Ruedemann Eyelid surgery

							                    Ruedemann Lecture

Good evening Dr. Tuck, Dr. Hawes, Mr. Acosta, members and
fellows of the Academy and American Society of Ocularists,
guests....friends. Thank you for the high honor you have bestowed
upon me this evening in naming me the 21st Ruedemann
Lecturer. I would like to first off thank my fellowship preceptors
Dick Dortzbach and Brad Lemke for teaching me that the asking
of “why” is the necessary first step in formulating “how”, the
highly skilled ocularists I have had the pleasure of working with:
Sue Alexander, Chuck Workman, Gene Fletecher and Carrie
Messer, and, not the least, my wife, Sandy, and children, Julie,
Scott and Steve, for having the patience to live with me in this
pursuit called medicine.


When I look at the roster of prior Ruedemann lecturers, I am
humbled, indeed, but....
(Slide)


Even a midget can expand the horizon by standing on the
shoulders of a giant.
(Slide)


Dr. Albert Darwin Ruedemann, Sr., was such a giant. He was
born in 1897, and died in 1971, when I was a freshman in medical
school. He left his mark at the University of Michigan, the
Cleveland Clinic and the Kresge Eye Institute in Detroit.
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(Slide)


He served as the secretary for instruction of the Academy from
1938 to 1962, and won numerous awards and accolades. In
describing him, Dr. William Benedict said, “His thinking is clear,
his learning is wide, his interest in instruction and education
intense, and his tolerance of ignorance nil”. Quite an epitaph.
(Slide)


He had a long interest in anophthalmia, and it was through his
effort that this joint meeting was established in 1957. He ushered
in the era of the integrated implant with his description, in 1946,
of a combination implant and prosthesis to be placed in the socket
after enucleation.
(Slide)


We share Dr. Ruedemann’s enthusiasm, for we have a common
interest in the restoration of as much function and cosmesis as
possible following the loss of an eye. The problem we face is that
seemingly consistent processes of enucleation and prosthesis
fitting are met with confoundingly variable results. Tonight we
will explore some possible reasons for this, and hopefully,
formulate a clearer understanding of the pathophysiology of
anophthalmia. The answers to these questions may both over-
and underwhelm you, so hang on.
(Slide)
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First, lets be clear about what we actually do when we remove an
eye. The eye is gone, unfortunately. We may, however, be guilty
of concentrating too much on what was removed, and not enouth
on what is left behind.
(Slide)


Secondly, let us make the general observation that, with certain
exceptions, our goal of normal function and cosmesis is best
served by performing the least amount of surgery. Again, leaving
more behind seems to be correlated with a higher degree of
“normalcy”.
(Slide)


For hundreds of years, it was enough that the patient survived
the enucleation. This is a handout from an Academy instructional
course in 1583. However, with the development of the Mules
implant in the 1880’s, new possibilities developed.
(Slide)


Inquiring minds began to ask questions. George de Schweinitz
remarked in 1900 that “An enucleation which pays no attention to
the preservation of the relationship between the conjunctiva,
ocular tendons and capsule of Tenon is a brutal operation.” A
year later Jose Barraquer stated, “ What is necessary is to place
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some soft tissue whose shape can easily adapt to the glass
prosthesis and that can persist indefinitely in Tenon’s Capsule.”
(Slide)


In 1917, John Wheeler, the father of ophthalmic plastic surgery
reflected on problems he identified in patients following
enucleation. These same problems, with slightly different twists
and emphases, have recurred throughout this century.
(Slide)


65 years after Wheeler, Tyers and Collin coined the term
“Postenucleation socket syndrome” to describe the constellation of
enophthalmos, deep upper lid sulcus, ptosis and stretching of the
lower lid.
(Slide)


In 1982, Lee Allen realized that the surgical practice of
imbrication of muscles over a spherical implant invariably led to
secondary changes in the muscle cone, and resulting iatrogenic
ptosis.
(Slide)


pause
(Slide)
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In 1987, Dr. Lars Vistnes, a truely Renaisance reconstructive
surgeon, recognized the same findings as Dr. Wheeler, with a
slightly different twist, and termed this the “anophthalmic orbit
syndrome”. We will revisit more of Dr. Vistnes’ thoughts later in
this lecture.
(Slide)


To explain some of these problems, Henry Baylis and his co-
authors, writing in Sonny McCord’s textbook of ophthalmic plastic
surgery, made a statement profound with it’s simple truth. “The
anophthalmic socket is a uniquely complex system of structural
and functional elements in which a change in any single element
profoundly affects the other elements.” The value of this
statement was recognized by ______Willis, and could probably
serve as a one-sentence text in socket surgery.
(Slide)


In 1988, Smerdon and Sutton attempted to delineate just what
factors were involved in cosmetic failure in anophthalmia. 56
enucleation patients were subjected to quantitative
measurements of sulcus depth and socket volume and qualitative
assessment of cosmetic appearance. Somewhat surprizingly,
cosmetic failure was not correlated with volume loss, but with
superior sulcus formation. Sulcus formation itself was not
correlated with volume loss. Younger patients were found to have
better cosmetic results.
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(Slide)


The decade of the 1990’s has seen the rapid presentation of
additional observations which have significantly increased our
knowledge of what clinical factors are responsible for cosmetic
failure in anophthalmia. ____Willis described the “post-
enucleation” syndrome and....
(Slide)


Emphasized that these factors are interdependent and self-
perpetuating over time if left untreated.
(Slide)


Neuhaus and Hawes pointed out that the loss of the inferior
fornix can be present even with adequate conjunctiva, and is due
to loss of the attachments of the lower eyelid retractors to the
conjunctival fornix.
(Slide)


Smit, Koornneef and the talented investigators in Amsterdam
presented perhaps the most important series of articles
explaining, anatomically, what is happening in those patients who
develop this post-enucleation constellation of pathological
changes. They observed the following abnormalities:
enophthalmos, retraction, not ptosis, of the upper eyelid,
deepening of the superior sulcus, backwards tilt of the prosthesis
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and stretching of the lower eyelid. This almost constant
correlation of deep upper eyelid sulcus with deep superior fornix
is, I think, a key element.
(Slide)


To analyse these patients, they performed sagital CT imaging,
superimposed the normal orbit on the anopthalmic orbit, and
noted the difference in key measurements.
(Slide)


They found: an anterior displacement of posterior Tenons, as
their implants were placed behind posterior Tenons, a rotatory
displacement of orbital contents, superior to posterior and
posterior to inferior and a retraction and apical displacement of
the vertical recti muscles.
(Slide)


pause
(Slide)


These anatomic findings, and their resolution after implant
placement, are even more dramatically represented in sagital
MRI imaging of an anophthalmic orbit before and after secondary
implant placement.
(Slide)
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Certainly, enucleation has the potential to cause changes in a
number of orbital and periorbital tissues. Smit’s observations are
pointing us towards the connective tissue component of the orbit.
Let’s dig a little deeper.
(Slide)


Tenon’s Fascia--everyone talks about it, but what is it? Is it
important? Why ask why? Well, it is extremely important in the
understanding of the pathophysiology of anophthalmia, but, as
Dwight stated in 1900, “The complications of this membrane are
limited only by the perverted ingenuity of those who describe it.”
How is it described? Is it Tenon’s Capsule, indicating it to be a
structure more closely related to the globe, or is it Tenon’s Fascia,
indicating a structure perhaps more related to the extraocular
muscles. The Motais school views Tenon’s as an extention of the
rectus muscle sheaths, while the view of Testut, Charpy and
Virchow was that the rectus muscle sheaths are formed from
Tenon’s .
(Slide)


Anatomic dissections do not always help, and yet, our
understanding of the teleologic significance of
Tenons...”whatever”, seems to be at the root of understanding the
changes in the anophthalmic orbit.
(Slide)
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Lester Jones can be credited, I think, with acting as a referee in
this debate. His classic descriptions of the levator muscle
involved a comparative anatomic study of mammals. He found in
marine mammals, a most convincing arguement. The primitive
rectus muscle divides into an ocular and palpebral head. The
palpebral head in turn divides into a true palpebral head, and a
capsular head, which corresponds to the human anterior Tenon’s
...FASCIA. The finding of smooth muscle cells in Tenon’s further
supports it’s close relationship to the ocular muscles, rather than
to the globe.
(Slide)


This view is further supported by the elegant and seminal work of
Koornneef in his description of the unity of the “musculo-fibrous
apparatus of the orbit”.
(Slide)


Pause
(Slide)


Pause
(Slide)


Henry Baylis, thank you again.
(Slide)
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It has been one of my pleasures to work with a number of fellows
in the basic science investigation into pathophysiologic changes in
the anophthalmic orbit. I would like to review the results of two
such investigations, as I think we are getting someplace now.
Sara Kaltreider studied the production of socket contraction in
the monkey orbit, and its correlation with myofibroblast
induction.
(Slide)


With our model, we could reliably produce socket contraction,
with resulting loss of socket volume and depth.
(Slide)


Cells consistent with myofibroblasts were found, with severe
anterior disruption of orbital anatomy and the formation of dense
scar bands from the optic nerve and recti muscles to the fundus of
the socket. What tissue unites the conjuctiva, rectus muscles and
optic nerve? Tenon’s fascia. Proliferation of contractile scar
tissue along this tissue plane will produce the contracted socket....
(Slide)


As evidenced in this sagital MRI.
(Slide)


It had been hypothesized that altered blood flow in anophthalmia
may contribute to fat atrophy and loss of socket volume with the
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production of the constellation of findings of the anophthalmic
socket syndrome. To investigate this, Jan Kronish investigated,
with arteriography and labeled microspheres, the blood supply of
the anophthalmic orbit.
(Slide)


No change in size of blood vessels was found, although their
course was somewhat more tortuous. Microsphere analysis
showed no difference in blood flow to the fat, muscles, connective
tissue or eyelids following enucleation.
(Slide)


Far from fat atrophy, a statistically significant 13% increase was
seen in fat and connective tissue, excluding muscle mass,
following enucleation. This is consistent with a similar increase
in soft-tissue orbital volume found by Manson and associates in
their investigation into orbital volumes following orbital floor
fracture.
(Slide)


Moreover, no difference in adipocyte morphophometry was found.
(Slide)


Our conclusions were that there was primarily a disturbance in
spatial architecture in anophthalmia with a redistribution of soft
tissue and contractile scar formation. The volume of the globe
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was lost, to be sure, but there was an actual increase in
connective tissue mass.
(Slide)


Remember this
(Slide)


Sooner or later, we must address the volume question. The
volume of the globe is 6.5-7.0 cc. The volume of the average
prosthesis is 2.5 cc. In order to match the volume lost in an
enucleation, an implant of @ 21 mm would be needed.
(Slide)


Pause
(Slide)


However, this may be overly simplistic. The ocularists point out
that fitting a prosthesis over a 21 mm implant would usually be
difficult. There is little room for building adequate chamber
depth. Remember too the finding of Smerdon and Sutton:
cosmetic failure was correlated not with volume loss, but with
superior sulcus formation. Our volume augmentation must be
directed, and, to counter the effects described by Smit, should be
intra-Tenons.
(Slide)
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Pause
(Slide)


Can we summarize these findings? The main problem in
anophthalmia is a rotational volume displacement, probably
caused by changes in Tenon’s fascia. This produces an apical
collapse of the muscle cone, with resulting deep superior fornix
and superior sulcus formation. Further rotational changes flatten
the inferior fornix with resulting pressure and secondary changes
on the lower eyelid. It is unclear whether there is ptosis or
retraction of the upper eyelid, but there is most certainly altered
rectus and probably levator function, with alterations in the
length/tension curve of the muscles.
(Slide)


There are no alterations in muscle mass or blood flow. The
fat/connective tissue compartment undergoes a significant
increase in mass, and there are varying degrees of myofibroblast
induction.
(Slide)


Let’s return to our enucleation, concentrating this time on what is
left behind, rather than on what is removed. It is clear, that to
block the changes which occur following enucleation, the ideal
orbital implant would duplicate the eye as closely as possible.
(Slide)
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The genius of Dr. Ruedemann is now even more apparent, as that
is what his plastic eye was designed to do. The theory was, and
is, sound. Technology and engineering are needed to make it
workable.
(Slide)


What are our requirements? Ideally, to solve the problems of Dr.
Ruedemann’s implant, the implant should be autogenous, or able
to be vascularized. The total volume and size of implant and
prosthesis should equal that of the globe. It should duplicate the
influence of the globe on Tenon’s fascia, recti muscles and
conjunctiva, and integration of the prosthesis and implant should
be possible. Judged by this strict criteria, in 1994 the ideal
implant from the pathophysiologic perspective would be an
evisceration, Vistnes’ eviscero-enucleation or a dermis fat graft.
(Slide)


Evisceration, especially with retention of the cornea, offers the
least pathophysiologic alteration in the orbit, and, not
surprizingly...
(Slide)


Gives excellent cosmesis and motility.
(Slide)
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The eviscero-enucleation of Vistnes, basically leaving the muscles
attached to a rim of sclera and placement of an implant behind
this, seems to be exceedingly difficult.
(Slide)


Dermis fat grafts can provide an excellent socket. Their
resorption is unpredictable, however.
(Slide)


The long and short of it is that all of these implant choices have
disadvantages. Hydroxyapatite and porous polyethylene, and
Allen and Universal implants also have their advantages and
disadvantages. How lucky we are that the ideal implant is yet to
be found. Perhaps a young investigator in the audience tonight
will be challenged enough to find it.
(Slide)


It may be quite different that we expect. We should not limit our
horizon to restoration only of cosmesis and motility. A number of
laboratories are actively investigating direct cortical stimulation
which may lead to a truely functioning artificial eye. I wish I
could say that in 5 or 10 years, “I’ll be back” to report on this, but
20/20 by 2020 is not beyond reason.
(Slide)
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At the beginning of this lecture, I said I thought you may be both
over and underwhelmed by its content. Such simple concepts,
really, yet so simple that they are easily invisible. Orbital
physiology is minimally altered by enucleation. The best results
can be expected when the underlying architecture, especially that
of Tenon’s Fascia, is minimally altered. Our technology can do
little to improve on the underlying basic design of the orbit, only
duplicate it as closely as possible.


I thank you for your kind attention.