Pseudophakic Bullous

Keratopathy
DANIEL M. TAYLOR, MD, BARRY F. ATLAS, MD, KENNETH G. ROMANCHUK, MD,
ALAN L. STERN, MD

Abstract: Pseudophakic bullous keratopathy (PBK) is a relatively new disease

that is rapidly becoming the prime indication for penetrating keratoplasty. From
1977 thru 1981 we performed 81 corneal transplants on 66 eyes for this
condition. In our experience, the incidence of PBK, with iris-supported lenses,
is five times greater than aphakic bullous keratopathy (ABK). A series of 800
intracapsular cataract extractions (IGGE) with implantation of iris-supported
lenses (1975-1979) were reviewed. Thirty-four patients (4.3%) developed PBK
(average two years after surgery). In a series of 3,000 simple IGGEs (1955-
1980), 24 patients (0.8%) developed ABK. Etiologic factors, methods of pre-
vention, and the results of penetrating keratoplasty are considered. PBK fol-
lowing IGGE is a serious disease entity, usually of multifactorial origin. Though
88% of the patients have clear grafts, a high incidence of associated posterior
segment disease tends to nullify the visual result. Planned extracapsular cat-
aract extraction and posterior chamber lens insertion (1979-1982) has reduced
our incidence of PBK to 0.3% (1/300). These results are promising but pre-
mature. [Key words: cataract surgery, corneal decompensation, corneal trans-
plantation, intraocular lenses, pseudophakic bullous keratopathy.] Ophthal-
mology 90:19-24, 1983

Pseudophakic bullous keratopathy (PBK), defined as
irreversible corneal edema in an aphakic eye with an
intraocular lens, is rapidly becoming the prime indica-
tion for penetrating keratoplasty. 1 Several corneal sur-
geons2- 6 have reported results of penetrating kerato-
plasty (PK) for PBK. The majority of these PBK cases
developed following intracapsular cataract extraction
with iris-supported intraocular lens implantation prior
to the development of Healon. The recent trend toward
extracapsular cataract extraction with posterior chamber
intraocular lenses may reduce the increasing incidence
From the Department of Ophthalmology, University of Connecticut Health
Center, Farmington, Connecticut, and the New Britain General Hospital,
New Britain, Connecticut.
of PBK. However, the majority of surgeons today still
employ the intracapsular technique.
The few previous reports on PBK do not thoroughly
discuss the condition of the eye prior to cataract ex-
traction or during the cataract and intraocular implant
surgery. To fill this void, we retrospectively reviewed 66
eyes with PBK, with particular reference to a variety of
etiologic factors, and the results of therapy by PK.
To confirm our suspicion that the incidence of corneal
decompensation following IOL insertion was signifi-
cantly greater than after simple cataract extraction, we
retrospectively reviewed almost 4,000 cataract proce-
dures from the senior author's practice from 1955 to
1979.

Presented at the Eighty-seventh Annual Meeting of the American Acad-
emy of Ophthalmology, San Francisco, Califomia, October 30-November
5,1982.
Reprint requests to Daniel M. Taylor, MD, 300 Kensington Avenue, New
Britain, CT 06050.
PATIENTS, MATERIALS, AND METHODS
From 1977 to 1981, we performed 81 penetrating
keratoplasties on 66 eyes for PBK (32 patients were re-
ferred and 34 were from our own practice). Twenty-four

0161-6420/83/0100/019/$1.10 American Academy of Ophthalmology 19

 OPHTHALMOLOGy" JANUARY 1983 VOLUME 90 NUMBER 1

Table 1. Visual Results of 37 Clear Grafts Table 3. Visual Aciuty <20/100-15 Clear Grafts

20/20-2 SMD 7
20/30-2 Chronic CME 4
20/40-6 Macular hole 2
20/50-1 Glaucomatous optic atrophy 1
20/60-2 Epithelial keratopathy 1
20/70-2
20/80-1 SMD = senile macular degeneration; CME = cystoid macular edema
20/200-7
20/400-2
CF -5 assumptions. (1) The incidence of coexisting eye disease,
HM -1 such as endothelial guttata, chronic controlled glau-
Undetermined-6 coma, diabetic retinopathy, etc, are presumed equal for
the two groups. The exact incidence of preexisting en-
CF = counting fingers; HM = hand motions. dothelial disease is not established because of our chang-
ing awareness and expertise in the recognition of subtle,
had significant pathology prior to cataract surgery con- but significant cellular changes. Allowance must also be
sisting of glaucoma surgery, traumatic corneal injury, made for less accurate recording of data in previous
inflammatory corneal scarring, or previous corneal decades in comparison with present day standards. The
transplantation, and were excluded from the study to assumption that the incidence of preexisting endothelial
reduce the number of variables. The remaining 42 eyes disease was similar for the two groups is reasonable and
with PBK were from an average cataract population. more accurate than an attempt to determine exact num-
They were reviewed for preoperative, operative, and bers by analysis of incomplete data under differing ex-
postoperative factors that might have contributed to the amination conditions. (2) The incidence of corneal de-
development of PBK. compensation in both series is presumed to be reason-
All eyes had undergone intracapsular cataract extrac- ably accurate since postsurgical cataract patients that
tion and implantation of iris-supported lenses. The in- undergo a marked visual change usually report for ex-
traocular lens styles were 20 Platina clip lenses, 16 Cope- amination unless precluded by severe illness, death, or
land lenses, 4 Sputnik lenses, and 2 Worst Medallion change in location. The latter fact precluding, follow-up
Iris suture lenses. There were 10 male and 32 female examination should be similar for the two groups.
patients, averaging 76.3 years of age. The PBK appeared
between 1 and 72 months postcataract extraction and
intraocular lens insertion, with a mean of 23 months. RESULTS OF PENETRATING
Follow-up time postkeratoplasty averaged 18 months, KERATOPLASTY
ranging from 3 to 55 months.
All corneal grafts were performed under local anes- Thirty-seven of the 42 eyes that received a penetrating
thesia with intravenous Inovar and mannitol. When keratoplasty for PBK ultimately have clear grafts. The
necessary, the donor corneal endothelium was protected IOL was removed in 7 of the 42 eyes and allowed to
from the pseudophakos by either Healon or the use of remain in 35 patients. Ten of the 42 patients (23.8%)
a lamellar endothelial cushion removed from the recip-
ient cornea. A 0.5-mm, oversized donor cornea button
was used in all cases. Table 4. PBK-Predisposing Factors-42 Eyes
A retrospective chart review was also accomplished
on a continuous series on 800 eyes on which we per- I. Preoperative
A. Corneal endothelial guttata 9 (21%)
formed ICCE with iris-supported lens implantation from B. Glaucoma (no prior surgery) (one patient had both) 5 (12%)
1975 to 1979 and a series of 3000 simple ICCE per-
formed from 1955 through 1979 to determine the in- 13 (31%)
cidence of postsurgical corneal decompensation requir- II. Operative
ing penetrating keratoplasty. Both series represent an A. Vitreous loss 4 (9%)
average cataract population of similar age that would B. Endothelial trauma (two patients had both) 10 (24%)
be encountered and operated upon in a routine clinical 12 (29%)
practice. The series are of sufficient size to make several
III. Postoperative
A. Uveitis/Vitritis 29 (69%)
Table 2. Visual Aciuty-31 Clear Grafts B. CME 13 (31%)
C. Glaucoma 7 (16%)
20/20-20/40 32% D. Trauma (IOL subluxation) 8 (19%)
20/20-20/80 51% 31 (74%)
20/100-LP 49%
PBK = pseudophakic bullous keratopathy; CME = cystoid macular
LP = light perception. edema; IOL = intraocular lens.

20
 TAYLOR, et al PSEUDOPHAKIC BULLOUS KERATOPATHY

required a regraft. The ten regrafts were necessary for

the following reasons: two corneal ulcers (one bacterial,
one fungal), one endophthalmitis following suture re-
moval, one glaucoma, and six irreversible. graft rejec-
tions. Of the ten regrafts, five are clear whIle five have Pre-op
varying degrees of graft edema or opacities. Of the five
patients with nonclear regrafts, one is a primary graft
failure, three have recurrent epithelial defects, and one 2
has poorly controlled glaucoma with graft edema.
Spectacle visual acuity was obtained in 31 of the 37
patients with clear grafts (Table 1). (Two patients had
unresolved vitreous hemorrhage, one had an inoperable
total retinal detachment, one is deceased, and two are
senile.) Of these 31 patients, 10 (32%) have vision 20/
40 or better 16 (51 %) have vision 20/80 or better, while
15 (49%) h~ve vision worse than 20/100 (Table 2). It is
expected that vision will improve as irregular astigma-
tism diminishes in patients who still have sutures to be
removed. The reasons for visual acuity worse than 20/
100 with a clear graft (15 patients) are: seven patients
have senile macular degeneration, two patients have
macular holes, four patients have chronic cystoid mac-
ular edema, one patient has glaucomatous optic atrophy,
and one patient has epithelial keratopathy (Table 3). Fig 1. PBK, predisposing factors, 42 eyes. Five patients had no pre-
disposing factors.

DISCUSSION
a continuous series of 800 eyes that received an ICCE
and iris-supported lens insertion from 1975 to 1979, 34
We divided the 42 patients with PBK into three eti- eyes (4.3%) are known to have developed PBK. This
ologically significant groups with respect to their cataract incidence of PBK compares favorably with the com-
surgery (Table 4). One group had preoperative pathol- bined experience of several authors7 using the intracap-
ogy, one group had operative complications, and the sular technique (Table 5). For comparative purposes we
third group had postoperative complications that we performed a retrospective review of 3,000 ICCE pe~
believe contributed to the development of PBK. The formed by the se\lior author from 1955 to 1979. Th~s
preoperative factors were endothelial guttata and med- revealed that only 24 patients (0.8%) developed aphakic
ically controlled glaucoma (with no prior surgery). Op- bullous keratopathy requiring penetrating keratoplasty.
erative factors were vitreous loss and endothelial trauma, Of this latter series, 5 had preoperative endothelial gut-
either from endothelial touch with the intraocular lens, tata, 2 had preoperative glaucoma with previous ~ltering
excessive manipulation, or excessive irrigation. Post- procedures, 15 had endothelial trauma at the tIme of
operative factors were chronic uveitis/vitritis, cystoid surgery, and 2 had postoperative vitreous-corneal ~d
macular edema, glaucoma, and endothelial trauma from herence (Table 6). In comparing this separate senes,
intraocular lens subluxation. where the patient age is similar and the incidence of pre-
The etiology of PBK is frequently multifactorial with existing, coexisting eye disease is presumed to be similar,
these eyes often being seriously diseased. Thirteen pa-
tients (31 %) had preoperative factors. Nine of these pa-
tients had endothelial guttata, five had glaucoma, and Table 5. Incidence of PBK
one had both. Twelve patients (29%) had operative fac-
tors. Ten of these patients had endothelial trauma, four Binkhorst 45/1005 4.5%
had vitreous loss, and two had both. Thirty-one patients Worst 44/1813 2.4%
(74%) had postoperative factors that frequently over- Hirschman 36/1011 3.6%
lapped. Twenty-nine of these patients had uveitis/vitri- Jaffe 5/500 1.0%
tis, 13 had CME, 7 had postoperative glaucoma, and 8 Drews 2/300 0.7%
had subluxated intraocular lenses with intermittent en- Tennant 4/160 2.5%
dothelial touch. Forty percent of these eyes had risk fac- Shepard 9/500 1.8%
Duffner 65/623 10.5%
tors from more than one group (Fig 1). Most interesting Berkowitz 14/226 6.2%
is that 5 of the 42 patients had no identifiable predis- Baggeson 13/203 6.4%
posing factors to PBK. Williamson 3/200 1.5%
To determine the senior author's incidence of postcat- Gentry 3/103 2.9%
aract extraction corneal decompensation requiring PK,
Total 240/6644 3.6%
our retrospective chart review revealed the following. In

21
 OPHTHALMOLOGY JANUARY 1983 VOLUME 90 NUMBER 1

Table 6. ABK Post-ICCE 24/3000 = 0.8%
I. Pre-operative factors
A. Corneal endothelial dystrophy
B. Glaucoma-previous filtering surgery
II. Operative factors
A. Endothelial trauma
1. Unplanned EECE c excessive manipulation
2. Endothelial damage from erisiphake
3. Cryosurgery-endothelial contact
B. Expulsive hemorrhage
III. Postoperative factors
A. Vitreous touch syndrome (Endothelial
dystrophy-1)
the incidence of PBK appears to be five times greater
than the incidence of simple ABK (X2 = 49.89, P
< 0.005).
The incidence of PBK in our series could have been
reduced from 4.3% to approximately 2% by a more se-
lective surgical approach. In the absence of compelling
circumstances, it seems wise to avoid lens implantation
in patients with low preoperative endothelial counts
(endothelial guttata or glaucoma), and to abort the in-
sertion of an intraocular lens in the presence of multiple
operative complications. Further reduction in the inci-
dence may have occurred if Healon had been available
from 1975 to 1979 by reducing the chance of endothelial
damage. Extracapsular cataract extraction with posterior
chamber lens insertion may have eliminated those cases
that were due to chronic irritation and inflammation
secondary to pseudophakodonesis or to anterior sub-
luxation of iris-fixated intraocular lenses.
Fifty percent of our cases of PBK were unavoidable
and were due to the presence of the intraocular lens.
While the majority of pseudophakic patients do well,
some respond to the presence of the intraocular lens
with chronic low-grade inflammation that can lead to
the development of cystoid macular edema and gradual
5 attrition of endothelial cells. Chronic glaucoma can have
2 a similar effect on the endothelium. Five eyes in this
7 series appear to have no explanation for endothelial de-
compensation. It has been reported, however, by Ra0 8
16 and Kraff,9 that the presence of an iris-supported lens
5 may result in gradual attrition of corneal endothelial
1
cells. This may be due to continuous bombardment of
10
2
the endothelium with shock waves resulting from pseu-
dophakodonesis, or internal motion of the iris-supported
18 intraocular lens following intracapsular cataract extrac-
tion. The added manipulation of intraocular lens im-
plantation following uncomplicated ICCE results in
2 greater loss of endothelium compared to a simple ICCE,
regardless of the skill of the operator. If the lens delivery
and intraocular lens insertion are traumatic, however,
corneal decompensation can occur even if the preop-
erative endothelial cell count was normal.
Our surgical results on penetrating keratoplasty for
PBK following ICCE parallel the results of other au-
thors2-6.1O (Table 7). Eighty-eight percent of our patients
have clear grafts, although ten required regrafting for
various reasons. The visual results are not as satisfactory,
however, as patients with poor vision have retinal pa-
thology to account for their final visual acuity. Fine2 also
shows retinal pathology to be responsible for diminished
vision with clear grafts. Of his ten patients with vision
worse than 20/40, four had senile macular degeneration,
four had cystoid macular edema, and two had glaucoma-
tous damage.
The patients described by Fine,2 Waltman,3 and
Meyer4 seem to have better visual acuity than those de-
scribed by Charlton,5 Arentsen,6 Welch,1O and this au-
thor. Direct comparisons are difficult to make, however.
Fine's follow-up is relatively short; Waltman does not
report visual acuities on patients followed less than one
year after surgery; and Meyer reports on a mixed series

Table 7. Penetrating Keratoplasty for PBK

Total % of Pts. with 10L Vision

Author No. Eyes No. PKs Clear Grafts Follow-up (months) Removal 20/20-20/40 20/50-20/100 20/200-NLP

Fine2 16 17 100% 6-12 5/16 37.5% 37.5% 25%

Waltman 3 36 38 94% 12 in 24 pts 5/36 54% 25% 25%
Meyer & Suga~ 25 25 88% 6-41 (mean 20) 11/25 52% 16% 32%
(18 ICCE)
Charlton, Binder & 19 ? ? mean 13.1 11/19 16% 42% 42%
Perl 5 (? no. of ICCE)
Arentsen & Laibson 6 36 36 94% 6 (ave. 18) 18/45 33% 56% 11%

Welch, Waring, Wilson 35 35 91% ?20 (part of larger series) 35/35 53% (20/80)
& Cavanaugh 10 47% (20/20-20/70)

Taylor, Atlas, 42 52 88% 1-51 (mean 14.8) 7/42 32% 19% 49%
Romanchuk & Stern

PBK = pseudophakic bullous keratopathy; PK = penetrating keratoplasty; 10L = intraocular lens; NLP = no light perception; ICCE = intracapsular cataract extraction.

22
 TAYLOR, et al PSEUDOPHAKIC BULLOUS KERATOPATHY
with 28% of patients undergoing extracapsular cataract
extraction,
The question of whether to remove the implant at the
time of keratoplasty remains unanswered. Welch et al
removed the intraocular lenses in 100% of their patients
with no apparent improvement in either graft clarity or
final visual acuity compared to patients of the other au-
thors. Charlton et al state, "There was no difference in
the ultimate visual acuities when an IOL was removed
or left in situ as far as achieving better than 20/100
vision." Arentsen states that, "Every effort should be
made to retain the intraocular lens. . . ." It has been
our policy to retain the implant whenever possible. We
have removed those lenses{7 out of 42) that we believed
were actively contributing to the corneal decompensa-
tion due to malposition, poor support, or chronic in-
flammation.
By late 1979, the rising incidence of serious CME and
corneal decompensation with relatively poor visual re-
sponse to penetrating keratoplasty led to a reevaluation
of cataract surgical methods and choice of implant.
Binkhorst,1I Worst,12 and others have argued for many
years that the presence of an intact posterior capsule
with containment of the vitreous within its normal con-
fines resulted in an anatomically stronger eye that ap-
proximates the normal phakic condition, thus reducing
the incidence of aphakic retinal detachment and CME.
This in turn permits a placement of a posterior chamber
intraocular lens into the capsule bag or ciliary sulcus,
which again closely approximates the normal anatomic
and physiologic position ofthe lens, resulting in stability
and normal iris function. The stable fixation of the im-
plant at a point furthest removed from the corneal en-
dothelium, with little or no chance of anterior sublux-
ation, reduces the opportunity for endothelial trauma.
Endophthalmodonesis and pseudophakodonesis are re-
duced to a minimum. The continuous shock waves from
internal motion are believed to play a significant role
in the development of cystoid macular edema, retinal
detachment, and endothelial cell attrition with subse-
quent corneal decompensation. Pseudophakodonesis
can lead to chronic iris irritation and liberation of in-
flammatory mediators (prostaglandins) that can cause
further attrition of the endothelium.
Belief in these concepts has led to a recent trend away
from intracapsular cataract extraction towards extra-
capsular cataract extraction (ECCE) with posterior
chamber (PC) lens insertion. In late 1979, we converted
to the extracapsular technique in an effort to improve
our long-term results. In over 300 patients, only one
(0.3%) developed PBK. The results to date of expert
extracapsular surgeons are equally as gratifying. Kratz 13
reports zero cases ofPBK following 2,500 cases of ECCE
and posterior chamber IOL implantations. These results
are premature, however, and may be misleading. Pseu-
dophakic bullous keratopathy usually does not occur
until one to four years or longer (average two years)
following lens implantation. More time is required to
judge the long-term effects of ECCE with PC lenses.
Furthermore, the conversion from the intracapsular
technique to the extracapsular technique is difficult for
even the expert intraocular surgeon. During the learning
experience, there will undoubtedly be instances of in-
advertent endothelial trauma that would not be en-
countered with the more familiar intracapsular tech-
nique. It is possible that a sudden mass shift from the
intracapsular technique to the extracapsular technique
might easily result in a marked rise in the incidence of
PBK. This could prove highly significant when one con-
siders that approximately one-half of all cataract ex-
tractions in the United States currently incorporate an
intraocular lens. 14
CONCLUSION
This review has led to the following conclusions: (1)
The implantation of an iris-supported intraocular lens
following intracapsular cataract extraction significantly
increases the long-term risk of corneal decompensation
through a variety of mechanisms. While the majority
of patients do well, a 4.3% incidence of pseudophakic
bullous keratopathy is unacceptable. This should lead
to a gradual reduction in the use of iris-supported in-
traocular lenses. (2) Eyes with guttata or chronic glau-
coma or previous ocular surgery should have careful
evaluation of endothelial health including specular mi-
croscopy prior to consideration of IOL surgery. (3)
Mounting evidence suggests that skillfully performed
extracapsular surgery with posterior chamber intraocu-
lar lens implantation in eyes with normal endothelium
will greatly reduce the incidence of long-term corneal
decompensation. More time is required, however, for
absolute proof. It is also recognized that the probable
benefits of extracapsular surgery can easily be off-set by
surgical inexperience.
ACKNOWLEDGMENT
The authors gratefully acknowledge Janet Snyder for typing
this manuscript.
REFERENCES
1. Smith RE, McDonald HR, Nesburn AB, Minckler OS. Penetrating ker-
atoplasty: changing indications, 1947 to 1978. Arch Ophthalrnol
1980; 98:1226-9.
2. Fine M. Keratoplasty for bullous keratopathy with intraocular lens.
Am Intraocullmplant Soc J 1978; 4:12-13.
3. Waltman SR. Penetrating keratoplasty for pseudophakic bullous ker-
atopathy: visual results. Arch Ophthalmol1981, 99:415-16.
4. Meyer RF, Sugar A. Penetrating keratoplasty in pseudophakic bullous
keratopathy. Am J Ophthalmol 1980; 90:677-81.
5. Charlton KH, Binder PS, Perl T. Visual prognosiS in pseudophakic
corneal transplants. Ophthalmic Surg 1981; 12:411-19.
6. Arentsen JJ, Laibson PRo Surgical management of pseudophakic
corneal edema: complications and visual results following penetrating
keratoplasty. Ophthalmic Surg 1982; 13:371-3.
7. Drews RC. Symposium: complications of modern surgical proce-
dures, inflammatory response, endophthalmitis, corneal dystrophy,
23
 OPHTHALMOLOGY JANUARY 1983
glaucoma, retinal detachment, dislocation, refractive error, lens re-
moval, and enucleation. Ophthalmology 1978; 85:164-75.
8. Rao GN, Stevens RE, Harris JK, Aquavella JV. Long-term changes
in corneal endothelium following intraocular lens implantation. Oph-
thalmology 1981; 88:386-97.
9. Kraff MC, Sanders DR, Lieberman HL. Does intraocular lens implan-
tation cause continuing endothelial cell loss? (Abstract) Ophthal-
mology 1981; 88(9s):52.
10. Welch NS, Waring GO III, Wilson LA, Cavanagh HD. Results of pen-
etrating keratoplasty in pseudophakic and aphakic corneal edema.
(Abstract) Ophthalmology 1981; 88(9s):71.
Discussion
by
W. Stanley Muenzler, MD
Doctor Taylor and associates provide us with data not pre-
viously reported. First, the incidence of pseudophakic bullous
keratopathy (PBK) does indeed appear to be significantly
greater than aphakic bullous keratopathy (ABK). They have
also given us insight into the etiology of PBK that we must
understand if we are to reduce the incidence. Arentson and
Laibson I point out that 50% of the contralateral eyes in their
series of 40 cases of PBK had endothelial dystrophy. In my
study of the endothelium 2 about 20% of those examined be-
tween ages 60 and 80 had guttata, with a much higher inci-
dence in women. The five patients the authors present with
no identifiable predisposing factors might be abnormal if ex-
amined with the specular microscope as suggested by Abbott
et al. 3 Cataract surgeons today are and must be more aware
of the endothelium and must continue to evaluate it under
high magnification. Sodium hyaluronate appears to protect the
endothelium, but does not eliminate damage to it. 45 Before
surgery we must be aware of the intermittent touch syndrome
recently described by Drews. 6 This consists of ciliary flush,
localized corneal edema, and cystoid macular edema. Elimi-
nation of the touch may reverse the syndrome.
The highest incidence of PBK would appear to be in a
woman with guttata and/or glaucoma, with an iris-fixated lens,
who has any sort of operative incident who requires any sec-
ondary procedure or develops uveitis or glaucoma before sur-
gery. No lens is immune. I have seen PBK with posterior cham-
ber lenses and in an increasing number with anterior chamber
lenses.
Most authors agree that the intraocular lens should be re-
tained if possible. This makes sense if the indication for the
lens was appropriate in the first place. Thus far, no mention
has been made of replacing the offending lens. If the lens could
not be fixated properly, had metal loops, or poor position, then
Hall and J1 replaced them with a more secure lens, usually
following vitrectomy. We replaced 40 implants in 62 cases,
and visual results have been as good or better than other series
reported. Whether replacing the lens will prevent long-term
decompensation of the grafted cornea only time will tell, but
that is our feeling.
From the Department of Ophthalmology, The University of Oklahoma
Health Sciences Center, Oklahoma City, Oklahoma.
24
VOLUME 90 NUMBER 1
11. Binkhorst CD. Corneal and retinal complications after cataract ex-
traction: The mechanical aspect of endophthalmodonesis. Ophthal-
mology 1980; 87:609-17.
12. Worst J. Extracapsular surgery in lens implantation. (Binkhorst lec-
ture) Part IV. Some anatomical and pathophysiological implications.
Am Intraocullmplant Soc J 1978; 4(1):7-14.
13. Boyd BF, Kranz RP. The contributions of posterior chamber intra-
ocular lenses-surgical technique. Highlights of Ophthalmology, Silver
Anniversary Volume, 1981; 950.
14. Boyd BF. What is the present status of intraocular lenses? Highlights
of Ophthalmology, Mini-Highlights 1981; IX, no. 16.
The high percentage of graft clarity and the relatively poor
visual results have been reported several times in PBK and
ABK. This is true, but most patients are improved. Although
Taylor and associates and others89 do not mention preoper-
ative visual acuities, I am certain that most of their patients
were in the finger counting range like those of Hall and I and
others. I ,7,1O Before surgery most patients are better than 20/
200 with about 60%, 20/80 or better, and relieved of the dis-
comfort that many of them have.
Finally, I have recently seen three patients with PBK whose
eyes looked entirely different at the time of keratoplasty than
they did a few months earlier while waiting for corneas. These
eyes showed a marked increase in corneal thickness and vas-
cularization, with shallowing to absence of the anterior cham-
ber. I recommend that patients with PBK be considered for
keratoplasty without long delays when possible.
REFERENCES
1. Arentsen JJ, Laibson PA. Surgical management of pseudophakic
corneal edema: complications and visual results following penetrating
keratoplasty. Ophthalmic Surg 1982; 13:371-3.
2. Muenzler WS. The Progression of Cornea Guttata. Poster presen-
tation. American Academy of Ophthalmology, Chicago, November
2-7, 1980.
3. Abbott RL, Fine BS, Webster RG Jr, et al. Specular microscopic and
histologic observations in nonguttate corneal endothelial degenera-
tion. Ophthalmology 1981; 88:788-800.
4. Lazenby GW, Broocker, G. Use of Sodium Hyaluronate (Healon) in
Intracapsular Cataract Extraction with Insertion of Anterior Chamber
Intraocular Lenses. Ophthalmic Surg 1981; 12:646-9.
5. Percival P. Protective role of Healon during lens implantation. Trans
Ophthalmol Soc UK 1981; 101 :77-8.
6. Drews RC. Intermittent touch syndrome. Arch Ophthalmol 1982;
100:1440-1.
7. Muenzler WS, Hall JA. Keratoplasty for pseudophakic bullous kera-
topathy. Presented at The University of Oklahoma, College of Med-
icine Sixth Annual Spring Meeting, April 3, 1982.
8. Waltman SA. Penetrating keratoplasty for pseudophakic bullous ker-
atopathy: visual results. Arch Ophthalmol 1981; 99:415-6.
9. Meyer RF, Sugar A. Penetrating keratoplasty in pseudophakic bullous
keratopathy. Am J Ophthalmol 1980; 90:677-81.
10. Charlton KH, Binder PS, Perl T. Visual prognosiS in pseudophakic
comeal transplants. Ophthalmic Surg 1981; 12:411-9.