Man experiences gradual onset of blurry vision in pseudophakic eye
Click Here to Manage Email Alerts
A 79-year-old white man presented to the ophthalmology clinic with a complaint of painless unilateral blurry vision that he described as a “gray haze” in his right eye over the past few months.
Five days before presentation, he felt it had worsened, prompting evaluation. The patient denied seeing any flashes of light, floaters, or curtain or veil over his vision. He denied any trauma or recent surgeries to the eye.
His ocular history was notable for complex cataract extraction in both eyes approximately 13 years prior, requiring Malyugin rings due to poor dilation and trypan blue to stain the anterior capsule. Additional ocular history included a macular hole of his left eye that underwent repair with a pars plana vitrectomy and membrane peel approximately 20 years prior, with baseline visual acuity of 20/200 in that eye after repair. He had an extensive medical history including atrial fibrillation, asthma, benign prostate hyperplasia, congestive heart failure, type 2 diabetes, hypertension and hyperlipidemia. His medications reflected his medical history. Socially, he was a former tobacco smoker for 40 years and denied any alcohol use.
Examination
Visual acuity was 20/30-2 in the right eye and 20/200-1 in the left eye without spectacle correction at distance. IOP was 18 mm Hg in the right eye and 19.5 mm Hg in the left eye measured via applanation tonometry. Pupils were 3 mm, round and reactive bilaterally without afferent pupillary defect. Extraocular motility and confrontation visual fields were full bilaterally. Ishihara color testing was full in both eyes. Slit lamp exam of both eyes revealed no conjunctival injection, clear corneas and no signs of anterior chamber inflammation. The right eye had a posterior chamber IOL with 1.5+ posterior capsular opacification inferiorly with a collection of hazy material that appeared to be located between the IOL and posterior capsule (Figure 1). There was no evidence of vitreous cells in either eye. Dilated fundus exam revealed a hazy view to the posterior pole in the right eye with trace epiretinal membrane visualized. The left eye had chronic pigmentary changes in the macula.
What is your diagnosis?
The features of decreased visual acuity in a patient with a history of complex cataract extraction 13 years prior who was found to have turbid material localized between the IOL and posterior capsule is most consistent with late-onset capsular bag distension syndrome. Upon recognition of fluid between the IOL and posterior capsule, it is important to rule out an infectious etiology. The most common infection that could manifest as this would be chronic endophthalmitis. Other etiologies include posterior capsular opacification; however, the presence of a fluid collection located posterior to the lens would be unusual.
Management
Arriving at an accurate diagnosis can be aided with the use of various anterior segment imaging modalities. Anterior segment OCT imaging confirmed a collection of turbid material between the posterior surface of the IOL and posterior capsule (Figure 2). OCT of the retina was performed to rule out any posterior involvement and revealed no pathology.
Given that the patient was symptomatic from the fluid collection and there was good visualization of the posterior capsule, the decision was made to perform a Nd:YAG capsulotomy, resulting in successful release of fluid into the vitreous cavity.
Discussion
Capsular bag distension syndrome (CBDS) is a rare complication that can occur during or after cataract surgery in which turbid fluid builds up between the IOL and posterior capsule. The incidence of this condition is reported as occurring in less than 1% of those who undergo phacoemulsification with posterior chamber IOL implantation. This condition can be classified based on the timing of onset. Intraoperatively, CBDS can occur due to high irrigation pressures during hydrodissection, which can cause hyperdistension of the posterior capsule. Cases with a small capsulorrhexis and aggressive hydrodissection are at highest risk. Most commonly, CBDS occurs during the early postoperative stage, which is classified as within a few days to weeks after surgery. Patients who present in this stage are typically symptomatic as there is commonly anterior displacement of the IOL causing a myopic shift in refraction with anterior chamber shallowing and IOP elevation. Postulated theories for this include incomplete intraoperative removal of viscoelastic posterior to the IOL. Rarely, patients can present in the late postoperative stage, which can occur months to years after surgery. On average, patients in this stage present around 4 years after their cataract surgery. It is theorized that a 360° adhesion occurs between the continuous curvilinear capsulorrhexis and the anterior surface of a posterior chamber IOL optic. This adhesion creates the potential for the formation of a sequestered space between the IOL and posterior lens capsule. In late CBDS, a turbid or milky fluid may form within this space, causing posterior distention of the capsular bag.
Patients with late-onset CBDS present with a gradual decline in their visual acuity months to years after cataract surgery. It is rare for a patient to have symptoms of eye pain, redness or irritation. On clinical examination, patients will have a decrease in their baseline visual acuity with a possible slight increase in IOP. Anterior segment examination may reveal shallowing of the anterior chamber with turbid fluid visualized between the posterior chamber IOL and posterior capsule. Some case reports describe the layering effect from the turbid fluid between the IOL and clear posterior capsule as a “retrolenticular pseudohypopyon.” There should be no signs of anterior chamber inflammation or hypopyon.
Anterior segment imaging can help detect early presymptomatic CBDS and classify the extent of capsular distension. Imaging modalities may include OCT of the anterior segment, ultrasound biomicroscopy (UBM) of the anterior segment or Scheimpflug-based photography. Anterior segment OCT and UBM will demonstrate hyperreflectivity localized behind the IOL. A Scheimpflug camera can also be used, but visualization is suboptimal compared with OCT and UBM.
Classification of CBDS based on clinical examination has been proposed in the literature. Type 1 is characterized by the presence of a transparent capsule with transparent liquid in the capsular bag that is barely noticeable on slit lamp biomicroscopy but can easily be visualized on anterior segment OCT or UBM. Type 2 presents with homogenous milky fluid in the capsular bag with a transparent posterior capsule. Type 3 includes the presence of liquid accumulation with posterior capsular opacification. Lastly, type 4 entails opaque liquid accumulation, posterior capsular opacification and addition of a Soemmering ring.
The pathophysiology regarding this condition has remained controversial. A proposed mechanism involves residual lens epithelial cells or retained lens material producing collagen, which creates a chronic inflammatory reaction leading to scarring and fibrosis between the anterior capsule capsulorrhexis edges and the IOL. This 360° adhesion creates a potential space for fluid to accumulate. Any substance trapped in this potential space causes an increase in osmotic pressure, thus triggering chronic fluid accumulation. Eifrig sampled this fluid collection, which demonstrated an accumulation of alpha-crystallin material, a common substance derived from residual lens epithelial cells. No evidence of gamma globulins was found, favoring against any antigen-antibody-mediated reaction. Kollias and colleagues aspirated the sequestered fluid and demonstrated growth of Propionibacterium acnes, indicating a possible chronic infectious etiology.
Studies have proposed possible risk factors that may predispose patients to development of this condition. These include a small continuous curvilinear capsulorrhexis of less than 5.5 mm, retained cortical lens material and longer axial length (26.26 ± 2.84 mm). This condition can occur many years after cataract surgery, as shown in our case, with the literature reporting the longest time of 14 years after surgery.
Treatment for CBDS can vary depending on the surgeon’s preference. Typically, the decision to observe or treat is dependent on the patient’s symptoms and presence of inflammation on clinical exam. If patients are asymptomatic with no signs of inflammation on exam, they can be observed closely without intervention. However, more commonly, patients are symptomatic, and the decision is made to proceed with treatment. The most common treatment involves the use of the Nd:YAG laser to perform a posterior capsulotomy, which allows for release of the entrapped fluid and return of the IOL to its previous location. If there are clinical signs of significant inflammation not responsive to topical anti-inflammatory medications or if there is poor visualization of the posterior capsule, more invasive intervention with a pars plana vitrectomy and manual capsulotomy may be required. This technique also provides the surgeon with the ability to aspirate a sample of the fluid to send for culture.
It is essential for patients to be closely followed after treatment as there is a rare chance of concurrent P. acnes endophthalmitis, which may present as significant postoperative inflammation. A small case series in 2011 described three cases of late-onset capsular bag syndrome that were associated with P. acnes. All three cases demonstrated no signs of intraocular inflammation before treatment with Nd:YAG posterior capsulotomy. The authors propose this may have been from the chronic sequestration of fluid, with the release of fluid and subsequent exposure of this organism to the anterior chamber after treatment inducing a pronounced inflammatory reaction.
Clinical course continued
Given that our patient was symptomatic and had no signs of intraocular inflammation, the decision was made to proceed with a Nd:YAG posterior capsulotomy. The procedure was completed successfully with visualization of the turbid material dispersing into the vitreous space. Slit lamp examination revealed disappearance of this material (Figure 3). One week after performing Nd:YAG capsulotomy, the patient’s visual acuity had improved to 20/20 without signs of intraocular inflammation.
- References:
- Almousa KS, et al. J Surg Case Rep. 2021;doi:10.1093/jscr/rjab278.
- Al-Mulla AH, et al. Cureus. 2021;doi:10.7759/cureus.19684.
- Dhaliwal DK, et al. Arch Ophthalmol. 2011;doi:10.1001/archophthalmol.2010.356.
- Eifrig DE. J Cataract Refract Surg. 1997;doi:10.1016/s0886-3350(97)80193-9.
- Galvin JC, et al. Am J Ophthalmol Case Rep. 2018;doi:10.1016/j.ajoc.2018.03.019.
- Kollias AN, et al. J Cataract Refract Surg. 2010;doi:10.1016/j.jcrs.2009.06.047.
- Zhu X, et al. Am J Ophthalmol. 2013;doi:10.1016/j.ajo.2013.07.028.
- Zhu XJ, et al. Eye (Lond). 2014;doi:10.1038/eye.2014.107.
- For more information:
- Edited by Jonathan T. Caranfa, MD, PharmD, and Angell Shi, MD, of New England Eye Center, Tufts University School of Medicine. They can be reached at jcaranfa@tuftsmedicalcenter.org and ashi@tuftsmedicalcenter.org.
Collapse
Read more about
Click Here to Manage Email Alerts