Cystoid Macular Edema Following DMEK
Cystoid Macular Edema Following DMEK
In this study, we observed a considerably elevated incidence of CMO (13%). The incidence of CMO following DMEK is higher than the frequency of CMO measured by OCT following uncomplicated cataract surgery (0.1%–2.4%). Many groups have not yet investigated the incidence of CMO following DMEK or other lamellar endothelial keratoplasty methods. In particular, we are not aware of any other homogenous large cohort study investigating CMO following DMEK on the basis of SD-OCT controls.
Dapena et al were the first to report a CMO risk of 0.7% in 135 uneventful DMEK surgeries. The incidence of CMO following DSAEK is reported to be higher: Suh et al indicate a CMO incidence of 5% following 118 DSAEK procedures. The difference between our data and the literature may be due to our routinely performed screening procedure with SD-OCT. After uncomplicated intraocular surgery, routine controls are performed less frequently, and SD-OCT often is not performed when BSCVA improves.
Do we overestimate the incidence of CMO in comparison with the background of Dapena et al? This could be the case if CMO is not clinically significant because it would have resolved spontaneously, as it is known to do following cataract surgery. However, we observed a significant correlation between CMO and BSCVA (p<0.01 in Pearson's correlation). The maximal central foveal thickness was measured at the time of onset of CMO (figure 3A), but BSCVA of the whole cohort improved continuously at that time point (figure 3B). Separating the eyes suffering from CMO in the trajectory of BSCVA (figure 2), there obviously is a lower BSCVA in the period following the first diagnosis of CMO confirming statistical significance in the Pearson's correlation (p<0.01). Thus, CMO may slow visual rehabilitation. Following (Triple-)DMEK, the correlation between CMO and BSCVA may be superposed by any other wound healing process, such as regression of corneal oedema. Therefore, no definite correlation of CMO and BSCVA can be drawn from our study.
To evaluate potential mechanisms for the development of CMO following DMEK, we assessed potential confounders.
We found a negligible difference of 13.3% CMO following Triple-DMEK and 12.5% following DMEK alone after 6 months of follow-up (figure 1). On first glance, this may seem to be a paradox: in Triple-DMEK, the risk for CMO could be higher, as more surgical manipulation is needed and the geometrical situation of the anterior segment is changed more severely than following DMEK alone.
In addition, pseudophacic eyes with endothelial insufficiency often have opaque and thick corneas because of previous complicated surgery. Because these corneas tend to have more haze blurring vision during surgery, they require more delicate unfolding procedures with more manipulation. Furthermore, all phacoemulsifications in the Triple-DMEK group were uncomplicated, so a low rate of CMO induction would have been expected. Laaser et al are the only other group to compare a Triple-DMEK and a DMEK cohort. They also reported no elevated complication rate in Triple-DMEK compared with DMEK alone.
Taken together, anatomical respectively geometrical conditions of the patients eye may be relevant for the development of CMO, whereas intraoperative or perioperative factors affecting the grade of inflammation do not seem to be relevant in our cohort. Compared with cataract surgery alone (without iridectomy or intracameral air), (Triple-)DMEK may lead to increased rate of CMO because of this regularly performed manipulation on the iris.
Open questions for further studies may be the rate of CMO following DMEK in phacic eyes without simultaneous cataract surgery as well as the rate of CMO following cataract surgery in eyes with previous DMEK.
In conclusion, we recommend considering SD-OCT during the first 6 months following DMEK or Triple-DMEK, at least in eyes with insufficient visual rehabilitation. Eyes with short axial length require special attention. DMEK-related CMO could be effectively treated with the first-line medical treatment routinely applied in CMO following cataract surgery. Concerning prophylactic therapy, the surgeon has to perform a thorough risk analysis because, on the one hand, frequency of CMO following DMEK seems to be higher than following cataract surgery. On the other hand, and in contrast to CMO following cataract surgery, DMEK-related CMO in one eye does not seem to increase the risk for the fellow eye.
Discussion
Incidence of CMO Following DMEK
In this study, we observed a considerably elevated incidence of CMO (13%). The incidence of CMO following DMEK is higher than the frequency of CMO measured by OCT following uncomplicated cataract surgery (0.1%–2.4%). Many groups have not yet investigated the incidence of CMO following DMEK or other lamellar endothelial keratoplasty methods. In particular, we are not aware of any other homogenous large cohort study investigating CMO following DMEK on the basis of SD-OCT controls.
Dapena et al were the first to report a CMO risk of 0.7% in 135 uneventful DMEK surgeries. The incidence of CMO following DSAEK is reported to be higher: Suh et al indicate a CMO incidence of 5% following 118 DSAEK procedures. The difference between our data and the literature may be due to our routinely performed screening procedure with SD-OCT. After uncomplicated intraocular surgery, routine controls are performed less frequently, and SD-OCT often is not performed when BSCVA improves.
Do we overestimate the incidence of CMO in comparison with the background of Dapena et al? This could be the case if CMO is not clinically significant because it would have resolved spontaneously, as it is known to do following cataract surgery. However, we observed a significant correlation between CMO and BSCVA (p<0.01 in Pearson's correlation). The maximal central foveal thickness was measured at the time of onset of CMO (figure 3A), but BSCVA of the whole cohort improved continuously at that time point (figure 3B). Separating the eyes suffering from CMO in the trajectory of BSCVA (figure 2), there obviously is a lower BSCVA in the period following the first diagnosis of CMO confirming statistical significance in the Pearson's correlation (p<0.01). Thus, CMO may slow visual rehabilitation. Following (Triple-)DMEK, the correlation between CMO and BSCVA may be superposed by any other wound healing process, such as regression of corneal oedema. Therefore, no definite correlation of CMO and BSCVA can be drawn from our study.
Potential Risk Factors for CMO Following DMEK
To evaluate potential mechanisms for the development of CMO following DMEK, we assessed potential confounders.
High axial length: the longer the patient's eyeball is, the longer the diffusion pathway to the macular region. In the case of inflammatory mediators, a gradient of the molecules forms along this distance, leading to an increasing dilution toward the macular region. The significant and protective impact of axial length on CMO following DMEK found in this study supports this hypothesis (Table 2).
Duration of surgery and amount of manipulation: it is known that manipulation of the iris causes inflammation. This may increase the risk of CMO. As Triple-DMEK and DMEK patients showed identical rates of CMO (figure 1) and Triple-DMEK was not a significant risk factor for CMO in the whole group (Table 2), this may not have had any impact on CMO in our cohort. But, in contrast to uncomplicated cataract surgery, (Triple-)DMEK includes more manipulation on the iris (eg, iridectomy and graft unfolding under intracameral air). This may explain an increased rate of CMO in Triple-DMEK compared with cataract surgery alone in standard cases.
Eyes with rebubbling: speculating on an increase in inflammation with repeated surgery and intracameral air, a negative effect of rebubbling on CMO could be expected. This was not the case (p=0.42, see Table 1) indicating that rebubbling only may cause minor stress on the ocular tissues.
Donor characteristics such as donor age or preoperative endothelial cell density do not seem to influence the risk of CMO (Table 2).
Diabetes mellitus does not seem to be a pronounced risk factor for CMO following Triple-DMEK in our cohort as no diabetic patient developed CMO.
Triple-DMEK Versus DMEK as Risk Factors for CMO
We found a negligible difference of 13.3% CMO following Triple-DMEK and 12.5% following DMEK alone after 6 months of follow-up (figure 1). On first glance, this may seem to be a paradox: in Triple-DMEK, the risk for CMO could be higher, as more surgical manipulation is needed and the geometrical situation of the anterior segment is changed more severely than following DMEK alone.
In addition, pseudophacic eyes with endothelial insufficiency often have opaque and thick corneas because of previous complicated surgery. Because these corneas tend to have more haze blurring vision during surgery, they require more delicate unfolding procedures with more manipulation. Furthermore, all phacoemulsifications in the Triple-DMEK group were uncomplicated, so a low rate of CMO induction would have been expected. Laaser et al are the only other group to compare a Triple-DMEK and a DMEK cohort. They also reported no elevated complication rate in Triple-DMEK compared with DMEK alone.
Taken together, anatomical respectively geometrical conditions of the patients eye may be relevant for the development of CMO, whereas intraoperative or perioperative factors affecting the grade of inflammation do not seem to be relevant in our cohort. Compared with cataract surgery alone (without iridectomy or intracameral air), (Triple-)DMEK may lead to increased rate of CMO because of this regularly performed manipulation on the iris.
Open questions for further studies may be the rate of CMO following DMEK in phacic eyes without simultaneous cataract surgery as well as the rate of CMO following cataract surgery in eyes with previous DMEK.
In conclusion, we recommend considering SD-OCT during the first 6 months following DMEK or Triple-DMEK, at least in eyes with insufficient visual rehabilitation. Eyes with short axial length require special attention. DMEK-related CMO could be effectively treated with the first-line medical treatment routinely applied in CMO following cataract surgery. Concerning prophylactic therapy, the surgeon has to perform a thorough risk analysis because, on the one hand, frequency of CMO following DMEK seems to be higher than following cataract surgery. On the other hand, and in contrast to CMO following cataract surgery, DMEK-related CMO in one eye does not seem to increase the risk for the fellow eye.
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