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      Tectonic Keratoplasty in Patients with Non-traumatic, Non-infectious Corneal Perforations

      , , , ,
      The Open Ophthalmology Journal
      Bentham Science Publishers Ltd.

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          Abstract

          Introduction:

          The study aims to report clinical results of tectonic keratoplasty for non-traumatic, non-infectious corneal perforations.

          Materials and Methods:

          The medical records of 12 patients who underwent tectonic penetrating keratoplasty between October 2014 and August 2018 at Ege University Ophthalmology Department were retrospectively reviewed.

          Results:

          The mean age of the patients was 52.92±30.34 (range, 2-82) years. The causes of corneal perforation were dry eye (neurotrophic keratopathy (n=4), limbal stem cell deficiency (n=2), exposure keratopathy (n=2) and graft versus host disease (n=1)) in 9 patients. In the remaining 3 patients, the etiology of perforation was not determined. The mean Visual Acuity (VA) was 2.98±0.39 (range, 1.8-3.1) LogMAR before the surgery. Despite conservative treatment, tectonic penetrating keratoplasty had to be performed in all patients in order to manage the perforation. Mean time in between initial examination and surgery was 10.75±12.04 (1-41) days. In 2 patients, allogenic limbal stem cell transplantation; in one patient, lateral tarsorrhaphy and in one patient symblepharon release with amniotic membrane transplantation were performed additional to tectonic keratoplasty. Mean follow-up time was 57.88±55.47 (4-141) weeks. Grafts were clear in 6 eyes and opaque in 5 eyes. The main causes of graft failure among opaque grafts were ocular surface disease (3), allograft rejection (1) and glaucoma-related endothelial failure (1). Phthisis bulbi was detected in one patient with congenital glaucoma due to vitreous loss at the time of perforation. The mean final VA in patients who had clear grafts was 1.83±1.03 (range, 0.8-3.1) LogMAR.

          Conclusion:

          To prevent serious complications in non-traumatic, non-infectious corneal perforations, providing anatomic integrity immediately is a must. If conservative treatment is inadequate or the perforation area is extensive, tectonic penetrating keratoplasty is indicated. Besides, it is important to manage the etiological risk factors in order to obtain successful clinical follow up.

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          Most cited references15

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          Management of corneal perforation.

          Corneal perforation may be associated with prolapse of ocular tissue and requires prompt diagnosis and treatment. Although infectious keratitis is an important cause, corneal xerosis and collagen vascular diseases should be considered in the differential diagnosis, especially in cases that do not respond to conventional medical therapy. Although medical therapy is a useful adjunct, a surgical approach is required for most corneal perforations. Depending on the size and location of the corneal perforation, treatment options include gluing, amniotic membrane transplantation, and corneal transplantation. Copyright © 2011 Elsevier Inc. All rights reserved.
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            Neurotrophic keratitis: current challenges and future prospects

            Neurotrophic keratitis (NK) is a degenerative corneal disease caused by damage of trigeminal corneal innervation, which leads to spontaneous epithelial breakdown and corneal ulceration. The impairment of corneal sensory innervation causes the reduction of both protective reflexes and trophic neuromodulators that are essential for the vitality, metabolism, and wound healing of ocular surface tissues. A wide range of ocular and systemic conditions, including herpetic keratitis, ocular chemical burns, corneal surgery, diabetes, multiple sclerosis, and neurosurgical procedures, can cause NK by damaging trigeminal innervation. Diagnosis of NK requires careful investigation of any ocular and systemic condition associated with the disease, complete ocular surface examination, and quantitative measurement of corneal sensitivity. The clinical stages of NK range from corneal epithelial alterations (stage 1) to persistent epithelial defect (stage 2) and ulcer (stage 3), which may progress to corneal perforation. Management of NK is based on clinical severity, and the aim of the therapy is to halt the progression of corneal damage and promote epithelial healing. Although several medical and surgical treatments have been proposed, no therapies are currently available to restore corneal sensitivity, and thus, NK remains difficult and challenging to treat. The purpose of this review is to summarize available evidence on the pathogenesis, diagnosis, and treatment of NK. Novel medical and surgical therapies including the topical administration of nerve growth factor and corneal neurotization are also described.
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              Stem cell differentiation and the effects of deficiency.

              Stem cells have several unique attributes, the key features being their potency and plasticity. They have the ability to give rise to multiple cell lineages and to transdifferentiate into totally different cell type(s) when relocated to a novel stem cell niche. Most self-renewing tissues are served by stem cells. At the ocular surface, the corneo-scleral limbus is believed to provide the niche for corneal epithelial stem cells. A large body of circumstantial evidence, both clinical and basic, supports this view. However, specific identification of limbal stem cells has proved elusive. Cytokeratin markers, vimentin, epidermal growth factor receptors, p63, and others have been used to identify epithelial cell populations at the limbus, which could harbour putative stem cells. In contrast, none of the known haematopoietic stem cell markers namely, CD34 and CD133, stain any specific subset of corneal or limbal epithelial cells. Singly or collectively, none of these markers point to any unique cell(s) that could be regarded as stem cells, supporting the notion that the corneal epithelium is served by 'committed progenitors' rather than by stem cells. Disease or destruction of the corneo-scleral limbus is associated with consequential events that eventually lead to visual impairment or blindness. Conjunctivalisation and vascularisation of the corneal surface and persistent or recurring epithelial defects are hallmarks of limbal deficiency.
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                Author and article information

                Journal
                The Open Ophthalmology Journal
                TOOPHTJ
                Bentham Science Publishers Ltd.
                1874-3641
                December 18 2020
                December 18 2020
                : 14
                : 1
                : 75-77
                Article
                10.2174/1874364102014010075
                8a544b09-f2f9-4762-a11e-0a04b3c4eb57
                © 2020

                https://creativecommons.org/licenses/by/4.0/legalcode

                History

                Medicine,Chemistry,Life sciences
                Medicine, Chemistry, Life sciences

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