Pseudophakic patient

The ocular adverse effects of latanoprost include conjunctival hyperemia, iris pigmentation, periocular skin color changes, anterior uveitis, and cystoid macular edema in pseudophakic patients (77,78). H. simplex dendritic keratitis has been reported after treatment with latanoprost (79). In patients with uveitic glaucoma, latanoprost can cause increased intraocular pressure and recurrence of inflammation (80). 

Amos JF, Semes Lfi Swanson MW, et al. Pupillary dilation for aphakic patients, pseudophakic patients, and patients with cataract. Optom CUn 1991 1 188-194. 

Also, we have noted that patients with unilateral cataracts after trauma or retinal detachment repair typically have very similar RRS carotenoid levels in the normal and in the pseudophakic eye. Thus, we have concluded that there is a decline of macular carotenoids that reaches a low steady state just at the time when the incidence and prevalence of AMD begins to rise dramatically. While this age effect has been noticed sometimes also in other studies using clinical populations and different MP detection methods (Sharifzadeh et al. 2006, Nolan et al. 2007), several groups have reported constant, age-independent MP levels. Examples include reflectance-based population studies in which respective average MP optical densities of 0.23 (Delori et al. 2001), 0.33 (Berendschot et al. 2002), and 0.48 (Berendschot and Van Norren 2004) were determined. 

Intravitreal triamcinolone injection is safe and effective for cystoid macular edema caused by uveitis, diabetic maculopathy, and central retinal vein occlusion, and for pseudophakic cystoid macular edema. Potential risks include glaucoma, cataract, retinal detachment, and endophthalmitis. Infectious endophthalmitis is extremely rare when appropriate sterile technique is practised. Seven patients developed a clinical picture simulating endophthalmitis after intravitreal injection of triamcinolone (71). The authors believed that this effect was a toxic reaction to the injected material and explained that the differential diagnosis of infectious endophthalmitis in eyes that have been injected with triamcinolone under sterile conditions includes a sterile toxic endophthalmitis that requires careful monitoring, perhaps every 8-12 hours, in order to determine whether the inflammation is worsening or improving. Resolution occurs spontaneously, and in the absence of eye pain unnecessary intervention can be avoided. 

Patients who have had cataract extraction with implantation of an intraocular lens (lOL) often have pupils that dilate less well than they did preoperatively.The poorer pupillary response probably relates to the amount of iris trauma occurring at surgery. The difference in mydriatic response may affect evaluating and treating peripheral retinal abnormalities in aphakic and pseudophakic eyes. However, even with maximally dilated pupils often the capsulotomy is the limiting fector. 

Figure 26-8 Diagram of the deep lamellar endothelial keratoplasty procedure for patients with Fuchs corneal dystrophy and pseudophakic bullous keratopathy. (Diagram courtesy of Dr. Mark Terry of the Devers Eye Institute in Portland, Oregon.)...

A variety of studies suggest that several of the currently available NSAIDs are effective in reducing postoperative anterior segment inflammation and early angiographic and clinically significant pseudophakic CME. Therefore topical NSAIDS may be used for this purpose pre- and postoperatively, especially for patients at higher risk for postoperative inflammation. 

Patients with a history of prior macular edema may be considered at greater risk of developing pseudophakic CME and may be pretreated with topical or injected steroids or topical NSAIDs. These patients may be given prophylactic topical NSAIDs postoperatively along with the usual steroid drops. Antiglaucoma prostaglandin analogue drops should be avoided or used judiciously in patients with an increased risk for postoperative CME. 

IVTA has been used in several small series of patients with pseudophakic CME reftactory to all therapies. The studies all noted initial benefit in both retinal thickness (monitored by optical coherence tomography) and in visual acuity, but differing amounts of triamcinolone were used (4, 8, and 25 mg) and outcomes varied, with most patients demonstrating recurrence of edema after 3 to 4 months. The most stable duration of benefit was seen with the highest dose (25 mg). 

Cystoid macular edema has been reported to occur in 2.8% of the patients receiving adrenaline especially in aphakic or pseudophakic eyes (13). Cystoid macular edema has also been seen after the use of dipivefrine, but in the classic case described in 1982 pretreatment with timolol maleate may have predisposed the eye to this complication (14). 

All patients received 90 minute HBO sessions at 2.0 or 2.5 ata (atmospheres absolute) for 19 to 36 sessions (mean of 28 6). Five of the patients were diabetic. One eye was pseudophakic. Twenty-six patients were followed prospectively in Devon. Patients were examined pre-, mid-, and post-HBO which were at approximately one month intervals, and thereafter at 3 months after conclusion of therapy. 

A total of 31 patients were followed prospectively (Table 1). In all patients examined, the myopic shifts ranged from none to a maximum of -3.00 diopters. Shifts were apparent by approximately one month after beginning HBO therapy and were resolved by 3 months after conclusion of the treatment regimen. The mean shift at one month was 1 diopter 0.6 for 20 eyes. The pseudophakic eye showed no myopic shift. No patient had a monocular myopic shift. However, 6 patients with a shift did not return for follow-up refraction after completion of HBO therapy. 

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