A 55-year-old white male presents with an anterior iritis and secondary glaucoma, O.D.
The patient has a history of cataract extraction without intraocular lens implantation in
1983. In 1987, an anterior chamber IOL was implanted. An ACIOL was chosen.
Theoretically, the optics provided by an ACIOL would be most identical with the gas
permeable contact lens he habitually wore.
After being treated elsewhere, he first presented to the Ophthalmology department. He
indicated being treated for increased intraocular pressure and reports using cosopt b.id.
brimonidine b.id., and atropine b.id. Also, acetazolamide 500mg b.id., of which he ran out
five days ago. Systemically, there is a history of hypertension, hyperlipidemia, and
hypothyroidism. Visual acuity at initial presentation was 20/60 improving two lines to
20/40, O.D. and 20/20 O.S. Intraocular pressure measured 35mmHg and 19mmHg, O.D.
and O.S., respectively. Biomicroscopy showed normal conjunctiva and cornea. There was
grade 1 cell and flare, O.D. O.S. is quiet. Gonioscopic evaluation of the angle revealed
some rubeosis and blood staining as well as small areas of synechiae near the ACIOL
haptics. Also, the implant appeared to be misplaced, with the superior haptic against iris
tissue, not with the angle. The inferior haptic is well-placed. Iris atrophy was present at
the area of contact with the ACIOL. Dilated examination showed some cells in the
vitreous. The cup–to-disc ratio was 0.6. Retinal examination was otherwise normal. It
seems that the source of the inflammation is the mechanical contact to the iris by the
misplaced haptic. That, the misplaced haptic’s chronic rubbing against the iris tissue
triggered the anterior chamber response. The patient was diagnosed with UGH syndrome.
He was instructed to continue with current medications; cosopt, brimonide, and atropine
b.id. Acetazolamide 500mg b.id. was restarted, and Lotemax q2h was added to reduce
intraocular inflammation. He was asked to return the next day for re-evaluation.
Two weeks later, the patient returns having missed his follow-up appointments, and is
scheduled with optometry. He reports taking all medications as prescribed, but was still
bothered by his right eye, noting occasional pain. Visual acuity dropped to 20/80, with
improvement by pinhole to 20/30, O.D. O.S. was 20/20. Slit lamp examination showed
some injection to the conjunctiva. The cornea was mildly inflamed with diffuse
microcysts and punctuate keratitis. A grade 1+ reaction was evident in the anterior
chamber. O.S. was unremarkable. Intraocular pressure measured 55mmHg, O.D., and
11mmHg, O.S. Gonioscopy was repeated. The angle was completely obscured with no
structures visible. Close examination revealed a crowded angle. Aqueous outflow was
blocked because the anterior chamber lens’ haptics pushed the peripheral iris tissue into the
angle. Dilation of the pupil with atropine, and the resultant fattening of peripheral iris
tissue combined with the effect of a misplaced ACIOL haptic resulted in angle closure.
The patient’s diagnosis, and thus treatment, of his UGH syndrome became complicated by
appositional angle closure. The patient was to discontinue atropine, allowing the iris tissue
to de-crowd the angle, thus restoring aqueous outflow. The patient was to continue all
other medications; brimonidine, cosopt, lotemax b.id., and acetazolamide 500mg b.id.
At follow-up three days later, the patient reports improved comfort and vision in his right
eye. Acuity measured 20/40, pinholing to 20/30, O.D. and 20/20 O.S. Slit lamp
examination showed mild conjunctiva injection. The right cornea showed mild
microcystic edema and SPK. There was a grade 1+ anterior chamber reaction, O.D. O.S.
was quiet. Intraocular pressure measured 26mmHg O.D. and 12mmHg O.S. The patient
was to continue with medications as previously scheduled, and will return in three days.
The patient continues to report comfort, O.D., as well as improving vision. Visual acuities
were 20/50, pinhole to 20/30, O.D., 20/20, O.S. There was some mild injection and
corneal edema present by biomicroscopic examination. A grade 1 anterior chamber
reaction was evident. Intraocular pressure was 22mmHg and 12mmHg. Despite better
intraocular pressure control, the best long term solution in UGH is IOL removal. The
patient was scheduled for explanation of the anterior chamber IOL in one week’s time.
Until then he will continue his medications as prescribed, and begin moxifloxacin t.id.
three days prior to surgery.
The surgery was performed without incident and the patient tolerated the procedure well.
He was instructed on ocular medications; brimonidine and cosopt b.id., acetazolamide 500
mg b.id., and tobradex ung q.id. Atropine was also re-started b.id. with the understanding
that its use would not result in angle closure as the misplaced haptic is no longer an issue.
At his one day post-operative appointment, the patient reported no pain or discomfort.
Acuity measured 20/100 with a +10 lens and a pinhole. The wound appeared intact and
sterile. There was a grade 2 anterior chamber reaction. Intraocular pressure measured
12mmHg, O.D. He was to continue with current medications and return in a few days.
In four days, he returns for follow-up without complaint. Visual acuity is 20/100. The
wound is healing well, and a 1+ anterior chamber reaction is present. Intraocular pressure
is measured at 8mmHg. He is to return in one week. Atropine was discontinued, tobradex
tapered, all other medications were maintained.
When he returned in one week, he is refracted to 20/30. Intraocular pressure is 12mmHg,
O.D. A grade 1 anterior chamber reaction is present. At this time, the patient’s
intraocular pressure has stabilized and his pressure medications will be tapered slowly.
Whether or not pressure will stay controlled is unsure given the uncertainty of damage to
the angle, trabecular meshwork, and the optic nerve.
Abstract
This describes an interesting case of UGH syndrome, which became complicated by
appositional angle closure resulting from a misplaced haptic. UGH syndrome is classically
defined as uveitis, an increase in intraocular pressure, and hyphema, and occurs as a direct
result of ocular insult to the blood-aqueous barrier by an intraocular lens. The patient
experienced moderate uveitis and a significant increased in intraocular pressure.
Additionally, the misplaced haptic it also contributed to appositional angle closure.
Surgical intervention became necessary. After the removal of the offending IOL,
inflammation was and intraocular pressure was controlled.
Introduction
Uveitis following cataract surgery, either from toxic lens syndrome or Uveitis-GlaucomaHypehma (UGH) syndrome, is attributed to faults of the intraocular lens (IOL). Toxic lens
syndrome, referring to the ocular reaction to the chemical finish placed on the IOL during
manufacturing, has largely been eliminated due to the advance in IOL lens design,
processing and production. UGH syndrome has become increasingly less common with
advances in both design and surgical techniques. Resulting from seemingly
uncomplicated cataract extraction surgery, chafing and erosion into the iris by the
intraocular implant disrupts the blood-aqueous barrier. Release of chemical mediators
drive inflammation and pressure increase. Hyphema develops as blood leaks into the
anterior chamber.
UGH syndrome has commonly been linked to anterior chamber IOLs, largely due the close
anatomical position with the iris. However, posterior chamber IOLs can cause UGH
syndrome. Consequences of UGH can lead to visual impairment from unchecked
glaucoma, chronic inflammation, or cystoid macular edema.
UGH was first described by Ellingson1, who noted post-surgical chronic uveitis with
keratic precipitate formation. Complications came from poor surgical technique or poor
lens design. When the footplate or haptic of an anterior chamber IOL is forcibly placed
into the anterior chamber angle, the edge can cut into the ocular tissue. Similarly, a
selected lens that is too large crowds the anterior structures of the eye. The damage is
evident as hemorrhage and chronic uveitis. Additionally, warpage to the IOL footplate, as
Ellingson observed, led to lens rocking and mechanical irritation resulting in uveitis,
glaucoma, and hyphema.
Furthermore, a poorly finished lens, one in which the footplate or haptic edge is rough, can
cause UGH syndrome. Keates and Ehrlich2 documented several patients with UGH
syndrome that required IOL removal. Close examination of the explanted lenses showed
serrated, uneven edges on the implant. The sharp, unfinished IOL, again, contact the uveal
tissue and erodes into the vascular ocular structures.
A review of the anatomy of the iris reminds us that iris tissue is highly vascularized. These
blood vessels lie superficial, within the anterior portion or the iris stroma. The anatomical
organization makes iris blood vessels susceptible to irritation from an IOL. Chronic
chafing or mechanical irritation against the iris can lead to erosion, a disruption of the
blood-aqueous barrier, and damage to the underlying vascular network3.
Symptoms and Signs
Patient symptoms may include intermittent blur, pain, redness, and photophobia. Some
patients have reported recurrent blurring of vision because of microhyphema and
microhypopyon. This blur has been described as sudden onset, slowing returning to
normal over the course of a few hours to a day. This is attributed to the release of blood
cells, proteins, and inflammatory debris. These are from the breakdown of the iris tissue
from friction against the IOL4. Cates5 describes patients’ UGH symptoms, noting a
complaint of haziness to vision. This, again, occurs suddenly, within minutes, with a
gradual resolution, hours to days. Also, complaint of ache in affected eye is common,
most likely due to uveitis and/or increased IOP.
Recurrent low-grade uveitis results from contact irritation between the iris or ciliary body
tissue and the IOL. Physically, there is erosion of ocular tissue and a breakdown of the
blood-aqueous barrier, specifically at the level of the tight junctions between the epithelial
cells. The chronic contact increases the possibility of release of substances within the eye
that may cause inflammation6. The degree to which the blood-aqueous barrier is disrupted
is in proportion to the severity of the patient’s symptoms and clinically evident signs7.
Clinical findings may be relatively slight, almost undetectable, or may be quite obvious. A
spectrum of clinical evidence exists, including pigment defects of the iris, pigment
dispersion, an increase in intraocular pressure, anterior chamber cell and flare, keratic
precipitates, microhyphema, or macrohyphema 7,8. The degree to which these findings
present, again, depend on the severity of damage to the blood-aqueous barrier 7,8. A
variable amount of any of these signs may occur, and not all may be present.
Microscopic evidence of hyphema may or may not be evident since blood is quickly
reabsorbed. A hyphema may have been present when the patient first began to have
symptoms, but the presence of this clinical finding is not necessary to make a UGH
diagnosis 4,5.
The increase in intraocular pressure is triggered by the ocular inflammation, again, induced
by IOL touch on the iris or ciliary body, may occur by several mechanisms. Occlusion of
the trabecular meshwork with inflammatory debris can cause blockage of aqueous outflow.
Pupillary block can also occur. The inflammatory proteins circulating within the anterior
chamber are sticky. The particles can attach the iris to the IOL restricting aqueous flow
from the posterior chamber. Mechanical injury to the trabecular meshwork, perhaps during
IOL implantation, may reduce outflow. Also, a response to topical steroids can trigger a
pressure increase9.
Anterior Chamber IOLs
UGH syndrome has most commonly been associated with anterior chamber IOLs.
However, not all anterior chamber IOLs carry the same risk. A closed loop anterior
chamber IOL carries a somewhat greater risk for UGH development than an open loop
anterior chamber IOL. This is essentially due to the physical structure of the lens design.
A closed loop lens, while being more difficult to size correctly and fit properly, makes
contact with a greater area of intraocular tissue. By combining a greater contact zone with
a lens that may be inappropriately placed, chances for complications increase.
Additionally, these lenses tend to be manufactured poorly, leaving a finished product with
rough, sharp edges. These coarse, irregular can damage uveal tissue quite easily, again,
especially if poorly sized. Conversely, an open loop IOL design, which was developed
later than the closed loop counterpart, are much easier to size, and are manufactured at a
higher quality. This lens design requires less area of contact between the lens and
intraocular contents. As a result, open loop IOLs carry less chance of complications when
compared with closed loop anterior chamber IOLs.
Posterior Chamber IOLs
Moreover, UGH syndrome is not unique to anterior chamber IOLs or iris-fixed IOLs and
can occur with a posterior chamber IOL. Posterior chamber intraocular lenses, although
rare, can also trigger UGH. Unstable lens fixation, misalignment of a haptic outside the
lens capsule, or physical touch to the posterior iris may be responsible. Erosion of the
posterior iris through chronic chafing may be responsible. Iris pigment defects or pigment
dispersion may be seen with little consequence. However, more seriously, intraocular
pressure increase, microhyphema, and recurrent uveitis may accompany these findings as
well8. Aonuma, et al10, report a case of UGH resulting from a posterior chamber
intraocular lens. Unstable sulcus fixation caused lens rotation, resulting in intermittent
blurred vision for two years. The lens was removed, a new implant inserted.
Van Liefferinge, et al11, describe two cases of UGH resulting from asymmetrical bagsulcus fixation of the IOL. Accordingly, the unbalanced lens shifted and eroded into the
ciliary sulcus. The chronic chafing between the IOL and the ciliary structures resulted in
inflammation and bleeding, and an increase in intraocular pressure.
Ultrasound Biomicroscopy
IOLs that are malpositioned can be detected with ultrasound biomicroscopy. Ultrasound
investigation can confirm proximity of a haptic and uveal tissue, confirming areas of
contact and chaffing, and a break in the blood-aqueous barrier. Additionally, assessment
of UGH can be made easier by determining the exact placement of IOL haptics. This is
especially helpful when a view is poor by slit lamp biomicroscopy alone. Ultrasound can
be used to determine the severity of UGH, which is important when determining treatment
plans8.
Nine cases were reviewed retrospectively, and ultrasound biomicroscopy showed
misplaced IOL haptics. Eight of these cases involved posterior chamber IOLs. Of these, it
was most common to find a haptic buried within the iris pigmented epithelium8.
Chen used ultrasound to evaluate surgical placement of haptics forom an open loop
anterior chamber IOL. Fourteen out of forty haptics studied were misplaced and shown to
be located with the iris tissue. All fourteen developed recurrent uveitis12.
Treatment
Treatment of UGH can be complicated and often ultimately necessitates IOL removal. The
goal of any treatment regimen is the resolution of patient symptoms. For this to occur, the
blood-aqueous barrier must remain intact and undisturbed. Pharmacologic manipulation of
the iris tissue through the use of miotics and mydriatics, often in an alternating manner,
may relieve the stress between the IOL and uveal tissue4. Perhaps, by moving iris tissue,
the integrity of the blood-aqueous barrier will unaffected. The IOL haptic can slide into
place where friction is reduced, or at least a position where the chance for complication is
reduced. Certainly, this is not successful in all cases, or even a viable option. Depending
on the degree of inflammation, a miotic pupil may invite synechiae. However, in a
relatively quiet eye, appropriate post-surgical timing, sooner rather than later, and with
haptics in a position where movement is possible, pharmacologic manipulation is an
option.
Initially, non-surgical methods, including use of pharmologic agents, are suggested.
Treating UGH may depend on the severity of the intraocular inflammation and symptoms.
Occasional, mild episodes may best be treated reactively, with topical pharmaceutical
agents. Bed rest is encourage to allow settling and resolution of hyphema, if present7. If
increased intraocular pressure is truly a product of inflammation, it should be controlled
well when topical steroids are administered properly. Aqueous suppressants, either
topically or orally, may be indicated also. It is important to avoid miotics and
prostaglandins in patients with UGH. If further intervention is required to control pressure,
despite the resolution of intraocular inflammation, glaucoma surgery, such as a filtration
procedure, may be required9.
Another option, when recurrent hyphema is dramatic and the predominant finding, is laser
treatment to the iris where the leakage originates. Argon laser photocoagulation applied to
areas of intraocular lens-iris contact is an effective may to control bleeding13. This
treatment option seems best reserved for an otherwise happy pseudophake, who
experiences mild, occasional visual symptoms, while inflammation and pressure are easily
controlled with topical medication. The resolution of late hyphema following IOL
implantation with laser aims for two results. First, closure of the leaking iris blood vessels
occurs. Second, a reduction of the contact area between the iris and the intraocuar lens
eliminates the area of touch. No chaffing can occur and hyphema and inflammation can be
avoided14. This creation of space negates the possibility of blood-aqueous barrier
disruption.
UGH and IOL Explanation
Surgical treatment, IOL rotation or more likely removal, for patients with UGH is
indicated when ocular inflammation and glaucoma are otherwise uncontrollable and the
risk to the eye is great. The IOL is the cause of the problems, through its breakdown of the
blood-aqueous barrier, and thus removal is necessary.
IOL exchange is done when possible. This is determined pre-operatively taking into
account the possibility of clinical improvement, further tissue destruction and
deterioration, and other ocular pathology. Severe glaucoma, corneal decompensation, and
neovascularization will prevent lens exchange. No secondary IOL is indicated when
severe ocular conditions prevent it, or increase the risk of further complications or longterm consequences15.
The selection of a secondary IOL is important. Lens type is determined pre-operatively
based on the support available within the eye16. A patient who has an anterior chamber
IOL removed, should do quite well with a posterior sulcus fit IOL.
A study by Doren, Stern, and Dreibe17, ranks UGH syndrome as the second leading cause
of IOL explantation. This review analyzes 101 cases of IOL removal from 1983 to 1987.
Pseudophakic bullous keratopathy was responsible for nearly seventy percent of IOL
removals. UGH accounted for almost ten percent, and IOL malposition was responsible in
nine percent of the cases. A breakdown of lens types show that these complications arose
with anterior chamber IOLs more frequently than any other lens type: 54 anterior chamber
IOLs in all, 33 closed-loop and 21 open loop. Of the nine cases of UGH, three resulted
from closed loop anterior chamber IOLs, four from rigid anterior chamber lenses, and 2
from iris-fixed lenses. No posterior chamber IOLs were indicated to have caused UGH.
The timing of UGH development proved to be soon after surgery, five cases within three
months, or years later, four cases all of which developed four or more years later. Postoperative results were mixed. Inflammation resolved in all cases. Two cases continued to
have glaucoma, although intraocular pressure was better controlled. The visual results,
however, were less encouraging. Although pre-operative visual acuity was poor, eighty
percent measuring worse than 20/200 due to cystoid macular edema, post-operatively,
patients failed to improve with the same eighty percent still failing to achieve better than
20/200. Patients who developed UGH syndrome had the worst visual outcome postoperatively versus PBK or IOL malposition.
Additionally, Sinskey, et al18, reviewed 79 cases of IOL explanation over a 12 year period,
determing frequency of lens type, primary reason for IOL exchange, and postoperative
results. Unique to this study, was the finding that posterior chamber IOLs were most
commonly involved. This is primarily explained by the fact that, currently, posterior
chamber IOLs are the most common lenses implanted. Complications with fifteen anterior
chamber IOLs were observed. The leading cause of explanation was corneal
decompensation. UGH syndrome was the offending complication in two cases. Iris fixed
IOLs accounted for sixteen of the cases, and UGH was found to be the leading
complication. Poster chambers IOLs, most commonly removed due to dislocation or
decentration, were responsible for UGH on one occasion.
The timing of lens removal varied by IOL type. Posterior chamber IOLs averaged 3.5
years, much sooner than anterior chamber IOLs, 4.3 years, or 7.9 years for iris-fixed IOLs.
The type of complications most associated with each lens type and post-operative timing of
the happening of symptoms, best explain this timeline. A displaced IOL or improper
power IOL may be diagnosed relatively quickly after surgery whereas chronic chaffing, for
example, may take years to develop and manifest symptoms.
Post-operative visual acuity after anterior chamber IOL removal improved; nine of 15
better than 20/40 and none worse than 20/200. Pre-operatively five cases were worse than
20/200. This review further indicates that the closer the association between the IOL and
the uveal tissue, the greater the chance of blood-aqueous barrier disruption and UGH
syndrome of developing.
Furthermore, a retrospective study by Mamalis, et al15, a review of 101 cases of IOL
removal from 1982 to 1989, concluded similar findings. Nearly sixty-seven percent of
IOLs explanated where anterior chamber lenses, with eighteen and sixteen percent irisfixed and posterior chamber IOLs, respectively. Indications for anterior chamber IOLs
ranked UGH second with 13 cases. Pseudophakic bullous keratopathy was the most
common reason numbering 27 cases. Comparing indications for removal of iris-fixed
IOLs, data parallels that of anterior chamber IOLs, PBK ranked first and UGH second.
Fifteen posterior chamber IOLs were removed. One case of UGH was indicated as the
reason for removal. More common indications were malposition and PBK.
Time intervals, implantation to explanation, were analyzed also. Again, iris-fixed IOLs
enjoyed the longest interval, nearly six years. Anterior chamber IOLs averaged three and a
half years. At just under a year and a half, posterior chamber IOLs had the shortest
interval.
IOL exchange was performed in all cases when possible. Most commonly, anterior
chamber lenses were used as the secondary IOL, seventy-two percent of all exchanges.
The remaining twenty-eight percent were posterior IOLs. Examining anterior chamber
IOL exchange results closely, pre-operative visual acuity improved nearly sixty-five
percent of the time. Seven patients with UGH fell into this category. Eleven cases
stabilized, including two UGH patients, accounting for twenty-two percent. In seven
cases, visual acuity worsened, with one case of UGH. When posterior chamber IOLs are
included, eighty five percent of patients improved or maintained their level of visual
acuity. Reasons why patients failed to improve included corneal decompensation,
glaucoma, and cystoid macular edema.
Mamalis19, in a second study showed that two-thirds of 102 patients requiring IOL removal
had anterior chamber IOLs. Again, UGH ranked second behind PBK. Overall, after IOL
removal or exchange, visual acuity improved in thirty nine percent of the patients, while
only fifteen percent worsened. Further corneal decompenstation, glaucoma, and cystoid
macular edema prevented these individuals from improving. Not surprisingly, the patients
who failed to improve were those with more severe complications prior to IOL removal. A
positive predicator of favorable results was early intervention, acting quickly to avoid
severe irreversible consequences
Lyle and Jin20 produced similar numbers in their evaluation of nearly 100 patients.
Improved acuity was measured in eighty-eight percent of cases. PBK, glaucoma and
cystoid macular edema, were the reasons for poor results. Furthermore, they found that
IOL exchange with a posterior chamber IOL produced better results than with an anterior
chamber IOL.
Conclusion
UGH, though uncommon today due to advances in surgical technique and IOL design, can
lead to devastating visual consequences. UGH should be included among differential
diagnoses for uveitis, increased intraocular pressure, and hyphema, occurring individually
or, of course, together. Suspicion of UGH should arise when an anterior chamber IOL is
present; especially one that appears displaced, tilted, or inappropriately fit. Ultimately,
treatment is aimed toward relieving inflammation and controlling intraocular pressure, but
early intervention will avoid damaging consequences and provide a good visual prognosis.
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