Tear film and ocular surface changes in a rabbit model of neurotrophic keratitis

The authors studied the tear film and ocular surface in a rabbit model of neurotrophic keratitis to determine the extent to which the surface disease of neurotrophic keratitis resembled keratoconjunctivitis sicca. After denervation, tear film osmolarity increased and remained significantly elevated for 14 weeks. The ocular surface developed decreased conjunctival goblet cell density, decreased corneal epithelial glycogen, and morphologic changes similar to those seen in keratoconjunctivitis sicca. Although the conjunctival changes were consistent with the increases in tear film osmolarity and the surface disease of keratoconjunctivitis sicca, the corneal changes observed with denervation, including slit-lamp findings, morphologic changes, and decreases in glycogen, were too severe and rapid in onset to be accounted for by osmolarity alone. Neurotrophic "keratitis" is an ocular surface disease composed in part of the surface disease of keratoconjunctivitis sicca. However, the data also support an additional mechanism for corneal disease that could be due to the trophic influence of the trigeminal nerve.     

糖胺聚糖与角膜透明度关系的研究

对12例正常角膜、12例斑块状角膜营养不良和1例全身性糖胺聚糖贮积症角膜进行形态学和胶性铁超微组化研究。结果表明正常角膜上皮下基底膜和前弹力层有硫酸软骨素,实质层胶原纤维间有硫酸软骨素和硫酸角质素,内皮细胞表面有透明质酸,各种细胞膜上有硫酸肝素存在。斑块状角膜营养不良实质层胶原纤维间硫酸软骨素明显增多,硫酸角质素缺乏,角膜实质细胞和内皮细胞胞质内合成了大量的细纤维状物质和异常的糖胺聚糖。全身性糖胺聚糖贮积症为硫酸肝素在细胞内的蓄积,病变细胞膜上硫酸肝素缺乏。作者认为角膜组织中一定量的糖胺聚糖维持了角膜透明,其分布部位、性质和数量变化均可导致角膜混浊。     

Simultaneous penetrating keratoplasty, cataract extraction and artificial lens implantation ("triple procedure") 1981-1987

Between June 1981 and March 1987, the authors performed simultaneous penetrating keratoplasty, cataract extraction, and intraocular lens implantation in 90 eyes. The main indications were Fuchs's corneal endothelial dystrophy (38 cases), corneal cicatrization (33 cases) and corneal or scleral perforation (7 cases). Extracapsular cataract extraction with posterior chamber lens implantation was performed in 82 patients. The posterior capsule ruptured in nine eyes, necessitating an anterior vitrectomy in four of them. The corneal transplant was rejected in nine eyes (10%). The mean preoperative visual acuity of 9/100 in 89 patients improved to 39/100 six months after surgery in 59 patients who were followed up and to 50/100 in the 29 patients with Fuchs's corneal dystrophy. The authors believe that in cases presenting with both cataract and medically uncontrollable corneal disease, simultaneous penetrating keratoplasty with extracapsular cataract extraction and implantation of a posterior chamber lens represents the treatment of choice.     

Confocal microscopy and corneal sensitivity in a patient with corneal manifestations of Tangier disease

PURPOSE: Tangier disease is an autosomal recessive disorder in which cholesterol-rich lipids are deposited at various tissues of the body including the cornea. In this case report, the corneal changes in a patient with Tangier disease are described. METHODS: A 72-year-old patient who was diagnosed with Tangier disease 25 years before received a complete eye examination including confocal microscopy and Cochet-Bonnet esthesiometry. RESULTS: Slit-lamp biomicroscopy and confocal microscopy showed bilateral corneal opacifications caused by lipid accumulation. Confocal microscopy showed that pathologic changes in the cornea in Tangier disease are limited to the stroma. Neither a reduced corneal sensation nor lid abnormalities as previously described in Tangier disease were found. CONCLUSION: Confocal microscopy helps to identify corneal changes in the stroma caused by Tangier disease easily missed in a slit-lamp examination. The ocular manifestations of Tangier disease do not necessarily include a reduced corneal sensitivity and lid abnormalities.     

Severe Corneal Changes following Intravitreal Injection of Bevacizumab

Purpose: To report a series of severe corneal changes following intravitreal injection of bevacizumab (Avastin) for age-related macular degeneration.

Design: Retrospective noncomparative case series.

Methods: The authors retrospectively reviewed the corneal changes that developed after the procedure in 1200 (460 patients) intravitreal injections of bevacizumab.

Results: Five significant corneal changes (1.1%) occurred in these patients within the 1st postinjection week. The severe corneal changes included corneal infiltrative keratitis (n?=?2) and corneal stromal edema and descemet folds (n?=?3). The findings depended on clinical examination and biomicroscopic and confocal evaluation. In terms of causality assessment, no rechallenge was possible. The appropriate treatment was applied and recovery was achieved in all patients during the follow-up period.

Conclusions: Intravitreal injection of bevacizumab may cause corneal changes. The safety and effects of bevacizumab on the cornea should be evaluated in detail.     

Penetrating keratoplasty in congenital corneal opacities

The clinical course and histopathological findings in 17 cases of congenital corneal opacity treated by penetrating keratoplasty are described. On the basis of the histopathological findings 9 of the cases of corneal opacity were diagnosed as Peter's anomaly, 5 cases as sclerocornea or mesenchymal dysgenesis, 2 as choristoma, and 1 case as leukoma. Only 2 of the corneal grafts performed in these infants remained clear. The underlying disease in the 2 cases where surgery was successful was Peter's anomaly, with a clear corneal periphery. From the analysis of the corneal buttons the authors deduce that graft failure in most such cases is due to severe structural changes of the host cornea. Three findings represented consistently unfavorable signs: (1) absence of Bowman's layer; (2) absence of Descemet's membrane and (3) corneal vascularization at the cut edge of the button. Immunoreaction or infection of the graft are rare causes of graft failure. Despite the extremely poor prognosis of bilateral congenital corneal opacities, penetrating keratoplasty should be attempted. The histopathological findings may be used as prognostic criteria for graft survival or the extent of anterior segment dysgenesis.     

Ocular findings in X-linked ichthyosis: a survey on 38 cases

The authors report on the occurrence of ocular abnormalities in X-linked ichthyosis (XLI) patients, in their carrier mothers and in healthy volunteers who served as controls. The diagnosis of XLI was based on: (1) demonstration of steroid sulfatase deficiency in cultured skin fibroblasts; (2) lack of hybridization of patient's deoxyribonucleic acid (DNA) with specific steroid sulfatase complementary DNA probe; (3) electrophoretic mobility of plasma lipoproteins. Cholesterol sulfate plasma levels were also determined. The incidence of corneal opacities was the same in XLI patients and in their carrier mothers (23.7 and 24.3%, respectively). Neither other corneal nor ophthalmological alterations were found. Moreover, in XLI patients the plasma levels of cholesterol sulfate were about twenty times higher than in controls. Our findings demonstrate that ocular changes do not seem to be an absolute criterion for a definite diagnosis of XLI and the fact that the pathogenesis of corneal opacities is not due to an accumulation of cholesterol sulfate, but rather that this compound probably induces physicochemical changes of the corneal tissue properties.     

Cogan's syndrome: ocular findings in an atypical case

Cogan's syndrome is an unusual multisystemic disease characterized by interstitial keratitis in association with vestibuloauditory dysfunction and possible irreversible deafness, classified into 2 clinical types: typical and atypical. There is disagreement in the literature about corneal disease in the atypical variety. A 32-year-old woman complaining of ocular hyperemia and ocular pain, photophobia and visual acuity loss in the right eye associated with sudden left hearing loss, vomiting, diarrhea, oliguria, oropharynx pain and fever. Previous history of similar disease in left eye and right hearing. There was intense conjunctival hyperemia, nodular scleritis, episcleritis, and circular infiltrates in the corneal stroma. The patient received pulse-therapy with methylprednisolone and cyclophosphamide. She exhibited significant ocular improvement but poor hearing results. The reported case may be a typical Cogan's syndrome (according to authors that assert the non-existence of corneal disease in the atypical type) with some findings characteristic of the atypical type or an atypical Cogan's syndrome (for those asserting that it is a corneal disease). Differential diagnosis is also discussed.     

Light and electron microscopy in one case of herpes zoster keratitis (author's transl)]

One case of herpes zoster keratitis studied after corneal graft is described. Light and electron microscopy investigations show severe pathological changes under the coneal epithelium: Bowman's layer disruption, superficial stromal alterations, sub-epithelial phagocyte proliferation with lipid and mucopolysaccharid vacuolar deposits, abnormal vascularization of the posterior stroma. The authors stress on this interesting ultrastructural study because of very rare cases of the same disease reported in the literature.     

Keratocyte survival following a controlled-rate freeze

One of the major drawbacks of cryorefractive surgery is the delay in the postoperative recovery of corneal clarity. The authors have hypothesized that this delay is due to the death of graft keratocytes caused by the freezing process, and the need for subsequent repopulation by host keratocytes to restore corneal clarity. By using a slow, controlled-rate freeze on a modified Barraquer cryolathe, the authors are able to maintain keratocyte viability in the graft corneal tissue, as assessed by standard histologic methods and by collagenase digestion. Maintenance of keratocyte viability results in the rapid return of corneal clarity following lamellar keratoplasty in the rabbit, with few of the histopathologic changes seen following standard rapid freezing of corneal tissue.     

Keratoendotheliitis fugax hereditaria. A clinical and specular microscopic study of a family with dominant inflammatory corneal disease

A peculiar hereditary corneal disease seen in one pedigree is presented. The disease manifests itself as transient attacks of kerato-endotheliitis. These attacks last from a few days to some weeks. Clinically, corneal oedema and endothelial guttata-like changes with very slight anterior chamber reaction can be seen; after many attacks there may be permanent opacities in the stroma. Endothelial specular photography during an attack reveals dramatic changes: large black nonreflecting areas between quite normal-looking hexagonal cells. Also between the attacks and among family members who have no clinical corneal disease, changes in the endothelium: black spots in the centres of endothelial cells and marked pleomorphism, are to be seen. Among the family members a high incidence of collagen diseases was found.     

Ocular manifestations of Fabry's disease

A 52-year-old black female teacher's aide presented for an eye examination with a complaint of progressively worsening vision, stinging and burning of the eyes, and occasional foreign body sensation. Examination revealed a dry eye syndrome and corneal dystrophy consistent with Fabry's disease, a cardiovascular disease with significant systemic as well as ocular findings. The patient was treated for the acute corneal symptoms and closely followed for progression of the dystrophic corneal changes.     

准分子激光角膜切削术动物实验初步观察

在兔眼行准分子激光角膜切削术，对其角膜进行临床、光镜及电镜观察，发现术后上皮愈合前实质浅层出现较明显的炎症反应，切削面胶原纤维无明显损伤，角膜基质内成纤维细胞明显增多，在兔角膜还观察内皮细胞有一过性的形态改变。对ＰＲＫ术后角膜创面的愈合及影响因素作了简要的讨论。     

Amniotic membrane transplantation in severe ocular surface disorders

PURPOSE: Amniotic membrane transplantation is currently being used as an alternative approach to treat severe corneal surface disorders refractory to medical therapy. The authors report complications of corneal surface disorders after successful amniotic membrane transplantation. METHODS: Case series. RESULTS: Twenty-eight patients with corneal surface disorders due to severe chemical burns, corneal ulceration, or persistent epithelium defects were treated with amniotic membrane transplantation. Four of these patients showed a spontaneous perforation and three patients developed a descemetocele within 6 weeks after the amniotic membrane transplantation. CONCLUSIONS: In this case series, descemetocele and corneal perforation occurred in 25% of the patients after amniotic membrane transplantation. This might be due to the severity of the underlying disease or to the impact of amniotic membrane on corneal fibroblasts and collagenases. The risk of corneal thinning and perforation should be considered in the decision of treatment with amnion and follow-up regimen.     

Management of neurotrophic keratopathy

Neurotrophic keratopathy is a degenerative corneal disease caused by an impairment of corneal sensitivity. Lack of the sensory nerve's trophic effect is responsible for the impairment in corneal healing and for the changes on the ocular surface that lead to corneal epithelial deficit, ulcer, and perforation. The etiology and recent advances in understanding of the pathogenetic mechanisms of neurotrophic keratopathy are reviewed here. An accurate history and a clinical examination that covers the function of cranial nerves often identify the cause of the disease. Clinical features and guidelines for the differential diagnosis and treatment are presented. Specific medical and surgical treatments, selected on the basis of clinical staging of the disease, can often halt disease progression. Future developments in medical treatment, including the use of neuropeptide and growth factors, are discussed. The identification of corneal anesthesia associated with an epithelial defect allows appropriate treatment and prevention of progression to stromal lysis and perforation.     

Our initial experience with the surgical correction of astigmatism by sectorial keratorrhaphy

The authors analyze the first experience with surgical correction of corneal astigmatism by sectorial keratorrhaphy (SKR). The operation consists in sewing an intralamellar nylon (9.00) suture perpendicular to poorly refracting meridian of the cornea. The mechanism of alteration of the corneal curvature resultant from SKR is similar to that in the known wedge-shaped resection of the cornea. The technique of surgery has been mastered in experiments with 12 isolated cadaver eyes. Morphologic studies of 16 eyes of 8 rabbits have lead the authors to a conclusion that prolonged presence of monofilament sutures in the corneal stroma induces the minimal changes in the adjacent tissues, these changes not augmenting over the follow-up period. 15 operations were performed in clinic, the follow-up periods were 4 to 14 mos. The data of the subjective examination of the refraction indicate that corneal astigmatism has reduced by 0.5 to 5.5 diopters, by 2.0-4.0 diopters in the majority of cases. The results evidence that SKR may be used as a method of choice for the surgical correction of hypermetropic or mixed astigmatism.     

Corneal topographic changes following strabismus surgery in Grave's disease.

A computerized topographic analysis system was used to evaluate corneal changes after strabismus surgery in eight eyes of five patients with Graves' disease. All patients underwent inferior rectus muscle recession; three eyes also had medial rectus recession. Corneal topographic analysis revealed that, postoperatively, corneas steepened inferiorly and inferotemporally at 1.5 mm from corneal apex (p less than 0.05). The opposite effect was observed in the superior quadrant (average flattening of 1.20 +/- 0.32 D at 1.5 mm from corneal apex, and 1.08 +/- 0.39 D at 3.0 mm from corneal apex; p less than 0.05). Superotemporally, the cornea flattened by an average of 0.65 +/- 0.26 D at 3.0 mm from corneal apex, and superonasally 0.72 +/- 0.19 D at 3.0 mm from corneal apex (p less than 0.05). Central, nasal, and temporal cornea did not show statistically significant changes. Spherical equivalent did not change significantly after surgery. The amount of restriction and upgaze measured preoperatively was correlated weakly with inferior corneal steepening (r2 = 0.44; p = 0.046). These results are indicative that corneal topography may be influenced by strabismus surgery for Graves' disease through alteration of extraocular muscle tension or intraocular pressure.     

Limbal stem cell transplantation in chronic inflammatory eye disease

OBJECTIVE: The goal of this study was to describe the outcome of limbal stem cell transplantation (LSCT) in patients with severe ocular surface disease caused by underlying chronic inflammatory eye disease. DESIGN: Retrospective noncomparative case series. PARTICIPANTS: Nine patients with limbal stem cell deficiency caused by an underlying ocular inflammatory disease who underwent LSCT. METHODS: The authors reviewed the records of 11 eyes of 9 patients with immunologically mediated ocular surface disease that underwent LSCT. MAIN OUTCOME MEASURES: The main outcome measures were reepithelialization of the corneal surface, restoration of corneal surface, and improvement in visual acuity. RESULTS: A total of 11 eyes underwent either autologous (n = 1) or HLA-matched living related donor (n = 10) LSCT for ocular surface disease secondary to inflammatory disease. Reepithelialization of the corneal surface in the immediate postoperative period occurred in 10 eyes (91%) within an average of 10 days (range, 3-21 days). Long-term restoration of the corneal surface was achieved in six (55%) eyes. Visual acuity improved in six eyes (55%). Reasons for poor outcomes included microbial infection, limbal stem cell graft rejection, and corneal ulceration. No donor eyes had complications. CONCLUSIONS: Patients with underlying immunologically mediated diseases, such as Stevens-Johnson syndrome, toxic epidermal necrolysis, or ocular cicatricial pemphigoid, who undergo LSCT have lower success rates than do those patients with noninflammatory ocular surface diseases.     

Corneal Donor Material Selection

The authors conducted the first long-range study to demonstrate possible negative effects on he recipients of corneal transplantation from donors who had died of a systemic malignancy or of chronic neurologic disease. The results are reported of a long-term retrospective analysis of 73 patients who received 86 grafts from donors with various systemic malignancies. These patients were followed for a mean of 127 months. There was no evidence of the transfer of the same malignancy to any of the recipients. There was no increased incidence of malignancy or earlier mortality in our patient population when compared with a reference population. Graft infection, endophthalmitis, or local tumor growth was not observed. The authors state that at the present time there is no basis for excluding donors dying of systemic malignancy as a source of material for use in keratoplasty. The authors examined the case histories of six patients who received grafts from donors who had died of a neurological disease with a suspected viral etiology. In a follow-up period ranging from 120 to 174 months, no evidence of neurologic disease developed in any of the patients. The sample was too small to provide data necessary for drawing conclusions concerning the safety of the use of material from this source. The authors strongly advise excluding any patient with a neurologic disease of suspected viral etiology as a source of corneal donor material.     

Lecithin:cholesterol acyltransferase deficiency

Lecithin:cholesterol acyltransferase (LCAT) deficiency is a rare familial disease inherited in an autosomal recessive pattern. It is characterized by a combination of plasma lipoprotein, corneal, erythrocyte and, in most patients, renal changes. The corneal changes consist of scattered stromal dots that are lipid deposits. Their composition is unique and suggests an intrinsic corneal metabolic defect. The corneal clouding is usually asymptomatic. Patients with the condition must be followed closely because renal failure may develop. We describe a patient with LCAT deficiency.