Cystoid Macular Edema Following DMEK
Cystoid Macular Edema Following DMEK
The cumulative incidence of CMO following Triple-DMEK and DMEK is displayed in figure 1.
(Enlarge Image)
Figure 1.
Kaplan–Meier estimation of CMO following DMEK and Triple-DMEK. Most CMO occurred in the early postoperative period. There was no considerable difference between DMEK and Triple-DMEK. CMO, cystoid macular oedema; DMEK, Descemet membrane endothelial keratoplasty; Triple-DMEK, DMEK combined with cataract surgery.
Follow-up data were available for 6 months in 146 eyes (94%). At the end of the follow-up period, 13% of all eyes had developed singular CMO (13.3% of eyes following Triple-DMEK and 12.5% of eyes following DMEK). The mean central foveal thickness was 401 μm in the CMO group and 303 μm in the group without CMO (p<0.001). There was a negative association between BSCVA and episodes of CMO (p<0.01; Pearson's correlation). Following the first diagnosis of CMO, these eyes showed lower BSCVA than eyes without CMO (figure 2). In both groups, there is an increase in BSCVA. The difference in BSCVA between both groups decreases with time.
(Enlarge Image)
Figure 2.
Trajectories of BSCVA in patients with and without CMO following the first diagnosis of CMO. Eyes suffering from CMO show lower BSCVA at the time of diagnosis compared with eyes without CMO. BSCVA, best spectacle corrected visual acuity; CMO: cystoid macular oedema.
All CMO except one (which had to be treated with intravitreal injections) disappeared with the aforementioned medical treatment followed by visual recovery (figure 3). There was no recurrence of CMO during the follow-up period. Among the 67 patients undergoing (Triple-)DMEK in both eyes, bilateral CMO did not occur. None of the diabetic patients developed CMO.
(Enlarge Image)
Figure 3.
Dynamics of central foveal thickness (A) and BSCVA (B) following (Triple-)DMEK. There is a spike in central foveal thickness at the time of occurrence (day 0). Afterward, the central foveal thickness constantly decreases (A). Following occurrence and medical treatment of CMO, BSCVA rises constantly during the entire investigated postoperative period (B). CMO, cystoid macular oedema; DMEK, Descemet membrane endothelial keratoplasty; Triple-DMEK, DMEK combined with cataract surgery; BSCVA, best spectacle corrected visual acuity.
In the proportional hazards Cox model of the whole group, none of the possible risk factors reached statistical significance (Table 2).
However, when looking at the Triple-DMEK patients (Table 2) alone, short axial length was statistically significantly associated with CMO (p<0.01, Table 2).
We observed the following complications:
Results
The cumulative incidence of CMO following Triple-DMEK and DMEK is displayed in figure 1.
(Enlarge Image)
Figure 1.
Kaplan–Meier estimation of CMO following DMEK and Triple-DMEK. Most CMO occurred in the early postoperative period. There was no considerable difference between DMEK and Triple-DMEK. CMO, cystoid macular oedema; DMEK, Descemet membrane endothelial keratoplasty; Triple-DMEK, DMEK combined with cataract surgery.
Follow-up data were available for 6 months in 146 eyes (94%). At the end of the follow-up period, 13% of all eyes had developed singular CMO (13.3% of eyes following Triple-DMEK and 12.5% of eyes following DMEK). The mean central foveal thickness was 401 μm in the CMO group and 303 μm in the group without CMO (p<0.001). There was a negative association between BSCVA and episodes of CMO (p<0.01; Pearson's correlation). Following the first diagnosis of CMO, these eyes showed lower BSCVA than eyes without CMO (figure 2). In both groups, there is an increase in BSCVA. The difference in BSCVA between both groups decreases with time.
(Enlarge Image)
Figure 2.
Trajectories of BSCVA in patients with and without CMO following the first diagnosis of CMO. Eyes suffering from CMO show lower BSCVA at the time of diagnosis compared with eyes without CMO. BSCVA, best spectacle corrected visual acuity; CMO: cystoid macular oedema.
All CMO except one (which had to be treated with intravitreal injections) disappeared with the aforementioned medical treatment followed by visual recovery (figure 3). There was no recurrence of CMO during the follow-up period. Among the 67 patients undergoing (Triple-)DMEK in both eyes, bilateral CMO did not occur. None of the diabetic patients developed CMO.
(Enlarge Image)
Figure 3.
Dynamics of central foveal thickness (A) and BSCVA (B) following (Triple-)DMEK. There is a spike in central foveal thickness at the time of occurrence (day 0). Afterward, the central foveal thickness constantly decreases (A). Following occurrence and medical treatment of CMO, BSCVA rises constantly during the entire investigated postoperative period (B). CMO, cystoid macular oedema; DMEK, Descemet membrane endothelial keratoplasty; Triple-DMEK, DMEK combined with cataract surgery; BSCVA, best spectacle corrected visual acuity.
In the proportional hazards Cox model of the whole group, none of the possible risk factors reached statistical significance (Table 2).
However, when looking at the Triple-DMEK patients (Table 2) alone, short axial length was statistically significantly associated with CMO (p<0.01, Table 2).
We observed the following complications:
Graft detachment or dislocation (20%; treated by air refilling of the anterior chamber)
Graft failure with persisting corneal oedema (2.6%; treated with repeated DMEK or with secondary PK)
Persistent CMO in one case (successfully treated with intravitreal injections).
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