Biomedical subjects

G Richard

Publications and source records attributed to G Richard.

At least 19 recordsLinked to original sources

PubMed2001

[Quantification of retinal nerve fiber thickness. A comparison of laser scanning ophthalmoscopy, polarimetry and optical coherence tomography in healthy and glaucomatous eyes].

PURPOSE: To evaluate the thickness of the retinal nerve fiber layer (RNFL) in healthy eyes and in eyes of patients with primary open angle glaucoma using the Heidelberg retina tomograph (HRT), the nerve fibre analyser (NFA) and the optical coherence tomograph (OCT). METHODS: In this prospective cohort study, 40 normal eyes and 86 eyes of age-matched glaucoma patients were compared by confocal scanning laser tomography using the HRT, scanning laser polarimetry (NFA) and optical coherence tomography (OCT). The RNFL thickness was measured in the superior, inferior, nasal and temporal regions as well as the total circumference. RESULTS: All three methods revealed a statistically significant difference between normal and glaucomatous eyes with respect to the mean RNFL thickness in the inferior and superior regions (p < 0.001). The mean RNFL thickness in the superior region was 329 microns (HRT), 87 microns (NFA) and 94 microns (OCT) in healthy volunteers compared to 275 microns (HRT), 72 microns (NFA) and 82 microns (OCT) in the patient group. In the inferior region, it was 323 microns (HRT), 87 microns (NFA) and 93 microns (OCT) in healthy subjects versus 240 microns (HRT), 74 microns (NFA) and 83 microns (OCT) in glaucoma patients. Cut-off points to differentiate between normal and glaucomatous eyes could not be defined. There was no difference in the RNFL thickness of right and left eyes. CONCLUSIONS: In RNFL thickness measurements using HRT, NFA and OCT, glaucoma patients showed a significantly thinner RNFL in the superior and inferior areas compared to healthy volunteers. These results confirm the known histological and fundus photographic findings of RNFL thinning near the optic disc in glaucoma patients. Although RNFL thickness cannot be used to diagnose glaucoma in individual patients due to the high interindividual differences, the quantitative assessment of RNFL thickness may complement the diagnostic armamentarium as a sensitive parameter for diagnosing and monitoring glaucomas.

Adult↗

PubMed2001

[Lacrimal duct treatment with ring intubation in injuries of the upper and lower eyelids].

BACKGROUND: Treating injuries of the lacrimal system with a silicon intubation is an approved method to prevent post-traumatic epiphora. MATERIALS AND METHODS: Between 1990 and 1999, operations were carried out on 44 patients with injuries of the canaliculi with silicon ring intubations. Interesting for us were the age distribution, causes of injuries, localisation and mid- to long-term postoperative complications. RESULTS: The age of the patients was between 1.75 and 74 years, 48% of the injuries were caused by household accidents, 23% by violence, 20% by traffic accidents and 9% by job-related accidents. The canaliculus inferior was injured in 68% of all patients. We found 10 postoperative complications, e.g. ectropia, a too long silicon ring or granuloma. We found a positive anatomical readapted lacrimal system in 88% and 12% of our patients complained of distinct to severe epiphora. CONCLUSIONS: The treatment of lacrimal laceration with a silicon intubation is an excellent method but special care should be taken with correct positioning of the lid margin.

Accidents, Home↗

PubMed2001

[Correlation of 55 samples of contact lens fluid and direct swabbings of the eye surface of symptomatic wearers of contact lenses].

BACKGROUND: The microbiological examination of contact lens storage solutions may reveal the etiological organisms responsible for keratitis and additionally harbour environmental contaminants. PATIENTS AND METHODS: From 1995 to 1998, conjunctival and corneal smears and scrapes, as well as the storage solutions of 55 soft contact lens wearers were examined microbiologically in a prospective non-randomised cohort study involving 53x unilateral and 2x bilateral cases of keraitis. RESULTS: In 42 of the in-use contact lens storage solutions, the following organisms were found: 8x Bacillus sp., 7x P. aeruginosa and 8x other pseudomonads, 6x Alcaligenes xylosans, 4x Serratia liquefaciens, 4x Enterobacter sp., 4x coagulase negative staphylococci, 3x Serratia marcescens, 3x S. aureus, 2x Streptococcus faecalis, 1x Klebsiella oxytoca and 5x Acanthameba. A significant correlation of ocular cultures was found for Pseudomonas, Enterobacter, Serratia, S. aureus, S. faecalis and Acanthameba, but not for Bacillus, Alcaligenes, and coagulase negative staphylococci. Fungi were not found. The more pronounced the clinical picture, the more Gram-negative bacteria were isolated. CONCLUSIONS: The microbiological examination of soft contact lens storage solutions of 55 keratitis patients confirmed that the microbes responsible were to be found in the fluid, in addition to environmental contaminants.

Acanthamoeba Keratitis↗

PubMed2001

[Thrombophilia factors as inducers of retinal vascular occlusion].

PURPOSE: Thrombophilic abnormalities and defects in the anticoagulant system, such as protein C or protein S deficiency, activated protein C resistance and factor V Leiden mutation, may produce retinal vascular occlusions. PATIENTS: Blood samples from 66 consecutive retinal vascular occlusion patients were obtained and analysed for protein C resistance and fibrinolysis activity. Other thrombophilic and standard laboratory coagulant tests were also carried out. RESULTS: An increased activity of factor VIII was found in 72% of the collective. Furthermore, 24% of all patients and 32% of patients younger than 45 years old were resistant to activated protein C. Nevertheless only one patient showed a homozygous factor V Leiden mutation. CONCLUSION: Thrombophilic activity in cases of protein C resistance or factor V Leiden mutation may result in severe thrombotic manifestations in ocular vessels. Compared to the elderly, younger people showed a higher activated protein C resistance which seems be one of the most common causes for retinal vascular occlusion in this age group.

Activated Protein C Resistance↗

PubMed2001

[Ocular hemodynamics and visual field in glaucoma treated with dorzolamide].

OBJECTIVE: It has been shown that oral carbonic anhydrase inhibitors improve visual function in glaucoma. Furthermore topical dorzolamide might improve ocular hemodynamics, as was demonstrated previously. This study was undertaken to evaluate whether topical dorzolamide affects visual function and ocular hemodynamics in glaucoma. METHODS: In a retrospective, open clinical trial, dorzolamide eye drops were administered to 28 patients with confirmed primary open angle glaucoma (POAG) in both eyes, 3 times daily for a mean follow up of 9 months. One eye was randomly chosen for evaluation. IOP, blood pressure, heart rate, pulsatile ocular blood flow (POBF) and Humphrey 30-2 visual fields were measured at baseline and after the start of the therapy. POBF was determined by pneumotonography. For statistical analysis the Wilcoxon-matched-paired test and the Bonferoni-Holm adjustment were used. RESULTS: In dorzolamide-treated patients the IOP dropped from 18 mmHg to 15.5 mmHg after 9 months therapy (p < 0.01) and the visual field improved significantly by 18% (p < 0.05). A statistically significant change was found for POBF from 543 microliters/min to 675 microliters/min (p < 0.05). CONCLUSIONS: The results showed the expected drop in intraocular pressure. Visual function and pulsatile ocular blood flow improved significantly which might be explained by an analogous, vasodilatory effect as was observed in orally applied carbonic anhydrase inhibitors.

Aged↗

PubMed2001

Molecular identification and expression of the peroxidase responsible for the oxidative burst in French bean (Phaseolus vulgaris L.) and related members of the gene family.

Molecular characterization has been accomplished for five members of the peroxidase gene family in French bean. The most important of these, designated FBPI, corresponds to the isoform believed to be responsible for the apoplastic oxidative burst demonstrated by suspension-cultured cells in response to fungal elicitor. Identification was made by a complete match of six peptide sequences derived from the native protein to the translated sequence of the cDNA. Modelling of the surface structure in comparison with two other members of the peroxidase family did not reveal any unusual features which might account for its role in the oxidative burst. However, FBP1 when expressed in Pichia pastoris generated H2O2 using cysteine at pH 7.2, a specific property of the native protein when isolated from suspension-cultured cells. FBP1, together with other members of the family, were all induced in cell cultures by elicitor action although they all showed some expression in non-induced cultured cells. They were also expressed in all tissues examined with varying levels of intensity of detection in northern blots. This was confirmed by in situ hybridization and FBP1 expression was confirmed in tissues where it has been previously detected by immunolocalization methods. Assigning roles to individual peroxidases is an important goal and molecular identification of the oxidative burst peroxidase allows further exploration of the relative roles of the different systems involved in generating reactive oxygen species.

Amino Acid Sequence↗

PubMed2001

Darier disease--novel mutations in ATP2A2 and genotype-phenotype correlation.

Darier disease (DD) is with a frequency of up to 1 in 36,000 a relatively common genodermatosis with autosomal dominant inheritance and late age of onset. The progressive skin manifestations are variable, but often debilitating and disfiguring, and may be associated with a wide range of neuropsychiatric problems, such as epilepsy and depression. On histology, acantholysis and dyskeratosis are prominent findings, implicating impaired functionality of desmosomes. Recently, mutations in the ATP2A2 gene encoding SERCA2, a calcium pump of the endo/sacrcoplasmic reticulum, have been identified as the molecular basis of DD. This slow-twitched calcium ATPase has two splice variants, one of which is highly expressed in epidermis, and maintains low intracellular calcium levels by facilitating transport of cytosolic calcium into the endoplasmic reticulum. Thus, it may confer a direct effect on the established calcium-dependent assembly of desmosomes. We screened ATP2A2 in a cohort of 24 DD families using conformation sensitive gel electrophoresis and direct sequencing, and detected 14 distinct mutations, 9 of which were novel. The mutational spectrum included 9 missense mutations, 1 nonsense mutation, 3 small in-frame deletions, and a 19-basepair insertion. Mutations were scattered over the entire gene with a slight preponderance in the first 8 exons, and affected exclusively residues conserved among all SERCAs. In addition, we found 2 silent polymorphisms, 1 of which occurred in 4 unrelated families. Comparison of molecular data and phenotypic features, such as severity and type of disease, occurrence of mucosal involvement, or association with neuropsychiatric disorders, did not reveal an obvious genotype-phenotype correlation in our cohort.

Calcium-Transporting ATPases↗

PubMed2001

Hypotrichosis with juvenile macular dystrophy is caused by a mutation in CDH3, encoding P-cadherin.

Congenital hypotrichosis associated with juvenile macular dystrophy (HJMD; MIM601553) is an autosomal recessive disorder of unknown etiology, characterized by hair loss heralding progressive macular degeneration and early blindness. We used homozygosity mapping in four consanguineous families to localize the gene defective in HJMD to 16q22.1. This region contains CDH3, encoding P-cadherin, which is expressed in the retinal pigment epithelium and hair follicles. Mutation analysis shows in all families a common homozygous deletion in exon 8 of CDH3. These results establish the molecular etiology of HJMD and implicate for the first time a cadherin molecule in the pathogenesis of a human hair and retinal disorder.

Adolescent↗

PubMed2001

Evidence for novel functions of the keratin tail emerging from a mutation causing ichthyosis hystrix.

Unraveling the molecular basis of inherited disorders of epithelial fragility has led to understanding of the complex structure and function of keratin intermediate filaments. Keratins are organized as a central alpha-helical rod domain flanked by nonhelical, variable end domains. Pathogenic mutations in 19 different keratin genes have been identified in sequences corresponding to conserved regions at the beginning and end of the rod. These areas have been recognized as zones of overlap between aligned keratin proteins and are thought to be crucial for proper assembly of keratin intermediate filaments. Consequently, all keratin disorders of skin, hair, nail, and mucous membranes caused by mutations in rod domain sequences are characterized by perinuclear clumping of fragmented keratin intermediate filaments, thus compromising mechanical strength and cell integrity. We report here the first mutation in a keratin gene (KRT1) that affects the variable tail domain (V2) and results in a profoundly different abnormality of the cytoskeletal architecture leading to a severe form of epidermal hyperkeratosis known as ichthyosis hystrix Curth-Macklin. Structural analyses disclosed a failure in keratin intermediate filament bundling, retraction of the cytoskeleton from the nucleus, and failed translocation of loricrin to the desmosomal plaques. These data provide the first in vivo evidence for the crucial role of a keratin tail domain in supramolecular keratin intermediate filament organization and barrier formation.

Amino Acid Sequence↗

PubMed2001

The spectrum of pathogenic mutations in SPINK5 in 19 families with Netherton syndrome: implications for mutation detection and first case of prenatal diagnosis.

The Comèl-Netherton syndrome is an autosomal recessive multisystemic disorder characterized by localized or generalized congenital ichthyosis, hair shaft abnormalities, immune deficiency, and markedly elevated IgE levels. Life-threatening complications during infancy include temperature and electrolyte imbalance, recurrent infections, and failure to thrive. To study the clinical presentations of the Comèl-Netherton syndrome and its molecular cause, we ascertained 19 unrelated families of various ethnic backgrounds. Results of initial linkage studies mapped the Comèl-Netherton syndrome in 12 multiplex families to a 12 cM interval on 5q32, thus confirming genetic homogeneity of Comèl-Netherton syndrome across families of different origins. The Comèl-Netherton syndrome region harbors the SPINK5 gene, which encodes a multidomain serine protease inhibitor (LEKTI) predominantly expressed in epithelial and lymphoid tissues. Recently, recessive mutations in SPINK5 were identified in several Comèl-Netherton syndrome patients from consanguineous families. We used heteroduplex analysis followed by direct DNA sequencing to screen all 33 exons and flanking intronic sequences of SPINK5 in the affected individuals of our cohort. Mutation analysis revealed 17 distinct mutations, 15 of which were novel, segregating in 14 Comèl-Netherton syndrome families. The nucleotide changes included four non-sense mutations, eight small deletions or insertions leading to frameshift, and five splice site defects, all of which are expected to result in premature terminated or altered translation of SPINK5. Almost half of the mutations clustered between exons 2 and 8, including two recurrent mutations. Genotype-phenotype correlations suggested that homozygous nucleotide changes resulting in early truncation of LEKT1 are associated with a severe phenotype. For the first time, we used molecular data to perform prenatal testing, thus demonstrating the feasibility of molecular diagnosis in the Comèl-Netherton syndrome.

Adolescent↗

PubMed2001

[Optical coherence tomography in geographic atrophy--a clinicopathologic correlation].

BACKGROUND: Optical coherence tomography was used for the examination of patients with geographic atrophy in different stages of age-related macular degeneration. Always compared with biomicroscopy and fluorescein angiography [4,7,8,10]. PATIENTS AND METHODS: 37 patients with geographic atrophy (n = 55 eyes) out of 150 with AMD (n = 169 eyes) were examined. The results of biomicroscopy, fluorescein angiography, optical coherence tomography and histological knowledge in age-related macular degeneration were studied. RESULTS: Fluorescein angiography always identified geographic atrophy and in 13.5% the findings additionally were similar to an occult choroidal neovascularisation with circular hyperpigmentation. Geographic atrophy shows a significant thinning of the neurosensory retina of 135 microns as an average in optical coherence tomography (p < 0.0005) which did not correlate to visual acuity. Typically an enhanced vertically sharp demarcated reflectivity of the choroid is found because of the lacking pigment epithelium. 43% of the geographic atrophies were identified by optical coherence tomography. 3 out of 55 eyes (5%) in optical coherence tomography only show macular holes additionally to geographic atrophy. CONCLUSION: A typical pattern of reflectivity is found by optical coherence tomography with enhanced reflectivity of the choroid because of lacking pigment epithelium and significant thinning of the fovea. Atypical macular holes moreover are found in 5% neither appearing in biomicroscopy nor in fluorescein angiography. An occult choroidal neovascularisation can be differentiated by optical coherence tomography from geographic atrophy because there is no spindle-like thickening of the pigment epithelium and no enhanced choroidal reflectivity. In borderline cases optical coherence tomography may be helpful and therapeutically decisive in differentiating geographic atrophy and occult choroidal neovascularisation and in detecting atypical macular holes.

Aged↗

PubMed2001

trans-dominant inhibition of connexin-43 by mutant connexin-26: implications for dominant connexin disorders affecting epidermal differentiation.

Dominant mutations of GJB2-encoding connexin-26 (Cx26) have pleiotropic effects, causing either hearing impairment (HI) alone or in association with palmoplantar keratoderma (PPK/HI). We examined a British family with the latter phenotype and identified a new dominant GJB2 mutation predicted to eliminate the amino acid residue E42 (DeltaE42) in Cx26. To dissect the pathomechanisms that result in diverse phenotypes of dominant GJB2 mutations, we studied the effect of three Cx26 mutants (DeltaE42, D66H and R75W) identified in individuals with PPK/HI, and another (W44C) present in individuals with non-syndromic HI on gap junctional intercellular communication. We expressed mutant Cx26 alone and together with the epidermal connexins Cx26, Cx37 and Cx43 in paired Xenopus oocytes, and measured the intercellular coupling by dual voltage clamping. Homotypic expression of each connexin as well as co-expression of wild-type (wt) Cx26/wtCx43 and wtCx26/wtCx37 yielded variable, yet robust, levels of channel activity. However, all four Cx26 mutants were functionally impaired and failed to induce intercellular coupling. When co-expressed with wtCx26, all four mutants suppressed the wtCx26 channel activity consistent with a dominant inhibitory effect. However, only those Cx26 mutants associated with a skin phenotype also significantly (P<0.05) inhibited intercellular conductance of co-expressed wtCx43, indicating a direct interaction of mutant Cx26 units with wtCx43. These results demonstrate, for the first time, a trans-dominant negative effect of Cx26 mutants in vitro. Furthermore, they support a novel concept suggesting that the principal mechanism for manifestation of dominant GJB2 mutations in the skin is their dominant interference with the function of wtCx43. This assumption is further corroborated by our finding that Cx26 and Cx43 focally colocalize at gap junctional plaques in affected skin tissue of two carriers of DeltaE42.

Adolescent↗

PubMed2001

The fate of heterotopically grafted neural precursor cells in the normal and dystrophic adult mouse retina.

PURPOSE: To study the integration and differentiation of heterotopically transplanted neural precursor cells in the retina of adult mouse mutants displaying apoptotic degeneration of photoreceptor cells. METHODS: Neural precursor cells were isolated from the spinal cord of transgenic mouse embryos ubiquitously expressing enhanced green fluorescent protein. Cells were expanded in vitro and transplanted into the retina of adult wild-type and age-matched beta2/beta1 knock-in mice. Beta2/beta1 knock-in mutants display apoptotic death of photoreceptor cells and were generated by placing the cDNA of the beta1 subunit into the gene of the beta2 subunit of Na,K-ATPase. The integration and differentiation of grafted cells in recipient retinas was studied 1 or 6 months after transplantation. RESULTS: Mutant retinas contained more donor-derived cells than wild-type hosts. Moreover, in mutants, donor cells integrated into deeper retinal layers. In both genotypes, grafted cells differentiated into astrocytes and oligodendrocytes. Only a few ganglion cell axons were myelinated by donor-derived oligodendrocytes 1 month after transplantation, whereas extensive myelination of the nerve fiber layer was observed 6 months after transplantation. Unequivocal evidence for differentiation of grafted cells into neurons was not obtained. CONCLUSIONS: Heterotopically transplanted neural precursor cells are capable of integrating, surviving, and differentiating into neural cell types in normal and dystrophic retinas of adult mice. The particular environment of a pathologically altered retina facilitates integration of transplanted precursor cells. In principle, neural precursors may thus be useful to substitute for or replace dysfunctional or degenerated cell types. Results of the present study also indicate that replacement of retinal cell types is likely to require more appropriate donor cells, such as retinal precursor cells.

Actins↗

PubMed2000

[Programmed cell death (apoptosis) in excised subretinal neovascularization].

BACKGROUND: The occurrence of apoptosis in choroidal neovascularizations (CNV) has only been described previously in a few cases. However, little is known about the extent and function of apoptosis. We analyzed the incidence of apoptosis in order to find new options in the therapy of CNV. Particular attention was given to the length of time that the process existed before surgery in patients with age-related macular degeneration (AMD). PATIENTS AND METHODS: In 34 patients (18 women, 16 men) ranging in age from 20 to 91 years (mean 70.3 years), CNV was detected by angiography. The majority of patients (n = 29) with CNV had AMD, which in most patients affected both eyes. In two patients CNV was due to post-traumatic proliferative vitreoretinopathy, in two other patients CNV occurred after a penetrating bulbus injury, and in one patient pseudoxanthoma elasticum was found. Thirty-four CNV membranes were excised by pars plana vitrectomy via retinotomy, fixed in formalin and embedded in paraffin. Sections were stained with PAS and H&E and examined microscopically. The in situ cell-detection kit (TUNEL) was used for immunohistochemical detection of apoptotic cells from fragmented DNA. RESULTS: In 74% (n = 25) of all patients and in 76% (n = 22) of patients with AMD, disseminated or focal apoptotic cells were detectable in the connective tissue, retinal pigment epithelium and in the vascular endothelium. In AMD patients with apoptotic cells, the SNV existed 1-12 months (mean 5.5 months) before surgical intervention. In patients without apoptotic cells, the CNV were present 5-36 months (mean 17 months) before surgery. At the time of surgery, the loss of reading ability had on average been going on 3 months; in patients with apoptotic cells, the mean time from the onset of this symptom was 2.4 months (1 week to 11 months); and in patients without apoptotic cells it was 5 months (1-12 months). CONCLUSION: Programmed cell death as a regulating pathomechanism was observed in all tissue parts of CNV with variable extension. In patients with AMD, a correlation existed between the length of time that CNV existed before surgery and the incidence of apoptotic cells. Apoptosis was found more frequently in recent CNV than in long-standing lesions. The various activity found in CNV suggests that the success of treatment may depend on the moment of intervention. To characterize the role of apoptosis further inducing and inhibiting factors have to be analyzed.

Adult↗

PubMed2000

[Endophthalmitis after cataract surgery: predisposing factors, infectious agents and therapy].

BACKGROUND: Infectious exogenous endophthalmitis is a serious complication after cataract surgery. Despite modern pharmacological and surgical methods, its treatment is still difficult. PATIENTS AND METHODS: In a retrospective study the records of all patients treated for endophthalmitis following cataract extraction at the Department of Ophthalmology of the University Hospital in Hamburg between January 1989 and December 1997 were assessed. RESULTS: Of 36 patients treated for endophthalmitis, 29 (80.6%) had been referred. In 14 (38.9%) of these 29 patients endophthalmitis had occurred after outpatient cataract surgery. Seven patients (19.4%) had been treated as inpatients at the University Eye Hospital Eppendorf. Vitrectomy was performed in 80.6% of the cases. An infectious agent was isolated from 50% of diagnostic probes. The most common organism isolated were coagulase-negative staphylococci (4 cases). Predisposing factors for the development of endophthalmitis were diabetes (27.8%), intraoperative loss of vitreous (19.4%), application of systemic steroids (13.9%) and wound dehiscence (11.1%). Of 27 patients (75%) followed up, 16 (59.3%) had a final visual acuity of 20/400 or better (mean 20/40). An enucleation had to be performed in 4 patients (13.8%). CONCLUSION: In this study, approximately 60% of patients with endophthalmitis following cataract extraction had their globes preserved and a good visual outcome after appropriate surgical interventions.

Adrenal Cortex Hormones↗

PubMed2000

[Ultrasound biomicroscopy in pigmentary glaucoma].

PURPOSE: To evaluate the anatomical relationships of the iris in pigmentary glaucoma before and after laser iridotomy and to evaluate the effect on intraocular pressure. METHODS: Ultrasound biomicroscopy (UBM, Humphrey-Zeiss) of the anterior segment was performed in 28 eyes of 28 patients (20 male, 8 female, mean age 43 years, mean untreated IOP 24.3 mmHg) with pigmentary glaucoma before and after laser iridotomy. The slope of intraocular pressure was documented. Mean follow-up was 9 months. For statistical analysis the Wilcoxon test was used. RESULTS: Ten out of 28 eyes showed iridozonular contact and concavity of the midperipheral iris. Laser iridotomy resulted in a significant pressure drop (P < 0.05) in these 10 eyes (24.6 mmHg to 18.3 mmHg). Eighteen eyes, however, did not show iridozonular contact and intraocular pressure did not drop sufficiently (P > 0.05; 25.1 mmHg to 23.1 mmHg) after laser iridotomy. CONCLUSION: The results show that iridozonular contact does not exist in every patient with pigmentary glaucoma. Therefore, it seems possible that more than one pathogenic mechanism is involved in pigmentary glaucoma. In patients with iridozonular contact, however, laser iridotomy significantly reduces intraocular pressure.

Adult↗

PubMed2000

[Prolonged wound healing after perforating keratoplasty. CPAP hyperbaric ventilators for sleep apnea as a risk factor].

Nasal hyperbaric respiration devices used at night to counteract sleep apnea may represent a concealed cause of delayed superficial wound healing following perforating keratoplasty. We report the cases of two patients whose respirators produced a continuous flow of pressurized air (nCPAP) onto the operated eyes, leading to conjunctival hyperemia, recurrent corneal erosion, infiltration of the puncture track and the cornea, and superficial punctate keratopathy. Microbiological investigation revealed no clearly identifiable pathogens. Healing improved consistently only after the pressurized air system had been modified so that no air escaped from the nostrils and the patients had been instructed in disinfection of the moisturizing system.

Adult↗

PubMed2000

Effect of perfluorodecalin on human retinal pigment epithelium and human corneal endothelium in vitro.

BACKGROUND: Perfluorocarbon liquids are useful intraoperative tools in complicated vitreoretinal surgery. They are usually removed at the end of the procedure, but small amounts may remain in the eye. Recently, contradictory results have been reported on the damage in association with residual perfluorocarbon liquids in the eye. This study examined the effects of perfluorodecalin on human retinal pigment epithelium and corneal endothelium in vitro. METHODS: Vitality and proliferative capacity of cell cultures were measured after incubation with perfluorodecalin. Vitality of cell cultures were measured using the Life-Dead assay. Cell proliferation was determined by measuring incorporation of 5-bromo-2'-deoxyuridine into cellular DNA. Furthermore, endothelium of organ-cultured human corneas was examined after incubation with perfluorodecalin by photodocumentation. RESULTS: Both cell types showed less extinctions in the Life-Dead assay after incubation with perfluorodecalin. After removing perfluorodecalin from the cultures, cells showed the same capacity of proliferation as the control cells. Compared to control corneas, perfluorodecalin induced a decrease in endothelial cell density. In four corneas, endothelial cell necrosis was observed. CONCLUSION: Decreasing extinctions in the Life-Dead assay after incubation with perfluorodecalin can be interpreted as showing a decreasing amount of vital cells. Because cell proliferation showed no significant changes the results suggest that perfluorodecalin may not be directly toxic to cells in vitro. It may exert an indirect or mechanical effect on cell function by impeding the normal metabolic exchange between endothelium and medium. Based on these results perfluorodecalin should be completely removed after operation.

Cell Count↗