PURPOSE: To describe the clinical and pathologic characteristics of mucin-producing sweat gland carcinoma of the eyelid and to determine whether neuroendocrine differentiation is of prognostic significance.DESIGN: Retrospective interventional case series.METHODS: Search of the New York Eye and Ear Infirmary pathology database between 1990 and 2011 identified 16 patients with mucin-producing sweat gland carcinoma. Clinical, histopathologic, and immunohistochemical analyses were performed on all identified cases.RESULTS: The patients presented with vascularized, focally cystic, nonulcerated eyelid margin lesions. Histopathologic evaluation showed that 4 lesions (25%) had a cystic, papillary, and solid growth pattern with an in situ component, 7 (44%) were pure invasive mucinous carcinomas, and 5 (31%) demonstrated both growth patterns. Immunohistochemical analysis of 15 tumors showed that pure cystic/papillary lesions had a significantly greater percentage of synaptophysin-immunoreactive cells (P = .036). There was no significant difference in the number of neuroendocrine markers expressed or in the intensity of immunostaining among the 3 different growth patterns. Re-excision for margin clearance was performed in 8 of 13 cases (61.5%). Two of 13 lesions recurred (15%); 1 of these was an in situ tumor with cystic morphology and neuroendocrine differentiation and the other was pure invasive mucinous carcinoma. None of the lesions metastasized.CONCLUSIONS: Mucin-producing sweat gland carcinoma pathologically represents a continuum, from an in situ lesion to a classic, invasive mucinous carcinoma. Immunohistochemical evidence of neuroendocrine differentiation can be observed in all lesions and does not appear to have a prognostic significance, arguing against the utility of immunohistochemical subtyping of mucinous sweat gland carcinomas. (Am J Ophthalmol 2013;155:585-592. (C) 2013 by Elsevier Inc. All rights reserved.)
PURPOSE: To report the presentation and subsequent management of a series of patients presenting with cosmetic iris implants.SETTING: New York Eye and Ear Infirmary, New York, New York, USA.DESIGN: Case series.METHODS: In this evaluation of patients with NewColorlris cosmetic iris implants, data collected included patient demographics, visual acuity, intraocular pressure (IOP), endothelial cell count, and slitlamp examination findings at presentation. Medical and surgical interventions and the postoperative course were recorded.RESULTS: Fourteen eyes of 7 patients (ages 22 to 60; 71% men) were identified. Nine eyes (64%) presented with decreased visual acuity, 7 (50%) had elevated IOP, 5 (36%) had corneal edema, and 5 (36%) had anterior uveitis. All 14 eyes had explantation of the iris prosthesis (range 4 to 33 months after placement). The minimum follow-up after implant removal in all eyes was 2 months (range 2 to 28 months). Intraoperative complications included suprachoroidal hemorrhage during explantation in 1 eye. Postoperative complications included corneal edema (8 eyes), cataract (9 eyes), and increased IOP/glaucoma (7 eyes). Secondary surgeries included Descemet-stripping automated endothelial keratoplasty (5 eyes), cataract extraction with intraocular lens placement (7 eyes), trabeculectomy (3 eyes), glaucoma drainage implant placement (3 eyes), and penetrating keratoplasty (1 eye).CONCLUSIONS: The cosmetic iris implants may result in severe ocular morbidity. Complications in our series included uveltis, glaucoma, corneal edema, and decreased visual acuity. Although explantation helped stabilize symptoms, additional medical and surgical intervention to control IOP and corneal decompensation was required in many cases.
Because the focus of our series was to report the serious complications and subsequent management of these patients, we did not focus on the actual surgical technique used in their removal. We respectfully disagree with Drs. Moshirfar and Kim's assertion that cosmetic iris implant removal causes significant morbidity associated with the implant removal and is comparable to IOL exchange. The NewColorIris implants cause the UGH syndrome, originally described in 1978 as a complication of intraocular chafing by first-generation anterior chamber IOLs.1 What the commentators neglect to note is that the UGH syndrome is not uniformly cured by removal of the implant. Early experience with anterior chamber IOLs demonstrated that the disease process may continue, the glaucoma may persist, and ultimately, many of the corneas fail, not from the IOL removal but from the chronic ongoing endothelial cell loss and the morbidity caused by the IOL.2 Most current IOLs are thicker than the NewColorIris implants and are harder to section. Their greater volume in the anterior chamber makes them slightly more difficult to debulk and remove. In contrast, once enveloped in the ophthalmic viscosurgical device (OVD) both below and above the iris implant, the NewColorIris implants are easily sectioned, even with a 25-gauge retinal scissor placed through a paracentesis. They are thinner and much more flexible than a typical IOL and pass readily through a 3.0 mm incision. Drs. Moshirfar and Kim suggest the loss in postoperative corrected distance visual acuity (CDVA) in 3 eyes in our series (Eyes 2L, 6L, 7R) as evidence of the potential morbidity in explantation. We disagree. Patient 2L in our series had intraocular pressures (IOPs) in the 40s and 50s for more than 6 months before implant removal. Despite our group's recommendation to explant the iris implants immediately, the patient delayed surgery for 7 months and developed a suprachoroidal hemorrhage from chronic elevated IOP. According to the operating surgeon, prior to explantation, the vision had dropped to the counting fingers level due to the IOP elevation, optic neuropathy, and worsening corneal edema. Patient 6L developed cornea edema after explantation because of progressive endothelial cell loss. The cornea was already in the process of decompensating. The preoperative endothelial cell counts were low. The CDVA after explantation is only relevant in that the patient had not had Descemet-stripping automated endothelial keratoplasty (DSAEK) surgery at the time of publication. Patient 7R in our series had trabeculectomy to control elevated IOP prior to DSAEK. The subsequent DSAEK and cataract surgeries were pending prior to publication. We do not believe the poor outcome is a consequence of the surgery but of the disease itself. Four different surgeons were involved in explanting all the iris implants except in the patient who developed the suprachoroidal hemorrhage. All removed the implant in similar fashion. After making one or more paracenteses, a dispersive OVD was placed behind and in front of the implant. A keratome measuring 3.0 mm was used to enter the eye. The surgeon used a Stern-Gill scissors (Katena Products, Inc.) or a Grieshaber single-use 25-gauge retinal scissors to cut the implant into 2 or more pieces and an MST microholding forceps or a 25-gauge Grieshaber single-use retinal forceps to carefully externalize the flexible iris implant segment through the wound with minimal difficulty; 10-0 nylon sutures were placed across the wound. We have included a video of one explantation surgery (Video, available at http://jcrsjournal.org). In addition, Eyetube.net has a narrated video of another iris implant removal technique.A