Scott DR, Quigley HA. Medical management of a high bleb phase
after trabeculectomies. Ophthalmology 1988; 95:1169.
6. Stewart RH, et al. Trabeculectomy and modifications of
trabeculectomy. Ophthalmic Surg 1979; 10: 76-80.
7. Mills K. Trabeculectomy: a retrospective long-term follow-up of 444
cases. Br J Ophthalmol 1981; 65: 790-5.
8. Gressel MG, Heuer DK, Parrish RK. Trabeculectomy in young
patients. Ophthalmology 1984; 91: 1242.
9. Miller RD, Barber JC. Trabeculectomy in black patients. Ophthalmic
Surg 1981; 12: 46-50.
55
56
55. Ewing RH, Stamper RL. Needle revision with and without 5fluorouracil for the treatment of failed filtering blebs. Am J Ophthalmol
1990; 110: 254-9.
56. Potash SD, Ritch R, Liebmann J. Ocular hypotony and choroidal
effusion following bleb needling. Ophthalmic Surg 1993; 24: 279.
57. Durcan FJ, Cioffi GA, van Buskirk EM. Same-site revision of failed
filtering blebs. J Glaucoma 1992; 1: 2-6.
58. Greenfield DS, Miller MP, Suner IJ, Palmberg PP. Needle elevation of
the scleral flap for failing filtration blebs after trabeculectomy with
mitomycin C. Am J Ophthalmol 1996; 122: 195-204.
59. Traverso CE, Tomey KF, Antonios S. Limbal- vs fornix-based
conjunctival trabeculectomy flaps. Am J Ophthalmol 1987; 104: 28.
60. Segrest DR, Ellis PP. Iris incarceration associated with digital ocular
massage. Ophthalmic Surg 1981; 12: 349-51.
61. Miller GR, Krustin J. Ruptured filtering bleb after ocular massage.
Arch Ophthalmol 1966; 76: 363.
62. MacRae SM, et al. The effects of sodium hyaluronate, chondroitin
sulfate and methylcellulose on the corneal endothelium and intraocular
pressure. Am J Ophthalmol 1983; 95: 332-41.
63. Ruderman JM, Jampol LM, Krueger DM. Visual loss caused by
subretinal hemorrhage and rupture of Bruchs membrane after digital
ocular massage. Am J Ophthalmol 1988; 106: 493-4.
64. Lieberman Mf. Suture lysis by laser and goniolens. Am J Ophthalmol
1983; 95:257.
65. Hoskins D, Migaliazzo CV. Argon laser treatment of filtering bleb
insufficiency. Klin Monatsbl Augenheilkd 1989; 195: 328.
66. Hoskins HD Jr, Migaliazzo C. Management of failing filtering blebs
with argon laser. Ophthalmic Surg 1984; 15: 731.
67. Ritch R, Potash Sd, Liebmann JM. A new lens for argon laser suture
lysis. Ophthalmic Surg 1994; 25: 126.
68. Lai JS, Tham CC, Lam DS. Argon laser suture lysis using Ritch lens
following cataract surgery. Indian J Ophthalmol 2002; 50: 131-2.
69. Savage JA, Condon GP, Lyth RA, et al. Laser suture lysis after
trabeculectomy. Ophthalmology 1998; 95: 1631-8.
70. Tomey KF. A simple device for laser suture lysis after trabeculectomy.
Arch Ophthalmol 1991; 109: 14-5.
71. Salamon SM. Trabeculectomy flap suture lysis with endolaser probe.
Ophthalmic Surg 1987; 18: 506-7.
72. Benson WE, Coscas G, Katz LJ. Revision of failing filtering blebs. In
Current Techniques in Ophthalmic Laser Surgery. Philadelphia:
Current Medicine 1994: 200-4.
73. Kapetansky FM. Laser suture lysis after trabeculectomy. J Glaucoma
2003; 12: 316-20.
74. Mudgil AV, To KW, Balachandran RM, Janigian RH, Tsiaras WG.
Relative efficacy of the argon green, argon blue-green, and krypton
red lasers for 10-0 nylon subconjunctival laser suture lysis. Ophthalmic
Surg Lasers 1999; 30: 560-4.
75. Aktan SG, Mandelkorn RM. Krypton laser suture lysis. Ophthalmic
Surg Lasers 1998; 29: 635-8.
76. Macken P, Buys Y, Trope GE. Glaucoma laser suture lysis. Br J
Ophthalmol 2000; 80: 398-401.
77. DiSclafani M, Liebmann JM, Ritch R. Malignant glaucoma following
argon laser release of scleral flap sutures after trabeculectomy. Am J
Ophthalmol 1989; 108: 597-8.
78. Ferrer H. Conjunctival dialysis in the treatment of glaucoma recurrent
after sclerectomy. Am J Ophthalmol 1941; 24: 788-90.
79. Fitzgerald JR, McCarthy JL. Surgery of the filtering bleb. Arch
Ophthalmol 1962; 68: 453.
80. Gillies WE, Brooks AMV. Restoring the function of the failed bleb.
Aust NZ J Ophthalmol 1991; 19: 49-51.
81. Morales J, Ritch R. Treatment of failing filtering blebs. Clin Decisions
Ophthalmol 1987; 11: 4-11.
82. Shin DH, et al. Needling revision of failed filtering blebs with adjunctive
5-fluorouracil. Ophthalmic Surg 1993; 24: 242.
83. Hayashi M. Use of the Hoskins lens in needle revision of a failed bleb
after filtration surgery. Am J Ophthalmol 1995; 119: 232-3.
84. Mathur R, Gazzard G, Oen F. Malignant glaucoma following needling
of a trabeculectomy bleb. Eye 2002; 16: 667-9.
85. Ramanathan US, Kumar V, ONeill E, Shah P. Aqueous misdirection
following needling of trabeculectomy bleb. Eye 2003; 17: 441-2.
86. Shingleton BJ, et al. Management of encapsulated filtration blebs.
Ophthalmology 1990; 97: 63-8.
87. Shin DH, Kim YY, Ginde SY, Kim PH, Eliassi-Rad B, Khatana AK,
Keole NS. Risk factors for failure of 5-fluorouracil needling revision
for failed conjunctival filtration blebs. Am J Ophthalmol 2001; 132:
875-80.
88. Liebmann JM, Ritch R. 5-fluorouracil in glaucoma filtration surgery.
Ophthalmol Clin NA 1988; 1: 125-31.
89. Broadway DC, Bloom PA, Bunce C, Thiagarajan M, Khaw PT.
Needle revision of failing and failed trabeculectomy blebs with
adjunctive 5-fluorouracil: survival analysis. Ophthalmology 2004;
111: 665-73.
90. Ophir A, Wasserman D. 5-fluorouracil-needling and paracentesis
through the failing filtering bleb. Ophthalmic Surg Lasers 2002; 33:
109-16.
91. Ophir A, Porges Y. Needling with intra-bleb 5 fluorouracil for
intractable neovascular glaucoma. Ophthalmic Surg Lasers 2000;
31: 38-42.
92. Durak I, Ozbek Z, Yaman A, Soylev M, Cingil G. The role of needle
revision and 5-fluorouracil application over the filtration site in the
management of bleb failure after trabeculectomy: a prospective
study. Doc Ophthalmol 2003; 106: 189-93.
93. Hodge W, Saheb N, Balazsi G, Kasner O. Treatment of encapsulated
blebs with 30-gauge needling and injection of low-dose 5-fluorouracil.
Can J Ophthalmol 1992;27:233-6.
94. Hawkins AS, Flanagan JK, Brown SVL. Predictors for success of
needle revision of failing filtration blebs. Ophthalmology 2002; 109:
781-5.
95. Ben-Simon GJ, Glovinsky Y. Needle revision of failed filtering blebs
augmented with subconjunctival injection of mitomycin C.
Ophthalmic Surg Lasers 2003; 34: 94-9.
96. Mardelli PG, Lederer CM Jr, Murray PL, Pastor SA, Hassanein KM.
Slit-lamp needle revision of failed filtering blebs using mitomycin C.
Ophthalmology 1996; 103: 1946-55.
97. Iwach AG, Delgado MF, Novack GD, Nguyen N, Wong PC.
Transconjunctival mitomycin-C in needle revisions of failing filtering
blebs. Ophthalmology 2003; 110: 734-42.
98. Smith MF, Doyle JW. Use of tissue plasminogen activator to revive
blebs following intraocular surgery. Arch Ophthalmol 2001; 119:
809-12.
99. Szymanski A. Promotion of glaucoma filter bleb with tissue
plasminogen activator after sclerectomy under a clot. Int Ophthalmol
1992; 16: 387-90.
100. Tym WH, Seah SKL. Augmentation of filtering blebs with
perfluoropropane gas bubble. An experimental and pilot clinical
study. Ophthalmology 1999; 106: 545-9.
57
58
INTRODUCTION
Modern implant glaucoma surgery has been influenced
by the invention of Dr Mateen Ahmed and the
introduction of his glaucoma valved implant in 1990.
The Ahmed valve was the first restrictive glaucoma
implant with a true valve mechanism developed. It was
designed to address the need to control intraocular
pressure (IOP) during the first day after surgery, reducing
at the same time the risk of hypotony and choroidal
detachment; a task hard to achieve with pre-existing nonrestricted implants.
Four different models are available for implantation
nowadays:
AGV S2: Three-piece design, polypropylene body,
silicone tube, 184 mm2 total area, intended for adult
eyes, axial length 20.5 mm or more
AGV S3: Three-piece design, polypropylene body,
silicone tube, 92 mm2 total area, for pediatric or
nanophthalmic eyes
AGV B1: Double plate design, polypropylene
body, silicone tube, 368 mm2 total area, second
plate can be fixed at either side of primary plate
AGV FP7: Flexible plate, silicone body, silicone
tube, 184 mm2 total area. The valved mechanism
is made of polypropylene protected by silicone to
avoid its contact with inflammatory cells. Its plate
also has new holes intended to limit the size of the
bleb and decrease chances of extrusion and/or
migration.
The tube is inserted into the anterior chamber or
into the vitreous cavity via pars plana in vitrectomized
eyes. The aqueous is transported to the valves body,
where it has to pass between two silicone elastomer foils,
INDICATIONS
The valve should be considered for any multioperated,
unresponsive glaucoma. It can also be a first line
procedure in phakic, aphakic, post-keratoplasty or
neovascular glaucoma, in eyes with previous retinal and/
or vitreous surgery, and in any eye with scarred
conjunctiva.
Children with glaucoma and eyes that have not
reached an axial length over 20.5 mm should receive
the AGVS3 model. Children with congenital or
secondary glaucomas and adult-size or buphthlamic eyes
should receive either model AGVS2 or FP7.
59
SURGICAL TECHNIQUE
Several modifications to the usual technique were
developed by Dr. Gil-Carrasco, at the Hospital de la
Asociacin Para Evitar La Ceguera en Mxico, Dr Luis
Snchez Bulnes or APEC. These include the use of 7-0
silk, the scleral tunnel technique and no-patch technique
as described previously.2
The eye is usually operated under peribulbar or
retrobulbar anesthesia, but in special cases where the risk
of perforation is too great, a combination of topical and
sub-Tenons can be used safely. General anesthesia can
be left for children and other uncooperative patients. A
bolus of mannitol and/or Honans balloon may be
necessary whenever the anterior chamber will have a large
incision due to combined cataract, IOL, or corneal surgery.
The preferred quadrant for valve implantation is the
superotemporal because of its easier access, less chances
of muscular restriction and a better-looking postoperative
aspect. Only in cases with marked scleral thinning,
dehiscent conjunctiva or when a second or third implant
is needed should the other quadrants be considered.
The inferotemporal or inferonasal quardant, as proposed
60
61
Fig. 6.6: One-stitch technique. Both ends of the suture are tied
under the tube. The suture must be tightened to avoid
displacements
62
63
Fig. 6.12: Widening the inner portion of the tunnel. Small side
to side movements are made using the cutting edge of the
needle to widen the tunnels inner opening
64
Fig. 6.13: Tunnel for pars plana insertion. The tunnel is started
5 to 6 mm from the limbus and at the 3 to 4 mm mark the needle
is directed posteriorly, behind the iris
65
66
67
68
69
70
71
Early postoperative
Late postoperative
Related to
conjunctival:
dissection/closure/
buttonholes
Ocular perforation
Related to tube
insertion/position/
cutting
Valves body
placement
Hyphema
Flat/shallow AC
Choroidal
detachment/
Expulsive
Hemorrhage
Vitreous loss/
malignant glaucoma
Traumatic cataract/
Lens trauma
Conjunctival
dehiscence/Seidel
Tube exposure
Valves body
displacement
Restrictive strabismus
Sub-acute choroidal
detachment
Malignant glaucoma
Cataract
Cataract
Intraoperative Complications
All intraoperative complications should be treated as soon
as they appear, except for lens trauma, which may be
observed if the capsular rupture is small; fibrosis may
form over the capsular rupture and the opacity may be
localized and not interfere with the visual axis. If the
rupture is too big or compromises the pupillary axis the
cataract may be extracted, preferably by phaco, and the
IOL implanted as a secondary procedure when the
biometry becomes available.
Most troubles related to conjunctival and scleral
dissection happen in eyes with previous retinal surgeries,
scleromalacia, scleral staphylomas, or previous ocular
72
73
74
75
the new tunnel, carefully dissecting out the tube from the
old tunnel aided by a sharp needle and place the tube
through the new tunnel before opening the capsule, so
the eye does not get too hypotonous. Care must be taken
not to accidentally cut the tube if dissecting with excessive
bleeding and poor visualization. After the tube is back in
place capsule dissection is performed as described
previously and conjunctival closure as for the primary
procedure.
Tube related late complications can be managed in
several ways. Tube retraction may need repositioning of
the tube through a new and more posterior tunnel, but
occasionally may need repositioning the valves body
more anteriorly. A more conservative but not always
available approach is to use New World Medicals tube
extender, avoiding making another tunnel, unless the
tube has been exposed.12
Tube exposure is a rare complication with the present
episcleral tunnel technique. Exposure can lead to
infection and even to endophthalmitis. Primary suturing
of the conjunctiva may work, but occasionally scleral,
76
CONCLUSIONS
The Ahmed valve has been the mainstay for immediate
control of IOP in difficult and complicated glaucoma
cases. Its properties have made it a reliable means of
managing simultaneously many tribulations in
problematic eyes. Regardless of its benefits, its use is not
always trouble-free or remedial. Many complications
during both the early and late postoperative periods can
be sight-threatening, and difficult to manage, not least
of all loss of long-term IOP control.
New materials, coatings, surgical techniques, antiscarring agents and drugs may improve the clinical
management of the postoperative period in eyes that
need an Ahmed valve. The role of eye massage to
increase the size of the filtering bleb has to be studied
further in order to determine if it is beneficial or
detrimental in the long run. Possible future risk factor
analysis and genetic tests may be able to predict which
patients, or at least which indications, will do better with
REFERENCES
1. Britt MT, LaBree LD, Lloyd MA, et al. Randomized clinical trial of
the 350 mm2 versus the 500 mm2 Baerveldt implant: longer term
results: is bigger better? Ophthalmology 1999; 106: 2312-8.
2. Gil-Carrasco F, Salinas-VanOrman E, Recillas-Gispert C, Paczka JA,
Gilbert ME, Arellanes-Garcia L. Ahmed valve implant for uncontrolled
uveitic glaucoma. Ocul Immunol Inflamm 1998;6:27-37.
3. Ayyala RS, Layden WE, Slonim CB, Margo CE. Anatomic and
histopathologic findings following a failed Ahmed glaucoma valve
device. Ophthalmic Surg Lasers 2001; 32: 248-9.
4. Parks MM. Causes of the adhesive syndrome. In Symposium on
Strabismus. St. Louis, CV Mosby, 1978.
5. Susanna R Jr. Latin American Glaucoma Society Investigators.
Partial Tenons capsule resection with adjunctive mitomycin C in
Ahmed glaucoma valve implant. Br J Ophthalmol 2003; 87:994-8.
6. Hill RA, Pirouzian A, Liaw L. Pathophysiology of and prophylaxis
against late Ahmed glaucoma valve occlusion. Am J Ophthalmol
2000; 129: 608-12.
7. Coleman AL, Mondino BJ, Wilson MR, et al. Clinical experience
with the Ahmed glaucoma valve implant in eyes with prior or
concurrent penetrating keratoplasties. Am J Ophthalmol
1997;123:54-61.
8. Al-Torbak A. Graft sur vival and glaucoma outcome after
simultaneous penetrating keratoplasty and ahmed glaucoma valve
implant. Cornea. 2003;22:194-7
9. Gil-Carrasco F, Paczka JA, Jimnez Romn J, et al. Experiencia
clnica inicial con la vlvula de Ahmed: reporte de 278 casos con
glaucoma incontrolable. St. Ophthal 1997;16:117-22
10. Malbran ES, Malbran E, Buonsanti J, Adrogue E. Closed-system
phacoemulsification and posterior chamber implant combined with
penetrating keratoplasty. Ophthalmic Surg 1993; 24(6):403-6.
11. Wilson MR, Mendis U, Paliwal A, Haynatzka V. Long-term follow-up
of primary glaucoma surgery with Ahmed glaucoma valve implant
versus trabeculectomy. Am J Ophthalmol 2003;136:464-70.
12. Rebolleda G, Munoz-Negrete FJ. Extender-tube for Ahmed glaucoma
valve implant. Arch Soc Esp Oftalmol. 2003;78:513-6.
INTRODUCTION
HISTORICAL BACKGROUND
78
79
Fig. 7.5: IOP after drainage by Molteno implant in a 47-yearold male with advanced traumatic glaucoma in a quiet eye.
Note hypotensive stage, hypertensive stage, and late stable
stage
80
Fig. 7.11: Diagramatic IOP graphs to illustrate effects of antiinflammatory drugs on IOP and final thickness and permeability
of final bleb capsule after insertion of Molteno implants with
immediate drainage of aqueous
81
82
Fig. 7.18: Diagramatic IOP graphs to illustrate effect of antiinflammatory drugs in reducing the hypertensive stage
inflammation and increasing the permeability of the fibrous
bleb capsule after insertion of Molteno implants with delayed
drainage of aqueous (vicryl tie technique)
83
Age
Infants less than 18 months old, irrespective of the
severity of the glaucoma, produce thin bleb capsules
and thus require only single plate implants. Older children
and adults produce thicker and less permeable bleb
capsules even in less severe cases of glaucoma and usually
require double plate implants. Old (>70 years) and frail
84
individuals, particularly those who have been on longterm systemic steroids, produce less fibrous bleb capsules
so that single plate implants provide adequate drainage
in the less severe cases.
Severity of Glaucoma
Mild cases in which the IOP can be reduced to normal
levels with hypotensive medication require single plate
implants while eyes with a preoperative IOP >25 mm
Hg on two or more hypotensive agents require double
plate implants even in older patients.
Preoperative Management
Preoperative management involves reviewing and if
necessary increasing the patients hypotensive medication
to reduce the IOP to as near the normal range as possible.
If the IOP can be kept low even for a short time, this will
reduce the final thickness and increase the long-term
permeability of the fibrovascular bleb lining (with
correspondingly better control of IOP).
85
86
87
Fig. 7.29: The track of the 22-gauge needle tip through the
tissues into the anterior chamber
Fig. 7.31: Feeding the tube down the needle track into the AC
88
89
Fig. 7.34: The tube buried under the lamellar scleral flap and
covered by a patch of donor sclera
B
Fig. 7.35: Sectional diagrams to show: (A) a fold of Tenons
tissue caught behind the episcleral plate, and (B) Tenons tissue
freed
90
Fig. 7.40: The tube trimmed at 45o so that its point overlaps
the limbus by 2.5 to 3 mm
Fig. 7.42: Tenons tissue starting to lift off the pressure ridge
10 to 14 days after operation
91
Cytostatic Agents
The perioperative or postoperative use of mitomycin-C
or 5-fluorouracil with implants does not improve control
of IOP. Both agents inhibit wound healing and may cause
exposure of implants due to breakdown of the overlying
tissues, therefore they should not be used.17
92
Early Complications
The postoperative complications after insertion of
implants are very similar to those that occur after
conventional drainage surgery and their management is
broadly the same.
1. Hyphema: Hyphemas are common given the type
of case being drained by implant and require no
special treatment.
2. Choroidal detachment: Choroidal detachments are
uncommon and tend to occur in terminally
advanced cases where thin sclera prevents watertight
insertion of the tube into the AC. They are managed
conservatively.
3. Leakage through tube: This should be prevented
by careful surgical technique but when it does occur
the eye is managed conservatively using topical
steroids and cycloplegic agents and relying on the
biological valve formed by the pressure ridge to
prevent hypotony.
4. Hypotony: Despite good surgical technique
hypotony may occur in terminal eyes as a result of
temporary suppression of aqueous secretion by the
ciliary body. These cases are best managed
conservatively. Very occasionally hypotony occurs
when a double plate implant is inserted in a case
where, in retrospect, a single plate implant should
have been used. These cases are initially managed
conservatively, however if the IOP does not rise
sufficiently within 2 to 3 weeks the second plate
should be removed. This is easily done as an
outpatient procedure. Using topical anesthesia the
conjunctiva is incised over the anterior edge of the
second episcleral plate. The plate is then grasped
with a pair of toothed forceps and pulled forwards
out of the bleb cavity. The connecting tube is
stretched and cut as short as possible so that it retracts
into the tissues. After this procedure connective tissue
Late Complications
1. Raised intraocular pressure: In cases where a single
plate has not given adequate control of IOP a second
plate can be added without direct intraocular
intervention. A single plate implant is placed in an
adjacent quadrant to the existing bleb. After suturing
the plate in position on the sclera and occluding its
drainage tube by a 5.0 vicryl ligature the tube is
trimmed to a length where it extends to the centre
of the existing first plate. The end of the tube is
beveled with the bevel facing down towards the
surface of the plate to prevent the end of the tube
from being occluded by contact with the inner
surface of the bleb capsule. A 22 gauge needle is
used to form a microkeratome as previously
described and a tapered incision made in the
fibrovascular bleb capsule to allow the tube to be
pushed into the cavity. Following this procedure a
preformed bleb lining forms around the second
plate and additional drainage of aqueous starts
automatically when the vicryl suture dissolves.
2. Thinning of the tissues over the tube: Late thinning
of the conjunctival tissues covering the drainage tube
is managed by raising a flap of conjunctiva and
placing a piece of donor sclera over the tube.
3. Late migration of the tube in the anterior chamber:
The tissues of growing eyes of young infants and
eyes with chronic uveitis are unusually soft and may
allow slow displacement of the tube from its original
position in the AC. The tubes position should be
routinely noted and any slow displacement in a
direction that threatens contact between the free
end of the tube and the cornea should be addressed.
The technique for re-siting the tube consists of raising
a fornix based flap of conjunctiva and Tenons tissue
to give access to the tube between the episcleral
plate and the limbus. A careful longitudinal incision
of the connective tissue sheath around the tube is
made. This allows the tube to be grasped by a fine
pair of forceps and withdrawn from the AC. A
93
ILLUSTRATIVE CASES
Special Considerations for
Certain Groups of Cases
Buphthalmos
Implants give outstanding results when used as a primary
procedure in cases of buphthalmos associated with
Sturge-Weber syndrome, neurofibromatosis, congenital
cataract surgery and severe cases of primary
hydrophthalmia.10 Similar short-term results can be
obtained in cases that have undergone many previous
procedures however, the long-term consequences of
multiple operations such as low grade inflammation,
retinal detachment, band keratopathy and corneal
decompensation sooner or later destroy the patients
vision despite adequate control of IOP. Thus implants
should be used where alternative procedures do not carry
a good long-term prognosis. With children donor sclera
is used to provide long-term cover for the tube and
constant vigilance is required to prevent the development
of amblyopia in otherwise successful cases. When
implants are used in cases of Sturge-Weber syndrome
the aqueous is absorbed into abnormal angiomatous
vessels that have a higher intravascular pressure than
normal capillaries causing the IOP to stabilize at 20 mm
Hg. Attempts to lower this pressure by adrenergic agents
give erratic results and such cases are best managed by
accepting an IOP at the upper limit of the normal range.
Illustrative case of simple buphthalmos: Case 1:
An 11-year-old girl with simple buphthalmos,
presented with an IOP of 60 mm Hg, advanced
cupping and a visual acuity of 6/60! She was
commenced on 3 hypotensive medications which
reduced the IOP to 30 mm Hg. Eleven weeks later
a double plate Molteno implant was inserted using
the vicryl tie technique and donor sclera. The
Fig. 7.44: Right eye of case 1 showing blebs over double plate
Molteno implant and donor sclera 9 years after insertion
94
B
Figs 7.48A and B: IOP curves of case 2 (A) right (b) left
95
Neovascular Glaucoma
It is possible to salvage useful vision in cases of acute
neovascular glaucoma by immediate reduction of IOP.
This involves the insertion of an implant with immediate
drainage of aqueous to reduce the IOP to normal levels
to clear the ocular media and restore circulation through
the diseased retinal vessels. The operation is followed by
urgent photocoagulation of the underlying retinal disease
combined with active treatment of the underlying vascular
and general disease states. In cases where a double plate
implant is used the connecting tube between the plates
is occluded by a 5.0 vicryl ligature.
Illustrative case of neovascular glaucoma: Case 4:
A 59-year-old male with type 2 diabetes treated by
diet and glibenclamide who had recently undergone
cataract extraction in both eyes, presented with an
elevated IOP in his right eye due to iris
neovascularization. This was treated by argon laser
photocoagulation and trabeculectomy. His left eye
was treated by argon laser photocoagulation at the
same time. Two months later his IOPs were 46 and
34 mm Hg respectively with iris new vessels
bilaterally. Both eyes were treated by insertion of
single plate Molteno implants with immediate
drainage of aqueous. The postoperative courses
were uneventful. The left visual acuity was 6/24.
He was prescribed oral prednisone, flufenamic acid
200 mg*** and colchicine for 6 weeks after
operation to reduce intraocular inflammation and
bleb fibrosis. These procedures were followed by
photocoagulation to the left eye. The IOP was well
***Flufenamic acid 200 mg tds is equivalent to diclofenac 50 mg tds
96
Fig. 7.52: Left eye of case 4 showing white quiet eye 6.5
years after insertion of implant
Illustrative case of uveitic glaucoma: Case 5: A 27year-old pregnant woman with Stills disease,
presented with an elevated IOP in her right aphakic
only eye. She had developed uveitis in both eyes at
5 years of age and had lost her left eye. Although
the uveitis was only minimally active her right eye
had been treated by three drainage operations, two
cataract extractions and one 180o cyclocryotherapy.
Preoperatively her IOP varied between 24 and 50
RESULTS
Primary Open Angle Glaucoma
The introduction of the delayed drainage technique for
inserting Molteno implants has led to their being used in
less severe cases of primary open angle glaucoma where
there are additional local and general risk factors. It is of
97
Fig. 7.55: Aphakic right eye of case 523 years after insertion
of double plate Molteno implant in a case uveitis associated
with juvenile rheumatoid arthritis
Fig. 7.57: Left eye of case 623 years after insertion of double
plate Molteno implant showing clear corneal graft and end of
tube visible at 11 oclock. This tube was inserted via the pars
plana
98
Secondary Glaucomas
In all groups the overall prognosis for control of IOP in
visually useful eyes is generally good with failure occurring
in terminal eyes, eyes that have undergone multiple
previous operations and cases of uveitis in which the
underlying disease cannot be controlled. The outcomes
of cases of buphthalmos, juvenile glaucoma, traumatic
glaucoma, uveitic glaucoma, secondary glaucoma
following previous intraocular surgery and neovascular
glaucoma treated by insertion of Molteno implants with
respect to IOP control and hypotensive medication use
are presented in Tables 7.3 and 7.4.
99
Table 7.1: Status of cases of primary open angle glaucoma treated by a trabeculectomy or Molteno implant at Dunedin
Hospital between 1986 and 2003 as of January 2004
Number
IOP control
(IOP = 5 - 21 mm Hg)
No medication
531
223
510
182
21
41
109
51
122
48
366 (69%)
153 (69%)
357 (70%)
135 (74%)
10 (48%)
20 (49%)
64 (59%)
39 (77%)
74 (61%)
34 (71%)
Fail
With medication
125 (24%)
70 (31%)
122 (24%)
47 (26%)
3 (14%)
21 (51%)
38 (35%)
12 (24%)
26 (21%)
(%)
40 (8%)
0
32 (6%)
0
8 (38%)
0
7 (6%)
0
22 (18%)
0
Table 7.2: Mean IOP and hypotensive medication use of cases of primary open angle glaucoma treated by trabeculectomy
or Molteno implant at Dunedin Hospital between 1986 and 2003
Number
Mean IOP (standard deviation) in mm Hg
Mean number of Hypotensive Medications
Preoperative
Trabeculectomy as first or subsequent operation*
Implant as first operation or following trabeculectomy*
Trabeculectomy as first operation
Implant as first operation
Trabeculectomy after trabeculectomy failure
Implant after failed trabeculectomy
Phacotrabeculectomy
Phaco/implant
Trabeculectomy and later cataract extraction
Implant and later cataract extraction
N=531
23.7 (6.6)
1.90
N=223
24.0 (6.5)
1.98
N=510
23.7 (6.5)
1.89
N= 182
23.9 (6.6)
1.96
N= 21
25.9 (8.7)
2.10
N= 41
24.6 (6.0)
2.07
N = 109
21.0 (6.0)
1.66
N= 51
21.7 (6.2)
1.87
N = 122
24.9 (5.6)
1.95
N = 48
23.8 (7.2)
1.75
Years postoperatively
1
10
15
N=445
15.0 (3.5)
0.23
N=182
14.4 (2.9)
0.59
N=431
15.0 (3.5)
0.21
N= 147
14.4 (2.8)
0.57
N=14
18.4 (4.7)
0.72
N= 35
14.7 (3.3)
0.73
N= 89
16.2 (3.2)
0.3
N= 47
14.0 (2.3)
0.51
N= 117
14.5 (3.7)
0.21
N= 46
14.8 (2.7)
0.48
N=377
15.0 (3.4)
0.29
N=160
14.2 (3.2)
0.54
N=365
15.0 (3.3)
0.27
N= 126
14.0 (2.8)
0.49
N=11
16.2 (5.4)
0.97
N= 34
14.8 (4.3)
0.72
N= 64
16.2 (3.6)
0.42
N= 38
13.5 (2.6)
0.48
N= 115
14.9 (3.8)
0.24
N= 43
14.6 (3.0)
0.39
N=224
14.9 (3.2)
0.42
N=87
14.2 (3.1)
0.48
N=216
14.8 (3.1)
0.38
N= 63
14.2 (2.9)
0.35
N= 9
16.7 (4.7)
1.22
N= 24
14.4 (3.7)
0.81
N= 28
15.2 (3.6)
0.57
N= 21
13.1 (2.9)
0.52
N= 86
15.3 (3.11)
0.43
N= 27
14.6 (3.6)
0.52
N=90
15.4 (4.2)
0.45
N=27
13.1 (3.3)
0.50
N=87
15.3 (4.3)
0.45
N=16
12.2 (2.5)
0.40
N= 5
15.7 (1.0)
0.80
N=11
14.3 (4.0)
0.66
N= 6
19.5 (7.0)
0.85
N=11
12.0 (2.3)
0.36
N= 47
14.8 (3.4)
0.30
N= 8
14.9 (4.6)
0.68
N=14
14.5 (4.1)
0.96
N=2
10.3 (0.4)
1.00
N=12
14.1 (4.3)
0.87
N=5
16.1 (2.4)
0.80
N=2
10.3 (0.4)
1.00
N=18
14.2 (3.2)
0.37
100
Table 7.3: Status of cases of buphthalmos, juvenile glaucoma, traumatic glaucoma, uveitic glaucoma, secondary glaucoma
and neovascular glaucoma treated by Molteno implant at Dunedin Hospital between 1977 and 2003 as of January 2004
Number
Buphthalmos
Juvenile glaucoma
Traumatic glaucoma
Uveitic glaucoma
Secondary glaucoma
Neovascular glaucoma
IOP control
(IOP = 5-21 mm Hg)
49
24
43
49
74
148
Fail
No medication
With medication
26 (53%)
9 (38%)
31 (72%)
33 (67%)
44 (60%)
40 (27%)
16 (33%)
11 (46%)
7 (16%)
11 (23%)
21 (28%)
39 (26%)
7 (14%)
4 (17%)
5 (12%)
5 (10%)
9 (12%)
69 (47%)
Table 7.4: Mean IOP and hypotensive medication use of cases of buphthalmos, juvenile glaucoma, traumatic glaucoma,
uveitic glaucoma, secondary glaucoma and neovascular glaucoma treated by Molteno implant at Dunedin Hospital between
1977 and 2003
Number
Mean IOP (standard deviation) in mm Hg
Mean number of Hypotensive Medications
Preoperative
Buphthalmos
Juvenile glaucoma
Traumatic glaucoma
Uveitic glaucoma
Secondary glaucoma
Neovascular glaucoma
N=49
32.9 (12.5)
1.67
N=24
27.8 (9.7)
2.00
N=43
32.7 (13.6)
1.86
N=49
31.4 (13.4)
1.87
N=74
31.2 (10.9)
2.02
N=148
40.0 (12.8)
1.30
Years postoperatively
1
10
15
20
N=43
15.0 (4.3)
0.40
N=20
17.1 (4.8)
0.81
N=35
15.9 (3.3)
0.44
N=43
15.9 (5.2)
0.58
N=65
16.4 (5.5)
0.68
N=100
19.6 (9.3)
0.77
N=42
15.2 (4.4)
0.38
N=19
17.1 (4.7)
0.58
N=34
15.4 (3.9)
0.31
N=39
15.5 (6.1)
0.46
N=60
15.9 (5.5)
0.53
N=75
19.1 (10.0)
0.72
N=36
15.5 (4.1)
0.39
N=18
16.3 (4.3)
0.77
N=29
15.5 (3.5)
0.36
N=29
14.8 (4.4)
0.52
N=37
17.4 (7.6)
0.65
N= 29
21.9 (11.0)
0.78
N=27
16.6 (3.5)
0.68
N=13
16.2 (2.6)
0.99
N=19
15.0 (4.4)
0.14
N=17
15.4 (4.6)
0.47
N=21
16.5 (4.1)
0.50
N=9
26.8 (10.7)
0.52
N=19
17.3 (3.7)
0.76
N=9
18.4 (8.8)
1.11
N=12
15.4 (3.8)
0.08
N=7
13.4 (5.5)
0.14
N=13
18.6 (6.9)
0.98
N=2
12.0 (5.7)
0.25
N=8
16.7 (3.0)
0.87
N=4
N=4
1.07
N=9
13.8 (4.4)
0.33
N=3
10.5 (4.9)
0.33
N=3
18.8 (13.3)
0.16
CONCLUSIONS
The current surgical techniques for inserting Molteno
implants provide very safe and highly effective ways of
preventing postoperative hypotony and reducing the IOP
to normal levels in most types of glaucoma. The only
groups in which results are uncertain are very advanced
cases that have undergone many previous operations,
cases of chronic uveitis that remain active despite
treatment and cases of neovascular glaucoma in which
the underlying vascular disease is not amenable to
treatment.
REFERENCES
1. Molteno ACB, Fucik M, Dempster AG, Bevin TH. Otago glaucoma
surgery outcome study. Factors controlling capsule fibrosis around
Molteno implants with histopathological correlation. Ophthalmology
2003;110:2196-2210.
2. Molteno ACB. New implant for drainage in glaucoma. Clinical
trial. Br J Ophthalmol 1969;53:606-15.
3. Molteno ACB, Dempster AG. Methods of controlling bleb fibrosis
around draining implants. In. Mills KB (Ed): Fourth International
Symposium of the Northern Eye Institute. Manchester: Pergammon
Press, 1988.
4. Vote B, Fuller JR, Bevin TH, Molteno ACB. Systemic antiinflammatory fibrosis suppression in threatened trabeculectomy
failure. Clin Exp Ophthalmol 2004;32:81-6.
5. Fuller JR, Bevin TH, Molteno ACB, et al. Anti-inflammatory fibrosis
suppression in threatened trabeculectomy bleb failure produces good
12.
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15.
16.
17.
101
102
8 Nonpenetrating Surgery
INTRODUCTION
In order to obtain a physiological per- and postoperative
IOP, the idea of nonpenetrating glaucoma surgery
(NPGS) was to create a reproducible postoperative
outflow resistance with the trabeculo-Descemets
membrane.
Several techniques of nonpenetrating filtering
surgeries based on the pioneer work of Krasnovs
sinusotomy have been described (Figs 8.1 and 8.2). In
primary and most cases of secondary open-angle
glaucoma, the main aqueous outflow resistance is thought
to be located at the level of the juxtacanalicular
trabeculum and the inner wall of Schlemms canal. These
two anatomical structures can be removed. This
technique has been called ab externo trabeculectomy. It
was first proposed by Delage in 1978, and later by
Zimmermann in 1984 and Arenas in 1991 (Fig. 8.3).
Another way to increase the aqueous outflow in a patient
with restricted posterior trabeculum outflow is to remove
the corneal stroma behind the anterior trabeculum and
Descemets membrane (Fig. 8.4). This has been called
deep sclerectomy and was first described by Fyodorov
and Kozlov and later by Stegmann (viscocanalostomy).
The most common techniques used today are deep
sclerectomy and viscocanalostomy. This chapter will
describe these two techniques.
DEEP SCLERECTOMY
In deep sclerectomy, the main aqueous outflow occurs
at the level of the anterior trabeculum and the Descemets
membrane (Fig. 8.4). This has been shown by Vaudaux
et al in an ex vivo model of deep sclerectomy (Vaudaux).
They have also reported that the outflow facility increased
from 0.19 0.03 to 24.5 12.6 l/min/mm Hg. To
VISCOCANALOSTOMY
The hypothetic mechanism of filtration in viscocanalostomy is different from those described in other nonpenetrating filtering surgeries. Stegmann thinks that the
aqueous humor filters trough the trabeculo-Descemets
membrane to the scleral space like in deep sclerectomy,
but that it does not form a subconjunctival filtering bleb
since the superficial scleral flap is tightly closed with
numerous nylon 10/0 sutures. From the scleral space,
the aqueous humor is supposed to reach the Schlemms
canal which is opened on either side of the deep
sclerectomy, and then flows into the aqueous episcleral
veins. Until now no scientific study has been able to
confirm this hypothesis, and in our hands, patients who
underwent viscocanalostomy presented in 50 percent
of the cases a subconjunctival filtering bleb. The long-
Nonpenetrating Surgery
103
104
Disadvantages
SURGICAL TECHNIQUE
When performing nonpenetrating glaucoma surgery the
surgeon looks at two aims: one to create the trabeculoDescemets membrane which will allow a reproducible
postoperative outflow resistance, thus decreasing the
immediate postoperative complication rate, and two, to
Nonpenetrating Surgery
105
106
Nonpenetrating Surgery
Fig. 8.12: In the anterior part of the scleral bed, the scleral
fibers are parralel to the limbus and represent the scleral spure.
This is an excellent landmark to find Schlemms canal which
is located just anterior to the scleral spure
107
108
Trabeculo-Descemets Perforation
In the learning phase of NPGS, the surgeon may
perforate quite often the thin membrane. It is important
when the iris prolapsed through the perforation, to
perform a peripheral iridectomy, followed by a tight
superficial scleral flap closure with 6 to 8 nylon 10/0
suture (Fig. 8.23) the scleral space should be filled with
high viscosity hyaluronic acid in order to reduce the
aqueous humor outflow (Fig. 8.24). When the anterior
chamber is shallow, viscoelastic may also be injected into
the anterior chamber through a paracentesis. This
Nonpenetrating Surgery
109
Fig. 8.23: Tight superficial scleral flap closure with 8 nylon 10/
0 sutures to increase the aqueous humor outflow resistance
POSTOPERATIVE MEDICATIONS
Patients are treated first with topical corticosteroid and
antibiotic for 2 to 3 weeks using 3 to 5 drops a day. This
110
BIBLIOGRAPHY
1. Ahmed II, Crandall AS. Viscocanalostomy vs trabeculetomy.
Ophthalmology 2002; 109(3):411-2.
2. Ambresin A, Borruat FX, Mermoud A. Recurrent transient visual
loss after deep sclerectomy. Arch Ophthalmol 2001;119(8):1213-5.
3. Ambresin A, Shaarawy T, Mermoud A. Deep sclerectomy with
collagen implant in one eye compared with trabeculectomy in the
other eye of the same patient. J Glaucoma 2002;11(3):214-20.
4. Arenas E. Trabeculectomy ab-externo. Highlights of Ophtalmology.
1991;19:59-66.
5. Argento C, Sanseau AC, Badoza D, Casiraghi J. Deep sclerectomy
with a collagen implant using the excimer laser. J Cataract Refract
Surg 2001; 27(4): 504-6.
6. Ates H, Andac K, Uretmen O. Non-penetrating deep sclerectomy
and collagen implant surgery in glaucoma patients with advanced
field loss. Int Ophthalmol 1999;23(3):123-8.
7. Ates H, Uretmen O, Andac K, et al. Deep sclerectomy with a
nonabsorbable implant (T-Flux): preliminary results. Can J
Ophthalmol 2003; 38(6):482-8.
8. Bauchiero L, Demarie A, Belli L, et al. Deep sclerectomy and
viscocanalostomy: critical revision of the results obtained during the
learning curve. Acta Ophthalmol Scand Suppl 2002;236:64-6.
9. Bylsma S. Nonpenetrating deep sclerectomy: collagen implant and
viscocanalostomy procedures. Int Ophthalmol Clin 1999
Summer;39(3):103-19.
10. Carassa RG, Bettin P, Fiori M, et al. Viscocanalostomy versus
trabeculectomy in white adults affected by open-angle glaucoma: a
2-year randomized, controlled trial. Ophthalmology.
2003;110(5):882-7.
11. Chiou AGY, Mermoud A, Hdiguer SEA, et al. Ultrasound
biomicroscopy of eyes undergoing deep sclerectomy with collagen
implant. Br J Ophthalmol 1997; 80:541-4.
12. Chiou AGY, Mermoud A, JP Underdahl, et al. An ultrasound
biomicroscopic study of eyes after deep sclerectomy with collagen
implant. Ophthalmology, 1998; 105:746-50.
13. Chiou AGY, Mermoud A, Jewelewicz D. Post-operative inflammation
following deep sclerectomy with collagen implant versus standard
trabeculectomy. Graefes Arch 1998; 236:539-96.
14. Chiou AGY, Mermoud A, Hdiguer SEA. Glaucome malin par blocage
ciliare aprs sclrectomie profondeImagerie par biomicroscopie
ultrasons. Klin Monatsbl Augenheikld 1996;208:279-81.
15. Chiselita D. Non-penetrating deep sclerectomy versus trabeculectomy
in primary open-angle glaucoma surgery. Eye. 2001;15 (Pt 2):197201.
16. Dahan E, Drusedau MU. Nonpenetrating filtration surgery for
glaucoma: control by surgery only. J Cataract Refract Surg 2000;
26(5):695-70
17. Dahan E, Ravinet E, Ben-Simon GJ, et al. Comparison of the
efficacy and longevity of nonpenetrating glaucoma surgery with and
without a new, nonabsorbable hydrophilic implant. Ophthalmic
Surg Lasers Imaging 2003;34(6):457-63.
18. Delarive T, Rossier A, Rossier S, et al. Aqueous dynamic and
histological findings after deep sclerectomy with collagen implant in
an animal model. Br J Ophthalmol 2003;87(11):1340-4.
Nonpenetrating Surgery
40.
41.
42.
43.
44.
45.
46.
47.
48.
49.
50.
51.
52.
53.
54.
55.
56.
57.
58.
59.
60.
61.
62.
63.
64.
65.
66.
67.
68.
69.
70.
71.
72.
73.
74.
75.
76.
77.
78.
79.
80.
111
112
INTRODUCTION
It was Krasnov, in 1966,1,2 who originally proposed the
removal of the external wall of the Schlemms canal and
coined the word sinusotomy for the procedure by which
he removed the external wall of Schlemms canal from
10 to 20 oclock over 120; the inner wall of Schlemms
canal was left untouched and then the conjunctiva was
closed. Alkseev, in 1978,3 proposed the removal of the
endothelium of the inner wall of Schlemms canal and
of the juxtacanalicular tissue in sinusotomy in order to
increase the permeability of the inner wall of the chamber
angle.
Zimmerman et al (1984)4 introduced nonpenetrating
trabeculectomy; Fyodorov et al (1984)5-6 proposed deep
sclerectomy and later, and together with Kozlov and
others (1989), nonpenetrating deep sclerectomy; Kozlov
et al (1990)7 perfected the method with the addition of
a cylindric collagen implant and later developed laser
goniopuncture, methods which were further developed
by Kozlov and Kozlova (1996)8 and by Kozlova (19962000).9-10 According to Kozlovs technique, in addition
to the resection of the external wall of Schlemms canal,
the inner wall of Schlemms canal with the endothelium,
together with the juxtacanalicular tissue and external
corneoscleral trabecular meshwork are removed. In
(1991), Arenas Archila11 proposed trabeculotomy ab
externo, by which the same tissues were removed, after
removal of the external wall of Schlemms canal, but
using a microtrephine working at a speed of 800 rpm.
In 1999 Stegman 12 reported his results with viscocanalostomy in black African patients. Sourdille et al.
(1999)13 used a triangular reticulated hyaluronic acid
implant of the same size as that of the second triangular
CONTRAINDICATION
The NPDS is contraindicated in narrow-angle or angleclosure glaucoma, congenital glaucoma and late
congenital glaucoma when the mesodermal remnants
reach Schwalbes line.
113
114
Fig. 9.1: Optic nerve fiber defect at the inferotemporal quadrant with rim notch. Visual field: normal according to SAP and Bebie
curve while Frequency Doubling Technology reveals a visual field defect topographically correlated with optic nerve and fiber
layer defects. It is not a hypertension, it is really a glaucoma. The intraocular pressure fails to be regulated with maximum therapy.
We indicated NPDS
Fig. 9.2: Damage at the inferotemporal quadrant of the optic nerve (rim volume: 0.14 mm3: phase IV). For conventional perimetry
(SAP), the visual field is normal. FDT: Visual field defect correlated topographically with the optic nerve damage. Since it is not
hypertension but a glaucoma in which the IOP is not regulated with maximum therapy, the indication is NPDS.
115
Fig . 9.3: Advanced optic nerve damage with a rim volume of 0.17 mm3 (phase IV). Moorfield regression analysis shows a
marked optic nerve damage at the superotemporal quadrant (in red) and a smaller defect at the temporal, inferotemporal,
superonasal and nasal quadrants (in yellow). SAP: normal, FDT: visual field defect correlated topographically with the damage
of the optic nerve. Brusinis GSS for SAP (bottom) and normal visual field on the left. On the right, FDT revealed that the visual
field is in stage 1. Intraocular pressure was not regulated with maximum therapy and NPDS was therefore indicated.
COMPLICATIONS OF SURGERY
Triangular Flap Dissected too Superficially
The dissection of the triangular flap is not deep enough
for the resection of the external wall of the Schlemms
canal. The graphic at the center of the figure shows the
key element for the surgeon to find the Schlemms canal.
The most posterior darker blue sector (between 3 and 4
of the blue area) indicates the location of the Schlemms
canal (Fig. 9.13).
The external wall of Schlemms canal must be
dissected with a cutting round spatula specially designed
for this purpose by Grieshaber (Fig. 9.14). This dissection
can be made with direct illumination or under
transillumination (Fig. 9.15A and B).
For the finding of the Schlemms canal it is very
important to view the surgical area with direct
illumination and with transillumination (Minskys
116
Fig. 9.4: Resistance on the conventional outflow pathway, which was removed by trabeculectomy (vertical red line). With NPDS
(vertical green line) we removed the external wall of Schlemms canal with collectors upon removing the triangular flap.
Removal of the internal tissues includes: internal wall of Schlemms canal, the juxtacanalicular tissue, the external part of the
corneoscleral trabecular meshwork. The internal part of the corneoscleral trabecular meshwork and the uveal trabecular
meshwork, which, together with Descemets membrane form the trabeculo-Descemets membrane, remain unmoved.
117
Fig. 9.6: In NPDS, the external wall of the Schlemms canal is removed with the second triangular scleral flap and with
Mermouds forceps, a membrane made up by the inner wall of the Schlemms canal, the juxtacanalicular tissue and the external
part of the corneoscleral trabecular meshwork are also removed. The tissues which are left in their place are: trabeculoDescemets membrane, made up by the internal part of the corneoscleral meshwork and the uveal meshwork. As stated by Dr
Mermoud, this membrane is strong enough to support the anterior chamber and also permeable enough to improve aqueous
humor outflow with the consequent intraocular pressure reduction.
118
Fig. 9.9: Removal of the second triangular scleral flap (Left), on which the external wall of Schlemms canal, identified by its
hazel- or brown-colored granulous appearance, can be seen. Center and right: Correlation of this photograph with the landmarks
119
Fig. 9.11: Dissection of the inner wall of Schlemms canal with its endothelium, juxtacanalicular tissue and the external corneoscleral
trabecular meshwork (Left). Schematic representation of the tissue removed and of its previous locations (Center), where only
the internal corneoscleral trabecular meshwork and the uveal trabecular meshwork, which, together with Descemets membrane
form the trabeculo-Descemets membrane, are left (Bottom-right).
120
Fig. 9.13: Image visualized if the dissection has failed to be done at the correct plane and it is not deep enough for the resection
of the external wall of the Schlemms canal by means of the triangular flap. All three areas are visible but the open Schlemms
canal is not (Left). The schematic representation at the center shows the key element for the surgeon to find the Schlemms
canal: the most posterior darker blue sector (between 3 and 4) of the blue area corresponds to the Schlemms canal
121
Figs 9.15A and B: Dissection of the external wall of the Schlemms canal (A) under direct illumination and (B) under
transillumination, done with an instrument specially designed for this purpose by Grieshaber
Figs 9.16A and B: Minskys maneuver (see text). In (A) under direct illumination of the Schlemms canal area, the location of
the Schlemms canal cannot be seen, which under transillumination (B) this can be seen very clearly (white arrows)
NPDS PEARLS
The goal of step number 1 (unroofing of the Schlemms
canal) is to remove the external wall in order to achieve
a good exposure of the canal. This step is perfectly shown
in Figure 9.20.
The second critical step is number 2, in which the
surgeon removes the external elements with Mermouds
LEARNING CURVE
See Figures 9.22A to H and 9.23A to C.
122
Figs 9.17A to C: The dissection of the external wall of the same case is shown in A, B and C. The external wall of Schlemms
canal is completely removed
A
B
C
Figs 9.18A to C: In this case when the surgeon tried to remove part of the second flap, the iris prolapsed because a perforation
of the internal wall had taken place (A, B and C). When this happens, the surgical procedure must invariably be turned into a
trabeculectomy
123
Figs 9.19A to C: The triangle flap whit the external wall of Schlemms canal
and the internal wall in place
124
Figs 9.21A to C: The second critical step is number 2. It is necessary to remove the internal elements, internal wall of Schlemms
canal, juxtacanalicular tissue and external part of the corneoscleral trabecular meshwork in order to regulate the intraocular
pressure. It should be kept in mind that between the internal and external part of the corneoscleral trabecular meshwork there
is a natural cleavage pane
Follow-up
All patients were examined at six-month intervals:
1. With a single IOP spot check.
2. With a diurnal curve. The IOP was measured at 6
am, 9 am, noon, 3 pm, 6 pm and 9 pm always
with applanation tonometry: at 6 am with the
patient in bed using a hand applanation tonometer,
125
Figs 9.22A to H: Step of the surgery when the triangle flap is remove and UBM of the same cases a different stage of the learning
curve, in the first 100 eyes, made in one year, in the first 3 months (A, B), at the 6 months (C, D) at the 9 months (E, F) and at 1
year (G, H).
126
127
Figs 9.25A and B: (A) chamber angle before NPDS; (B) chamber angle after NPDS. The chamber angle studied
with an optical cut made by the slit lamp, shows that after NPDS that half of the Schwalbes line and scleral spur
where removed, and the optical cut between this two element is concave because this is the place of the scleral
lake filled with humor aqueous
Fig. 9.26: Nd: Yag laser goniopuncture: at the left the right place to performed goniopuncture:
at the Schwalbes line, at the posterior corneal surface and in the trabecular meshwork. At
the right there is a goniophotograph showing Schwalbes line, the scleral spur and blood
coming of the Schlemms canal, after goniopuncture
128
Figs 9.27A to C: (A) Microperforation during surgery, (B) Ocular hypertension due to dyscoria, (C) Iris incarceration
129
Figs 9.29A and B: (A) Ultrasound biomicroscopy showing, from left to right: conjunctival tissue whit
aqueous humor, separating it from the cuadrangular scleral flap and two parallel lines behind it
corresponding to the implant, where the nylon suture securing it can be seen. The implant is
surrounded by aqueous humor and the scleral lake is seen behind it. (B) The intraescleral lake and
the trabeculo-Descemets membrane, 8 months later. The implant is reabsorbed
REFERENCES
1. Krasnov MM. Glaucoma surgery in the region of the outer and inner
wall of Schlemms canal. In Proceedings of the III Congress of
130
2.
3.
4.
5.
6.
7.
8.
9.
H Roux, T Shaarawy
10 Deep Sclerectomy
INTRODUCTION
SURGICAL STEPS
132
133
C
Figs 10.4A to C: A further 4 by 4 scratch incision is done in order to fashion a deeper flap using a diamond blade or a No. 11
stainless steel blade. The incision commences close to the cornea, and should be started superficially and gradually increasing
the depth as the incision is extended towards the margins of the superficial dissection
Fig. 10.5: Starting to dissect the deep flap, it is always important to expose the choroid. Exposing the choroid gives a clear
indication on the dissection depth. Choroid exposition should be done in one of the two posterior corners of the deep flap (rightsided, with a right-handed surgeon), and as mentioned before, is done only to comprehend the dissection depth. As soon as the
choroid is exposed, dissection should be started anteriorly a few microns superficial to the choroid. Blind dissection without
observing the choroids, often enough, results in superficial dissection, missing Schlemms canal and subsequent failure
134
Figs 10.6A and B: Dissecting the deep flap entails at all times, the proper stretching of the grasped scleral tissue. In this way a
clear line of dissection is obvious.
Dissecting at this line allows for same level of dissection, going above the line will superficialise the plane of dissection, and
going below the line will, obviously, deepen the plan
Figs 10.7A and B: Continuing on the same plane after observing the choroid, will result in the opening of Schlemms canal,
dividing it into two parts; a superficial part within the dissected deep flap, and a deeper part (floor) in the dissection bed
135
Figs 10.9A and B: Further lateral dissection on both sides with a diamond knife or preferably with a No. 11 steel blade will offer
an extension of the dissection into clear cornea. The blade should be bevel up and angled laterally to avoid perforation. This is
probably the most sensitive part of dissection and assuring the up and lateral direction of the blades bevel is probably the safest
method to dissect. Dissection should be done in as a dry field as possible and under high magnification
136
10.12
10.13
Figs 10.12 and 10.13: The inner wall of the Schlemms canal and the Juxtacanalicular trabeculum is peeled off using fine
forceps. One option is the use of the Mermoud forceps (Hucovision, AG), or fine tying forceps. It is a fact that major obstruction
to aqueous outflow is, in primary and secondary open angle glaucoma, the inner wall of Schlemms canal and the juxtacanalicular
trabeculeum, and proper peeling off this portion is key to success
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Figs 10.14A and B: An implant inserted in the scleral dissection seems to act as a space occupier; bridging the period of
maximal wound healing activity, and is associated, in randomised controlled trials, with improvement in success rates
138
Management
The two factors that determine the management of a
TDM perforation are the depth of the anterior chamber,
as well as the presence of an iris prolapse.
Small holes with no iris prolapse or loss of AC depth
could be ignored and the surgery continued normally.
Small or large perforations with shallow or flat AC and
no iris prolapse should be dealt with in order to prevent
subsequent iris prolapse or peripheral anterior synechia
formations. Viscoelastic material should be injected,
through a paracentesis, into the AC under the TDM
window to reposition the iris. The smallest possible
amount of viscoelastic material should be used to avoid
a postoperative ocular pressure spike. In addition, an
implant resting on the perforation site may be used to
tamponade the hole. The superficial scleral flap should
also be tightly sutured with 6 to 8 10/0 nylon sutures.
Iris prolapse accompanying a long tear or a large
hole calls for a peripheral iridectomy, the superficial flap
should be tightly closed and viscoelastic material injected
in the surgically created scleral space to increase the
outflow resistance.
Any perforation of the TDM during deep sclerectomy
transforms a non-penetrating filtering surgery into a
penetrating one. Because the scleral space left after deep
sclerectomy decreases the aqueous-humor outflow
resistance, a very tight superficial scleral-flap closure is then
of great importance. This operation can be compared to
a trabeculectomy with an additional deep sclerectomy.
Results of NPGS
Prospective non-randomized trials of deep sclerectomy
and viscocanalostomy provide sufficient evidence that
the procedure can reduce IOP to acceptable levels.
Randomized controlled trials comparing NPGS to
trabeculectomy are at a consensus on the superior safety
profile of NPGS. On efficacy there are controversial
reports. This disparity in results can be attributed to a
number of factors; namely the fundamental differences
between various NPGS techniques, the long-learning
curves, and the use of gniopunctures to achieve target
IOPs. However, one should keep in mind, when browsing
through results that it is all about technique. Issues related
139
FURTHER READING
1. Mermoud A, Schnyder CC, Sickenberg M, et al. Comparison of
deep sclerectomy with collagen implant and trabeculectomy in openangle glaucoma. J Cataract Refract Surg 1999;25:323-31.
2. Mermoud A. Sinusotomy and deep sclerectomy. Eye 2000;14:
531-5.
3. Shaarawy T, Karlen M, Schnyder C, Achache F, Sanchez E, Mermoud
A. Five-year results of deep sclerectomy with collagen implant. J
Cataract Refract Surg 2001;27:1770-8.
4. Shaarawy T, Mermoud A. Deep sclerectomy in one eye vs deep
sclerectomy with collagen implant in the contralateral eye of the
same patient: long-term follow-up. Eye 2005;19(3):298-302.
5. Shaarawy T, Mansouri K, Schnyder C, Ravinet E, Achache F,
Mermoud A.Long-term results of deep sclerectomy with collagen
implant. J Cataract Refract Surg 2004;30(6):1225-31.
6. Shaarawy T, Flammer J, Smits G, Mermoud A. Low first postoperative
day intraocular pressure as a positive prognostic indicator in deep
sclerectomy. Br J Ophthalmol 2004;88(5):658-61.
140
INTRODUCTION
To control the intraocular pressure safely by a surgical
procedure is the philosophers stone of glaucoma. Cairns
trabeculectomy 1 has been associated with a high
incidence of immediate postoperative complications
linked to the opening of the anterior chamber. The new
techniques of nonpenetrating glaucoma surgery
(NPGS), such as deep sclerectomy2 and viscocanalostomy 3 were developed in order to prevent those
problems and have recently gained popularity as a safe
and efficient alternative to conventional penetrating
glaucoma surgery. There is unanimous agreement that
in NPGS postoperative rehabilitation is faster and is not
considered to require the same precautions as following
trabeculectomy.
Nevertheless, the first postoperative weeks are crucial
for the success of NPGS. Experience has shown that
appropriate postoperative management (especially within
the first 2 weeks) can have the same magnitude of
influence on surgical outcome as surgery itself.
POSTOPERATIVE MEDICATION
Routine medications used in the immediate
postoperative period (first 2 to 3 weeks) include a topical
regimen of corticosteriods and antibiotics.
Corticosteroids are used to inhibit postoperative
inflammation in the anterior segment by reducing the
rate of conjunctival epithelialization and angiogenesis. It
has been shown that these agents significantly improve
the outcome of filtering surgery. 4 The effect of steroids is
dose-dependent and greatest in the first three days after
surgery.
Prednisolone acetate 1.0 percent is administered
beginning on the first postoperative day. Drops are given
every 4 hours during waking hours for at least two weeks
and then generally tapered over the next 2 to 4 weeks.
If used longer, they may lead to a steroid-induced IOP
rise.
A broad-spectrum antibiotic (e.g. fluochinolone) is
recommended as a prophylaxis for postoperative bleb
infection and endophthalmitis.5 We prescribe antibiotics
for 1 to 3 weeks. There is, however, no consensus among
surgeons for the ideal duration of their use.
Several studies have shown the beneficiary effect of
non-steroidal anti-inflammatory drugs (NSAIDs) such as
indomethacin and diclofenac on postoperative
inflammation and pain. 6,7 In recent years, new
combinations of antibiotics/NSAID have entered the
market that facilitate the surgeons treatment regimen.
Management
Failed-filtering blebs should be treated with needling
procedures with or without adjunctive antimetabolite
injection. The needling revision attempts to create an
opening in the thickened wall of a bleb or to elevate the
scleral flap in order to re-establish filtration.
Under the slit lamp, after a 30-gauge needle is
introduced beneath the conjunctiva, the conjunctiva is
ballooned at the site with the injection of a topical
anesthetic. The tip of the needle is then moved into the
fibrous cyst and several tears are made in the capsule. It
could also be moved in sweeping motion to mechanically
separate adhesions at the edges of the flap. Tonometry
and Seidel testing should be done 15 minutes after this
procedure. The procedure can also be performed in the
operating room to ensure a safer environment. Reported
success rates vary between 68 to 93 percent. 9-11
Complications of needle revision are conjunctival
hemorrhage, transient wound leak, hyphema, choroidal
effusion, and hypotony. In general they are minor and
resolve without sequelae.
141
Nd:YAG Goniopuncture
When percolation of aqueous humor through the
trabeculo-Descemets membrane (TDM) is considered
to be insufficient, a goniopuncture can be performed in
the membrane using a neodymium:yttrium-aluminium
(Figs 11.3 and 11.4) garnet laser shortly after surgery. 12
A lack of surgical dissection can be the reason for a
mounting IOP in the first postoperative period. If
goniopuncture is required later than approximately 9
months after surgery, it may be due to fibrosis of the
TDM. It may be needed in up to 51 percent of
nonpenetrating procedures over a period of eight years
and is successful in lowering postoperative IOP in 80
percent of cases as reported by Shaarawy and coworkers. 13
Complications associated with goniopuncture are rare.
Mermoud et al have reported two cases of choroidal
detachment. There is one reported case of peripheral
iris synechiae to the TDM.14 More recently, Vuori15
reported three cases of spontaneous iris prolapse in her
series of 31 patients. The extent of IOP increase after iris
prolapse (39 mm Hg, 59 mm Hg, and 71 mm Hg in the
3 cases) required surgical intervention, which transformed
the procedure to a trabeculectomy. These reports show
that there are potentially sight-threatening complications
to Nd:YAG goniopuncture.
Gonioponcture with the Nd:YAG laser should be
considered as an useful adjunctive procedure that
converts a nonpenetrating procedure into a microperforating one and can sometimes by the key to successful
surgery.
Antimetabolites
The goal of glaucoma filtering surgery is to maintain an
intrascleral fistula by reducing the wound-healing process
and thereby to keep the IOP in the low teens.
One of the most frequent causes of failure of NPGS is
fibrosis of the conjunctiva and episclera associated with
bleb fibrosis. The use of topical antifibrotic agents such as
Mitomycin-C (MMC) and 5-fluorouracil (5-FU) for wound
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Mitomycin-C
The MMC is an antibiotic that is isolated from
Streptomyces caespitosus. It has antineoplastic and
cytotoxic properties which have made it popular for
patients with a high risk of filtration failure. MMC has
been shown to be more potent than 5-FU in inhibiting
fibroblast synthesis and proliferation. 16 Several studies
have demonstrated that the use of intraoperative MMC
significantly reduces the postoperative IOP and increases
the success rate of deep sclerectomy. 17,18 It is the single
most important parameter for obtaining desired bleb
morphology.
An MMC is usually applied intraoperatively on a
cellulose sponge to the episclera or the conjunctiva.
Concentrations range from 0.2 to 0.5 mg/ml, for 2 to 5
minutes (some surgeons prefer shorter application times
for patients with thinner structures). Mitomycin-C can
also be administered in the framework of a postoperative
needling revision for failing blebs.
Adverse side effects of MMC use are the toxicity to
corneal endothelium and blood vessels. MMC-associated
blebs have a cystic and avascular aspect. The thin wall
can lead to wound leaks (positive Seidel test). It might
also increase the risk of scleral ectasia and iris prolapse
and should be used cautiously.
5-Fluorouracil
5-FU is a fluorinated pyrimidine antagonist that selectively
inhibits the fibroblast cell cycle, thereby decreasing
fibroblast proliferation. It was the first antimetabolite that
was used by glaucoma surgeons. It reduces scar formation
at the surgical site by reducing the proliferation of Tenons
capsule fibroblasts. Intraoperative application has been
shown to reduce postoperative IOP and the need for
postoperative glaucoma medication. 19,20
143
Ocular Hypertension
Hypotony
Bleb Leak
Conjunctival bleb leaks can occur early after surgery and
are the most frequent cause of a flat anterior chamber.
We regularly perform a Seidel test during the early
postoperative period.24 However, wound leaks can also
occur with normal IOP. For this reason, routine Seidel
testing should be performed during the weeks following
surgery, especially for eyes which received antimetabolites
and for blebs with a thin, avascular appearance. Late
spontaneous bleb leaks in-patients with severe coughing
have been reported in trabeculectomy cases. 25 Although
no such case has been described in NPGS, surgeons
should be aware of these potential in-patients with chronic
obstructive pulmonary disease.
144
Hyphema
Hyphema is a complication with a low incidence after
NPGS. 21,27 Anterior chamber bleeding usually originates
from a rupture of small iris vessels, ciliary processes, or
from leakage of red blood cells through the TDM.
Management: In case of levelled hyphema no particular
treatment (i.e. surgical washout) is required since the
AC usually clears itself from present erythrocytes.
Inflammation
The low incidence of inflammation is one major
advantage of nonpenetrating over penetrating filtering
surgeries. The very nature of NPGS being an
extraocular intervention without the need for an
iridectomy explains why anterior chamber inflammation
is mild in the initial postoperative phase and practically
non-existent thereafter. 28
We have observed a higher rate of inflammation inpatients with more complicated diagnosis (pseudoexfoliative, pigmentary, and uveitic glaucoma). There also
seems to be a tendency for increased rates of inflammation in combined phacoemulsification-deep
sclerectomy procedures.29
Management: Topical steroids are given over a six week
period.
Choroidal Detachment
When fluid accumulates between sclera and choroid, an
elevation of the choroids resulting in choroidal
detachment occurs. This complication is often observed
Suprachoroidal Hemorrhage
It is a serious but fortunately extremely rare complication
that can lead to permanent loss of vision. There is one
published report in the literature of this complication
occurring after deep sclerectomy.35 In this case, the
suprachoroidal hemorrhage resolved spontaneously by
three weeks. Hemorrhage into the suprachoroidal space
can occur during surgery or in the immediate postoperative period, but generally within the first 48 hours.
The patient experiences severe, uncontrollable pain, loss
of vision and a high IOP. Prolonged hypotony has been
clearly identified as the main risk factor in trabeculectomy
eyes. 36 Another risk factor is aphakia. Since visualization
is normally poor, echography can be useful to detect a
hemorrhage.
TDM Rupture
The thin remaining trabeculo-Descemets membrane can
rupture at any point of time after surgery. Patients should
be warned not to rub their eyes too vigorously and to
avoid Valsalva maneuvers. But the risk of this
complication, normally decreases with time due to
increasing post-membrane outflow resistance. Clinically,
often an accompanying iris prolapse with a decentralized
pupil and darkening of the subconjunctival space can
be seen.
Management: No treatment is needed when IOP remains
stable. If, however, the concomitant iris prolapse impedes
145
Cataract Formation
Surgery-induced cataract is a common complication of
trabeculectomy, 40 whereas nonpenetrating glaucoma
surgery is associated with very low incidence of cataract.
Aside from the vision impairing effect of cataract
development, cataract extraction in a previously
operated eye may be accompanied by a surgically
induced malfunction of the filtering bleb. 41
Malignant Glaucoma
Malignant glaucoma was first described by von Graefe42
as a form of postoperative glaucoma that often led to
blindness. It is usually characterized by a shallow anterior
chamber and an increase in IOP. Predisposing factors
resulting in malignant glaucoma are (intra)ocular surgery
(e.g. trabeculectomy and cataract surgery) and anterior
segment laser procedures. Due to the property of NPGS
being extraocular, this complication is quite infrequent.
Chiou and co-workers43 reported one case with narrowangle glaucoma who developed malignant glaucoma after
deep sclerectomy.
146
Bleb Fibrosis
A frequent cause of an increasing IOP is bleb failure due
to conjunctival or episcleral fibrosis which is slightly more
frequent after NPGS than after trabeculecomy . Signs of
an early bleb fibrosis are an in elevated IOP, diffuse
conjunctival injection, and the presence of large vessels.
Predisposing factors are inflammation in the anterior
chamber and subconjunctival hemorrhage.
Management: If despite the presence of a fibrotic bleb
IOP remains normal, no treatment is needed. In case of
increasing IOP, subconjunctival injections of an
antimetabolite are required to stop the scarring process.
Cataract Progression
It was reported that cataract progression is not influenced
by deep sclerectomy contrary to trabeculectomy.45 This
lack of progression is probably due to the absence of
postoperative hypotony and the integrity of the anterior
chamber and the globe as a whole.
Shaarawy and co-workers46 followed 104 patients for
up to 48 months and showed progression of existing
senile cataract in 21 percent of eyes.
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147
Scleral Ectasia
Fig. 11.2: Anterior peripheral synechiae on TDM
148
REFERENCES
1. Cairns JE. Trabeculectomy. Preliminary report of a new method.
Am J Ophthalmol. 1968;66(4):673-9.
2. Kozlov VI, et al. Nonpenetrating deep sclerectomy with collagen.
Ophthal Surg 1990;3:44-6.
3. Stegmann R, Pienaar A, Miller D. Viscocanalostomy for open-angle
glaucoma in black African patients. J Cataract Refract Surg.
1999;25(3):316-22.
4. Roth SM, Spaeth GL, Starita RJ, et al. The effects of postoperative
corticosteroids on trabeculectomy and the clinical course of glaucoma:
five-year follow-up study. Ophthalmic Surg 1991;22:724-9.
5. Sunaric-Mgevand G, Pournaras CJ. Current approach to
postoperative endophthalmitis. Br J Ophthalmol 1997;81:1006-15.
39.
40.
41.
42.
43.
44.
45.
46.
47.
48.
149
150
12 Trabeculotomy Ab Externo
INTRODUCTION
Trabeculotomy is receiving increased interest as a
glaucoma procedure not only in developmental, but also
in adult-onset open-angle glaucoma. Together with
goniotomy, it occupies the forefront in the management
of developmental glaucoma. Except for cases with
anterior segment dysgenesis, trabeculotomy has the
advantages of being possible to perform in virtually all
cases, regardless the presence or absence of corneal
opacity. There is less need for repeated surgeries. Recent
reports have reported success even in conditions it was
thought previously unsuccessful as aniridia and SturgeWeber associated glaucoma.1,2 In recent years, it has been
increasingly performed in adult POAG cases3 with good
results and less complications as compared with
trabeculectomy. It has been also reported in many series
of combined phacotrabeculotomy, with good results.4-6
In these eyes, it is associated, not only with a high success
rate, but also with much fewer complications as
compared with phacotrabeculectomy.
The idea was first introduced in the late sixties and
early seventies,7,8 and is simply to approach the canal of
Schlemm from outside the eye (ab externo), introduce
specially designed probes into them, rotating these into
the anterior chamber. In doing so the inner wall of the
canal, the trabeculum, usually offering the most resistance
to aqueous outflow, and any associated developmental
anomaly, are severed. In eyes with no previous surgical
intervention, it is possible to probe the canal of Schlemm
along the full length of the trabeculotome in virtually all
cases. The often acclaimed branching canal is not met
Trabeculotomy Ab Externo
151
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152
Figs 12.4A and B: Diagrammatic representation of the layout of surgery: Surgery is usually carried out at the 12 oclock position,
unless this site is jeopardized by previous surgery, in which case a lateral (or even inferior) approach can be used. Trabeculotomy
probes are introduced into both sides of the cut ends of Schlemms canal. Both probes should be introduced before rotating the
first probe to reduce the difficulty of inserting the second probe in a collapsed canal
Figs 12.4C and D: Probes are then rotated, one after another into the anterior chamber. In doing so, the trabecular meshwork
is cut along the length of the probes connecting the Schlemms canal directly to the anterior chamber
Trabeculotomy Ab Externo
153
154
Fig. 12.9: The radial incision is very gradually deepened, extending anteriorly or posteriorly if the need arises, till the canal is
reached. Opening of the canal is recognized by one or more of the following:
Gentle egress of aqueous; a gush or an efflux of aqueous denotes opening the anterior chamber rather than the canal
Direct (dry) visualization of the canal; most commonly in stretched out buphthalmic eyes. This is usually associated afterwards
by the exudation of aqueous
Rarely; in congested eyes, egress of blood from the canal site can be the main sign of its opening
Trabeculotomy Ab Externo
155
Fig. 12.13: The lip of the radial incision is held by the nondominant hand, while the trabeculotomy probe is held by the
dominant hand and gently directed towards the cut end of the
canal.
Fig. 12.14: The probe is gently introduced into the canal; the lip
of the incision is released. Depending on the depth of dissected
scleral flap, the internal probe can usually be visualized in its
tight path in the canal (arrows). The external probe is always
there to assess the conformity of the trabeculotome to the limbic
circumference, and that it has not gone astray. A correctly places
trabeculotome only moves along its axis. If correctly placed, it
should not rotate. It is a blunt pin in a conforming tube!
156
Fig. 12.16
Figs 12.16 and 12.17: The same is repeated with the second
probe
Fig. 12.19: The two probes nicely in place; the outer probes
are parallel to the limbus. They are not freely mobile either
anteriorly into the AC, or posteriorly into the supraciliary space
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Trabeculotomy Ab Externo
157
Fig. 12.21: The outer probe betrays a faulty insertion into the
supraciliary space; the trabeculotome is freely mobile
anteroposteriorly. This has to be removed completely, and
reinserted carefully (temporal secondary trabeculotomy in an
eye with previous trabeculectomy at 12 oclock position)
158
Fig. 12.25
Fig. 12.26
Figs 12.25 and 12.26: The trabecular meshwork to be cut during trabeculotomy is a soft structure. Cutting it does not involve any
force. On rotating the trabeculotome into the AC, the tip makes the first cut, and appearance in the AC (arrows), then follows the
rest of the internal probe (inset). This tactile lag between appearance of only the tip first, with no limbal or corneal distortion, and
then the rest of the probe (Khalils sign), is an important sign of success. The need for force, with corneal or limbal distortion
(Fig.12.8) simply means that the trabeculotome is not properly placed. On the other hand, if rotation meets no resistance at all,
with simultaneous appearance of the whole length of the internal probe in the AC means that it was lodged in the anterior
chamber angle rather than in the canal
Fig. 12.27: After rotating of the full length of the probe into the
AC, the probe is gently withdrawn, paying care not to touch the
iris-lens. This is especially important with the second probe
when the anterior chamber gets shallower
Trabeculotomy Ab Externo
159
Fig. 12.29
Fig. 12.30
Figs 12.29 and 12.30: Hyphema on rotating the trabeculotome is not uncommon. It is usually self-limited, and absorbed by the
second postoperative day. Injection of air into the AC helps control a more active bleeding
Fig. 12.32
Fig. 12.33
Figs 12.32 and 12.33: The conjunctiva is then closed by running 8/0 vicryl
160
Fig. 12.34
Fig. 12.35
Figs 12.34 and 12.35 (optional addition): In the rare event of inability to locate the canal, the procedure can be easily
converted to a trabeculectomy.
REFERENCES
1. Adachi M, Dickens CJ, Hetherington J Jr et al. Clinical experience
of trabeculotomy for the surgical treatment of aniridic glaucoma.
Ophthalmology 1997;104(12):2121-5.
2. Irkec M, Kiratli H, Bilgic S. Results of trabeculotomy and guarded
filtration procedure for glaucoma associated with Sturge-Weber
syndrome. Eur J Ophthalmol 1999;9(2):99-102.
3. Chihara E, Nishida A, Kodo M et al. Trabeculotomy ab externo: An
alternative treatment in adult patients with primary open-angle
glaucoma. Ophthalmic Surg 1993;24(11):735-9.
4. Gimbel HV, Meyer D. Small incision trabeculotomy combined with
phacoemulsification and intraocular lens implantation. J Cataract
Refract Surg 1993;19(1):92-6.
INTRODUCTION
Laser Trabeculoplasty (LTP)
The first pilot study using laser energy on the trabecular
meshwork (TM) to reduce intraocular pressure was
described by Wise and Witter in 1979.1 Many articles
have since been published on the evidence base of the
clinical effectiveness of laser trabeculoplasty using argon
lasers, Dye lasers and Diode lasers. The laser wavelengths
used in the majority have been those provided by the
continuous wave argon lasers traculoplasty (ALT), with
wavelengths between 450 nm (blue) and 520 nm
(green), and with a spot size of 50 m at a pulse duration
of 200 msec, producing powers between 700 and 1000
mW titrated by expected visible reaction on the TM. This
energy absorption at TM produced thermal coagulation
effects detectable by most histopathology techniques.
Clinically this energy absorption produced a drop in
intraocular pressure in approximately 90 percent of
patients treated through 360o (first year, with decreasing
efficiency of 5 to 10% per year)2 and inflammatory
changes sufficient to induce peripheral anterior synechiae
and trabecular scarring. The mechanism of action of LTP/
ALT has been unknown to date with scientific speculation
indicating the likely mechanisms being either mechanical,
by postcoagulative collagenous contracture stretching the
TM open, or ultra-structural, by TM endothelial renewal
following laser induced TM endothelial loss. Later in
vitro studies have confirmed coagulative damage at the
edge and base of ALT craters as well as disruption of
collagen beams, associated fibrinous exudates, lysis of
endothelial cells, and nuclear and cytoplasmic debris.3
In view of the great potential benefit of this form of
treatment, in terms of effectivity, compliance and quality
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162
SLT LASER
Lumenis (Coherent) has designed a laser that provides
the necessary energy. The first of these lasers is the Selecta
7000 pictured in Figure 13.2.
Fig. 13.2: The Selecta 7000 SLT Laser. The first produced by
Lumenis (Coherent)
163
Fig. 13.4
Fig. 13.6: Melanin laden pigmented TM endothelial cells
164
EFFECTIVITY OF SLT
165
166
DELIVERY OF SLT
The SLT on all studies has demonstrated ease of delivery,
minimal discomfort for the patient during delivery of
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COMPLICATIONS OF SLT
168
SUMMARY
Selective Laser Trabeculoplasty is a safe and effective
procedure for the treatment of POAG, OHT, and some
of the secondary open-angle glaucomas such as
pigmentary and pseudoexfoliative glaucoma. The
treatment can be applied as both a secondary treatment
profile following poor control on MTMT and as a primary
treatment on the diagnosis of the onset or potential onset
of a glaucomatous optic neuropathy.
Primary treatment offers patients significant
advantages by reduction of medication and possibly no
medication requirement, which is particularly useful in
the elderly or infirm, or in those who are often in the
prime of their lives where inadvertent poor compliance
can be a problem. In addition the effect of the treatment
seems to be better when the treatment is offered when
the intraocular pressures are high and the eye is untreated
by medication.
The modern treatment of glaucoma, which has
involved many new medical agents as well as SLT, has
reduced the need for filtering surgery in many ophthalmic
units. The part SLT plays in this reduction in those units
having this device is difficult to estimate.
The patients who have had SLT are happy but the
need for follow-up in these patients needs to be stressed
as the apparent decrease in the need for medication can
be misconstrued as a cure, careful discussion with the
patients receiving this treatment, particularly as a primary
treatment will avoid this happening.
ACKNOWLEDGEMENT
Thanks and appreciations go to George Marcellino and
his Lumenis company colleagues for their assistance in
the provision of graphic material.
REFERENCES
1. Wise JB, Witter SL. Argon Laser therapy for open-angle glaucoma:
A Pilot study. Arch Ophthalmol 1979; 97(2):319-22.
2. Lund OE, Zink H. Long-term results following argon laser
trabeculoplasty. Klin Monatsbl Augenheilkd. 1988;193(6):572-8
German.
169
170
SPECIAL CONSIDERATIONS
Conjunctival scarring from previous surgery makes
dissection difficult and increases the failure rate of
glaucoma surgery, as well as increasing the risk of
conjunctival tear and buttonhole. Long use of meiotics
makes the pupil difficult to dilate and makes cataract
surgery difficult specially capsulorrhexis and
phacoemulsification.11
Patients with pseudoexfoliation syndrome are more
prone to develop cataracts, and a higher association of
glaucoma . The management of such a case is challenging
because 1. A tendency towards incomplete mydriasis
with a subsequent small pupil that can complicate cataract
extraction. 2. weak zonules that increases the risk of
zonular dialysis with vitreous loss and lens dislocation
during cataract surgery and again this increases the failure
rate of the glaucoma procedure.17 3. A cornea that might
be more prone to endothelial damage. 4. A tendency
towards hyphaema during surgery. 5. A tendency
towards total zonular loss that will cause even in the bag
lens to fall into the vitreous. If zonular dialysis and lens
subluxation is noted preoperative by phacodenesis this
necessitates a special preparation of either capsular
tension rings with careful Phacoemulsification, or if it is
SURGICAL OPTIONS
The coexistence of cataract and glaucoma in the same
patient gives one of three options for management either
doing both procedures in the same time, starting with
the cataract procedure or starting with the glaucoma
procedure.
171
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173
SURGICAL PROCEDURE
Preoperatively meiotics should be discontinued a few
days prior to surgery to allow for pupillary dilatation if
the IOP is still high other medical options should be used
till the surgery date.
Preoprative the pupil is dilated using phenylephrine,
cyclopentolate and tropicamide and flurbiprofen.
Anaesthesia can be topical, local or general. Local
anaesthesia with sedation is the best option. In this
procedure a 1:1 mixture of 2 percent lidocaine with
bupivacaine, together with 150 units of hyaluronidase
in 10 cc of this mixture, are injected. This same mixture
is used for the facial block either with the van Lint or the
OBrien block. Gentle massage of the lids is used to
soften the globe, intermittently for 5 minutes following
174
Conjunctival Flap
Hemostasis
Traction Suture
175
Mitomycin-C
After dissection of the conjunctiva and Tenons capsule a
mitomycin-C 0.3 mg/cc soaked Weck-Cel is inserted
underneath the conjunctiva, the cut edje of the
conjunctiva is not allowed to touch the pledget. It is left
in place for 2 to 3 minutes, depending on the race of
the patient, age and whether or not he underwent
previous surgery. The pledget is then removed and the
whole area is thouroughly irrigated with 15 cc of balanced
salt solution. It is important to avoid accidental inoculation
of MMC into the eye. To avoid this no entry into the
anterior chamber is allowed prior to the application of
MMC, and no instrument is allowed to touch MMC and
if this happens it is soaked well before use.
Scleral Flap
A half thickness triangular or rectangular scleral flap is
fashioned, with dimensions equivalent to the width of
the intraocular lens to be inserted if a one site
phacotrabeculectomy procedure is planned, usually a
3.2 mm is adequate for a foldable IOL and a bigger one
is for rigid IOLs. The scleral flap is outlined by a Grieshaber
681.01 blade or a Beaver 69 blade or an Alcon
superblade 30 degrees. A 0.12 toothed forceps as a
Phacoemulsification
Entry into the Anterior Chamber
A 3.0 mm Keratome is used to enter the eye at the
anterior most point beneath the scleral flap, the keratome
176
Fig. 14.9: After injecting the capsular stain onto the capsule
viscoelastic is again injected after washing the stain and rhexis
performed
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Capsulorrhexis
It is started with the cystotome and continued with it or
with the Utrata forceps. The capsule is then brought out
using the forceps, and then hydrodissection is done with
balanced salt solution using a 27-gauge cannula,
hydrodissection (injecting the BSS between the capsule
and cortex) and hydrodelineation (injecting BSS between
the cortex and nucleus) is done, sometimes the golden
ring is apparent denoting complete hydrodelineation.
177
Phacoemulsification
The normal steps of phaco are carried out either crack
and conquor or chip and flip method.
IOL Insertion
Fig. 14.10: Hydrodissection is performed underneath the
rhexis to envelop the nucleus
178
Fig. 14.15: Final adjustment of the IOL into the capsular bag
Sclerectomy
Following IOL placement, viscoelastic is aspirated from
the eye, carbachol is injected into the eye to constrict
the pupil, then viscoelastic is injected again into the
anterior chamber and specially in the site of the
sclerostomy. The assistant then retracts the flap and a
rectangular sclerectomy is done using the super blade
or the Kelly-Descemets punch.
179
Limbus-based Flap
The conjunctiva is closed with a 9-0 monofilament vicryl
in a continuous locking sutures and a bite of the posterior
Tenons is taken every 2 or 3 sutures.
Tenonectomy is performed with either technique
especially if there is a thick Tenon obscuring view of the
scleral flap for suture lysis later on.
After closure of the conjunctiva the viscoelastic is
washed from the eye and the phaco wound is hydrated
and taken one suture in for tight closure and if massage
is needed postoprative leak is guarded from.
180
Postoperative Care
The patient is put on frequent antibiotic steroid
combination for 4 wees with a decreasing rate through
the time and followed up every three days in the first
two weeks then weekly after that.
The need for laser suturelysis is when the pressure
gets high accoring to the condition of the optic nerve
and the target pressure needed, in that case a Hoskins
lens is used with the argon laser adjusted on 50 Mm
spot size 700 MJ and 0.1 sec time usually through a
clear conjunctiva one shot is enough to cut the suture,
mild massage can be done after the suturelysis to
maintain an aqueous drainage.
15.
16.
17.
18.
19.
REFERENCES
1. Anand N, Menage MJ, Bailey C. Phacoemulsification trabeculectomy
compared to other methods of combined cataract and glaucoma
surgery. Acta Ophthalmol Scand. 1997 Dec;75(6):705-10.
2. Borggrefe J, Lieb W, Grehn F. A prospective randomized comparison
of two techniques of combined cataract-glaucoma surgery. Graefes
Arch Clin Exp Ophthalmol. 1999 Nov;237(11):887-92
3. Caprioli J, Park HJ, Weitzman M Temporal corneal
Phacoemulsification combined with superior trabeculectomy: a
controlled study.. Trans Am Ophthalmol. Soc. 1996 ; 94: 451 63;
discussion 463 8.
4. Casson RJ, Salmon JF.. Combined surgery in the treatment of patients
with cataract and primary open-angle glaucoma. J Cataract Refract
Surg. 2001 Nov;27(11):1854-63.
5. Chia WL, Goldberg I.. Comparison of extracapsular and phacoemulsification cataract extraction techniques when combined with
intra-ocular lens placement and trabeculectomy: short-term
results.Aust N Z J Ophthalmol. 1998 Feb;26(1):19-27
6. Collignon-Brach JD, Ravet O, Robe-Collignon N. Surgical
indications in coexisting cataracts and glaucoma Bull Soc Belge
Ophtalmol. 2000; (Suppl):11-36.
7. Donoso R, Rodriguez A. Combined versus sequential
phacotrabeculectomy with intraoperative 5-fluorouracil. J Cataract
Refract Surg. 2000 Jan;26(1):71-4.
8. El Sayyad F, el-Maghraby A.. The contribution of phacoemulsification
to combined cataract and glaucoma surgery.Curr Opin Ophthalmol.
1998 Apr;9(2):95-100
9. El Sayyad F, Helal M, el-Maghraby A, Khalil M, el-Hamzawey H..
One-site versus 2-site phacotrabeculectomy: a randomized study. J
Cataract Refract Surg. 1999 Jan;25(1):77-82.
10. El-Sayyad FF, Helal MH, Khalil MM, El-Maghraby MA.
Phacotrabeculectomy versus two-stage operation: a matched study.
Ophthalmic Surg Lasers. 1999 Apr;30(4):260-5.
11. Epstein, David, Allingham, Rand, Shauman, Joel S., Chandler and
Grants Glaucoma. Fourth edition, Williams & Wilkins, 1997.
12. Friedman DS, Jampel HD, Lubomski LH, Kempen JH, Quigley H,
Congdon N, Levkovitch-Verbin H, Robinson KA, Bass EB.. Surgical
strategies for coexisting glaucoma and cataract: an evidence-based
update. Ophthalmology. 2002 Oct;109(10):1902-13
13. Galand A Cataract surgery in primary open angle glaucoma., Bull
Soc Belge Ophthalmol. 2000 (Suppl): 37 44.
14. Gianoli F, Schnyder CC, Bovey E, Mermoud A.. Combined surgery
for cataract and glaucoma: phacoemulsification and deep
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
181
44. Tezel G, Kolker AE, Kass MA, Wax MB. Comparative results of
combined procedures for glaucoma and cataract: I. Extracapsular
cataract extraction versus phacoemulsification and foldable versus
rigid intraocular lenses. Ophthalmic Surg Lasers. 1997 Jul;28(7):53950
45. Tow SL, Aung T, Oen FT, Seah SK. Combined phacoemulsification,
intraocular lens implantation and trabeculectomy for chronic angle
closure glaucoma, Int Ophthalmol 2001;24(5):283-9.
46. Urban V, Kammann MT, Sturmer JP. Glaucoma and cataract:
combined operation or trabeculectomy first and cataract extraction
later?] Klin Monatsbl Augenheilkd. 2000 Feb;216(2):105-11
47. Wishart PK, Austin MW. Combined cataract extraction and
trabeculectomy: phacoemulsification compared with extracapsular
technique.Ophthalmic Surg. 1993 Dec;24(12):814-21
48. Wu WC, Wu SC, Lin SM. Surgical outcome of combined
phacoemulsification and trabeculectomy. Changgeng Yi Xue Za
Zhi. 1999 Dec;22(4):572-8.
49. Wyse T, Meyer M, Ruderman JM, Krupin T, Talluto D, Hernandez R,
Rosenberg LF. Combined trabeculectomy and phacoemulsification:
a one-site vs a two-site approach. Am J Ophthalmol. 1998
Mar;125(3):334-9.
50. Zacharia PT, Schuman JS. Combined phacoemulsification and
trabeculectomy with mitomycin-C. Ophthalmic Surg Lasers. 1997
Sep;28(9):739-44.
51. Raitta C, Setala K. Intraocular lens implantation in exfoliation
syndrome and capsular glaucoma, Acta ophthalmol 1986;64:130.
52. Dosso AA and others: Exfoliation syndrome and phacoemulsification.
J Cataract Ref Ract Surg 1997;23:122.
53. Jakeman CM and others: Cataract surgery with intraocular lens
implantation in Fuchs heterochromic cyclitis, Eye 1990;4:543.
54. Jones NP: Extracapsular cataract surgery with or without intraocular
lens implantation in Fuchs heterochromic uveitis, Eye 1991;5:662.
55. Jones NP, Glaucoma in Fuchs heterochromic uveitis aetiology,
management and outcome, Eye 1991;5:662.
56. Poliner LS and others: Neovascular glaucoma after intracapsular
and extracapsular cataract extraction in diabetic patients, Am J
Ophthalmol 1985;100:637.
57. Aiello LM and others: Neovascular glaucoma and vitreous
haemorrhage following cataract surgery in patients with diabetes
mellitus, Ophthalmology 1983;90:814.
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182
15 Management of Angle-closure
INTRODUCTION
Angle-closure is an anterior segment disease caused by
anatomical disproportion. The defining characteristic is
contact between iris and trabecular meshwork sufficient
to cause a significant reduction of aqueous outflow
(whether permanent or transient). Angle-closure is a risk
factor for glaucomatous optic neuropathy, which is
rapidly progressive in comparison with primary openangle glaucoma (POAG). Population surveys suggest that
untreated angle-closure glaucoma blind about half of
those affected. Most cases are not symptomatic.
However, cases of primary angle-closure (PAC)
encountered in hospital practice characteristically present
with a symptomatic rise in intraocular pressure (IOP) or
relatively advanced optic disk damage and visual field
loss. The management of these cases must be tailored
to the individual case. However, there are three basic
principles of managing people with angle-closure:
1. Immediate control of symptoms and raised IOP.
2. Change angle configuration, preventing further
closure.
3. Detect and control continuing optic disk and visual
field damage.
Management of Angle-closure
Once intraocular pressure is controlled, the primary
aims of management are to open the drainage angle,
and to identify and monitor if glaucomatous optic
neuropathy is present and likely to progress.
Most cases (75%) of angle-closure are the result of
primary pupil block. This is dealt with by laser iridotomy
or surgical iridectomy. In about 10 to 12 percent of cases,
the primary mechanism is anterior non-pupil block
closure. This includes people with plateau iris syndrome,
in whom an anteriorly-rotated ciliary body causes a
pronounced angulation in the peripheral third of the iris
that brings the iris close to the trabecular meshwork.
Another anterior non-pupilblock mechanism is
peripheral iris crowding. In these cases, a thick, bulky iris
with prominent circumferential rolls inserts into the
anterior edge of the ciliary body. Dilation of the pupil
exaggerates the peripheral rolls, and leads to
iridotrabecular apposition.
183
Procedure
Anesthetize the eye with amethocaine and apply a Wise
or Abrahams iridotomy contact lens. Check the defocus
is set to zero. Look for iris crypts or thin areas, and treat
an area as peripheral as possible between 11 and 1
oclock. Blue eyes usually require single 1 to 2 mJ shots.
Total power consumption should be less than 30 mJ.
For green and brown eyes where radial fibers are visible
(i.e. thin iris) use single 2 to 3 mJ shots, expecting a
maximum total power of around 50 mJ. For thick brown
irides that have had CWL pretreatment, settings and
power consumption should be similar. If any hemorrhage
is encountered, gentle pressure will help this to stop.
Enlarge the iridotomy circumferentially up to 200
microns diameter.9 Verify by direct inspection that the
iridotomy extends through the iris-pigment epithelium.
184
Laser Iridoplasty
Aftercare
Intraocular pressure should be measured at one to two
hours after treatment. If the IOP is high, oral
acetazolamide plus or minus additional topical agents
should be used as required. All patients should receive a
strong topical steroid (prednisolone 1% or
dexamethasone 0.1%) hourly for 24 hours (taking a
break through the night), and then 4 times a day. All
patients should be seen 1 week later in clinic and regonioscoped. Stop steroid unless there is evidence of
continued inflammation. If the IOP is raised and there is
anterior segment inflammation, swap to a topical NSAID.
Surgical Iridectomy
A randomized clinical trial of surgical iridectomy versus
laser iridotomy identified no difference in IOP control
and visual acuity at 3 years post-treatment.10 Surgical
iridectomy should be performed in African and AfroCaribbean patients in whom a laser iridotomy has been
difficult.
Procedure
Anesthetize the eye with amethocaine, apply a Wise or
Abrahams iridotomy contact lens. Any continuous wave
laser used in pan-retinal photocoagulation may be used
to perform iridoplasty. Different classes of lasers vary
somewhat in their efficacy relative to power, and there is
substantial variation in power uptake between eyes. As
a general rule, you should start with a low power and
increase until the desired effect is achieved. Starting from
100 mW, the desired response is usually achieved at
between 180 mW and 300 mW: Pulse duration 0.5 to
0.7s, and spot size 500 microns. Burns should be applied
as peripherally as possible, throughout 360. A full
treatment requires about 25 to 35 shots, each burn being
placed about 2 aiming beam widths from the area of
discoloration marking the previous shot. The ideal endpoint is a brisk contraction of the iris stroma, without
Management of Angle-closure
charring or a pop (if these occur, turn the power down).
The aiming beam should be crisply focused in a regular
circle. Varying the direction of gaze of the subject often
helps clear visualization of the area to be treated. Most
often, directing gaze away from the quadrant being
treated improves the view.
The procedure is the identical for treatment of acute
cases. The view may be improved a little using topical
glycerine to clear a steamy cornea. The AC should be
examined carefully to determine where the cornea and
iris are in contact. These areas should not be treated
unless no alternative exists. If there is 360 peripheral
iridocorneal apposition, start the treatment more
centrally, and as the burns pull open the angle, rapidly
spiral the treatment into the extreme periphery.
Aftercare
This is exactly the same as for cases having laser PI. In
addition, any cases with PAS should be given pilocarpine
(blue eyes: 2%, brown eyes: 4%) to use qid for 1 week.
All patients are seen 1 week later in clinic and regonioscoped. Stop steroid unless there is evidence of
continued inflammation. If the IOP is raised and there is
anterior segment inflammation, swap to a topical NSAID.
Pilocarpine should be discontinued at 1 week, and the
gonioscopy repeated 3 to 4 weeks later to assess the
effect of iridoplasty on angle configuration.
In selected cases of pure plateau iris syndrome, laser
iridoplasty appears to be highly effective, changing angle
width from 0 to 20 in all cases in a reported series (often
to 30). The changing in angle width is relatively longlasting, with 20/23 eyes retaining open angles throughout
the follow-up period of at least 6 years. The other three
in whom the effect wore off were retreated with a further
change in angle width, suggesting that retreatment is
appropriate in certain selected cases.12
185
186
REFERENCES
1. Anderson DR, Davis EB. Sensitivities of ocular tissues to acute
pressure-induced ischaemia. Arch Ophthalmol 1975;93:267-74.
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Management of Angle-closure
21. Foster PJ, Devereux JG, Alsbirk PH, et al. Detection of gonioscopically
occludable angles and primary angle closure glaucoma by estimation
of limbal chamber depth in Asians: modified grading scheme. Br J
Ophthalmol 2000;84:186-92.
22. Devereux JG, Foster PJ, Baasanhu J, Uranchimeg D, et al. Anterior
chamber depth measurement as a screening tool for primary angleclosure glaucoma in an east Asian population. Arch Ophthalmol
2000;118:257-63.
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188
INTRODUCTION
The wound healing response is the single most important
determinant of the final intraocular pressure after
trabeculectomy, with excessive postoperative scarring
significantly reducing success.1,2 Over the last 20 years
there has been increasing use of agents to modulate this
response and produce an improved outcome from
filtration surgery. Recent advances in molecular and cell
biology have made a major impact on our understanding of the wound healing process and its
modification. This is leading to the advent of new agents
as modulators of the scarring response following
glaucoma surgery.
The glaucoma surgeon has the opportunity to assess
and modulate the wound healing response before,
during and after surgery. In this chapter we look at these
three stages in turn and review the spectrum of antiscarring therapies that are either currently available or
in development for use in each situation. Finally, since
the wound healing response is involved in the
pathogenesis of glaucoma by several different mechanisms, we briefly comment on the potential of modulating other important sites implicated in this disease, such
as modifying the growth factor, TGF- in the trabecular
meshwork and optic nerve head (Table 16.1).
PREOPERATIVE STRATEGIES
Careful preoperative assessment of the patient allows
the glaucoma surgeon to estimate the risk of failure of
drainage surgery. A number of factors are known to
increase the chance of scarring, as summarized in Table
16.2. This knowledge can then be applied to the
individual patient, taking into account their particular
Preoperative strategies
Topical steroid
Oral steroid
Intraoperative strategies
5-Fluorouracil
Mitomycin-C
Beta irradiation
Photodynamic therapy BCECF-AM
TGF antibody
Suramin
Postoperative strategies
Topical steroid
5-Fluorouracil
Tranilast
Interferon alpha 2
Future strategies
Table 16.2: Risk factors for scarring and failure after glaucoma
filtration surgery
Risk factor
Comment
Age
Race
Previous topical
medication
Uveitis
Chronic conjunctival
inflammation
Previous failed
glaucoma surgery
Previous conjunctival
surgery
Recent cataract surgery
Neovascular glaucoma
Aphakia
189
INTRAOPERATIVE STRATEGIES
The most common stage to begin modulating the wound
healing response is during surgery. Any preplanned
strategies based on known risk factors may be altered at
this stage by the flexible glaucoma surgeon, who will be
aware of intraoperative findings such as unexpectedly
thin conjunctiva. The introduction of the antiproliferative
agents mitomycin-C and 5-fluorouracil has greatly
improved the outcome from glaucoma filtration surgery,
particularly in patients known to be at high risk of
scarring.8-10 These adjuncts are now in widespread use,
but their toxic cellular effects have been associated with
severe complications, such as hypotony, bleb leaks and
infections.11-14 This has led to the continued search for
alternative intraoperative antiscarring treatments, which
are also discussed below.
5-Fluorouracil
5-Fluorouracil (5-FU) is a cytotoxic agent that
antagonizes pyrimidine metabolism, causing inhibition
of DNA synthesis. In the context of glaucoma surgery,
5-FU has the role of inhibiting proliferation of conjunctival
and Tenons capsule fibroblasts. Surgery is seen by the
body as an injury and immediately stimulates the start
of a cascade of events that are the wound healing
response. A key step in this chain of events is the
proliferation of fibroblasts as these cells synthesize collagen
to form a scar, are responsible for wound contraction
190
Mitomycin-C
The first antiproliferative agent to be used successfully to
enhance the outcome from trabeculectomy was
mitomycin-C.9 Mitomycin-C is an antibiotic agent that is
activated by reduction into an alkylating agent. It has
potent effects on cellular function, inhibiting DNA
replication, mitosis and protein synthesis. In the context
of glaucoma surgery it acts to modulate the wound
healing response at a similar stage to 5-FU, inhibiting
fibroblast proliferation. It is, however, both stronger in
its effect and potentially more toxic than 5-FU.
Khaw and co-workers showed that at clinical
concentrations mitomycin caused cell death and
permanent inhibition, whereas there is only temporary
inhibition of proliferation with late recovery occurred
with 5-FU.20-22 The use of a single five-minute exposure
to mitomycin-C provides a superior surgical success rate
compared to 5-FU injections in many high risk patients
but unfortunately can also result in a greater chance of
bleb leaks and possible infection.14, 31-33 The use of
intraoperative MMC has, however, dramatically
improved the outcome from surgery in patients who
previously had a low chance of successful filtration
surgery, such as people with cicatricial conjunctiva and
young patients with congenital glaucoma.34-36
Adjunctive MMC usage in tube (glaucoma drainage
device) surgery is also now increasingly common.
Although there is relatively little evidence for this practice,
MMC use in this clinical situation could be expected to
be beneficial as tube surgery is most commonly
performed in eyes with complex glaucoma and multiple
risk factors for trabeculectomy failure. Perkins et al studied
the effect of MMC in patients undergoing Molteno tube
surgery and found that it increased the chance of good
IOP control without medications compared to placebo.37
There is no standardised method for the
intraoperative application of MMC and there is great
variation between clinicians in the dose used. Many will
also alter the dose depending on the case and risk factors
for scarring, tailoring the antiproliferative effect to fit an
individual patients requirements. Use of a concentration
between 0.2 mg/ml and 0.5 mg/ml, applied for 2 to 5
minutes is most usual.38 The size of the MMC treatment
Beta Irradiation
Beta radiation was proposed for use as an adjunct to
glaucoma surgery in the late 1960s to early 1970s, long
before modern chemical antiproliferatives.40, 41 It is simple
to use in practice and became established in certain
centres for intraoperative use in the treatment of complex
cases, such as congenital glaucoma. 42 More recent
scientific study has shown in vitro and in vivo that a single
application of beta radiation inhibits proliferation of
human Tenons fibroblasts, causing growth arrest but not
cell death.43 This has led to a renewed interest in the use
of intraoperative beta irradiation in trabeculectomy,
although it has not yet convincingly been proven to be
effective in a randomised controlled trial of routine
glaucoma patients.44-46 The simplicity of its application
and the suggestion that it may avoid some of the side
effects of other chemical antimetabolites, has caused
some clinicians to believe that beta radiation may be
particularly appropriate for use in developing countries.
A study in South Africa has recently been completed
and is due to report on the effect of a single intraoperative
application of -irradiation.
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Suramin
Suramin is a growth factor suppressing agent which has
been shown to inhibit wound healing in an animal model
of filtration surgery.59 The first clinical study of this agent
compared 10 patients undergoing trabeculectomy with
intraoperative applications of Suramin with a matched
group in whom mitomycin was used.60 They found the
success rates and IOP lowering to be similar to mitomycin,
but had no cases of hypotony associated with Suramin;
in this study hypotony lasting more than 3 months
occurred in 50 percent of the mitomycin group.
POSTOPERATIVE STRATEGIES
Postoperative Topical Steroid
The use of topical steroid use following trabeculectomy
is well established, although there is wide variation in
clinical practice regarding dosage and treatment period.
The amount steroid used will also obviously be altered
depending on the case and the postoperative progress.
The hallmark trial by Starita et al showing the benefit
of topical steroids after trabeculectomy was published in
1985.61 This randomized prospective trial divided 68 eyes
Tranilast
Tranilast (N- (3, 4-dimethoxycinnamoyl) anthranilic acid)
produces an antiscarring effect by suppressing TGF-
activity. In experimental models of eye disease, it has
been found to inhibit progression of proliferative
vitreoretinopathy, reduce choridal neovascularization and
limit subepithelial haze after photorefractive keratectomy.66-68 In vitro assessment of Tranilasts effect on
Tenons capsule fibroblasts has shown that it inhibits cell
proliferation and collagen synthesis.69 This led to the first
prospective randomized controlled trial of postoperative
Tranilast in trabeculectomy patients.70 The 52 patients in
the study were randomized to receive either 0.5 percent
Tranilast drops or saline placebo four times daily for 3
months after surgery. No sight threatening side effects
were found to be associated with Tranilast and the treated
group had greater IOP reduction and larger blebs than
the placebo group over 2 years follow-up.
Interferon Alpha 2
193
FUTURE STRATEGIES
Modulation of TGF-
in the Trabecular
Meshwork
Transforming growth factor beta (TGF), as discussed
earlier in this chapter, is a key growth factor in the process
of wound healing and tissue repair, with its sustained
overproduction resulting in tissue fibrosis.51 Tripathis
group have demonstrated that trabecular cells express
the TGF 2 gene and secrete this cytokine into the
aqueous. 72 This group and others have found that
glaucoma patients have higher levels of TGF2 in their
aqueous humour than normal subjects.56 They have
suggested that this overproduction of TGF 2 in
glaucomatous eyes has a role in the pathogenesis of
primary open-angle glaucoma: it may cause an increase
in the extracellular matrix (ECM) deposition in the
trabecular meshwork and so increase outflow resistance.71
More recently, Tripathis group have also shown that
TGF2 modulates the pre-mRNA splicing of the ECM
molecule fibronectin in trabecular cells, stimulating the
synthesis and secretion of fibronectin in a dose-dependent
fashion.73 It may be possible in the future to modulate
this process and so alter the disease process in glaucoma.
Modulation of TGF-
in the Optic Nerve Head
The primary site of glaucomatous damage is at the optic
nerve head. The process of extracellular matrix
remodeling at this structure is increasingly implicated in
the development of disease, although the exact
mechanisms responsible have not been elucidated. It is
believed that the physical force of elevated IOP plays a
role in causing the posterior deformation and bowing of
the lamina cribosaa hypothesis supported by
biophysical modeling data and histological evidence.74-77
The expression of TGF has been shown to be increased
at the optic nerve head in glaucomatous human and
animal model eyes, and it is suggested that this growth
factor is responsible for the remodeling of the lamina
cribosa by activating local cells.78-80, Furthermore, Yuan
194
CONCLUSIONS
Modulation of wound healing is required to enable us
to achieve the ideal of a successful outcome from
glaucoma surgery in all our patients. Currently the most
reliable approach is to use the antiproliferative agents
mitomycin and 5-fluorouracil. However, these agents
are far from perfect and so there is now a search for
new agents to control the wound healing process more
safely.
Increased scientific knowledge of the events involved
in tissue repair is allowing the targeting of biological
molecules to find effective treatments that are potentially
safer, with minimal complications. As in other areas of
medicine, a combination of therapies may be required
to achieve good control of postoperative scarring.
Improved understanding of the wound healing process
and the postoperative period should allow clinician and
scientist to come together to find these more specific,
focal and titratable treatments. It may also be possible in
the future to manipulate the glaucomatous disease
process itself by controlling wound-healing factors, such
as TGF , in the trabecular meshwork and optic nerve
head.
REFERENCES
1. Hitchings R, Grierson I. Clinicopathological correlation in eyes with
failed fistulizing surgery. Trans Ophthalmol Soc UK 1983;103:84-8.
2. Addicks E, Quigley H, Green W, et al. Histologic characteristics of
filtering blebs in glaucomatous eyes. Arch Ophthalmol 1983;101:7958.
3. Broadway DC, Grierson I, Sturmer J, Hitchings RA. Reversal of
topical antiglaucoma medication effects on the conjunctiva. Arch
Ophthalmol 1996;114:262-7.
4. Broadway DC, Grierson I, Hitchings R. Adverse effects of topical
antiglaucoma medications on the conjunctiva. Br J Ophthalmol
1993;77:790-6.
5. Broadway DC, Grierson I, OBrien C, Hitchings RA. Adverse effects
of topical antiglaucoma medication: I. The conjunctival cell profile.
Arch Ophthalmol 1994;112:1437-45.
195
196
71. Gillies MC, Brooks AMV, Young S, et al. A randomized phase II trial
of interferon-alpha 2b versus 5-fluorouracil after trabeculectomy.
Aust New Zealand J Ophthalmol 1999;27:37-44.
72. Tripathi RC, Chan WF, Li J, Tripathi BJ. Trabecular cells express
the TGF-beta 2 gene and secrete the cytokine. Exp Eye Res
1994;58:523-8.
73. Li J, Tripathi BJ, Tripathi RC. Modulation of pre-mRNA splicing
and protein production of fibronectin by TGF-beta2 in porcine
trabecular cells. Invest Ophthalmol Vis Sci 2000;41:3437-43.
74. Bellaza AJ, Hart RT, Burgoyne CF. The optic nerve head as a
biomechanical structure: infinite finite element modeling. Invest
Ophthalmol Vis Sci 2000;41:2991-3000.
75. Hernandez MR, Andrzejewska WM, Neufeld AH. Changes in the
extracellular matrix of the human optic nerve in primary open-angle
glaucoma. Am J Ophthalmol 1990;109:180-8.
ophthalmologyebooks.com
197
Pupillary Block
Situation arising from an obstruction of aqueous humor
circulation from the posterior to the anterior chamber
caused by touch between the phakic IOL and the
pupillary border (Fig. 17.2). Typically the patient presents
with intense pain and photophobia, and examination
shows a narrow angle, with forward displacement of the
iris, crystalline lens and phakic IOL in the absence of a
patent iridotomy. This can be caused by any kind of
phakic IOL but is more likely after posterior chamber
phakic IOLs. Reported incidences are 0 to 11.5 percent
for angle-supported phakic IOLs,1-4 0 to 0.8 percent for
iris-fixated phakic IOLs5-11 and 0 to 12.5 percent for
posterior chamber phakic IOLs.12-16 Pupillary block is
avoided by making permeable iridotomies with the
Nd:Yag laser preoperatively or by performing a surgical
intraoperative iridotomy or iridectomy. It is important to
make sure that both layers of the iris are perforated by
observing the anterior capsule of the crystalline lens or
the zonular fibers through the iridotomy. In the presence
of a pupillary block after anterior chamber phakic IOL
implantation, miosis with pilocarpine may help to unblock
the pupil separating it from the IOL before iridotomies
are enlarged surgically or with the Nd:Yag laser. In the
presence of pupillary block after posterior chamber phakic
IOL implantation, the chamber is very flat, the IOL looks
overvaulted, and the treatment implies dilating the pupil
with phenylephrine 10 percent and atropine 1 percent,
and performing a new peripheral iridotomy or enlarging
198
Malignant Glaucoma
This situation implies a peripheral block at the trabeculum
and reversed aqueous flow towards the vitreous. It can
follow pupillary block when aqueous accumulates in the
posterior chamber and pushes the iris forward (Figs
17.3A and B). The incidence of malignant glaucoma
after phakic IOL implantation is very rare, but seems to
be more common after posterior chamber phakic IOL,
ranging from 0.1 to 1.4 percent.12-16 Typically intense
pain, vomiting, photophobia and very high IOP are
present, and the slit-lamp exam shows corneal edema,
a non-reactive pupil with mydriasis, and a narrow
199
Angle Closure
In larger than needed posterior chamber phakic IOLs,
the angle can be closed by excessive pushing of the
peripheral iris forward. This is called excessive vault (Figs
17.4 and 17.5). Angle closure is more frequent in
hyperopic patients because the anterior chamber angle is
usually narrower. On average, a properly sized posterior
chamber phakic IOL reduces the iridocorneal angle width
by 15 to 20 percent. Changing the lens for a smaller one
with smaller vault, or extracting the PIOL can solve the
situation. In the presence of an angle-supported phakic
IOL, angle closure can be caused by anterior synechiae,
but this is an extremely infrequent situation (Fig. 17.6).
Pigment Dispersion
Excluding the cases produced by excessive surgical
trauma, this is a very rare complication after phakic IOL
surgery. It has been reported after the use of posterior
chamber phakic IOLs with excessive vault and IOLperipheral iris touch, together with the development of
cataract (Figs 17.7A and B).
Steroid-induced Glaucoma
It has been reported in 13 to 30 percent of patients after
phakic IOL implantation for high myopia.1-3
The IOP raises between the second and the fourth
week after surgery while topical steroids are used.
Recently marketed topical steroids such as rimexolone
can help to decrease the incidence of steroid glaucoma.
In the presence of steroid glaucoma after phakic IOL
implantation, topical steroids should be discontinued and
non-steroidal antiinflammatory drugs together with antiglaucomatous agents should be used until the IOP
normalizes. Phakic IOLs do not seem to produce IOP
elevation in the long-term.1,3,15
In summary, in the presence of IOP increase in the
first few days after phakic IOL implantation:
Check the patency of the iridotomy and if in doubt
enlarge it with the Nd:Yag laser. Sometimes the
haptic of the IOL may be closing the iridotomy
200
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REFERENCES
1. Muoz G, Ali JL, Monts-Mic R, et al. Angle-supported phakic
intraocular lenses followed by lasik for the correction of high myopia.
Am J Ophthalmol 2003;136:490-9.
2. Baikoff G, Arne JL, Bokobza Y, et al. Angle-fixated anterior chamber
phakic intraocular lens for myopia of -7 to -19 diopters. J Refract
Surg 1998;14:282-93.
3. Ali JL, de la Hoz F, Perez-Santonja JJ, et al. Phakic anterior chamber
lenses for the correction of myopia: A 7-year cumulative analysis of
complications in 263 cases. Ophthalmology 1999;106:458-66.
4. de Souza RF, Forseto A, Nose K, et al. Anterior chamber intraocular
lens for high myopia. J Cataract Refract Surg 2001;27:1248-53.
5. Guell JL, Vazquez M, Gris O. Adjustable refractive surgery: 6-mm
Artisan lens plus laser in situ keratomileusis for the correction of high
myopia. Ophthalmology 2001;108:945-52.
6. Ali JL, Mulet ME, Shalaby AMM. Artisan phakic iris claw intraocular
lens for high primary and secondary hyperopia. J Refract Surg
2002;18:697-707.
7. Prez-Santonja JJ, Bueno JL, Zato MA. Surgical correction of high
myopia in phakic eyes with Worst-Fechner myopia intraocular lenses.
J Refract Surg 1997;13:268-81.
8. Menezo JL, Cisneros AL, Rodriguez-Salvador V. Endothelial study
of iris-claw phakic lens: four year follow-up. J Cataract Refract Surg
1998;24:1039-49.
9. Dick HB, Ali J, Bianchetti M, et al. Toric phakic intraocular lens:
European multicenter study. Ophthalmology 2003;110:150-62.
Index
203
Index
type 1 45
type 2 45
type 3 45
A
Abexterno trabeculectomy 103
Ahmed valve 58
Ahmed valve combined with
secondary and sutured intraocular
lens implantation 69
Ahmed valve implantation and vitreoretinal surgical procedures 70
Ahmed valve in combined procedures
68
cataract extraction and Ahmed valve
implantation 68
complications and their management
71
early postoperative complications
73
intraoperative complications 71
late postoperative complications
74
indications 59
models for implantation 58
AGV-B1 58
AGV-FP7 58
AGV-S2 58
AGV-S3 58
penetrating keratoplasty and Ahmed
valve implantation 67
surgical technique 59
technique for double plate Ahmed 66
Anesthesia 11
general 11
local 12
Antimetabolite related complications 16
Antimetabolites 141
Antiscarring agents 17
Argon and Nd:YAG lasers 49
Argon lasers traculoplasty 161
B
Bleb 45, 141
encapsulated 45
C
Cairns technique 36
Capsulorrhexis 177
Closure of the scleral flap 179
Combined cataract glaucoma surgery 170
choice of the procedure 172
special considerations 170
surgical options 171
cataract surgery alone 171
combined cataract and glaucoma
procedure 171
glaucoma surgery first 172
surgical procedure 173
closure of the conjunctiva 179
conjunctival flap 174
hemostasis 174
mitomycin-C 175
phacoemulsification 175
postoperative care 180
scleral flap 175
traction suture 174
Complications of transscleral Nd:YAG
cyclophotocoagulation 38
Control of bleb fibrosis by antiinflammatory agents 80
Control of bleb fibrosis by delayed drainage
of aqueous 81
Control of intraocular pressure 98
Cyclocryocoagulation 38
Cyclodestruction in glaucoma 37
current cyclodestructive procedures 38
infrared 810 nm diode laser
cyclophotocoagulation 38
red 647 nm krypton and 670 nm
diode laser
cyclophotocoagulation 41
early cyclodestructive procedures 37
cyclodiathermy 37
Nd:YAG cyclophotocoagulation
38
indications for partial cyclodestruction
42
mechanism of intraocular pressure
reduction 42
Cyclodiathermy 38
D
Deep sclerectomy 102, 131
management 137
Nd:YAG goniopuncture after NPGS
138
perforation of trabeculo-Descemets
membrane 137
results of NPGS 138
surgical steps 131
Diffuse lamellar keratitis-like reaction 200
Digital ocular massage 141
Diurnal pressure curve 126
E
Extracapsular method for combined
surgery 179
F
5-Fluorouracil 142
Failing filtering bleb 45
Filtering surgery 46
Filtration surgery-preoperative details 12
Fornix-based flap 179
Frequency doubling technology 112
G
Glaucoma 1
Glaucoma filtration surgery 23
intraoperative complications 24
conjunctional, scleral and iris
bleeding 25
conjunctival tear 24
204
H
Haemophilus 30
Holy Grail of glaucoma treatment 1
I
Intraocular pressure 1
economical burden of IOP lowering
strategies 7
ideal treatment to reduce IOP 1
in surgery better than drugs 1
issue of compliance and persistence 4
long-term IOP reduction 2
K
Kelly-Descemets punch 178
L
Laser trabeculoplasty 2, 161
Limbus-based flap 179
M
Management of angle-closure 182
change angle configuration and
prevent further closure 183
cataract surgery and lens extraction
185
laser iridoplasty 184
laser iridotomy 183
medical management of angleclosure 185
surgical iridectomy 184
detection and control of continuing
optic disk and visual field damage
186
immediate control of symptoms and
raised IOP 182
prevention 186
Management of filtration failure 50
bleb needling 52
bleb reconstruction 54
digital compression 50
laser cautery of bleb vessels 54
laser suturelysis 50
complications 51
historical aspects 50
indications 50
technique 50
trephination 52
technique 53
Minskys maneuver 121
Mitomycin-C 32, 142
N
Nd:YAG goniopuncture 141
Nd:YAG laser 27
Nd:YAG laser cyclophotocoagulation 37
Neovascular glaucoma 95
New technique versus classic
trabeculectomy 36
O
Ocular hypotensive medications 6
One-stitch technique 61
Index
P
Pars plana tunnel 64
Peripheral iridectomy 35
Phaco and Ahmed valve combined
procedure 68
Phacoemulsification 177
Phacotrabeculectomy 98, 150
Pilocarpine 182
Pre-and intraoperative drops 12
hypotensive agents 13
nonsteroidal anti-inflammatory drugs
13
parasympathetic agonists 12
povidone-iodine 12
steroids 12
sympathetic agonists 12
Primary open-angle glaucoma 4, 97, 182
R
Risk factors for filtration failure 46
Risk factors for scarring and failure after
glaucoma filtration surgery 188
S
Schlemms canal 102, 103, 122
Schwalbes line 137
Scleral-tunnel technique 36
Sclerectomy 178
Secondary glaucomas 98
Selective laser trabeculoplasty 161
complications of SLT 167
delivery of SLT 166
effectivity of SLT 164
place of SLT in relation of ALT 161
SLT laser 162
Severity of glaucoma 84
Signs of filtration failure 47
bleb encapsulation 49
due to blockage external to the ostium
49
due to blockage of the internal ostium
48
Sinusotomy 103
Stegmanns technique 107
Streptococcus 30
Sub-Tenons space 33
T
TDM holes 137
Tenons capsule 45
Trabeculectomy 1,11, 32, 98
surgical modifications 32
surgical technique for 13
antimetabolite treatment duration
and washout 18
205
V
Vicryl tie technique 81
Viscocanalostomy 102
W
U
Use of Molteno implants 77
current surgical technique 83
choice of surgical technique 84
cytostatic agents 91
direct control of bleb fibrosis by
systemic anti-inflammatory
agents 91
early complications 92
indications 83
indirect control of bleb fibrosis by
hypotensive agents 91
late complications 92
long-term management (all cases)
91
postoperative management in eyes
drained by delayed drainage
of aqueous (vicryl tie
technique) 90
postoperative management of
cases with immediate drainage
of aqueous 91
preoperative management 84
selection of implant area 83
surgical technique for delayed
drainage of aqueous 84
surgical technique for immediate
drainage of aqueous 88
surgical technique for neovascular
glaucoma 89
Y
YAG laser capsulotomy and hyaloidotomy
74