Early postoperative capsular block syndrome is considered a complication of capsulorhexis.1–3 Typical findings of this condition appear between 1 day and 2weeks after surgery1 and comprise slight to moderate myopia, a shallow anterior chamber, and a potential intraocular pressure (IOP) rise. The underlying phenomenon that promotes these signs is hyperexpansion of the capsular bag by fluid. Slitlamp examination reveals a forward displacement of the anterior capsule and the intraocular lens (IOL) optic and a backward displacement of the posterior capsule.
The origin of the fluid trapped in the capsular bag remains unclear. It has been suggested that retained viscoelastic substance or endocapsular epithelial cell products produce an osmotic gradient that drives water into the capsular bag.2,4 That hyperexpanded capsular bags can be detected as soon as 24 hours after surgery and that the osmotic forces potentially involved are considered too weak to move fluid across the lens capsule2 have led to a complementary theory to explain the pathogenesis of early postoperative capsular block syndrome.
I propose that saccadic eye movements may have a role in the introduction of fluid into the capsular bag. It is accepted that saccadic eye movements can reach rotational speeds up to 1000 degrees per second in normal patients. This is equivalent to a linear displacement of approximately 17 cm per second at the capsulolenticular plane of a normal eye. The high accelerations and decelerations involved in this rapid movement can promote a net flow of aqueous humor into the capsular bag.
This inflow seems to require particular anatomic conditions and elevation of a portion of the capsular rim above the anterior IOL surface. This partial elevation can usually be seen at the end of surgery and soon after (Figure 1, A). A valve-like structure must exist between the capsulorhexis rim and the IOL's anterior surface to retain the inflow inside the capsular bag (Figure 1, B). A glue-like tissue at the capsular rim adhering the capsule to the IOL surface has also been described in the early postoperative period.4 This tissue may help create this proposed valve (Figure 2). Aqueous humor could then be pumped into the capsular bag by rapid eye movements that produce an inertial unidirectional displacement of fluid toward the capsular bag.
Materials and Methods
An in vitro setup was created to simulate the anatomic and kinetic conditions in the early period after cataract surgery. This setup consisted of a reproduction of the globe, an extracapsular space, and an intracapsular space, separated by a capsulolenticular array (Figure 3). The extent of the adhesion between the perimeter of the capsule and the IOL surface was varied by applying a plastic adhesive between the capsular rim and the underlying IOL optic to different extents. The purpose was to reproduce the conditions that may cause early postoperative capsular block syndrome.
The globe was mounted with the rotation center parallel to the capsulolenticular plane. The extracapsular and the intracapsular spaces were separately connected to a differential pressure transducer (NovaSensor 410 0050D3L). Tubing exiting the globe was conducted through the axis of rotation to avoid centrifugal forces that would interfere with the experiments. A constant IOP of 20 mm Hg was applied during the extracapsular chamber experiments. A 3-way stopcock controlled the flow of balanced salt solution to the extracapsular space alone or transiently connected it with the intracapsular space to equalize pressures and reset the gradient to zero. Motion was applied to the eye model with a computer-controlled electromechanical transducer.
The perimeter of adhesion between the IOL and the capsular rim was always set symmetrical to the plane of rotation of the globe, promoting a free overlapping rim zone that would always travel parallel to the direction of movement. Experiments were divided in 4 groups: Group A, no capsular rim adhesion; Group B, 30% to 50% adhesion; Group C, 50% to 70% adhesion; Group D, 70% to 90% adhesion (Figure 4). The capsular setup was repeated 3 times in Groups A, B, and C and 8 times in Group D. After motion was applied with the nonadhered capsular rim lying flat over the IOL surface, the free capsular rim was manipulated with a blunt forceps to create a degree of elongation, avoiding flat contact with the underlying IOL and approximating the capsule configuration in Figure 1, B. Several experiments were performed with each capsule–IOL array.
The movement pattern applied to the artificial globe followed a waveform that simulated saccadic eye movements. This waveform was extracted from an actual digitized electro-oculogram (EOG) recording of a normal eye (Figure 5) and fed through a digital-to-analog converter to the electromechanical transducer. A motion sensor was used to monitor the actual waveform of the globe's rotation. A drawing and a photograph of the experimental setup are shown in Figures 6 and 7, respectively.
No pressure rise was observed in Groups A, B, and C with or without free capsular rim deformation. Group D showed different degrees of motion-related progressive intracapsular pressure development. A pressure gradient was measured in 4 of the 8 capsule setups in Group D and only after deformation was applied to the free border, avoiding flat contact with the underlying IOL. Figure 8 shows pressure-gradient measurements from 3 experiments in Group D.
Pressure rise reached a plateau of stabilized differential pressure after approximately 10 minutes of permanent saccadic movements. Different maximum pressure gradients extending above 4 mm Hg occurred in the intracapsular space (Figure 8, C). The pressure rise was inconstant, and repeated runs with the same capsulolenticular setup yielded different amounts of pressure buildup (Figure 9).
An artificial model was used to test the hypothesis that saccadic eye movements can force fluid into the capsular bag in the early postoperative period. Adhesion between the capsular rim and the IOL surface and some amount of capsular rim deformation were necessary to create a motion-dependent pressure gradient. Early adherence of the capsular rim to the IOL is commonly observed in vivo. The capsule's disposition over the IOL is variable and depends on the capsulorhexis shape and size, IOL position, progressive rim cell proliferation adhering to the IOL optic, and capsule characteristics of individual patients, among other factors.
It is possible that a valve-like mechanism can be formed between the anterior capsule and the underlying IOL when a combination of these factors occurs. Rapid eye movements can then act as a motor that pumps fluid inside the capsular bag, potentially reaching pressures able to distend the capsular bag. There are recent reports of capsular block syndrome occurring with sulcus-implanted IOLs. In this situation, the IOL optic was overlying, not underlying, the capsular rim. An adhering tissue between the capsulorhexis margin and the IOL optic is a constant observation.5 Early postoperative capsular block syndrome has also been reported after cataract surgery when no viscoelastic substance was used.5 These findings confirm that at least in some cases, the theory that retained viscoelastic substance is responsible for capsular block syndrome cannot be sustained.
Single saccadic eye movements in a proper direction can force the entrance to the capsular bag of small amounts of fluid from the extracapsular space to be retained inside the capsular bag by the valve-like nature of a favorable capsulolenticular relationship. A constant factor in the production of capsular block syndrome appears to be the adhesion of the anterior capsule to the IOL.
Repetition of rapid eye movements would keep fluid flowing into the capsular bag until a pressure equilibrium is reached. At this moment, the glue-like tissue grows to completely seal the capsular opening, keeping the pressurized fluid entrapped within the capsular bag, tending to chronicity. Thus, later changes in fluid composition may occur.
This study shows that rapid eye movements can produce a unidirectional fluid flow into the capsular bag in the presence of a mixture of favorable anatomic conditions. It cannot be stated from these experimental results that early postoperative capsular block syndrome is fully dependent on saccadic eye movements. What is suggested is that saccadic eye movements can promote aqueous humor flow into the capsular bag and that this inflow can be retained by the valve-like nature of the capsule–IOL relation initiating a capsular block condition. Other factors such as osmotic gradient or cellular by-products could also participate in the genesis, maintenance, and aggravation of the condition.
1. Miyake K, Ota I, Ichihashi S, et al. New classification of capsular block syndrome. J Cataract Refract Surg 1998; 24:1230-1234
2. Holtz SJ. Postoperative capsular bag distension. J Cataract Refract Surg 1992; 18:310-317
3. Masket S. Postoperative complications of capsulorhexis. J Cataract Refract Surg 1993; 19:721-724
4. Davison JA. Capsular bag distension after endophacoemulsification and posterior chamber intraocular lens implantation. J Cataract Refract Surg 1990; 16:99-108
5. Geyer O, Goldstein M, Rothkoff L, Lazar M. Capsular bag distension associated with sulcus implantation of intraocular lenses. J Cataract Refract Surg 1998; 24:1538-1540