Post-vitrectomy Cataract Acceleration in

Phakic Eyes: A Review

Published on December 26, 2017

Author: Khusbu Keyal

Specialty: Ophthalmology
Institution: Department of Ophthalmology, Shanghai Tenth People's Hospital Affiliated to Tongji University School
of Medicine
Address: Shanghai, 200072, China
Author: Xin Liao
Specialty: Ophthalmology
Institution: Department of Ophthalmology, Shanghai Tenth People's Hospital Affiliated to Tongji University School
of Medicine
Address: Shanghai, 200072, China
Author: Guodong Liu
Specialty: Ophthalmology
Institution: Department of Ophthalmology, Shanghai Tenth People's Hospital Affiliated to Tongji University School
of Medicine
Address: Shanghai, 200072, China
Author: Shuai Yang
Specialty: Ophthalmology
Institution: Department of Ophthalmology, Shanghai Tenth People‘s Hospital, Tongji University School of
Medicine
Address: Shanghai, 200072, China
Author: Fang Wang
Specialty: Ophthalmology
Institution: Department of Ophthalmology, Shanghai Tenth People's Hospital, Tongji University School of
Medicine
Address: Shanghai, 200072, China

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Abstract: Vitrectomy is considered the standard therapy for the treatment of posterior segment
disease; however, after a significant improvement of the visual acuity, there is a reduction in
visual acuity due to cataract formation, which requires further surgery. Nuclear sclerotic cataract
(NSC) is the most common type of cataract seen after vitrectomy. The pathogenesis of post-
vitrectomy NSC is unclear; several hypotheses have been formulated without any conclusions. In
order to correct post-vitrectomy NSC, phacoemulsification with intraocular lens implantation is
performed. This surgery itself has some complications, such as longer surgical time and the
increased risk of capsular rupture as compared to phacoemulsification done alone. In this review,
different hypotheses proposed by different authors in their studies and possible measures that
are known so far to prevent post-vitrectomy NSC are discussed along with its treatments and
their complications. Moreover, we aim to describe the pathophysiology of the formation of post-
vitrectomy NSC.

Introduction
In 1971, Robert Machemer introduced pars plana vitrectomy for ophthalmologic surgeries
(Machemeret al., 1971). Since then, the progress in biomedical engineering has led to the
invention of small gauge vitrectomy, which is considered minimally invasive
vitreous surgery (MIVS). As studies have been reported in the past, MIVS can be done by
various approaches, for example, the 25-G sutureless transconjunctival vitrectomy system
(TCVS) introduced by Fujii et al. (2002), 23-G sutureless vitrectomy system introduced by
Eckardt (2005), and the 27-G sutureless transconjunctival vitrectomy system introduced by
Oshima et al. (2010). With advances in such surgical techniques and instrumentation, vitrectomy
has become a common surgical procedure for posterior segment disorders such as non-clearing
vitreous hemorrhage due to diabetic retinopathy or vein occlusions, retinal detachment, macular
hole, macular pucker, vitreomacular traction, tractional macular edema, and others. However,
like all other surgeries, vitrectomy also has some early and late complications. Early
complications include a rise in intraocular pressure (IOP), cannula retraction, retinal break
formation, hypotony, retinal toxicity, etc., and late complications include formation or acceleration
of NSC in phakic eyes (Cherfan et al., 1991; de Bustros et al., 1988; Khanduja et al., 2013). NSC
is the most common cause of the postoperative decrease in visual acuity after successful
treatment of the disease. This limits the visual acuity, which further requires surgical correction.
The preferred method of surgery to correct NSC is phacoemulsification and intraocular lens
implantation. This surgery has two challenging features: (1) hardening of the nucleus as
compared to the age-related nuclear sclerosis, which requires a longer phacoemulsification time
during the procedure, and (2) more mobility of the posterior capsule due to the absence of
vitreous in the posterior segment, which increases the risk of capsular rupture. Thus, surgery for
post-vitrectomy NSC may have a higher probability of complications (Do et al., 2008). The
purpose of the present review is to summarize the hypotheses proposed by different authors in
their studies and possible measures that are known so far to prevent post-vitrectomy NSC along
with its treatment and its complications. Moreover, we aim to describe the pathophysiology of the
formation of post-vitrectomy NSC.
Pathophysiology
NSC is the increase in the stiffness of nuclear cytoplasm of the lens that causes lens
opacification. The mechanism of development of post-vitrectomy NSC is still unclear. To prevent
NSC, a clear understanding of the pathogenic mechanisms of lens opacification is needed.
Transparency and the refractive power of the lens are maintained by a very high protein
concentration. These proteins are protected from oxidation by the low-oxygen environment
around the lens with the help of reducing substances, like glutathione (GSH) and ascorbate
(Beebe et al., 2011). Oxygen levels in the eye are generally low and tightly regulated. In the
normal eye, much of the oxygen is metabolized by the adjacent retinal tissue and molecular
oxygen diffuses into the vitreous gel from the retinal vasculature(Alder et al., 1986), while some
are consumed by reacting with ascorbate in the vitreous gel (Beebe et al., 2014′; Shui et al.,
2009) decreasing the oxygen gradient from the retina to the lens. Thus, oxygen consumption by
the vitreous assures that the crystalline lens remains in a low oxygen environment, which is
thought to be an important factor for the maintenance of lens transparency (Eaton, 1991). The
concentration of antioxidant molecules, such as glutathione, is lowest in the nucleus and highest
on the lens surface (Sweeney et al., 2003). With increasing age and exposure of lenses to
hyperbaric oxygen, glutathione levels markedly decrease in the nucleus, making the nucleus of
the lens sensitive to oxidative insult and resulting in cataract formation (Beebe et al., 2011). A
study (Shui et al., 2009) has demonstrated that ascorbate levels were significantly lower in eyes
with increased vitreous liquefaction or previous vitrectomy, due to a greater mixing of the vitreous
fluid with oxygen, degrading a larger portion of the ascorbate. Therefore, loss of the vitreous gel
structure correlated with loss of vitreous function. According to Calvin et al. (1991), information
about the role of GSH in maintaining lens transparency was found in the intact lens when an
experimental depletion of glutathione by L-buthionine-(S,R)-sulfoximine (BSO), an inhibitor of
GSH biosynthesis, leads to a rapid cataract formation. The lens is an avascular tissue which
depends on diffusion from the retina for its oxygen supply, so elevated oxygen tension in the
vitreous leads to elevated oxygen tension in the crystalline lens which may play a key role in
NSC (Barbazetto et al., 2004). In a normal individual, there is a concentration gradient of oxygen
from the retina into the vitreous gel, when the vitreous gel is intact. If vitreous gel liquefies with
age or is removed by vitrectomy surgery, vitreous fluid can circulate delivering more oxygen to
the lens (Harocopos et al., 2004). A study (Holekamp et al., 2005) has shown an increased
oxygen level in the lens after vitrectomy, which leads to acceleration of NSC (Cherfan et al.,
1991; de Bustros et al., 1988; Margherio et al., 1985; Melberg and Thomas, 1995; Ogura et al.,
1991; Thompson et al., 1995). The incidence of NSC progression is greater in older patients
(Cherfan et al., 1991; Melberg and Thomas, 1995; Novak et al., 1984; Ogura et al., 1991), and
risk increases due to the loss of vitreous gel (Harocopos et al., 2004), as the liquefied vitreous
fluid has a diminished capacity to consume oxygen (Shui et al., 2009). The decrease in
antioxidants such as GSH and ascorbate (Giblin et al., 1995), the oxidation of nuclear proteins at
the center of the crystalline lens (Giblin et al., 1995), and the accumulation of insoluble lens
proteins and pigments (Spector, 1984) are some factors that result in loss of transparency of
the aging lens. When nuclear sclerosis occurs due to aging, it usually develops bilaterally, as
compared to operating eyes that progress unilaterally. Inhaled oxygen concentration influences
oxygen concentration of vitreous gel, as inhaling large percentages of oxygen while receiving
general anesthesia or previous vitrectomy surgery significantly increased intraocular oxygen
tension (Holekamp et al., 2005). While using long-term hyperbaric oxygen therapy, nearly 50% of
patients developed a nuclear cataract in 1 to 3 years. The cataractogenic effect of hyperbaric
oxygen in humans (Palmquist et al., 1984), mice (Schocket et al., 1972), and older guinea pigs
(Giblin et al., 1995) was observed as there was a rapid development of NSC in those who were
exposed to hyperbaric oxygen, which strongly supports the oxidative theory of NSC formation.
Myopia is known to have a higher prevalence of nuclear cataract but the mechanism is not yet
clear. Holekamp et al. (2008) suggested that it is related to the early vitreous degeneration that
accompanies axial elongation. Still, other authors found that patients with high myopia tend to
have vitreous liquefaction and the development of NSC (Bishop, 2000; Morita et al., 1995).
Hypothesis
A number of hypotheses have been postulated regarding the mechanism of the development of
post-vitrectomy NSC, yet it is not clear. Similarly, various preventive measures have been taken
to prevent post-vitrectomy NSC without satisfying results. Multiple factors may contribute to the
development and progression of post-vitrectomy NSC which includes the following.

Infusion solution composition and temperature

Infusion fluids used during vitrectomy may contribute to post-vitrectomy NSC; this may be due to
physiologic differences between the vitrectomy infusion solution and the native vitreous during
vitrectomy. The BSS (balanced salt solution) Plus irrigating solution has been found to cause
less damage to the corneal endothelium than Ringer’s lactate solution (Edelhauser et al., 1978).
But both solutions appeared to have similar effects on nuclear sclerosis progression (Cherfan et
al., 1991). Sawa et al. (2005) suggested that there may be a relationship between BSS and the
progression of nuclear sclerosis. It was thought that high glucose concentrations in the irrigating
solution used for diabetic patients might cause nuclear sclerosis in nondiabetic patients, as it was
observed that glycosylation of lens proteins in patients with elevated glucose levels
from diabetes increased cataract formation. High glucose has been shown to cause non-
enzymatic browning of lens proteins and cataract formation (Stevens et al., 1978). However,
there was a similar nuclear sclerosis progression with a hyperglycemic infusion solution and a
normoglycemic infusion solution (Cherfan et al., 1991). Nonvitrectomizing vitreous surgery was
performed without using a solution or gas for idiopathic epimacular proliferation that prevented
progression of NSC after surgery. This result also suggests that intraocular irrigating solutions
might play an important role in the development of NSC (Sawa et al., 2001). There could be
biochemical changes in the lens, causing increased nuclear sclerosis with temperature
differences between the room-temperature infusion solution and body-temperature crystalline
lens, but it does not appear to increase cataract formation with increased duration of exposure of
the lens to room-temperature infusion solution (Cheng et al., 2001).
Light toxicity
Light toxicity may also be a possible mechanism for cataract progression (Cherfan et al., 1991;
de Bustros et al., 1988). Mitchell et al. (1965) showed that the antioxidant enzyme “catalase” can
be inactivated in the presence of light, suggesting that intensive light exposure from an operating
microscope can be a facilitating factor in post-vitrectomy NSC formation. But the absence of
NSC progression after nonvitrectomizing vitreous surgery suggests that ultraviolet light from the
operating microscope is not the cause of increased nuclear sclerosis following vitrectomy
(Sawa et al., 2001).
Duration of vitrectomy
Initially, it was thought that the duration of vitrectomy increases the risk for NSC progression.
However, according to Cheng et al. (2001), 98% of the NSC incidents progressed at one-year
follow-up and there was no association found between the duration of vitrectomy and vitrectomy-
associated NSC which was observed with vitrectomy duration of 20 to 135 minutes.
Use of tamponade
As stated by previous two studies (de Bustros et al., 1988; Ogura et al., 1991) there is no definite
increase in post-operative NSC with the use of intraocular gas bubbles (air or sulfur hexafluoride)
compared to eyes without intravitreal gas bubbles. However, recent reports found the evidence
of increased nuclear sclerosis in eyes treated with gas tamponade (Hsuan et al., 2001;
Thompson, 2003). Thompson (2003) mentioned that there is a difference in the rate of increase
in nuclear sclerosis with the use of intraocular gas bubbles as compared to eyes without the use
of intraocular gas bubbles. Nuclear sclerosis increased by 60% with intravitreal gas bubbles,
compared to eyes without the use of gas bubbles. According to Hsuan et al. (2001), nuclear
cataract was found in 67% of tamponade cases and 30% of non-tamponade cases. Van
Effenterre et al. (1992) noted that in gas-filled eyes, nuclear sclerosis occurred in 63%. Nuclear
density increased almost 24 times from the baseline value post vitrectomy and gas tamponade
(Wong et al., 2012). A report on a prospective consecutive series showed that vitrectomy done
with long-acting intraocular gas tamponade used for macular hole repair leads to substantial
progression of post-vitrectomy NSC (Thompson et al., 1995).
A gauge of vitrectomy instrumentation
A study (Almony et al., 2012) has shown that the removal of the vitreous gel using any-gauge
vitrectomy surgery leads to significant progression of nuclear sclerotic cataract. It is independent
of the gauge of vitrectomy instrumentation. The finding supports the theory that the vitreous gel
is responsible for protecting the lens from exposure to molecular oxygen within the eye.
Intraoperative oxidation of lens proteins
Increased oxygen exposure to the lens following vitrectomy (Holekamp et al., 2005;
Petermeier et al., 2010) and intraoperative oxidation of lens proteins can be possible
mechanisms (Ogura et al., 1991) for post-vitrectomy NSC, which may be caused by molecular
oxygen from the retinal vasculature reaching to the lens because vitrectomy and vitreous
degeneration increase fluid circulation within the eye (Shui et al., 2009). Mitchell and Anderson
(1965) showed that the antioxidant enzyme “catalase” can be inactivated in the presence of
oxygen and inactivation of antioxidant enzymes in the lens may further promote oxidation of the
lens proteins (Fecondo and Augusteyn, 1983) resulting in NSC acceleration.
Changes of the lens’ biochemical microenvironment
Vitrectomy replaces the gel vitreous with liquid; there are changes in the microenvironment
surrounding the lens, and the fluid flow in the vitreous chamber diffuses oxygen from retina
throughout the eye, instead of being taken up by the adjacent retina, exposing the crystalline
lens to abnormally high oxygen, which may lead to post-vitrectomy NSC formation (Alder and
Cringle, 1985; Holekamp et al., 2005). Removal of the barrier function provided by the vitreous
results in permeability changes in the lens capsule, leading to cataract progression (Cheng et al.,
2001; Thompson et al., 1995). In a study by Holekamp et al. (2010), it was observed that the
source of oxidative damage and NSC is most likely coming from molecular oxygen arising from
the retinal vasculature and if this is not adequately metabolized by the vitreous gel or protective
mechanisms within the lens itself. After nonvitrectomizing vitreous surgery by Sawa et al. (2001),
there was no progression of nuclear sclerosis, supporting the theory of changes in permeability
that causes nuclear sclerosis. Moreover, permeability changes seem most likely, because there
is an increased incidence of nuclear sclerosis in patients with severe myopia and in those with
the Wagner-Stickler syndrome, both of which are associated with large fluid-filled spaces in the
vitreous cavity.
Treatment and Its Complications
In order to correct post-vitrectomy NSC, phacoemulsification with intraocular lens implantation is
performed. Phacoemulsification in vitrectomized eyes can be challenging but is beneficial.
According to different authors as stated below there was a significant improvement in visual
acuity after surgery. In the study by Grusha et al. (1998), the median visual outcome improved
from 20/125 before cataract surgery to 20/30 on the final examination. According to Hutton et al.
(1987), 43% of patients obtained visual acuity of 20/40 or better. According to Titiyal et al.
(2017), the mean improvement in visual acuity by more than two Snellen lines was 79.20% in
silicone oil group and 73.20% in air/gas group. The mean postoperative log mar visual acuity
was better in eyes with air/gas than with oil. Diaz et al. (1998) similarly noted improvement in
visual acuity by more than two Snellen lines in 73.91% eyes. Some disadvantages have also
been reported. A study by Sneed et al. (1986) observed that lens removal may be more
hazardous due to the weakness of the vitreous base support. Grusha et al. (1998) found a 2.3%
incidence rate of posterior capsule tear after vitrectomy. In a few cases, surgery was made
difficult by unusual fluctuations in anterior chamber depth and lens zonule instability, making the
patients more aware of pressure changes (Patel and Miller, 2001). In the study by McDermott et
al. (1997), it was associated with inadequate papillary mydriasis, iris lens excursions, and flaccid
posterior capsule. Cataract tends to be denser than that of normal eyes, increasing the difficulty
of ultrasonic emulsification and the risk of endothelial trauma and thermal corneal injury. The
possibility of occult posterior capsule rupture in the post-vitrectomy eye must be considered
because of capsule instability which occurs due to the absence of vitreous gel. According to
Do et al. (2008), post-vitrectomy phacoemulsification has challenging features, which include
hardening of the nucleus as compared to age-related nuclear sclerosis, requiring longer time
during the procedure, and more mobility of the posterior capsule due to the absence of the
vitreous, increasing the risk of capsular rupture. According to Titiyal et al. (2017) who compared
the surgical outcomes of phacoemulsification in post 23G vitrectomized eyes in silicone oil
versus an air/gas group, pupillary abnormalities were significantly more in oil (31.25%) than in
air/gas group (9.76%).
Preventive Measures
It seems feasible to formulate strategies to delay or prevent post-vitrectomy NSC, which include:
replacing the vitreous gel after vitrectomy, restoring the structure of the remaining vitreous after
limited vitrectomy (Beebe et al., 2014; Harocopos et al., 2004), restoring the gel vitreous after
vitrectomy or supplementing ascorbate to the vitreous cavity (Shui et al., 2009), sparing more of
the vitreous gel behind the crystalline lens (Cherfan et al., 1991), surgical technique that spare
the anterior vitreous behind the lens (Margherio et al., 1985), new hydrogels as vitreous
substitutes that might have a beneficial influence on intraocular partial oxygen tension
(Petermeier et al., 2010), and others. According to studies by Garland (1991) and Rose et al.
(1998), the ability of ascorbate to scavenge free radicals and the high level of ascorbate in the
eyes of diurnal animals suggest that the vitamin might protect against oxidative or photo-
oxidative damage. In a study by Smiddy and Feuer (2004), the surgery rate for post-vitrectomy
cataract was lower in diabetic than in nondiabetic individuals. Diabetic retinopathy is associated
with a decreased oxygen supply to the inner retina. Because the retina is the source of most of
the oxygen in the vitreous body, it seems likely that diabetic patients would have decreased
levels of oxygen in the vitreous body. Holekamp et al. (2006) reported a study which showed that
eyes of diabetic patients have a significantly lower intraocular oxygen tension in the center of the
vitreous body and near the lens than the eyes of nondiabetic patients. A second study
Holekamp et al. (2010) was reported by the same authors and it was observed that eyes with
ischemic diabetic retinopathy had less post-vitrectomy NSC at 6 months and at 12 months than
nonischemic diabetic and nondiabetic eyes. Post-vitrectomy NSC in nonischemic diabetic eyes
and nondiabetic eyes developed at the same rate. Hence, it is suggested that reducing the
amount of molecular oxygen reaching the crystalline lens may be a successful strategy to
prevent or delay a post-vitrectomy NSC formation. The large epidemiologic studies revealed that
diabetic patients may have a lower risk of nuclear cataract. The Age-Related Eye Disease Study
(2001), which examined 4,477 individuals of 60 to 80 years of age, found that moderate nuclear
opacities were less common in persons with diabetes mellitus, with the net result showing a
lower prevalence and incidence of nuclear sclerotic cataracts. Some studies have described
modified techniques for epiretinal membrane (EMP) removal to try to minimize the development
of post-vitrectomy NSC known as “nonvitrectomizing” vitreous surgery (Saito et al., 1999;
Sawa et al., 2005; 2001). According to Saito et al. (1999), nuclear sclerosis could be prevented
by a minimal operative invasion of the eye. Therefore, they performed EMP surgery on 21 eyes
of patients older than 50 years without intraocular irrigation or core vitrectomy and named this
procedure “Nonvitrectomizing Vitreous Surgery.” They measured visual acuity, objective
refraction with an automatic refractometer, and slit-lamp photography. Scheimpflug photographs
were also taken for several patients. The study concluded that a nonvitrectomizing vitreous
surgery seems to decrease the incidence of nuclear sclerosis in surgical eyes compared to fellow
eyes during a mean follow-up of 9.7 months. A second study (Sawa et al., 2001) was reported by
the same authors using these techniques on 41 eyes of patients older than 50 years with a
follow-up of 22 months. They quantitatively evaluated the changes in nuclear sclerosis using
refractive error and image analysis of densitometry with Scheimpflug photographs and confirmed
the benefit of nonvitrectomizing vitreous surgery in preventing postoperative NSC. This study
might support the theory of changes in permeability that causes nuclear sclerosis. The above two
studies suggest that when retinal surgery is performed in a manner that preserves the structure
of the vitreous body, the formation of cataract and the accompanying changes in the refractive
power of the lens are not accelerated; it is the removal of the vitreous gel itself that directly or
indirectly produces nuclear sclerosis after vitrectomy in elderly patients (Saito et al., 1999;
Sawa et al., 2001). Sawa et al. (2005) performed a quantitative assessment of the progression of
nuclear sclerosis by densitometry analysis using Scheimpflug photography. The untreated eye
served as a control for analysis. One major finding of this study was that there was no
progression of nuclear sclerosis after nonvitrectomizing vitreous surgery for ERM even with the
long follow-up period (mean, 72.2 months); another major finding was that there was relatively
high recurrence rate of the ERMs (33%) than those reported previously with conventional
vitrectomy, which ranges from 4% to 12% (de Bustros et al., 1988; Grewing and Mester, 1996;
Margherio et al., 1985). The study concluded that the nonvitrectomizing vitreous surgery seems
to prevent the progression of nuclear sclerosis. However, it seems to carry a higher risk of ERM
recurrence.
Summary
Continuing evolution in vitrectomy techniques, instrumentation from 17G to 27G, and vitreous
substitutes, namely, silicone oil, air, or gas, have steadily changed the surgical and visual
outcome; however, post-vitrectomy NSC remains the most common complication. With
vitrectomy being the common ophthalmic surgery, its complication and the prevention of it are
challenging to the surgeons. Post-vitrectomy cataract preventive studies are required in a more
extended way. In order to correct post-vitrectomy NSC, phacoemulsification with intraocular lens
implantation is done which itself has some complications. The key to the prevention of post-
vitrectomy NSC formation is still elusive; factors that might increase the protective or repair
systems are so far not available. It should be feasible to formulate strategies to delay or prevent
NSC and measures to reduce the incidence of post-vitrectomy NSC. Despite extensive studies
on the understanding of the mechanism and preventive measures of post-vitrectomy NSC,
results are not so satisfactory. Therefore, more extended research in this field is highly desirable.

Acknowledgment
This project was supported by National Natural Science Foundation of China (No. 81700840).

Disclosure
The authors declare no conflicts of interest.

Corresponding Author
Prof. Fang Wang, M.D., Ph.D., Department of Ophthalmology, Shanghai Tenth People’s Hospital
Affiliated to Tongji University School of Medicine, 301 Middle Yan Chang Rd., Shanghai 200072,
China.
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Categories: Cataract, Ophthalmology, Vitrectomy