Bilateral Corneal Edema Research Articles

Primary Congenital Glaucoma presenting with Acute Corneal Hydrops: a challenging approach to amblyopia prevention

Introduction: Acute hydrops is a rare initial manifestation of Primary Congenital Glaucoma (PCG). It can result in significant corneal opacity, posing an additional risk for amblyopia development in PCG patients. We report a case of a newborn with PCG presenting with acute corneal hydrops and significant corneal scarring, discussing the management and challenges of amblyopia prevention. Case Presentation: A 3-day-old female newborn was referred to our department due to bilateral corneal clouding. Anterior segment examination revealed bilateral corneal edema, with severe corneal prolapse in the right eye consistent with acute hydrops. The anterior chamber structures of the right eye were indiscernible due to significant corneal edema. The left eye presented a deep, quiet anterior chamber with no dysgenesis of anterior segment structures. Intraocular pressure (IOP) measurements were >40 mmHg in both eyes. Corneal diameters were 10 mm OD and 12 mm OS. Fundoscopic posterior segment assessment was not possible due to unclear media. B-scan ultrasonography revealed no significant changes. The patient underwent urgent bilateral trabeculotomy. Postoperatively, intense mechanical stretching induced by severely increased IOP was visible, with the right cornea exhibiting a central opacity managed with topical corticosteroids and showing improvement. Right corneal opacity spared the superior cornea, and atropine drops combined with left eye occlusion were employed to mitigate right eye deprivation amblyopia. Eighteen months later, the patient can fixate and follow objects with the right eye. Left eye corneal transparency was restored, and bilateral IOP control was achieved. Conclusion: Despite prompt surgical treatment, acute hydrops presents a postoperative management challenge and may result in irreversible corneal scarring. Timely management of corneal opacities is crucial to prevent amblyopia. A multidisciplinary approach is essential for the best visual outcome.

A Case of Irreversible Corneal Endothelial Damage Associated with Amantadine Use

Purpose: To report a case of irreversible corneal endothelial cell damage associated with amantadine administration.Case summary: A 60-year-old female patient was referred with bilateral painless corneal edema. There was no history of ocular trauma or surgery. The was no sign of ocular surface inflammation, such as, conjunctival injection, either. At presentation, her best corrected visual acuity (BCVA) was 20/100 in the right eye and 20/50 in the left eye. Review of the past medical history revealed that she had been diagnosed with Parkinson’s disease and had been taking amantadine (100 mg, twice a day) for 3 years. At 7 weeks after cessation of amantadine, corneal edema was resolved bilaterally and BCVA improved to 20/30 in the right eye and 20/20 in the left eye. However, specular microscopy showed low endothelial cell density (ECD) with 886 ± 297/mm2 in the right eye and 926 ± 374/mm2 in the left eye. At 4 months after cessation, there was no corneal edema and BCVA was 20/25 in the right eye and 20/20 in the left eye. However, ECD was low with 852 ± 249/mm2 in the right eye and 903 ± 332/mm2 in the left eye.Conclusions: In cases with bilateral corneal edema without no obvious pathology, the history of medication, such as, amantadine, should be reviewed. Although cessation of amantadine can lead to improvement of corneal edema, irreversible damage of the corneal endothelial cells may remain. Serial evaluation of corneal endothelial cells is therefore recommended in patients with systemic amantadine administration.

Bilateral Irreversible Amantadine-Related Corneal Edema Successfully Treated With Descemet Membrane Endothelial Keratoplasty (DMEK)

Corneal edema is a recognized adverse reaction of chronic amantadine hydrochloride use. Fortunately, it is usually reversible with prompt discontinuation of the medication. We report a case of a patient with schizoaffective disorder–bipolar treated with high doses of amantadine for drug-induced akathisia, who developed irreversible bilateral severe corneal edema, and was successfully treated with Descemet membrane endothelial keratoplasty (DMEK). This case highlights the importance of recognizing amantadine-induced endothelial toxicity and confirms the utility of DMEK in the treatment of the condition.

Unusual bilateral corneal edema seen in a case of Behcet's like syndrome

Unusual bilateral corneal edema seen in a case of Behcet's like syndrome

Bilateral keratoconus hydrops in a patient with Down Syndrome: a case report

Background: Keratoconus has been reported in as many as 8% to 36% of people with Down syndrome. Corneal hydrops, a complication of advanced keratoconus, is characterized by the sudden onset of severe stromal and epithelial edema resulting from descemet membrane rupture. According to previous studies, acute corneal hydrops occurs in between 0.2% and 2.8% of keratoconus patients, while the incidence of corneal hydrops in Down syndrome patients with keratoconus is unclear. This study aims to evaluate the bilateral keratoconus hydrops in a patient with Down Syndrome. Case Presentation: We reported a case of bilateral corneal hydrops in a Down syndrome patient aged 28. Upon arrival, his bilateral visual acuity was fixed to follow the object. Slit-lamp examination revealed bilateral corneal edema and apical corneal scarring, and grade 4 plus keratoconus were seen on the Scheimpflug camera system. The patient receives medical treatment to lessen the patient's symptoms while they wait for a cornea donor to do a transplant. Conclusion: Patients with Down syndrome could experience bilateral corneal hydrops. Strong symptom communication, quick referral, and good cooperation during eye examinations are needed for early detection of this eye condition.

Long-term complications of cosmetic iris implants

BackgroundAdditive cosmetic implants (NewColorIris, Kahn Medical Devices, Panama City, Panama) are placed in the anterior chamber, in order to externally change iris color. There is a lack of robust clinical long-term prospective studies regarding the safety of these devices, as they have been related to the early-onset presentation of corneal decompensation, elevated intraocular pressure (IOP), uveitis and hyphema. However, in this case report some mild complications started to manifest unexpectedly late: 15 years after an uneventful procedure.Case presentationA 41-year-old Caucasian woman presented with blurred vision in both eyes over the last 6 months. Fifteen years earlier, she had undergone bilateral implantation of additive iris implants for aesthetic purposes, without any complication or ocular trauma during the follow-up. Ocular examination showed bilateral mild corneal edema, iris atrophy, and presence of pigment in the endothelium. Increased IOP (28 mmHg) was identified in the right eye. Anterior segment optical coherence tomography (AS-OCT) confirmed the decentration of the iris implant from the pupillary axis in that eye. Gonioscopy demonstrated pigment dispersion in both eyes, as well as a tendency to bilateral angle closure, that was also illustrated by AS-OCT analysis. Endothelial cell count was 1268 cells/mm2 in the right eye and 1122 cells/mm2 in the left eye.The presence of both implants was affecting corneal endothelium and anterior chamber angle in both eyes, and additionally, the decentration of the device in the case of the right eye led to secondary ocular hypertension in that eye.ConclusionsCosmetic implants in contact to the iris can remain quiescent for years, leading to possible complications that can present even in the long-term. The degree of implant decentration, the stage of angle closure disease and the magnitude of pigment dispersion may be some important factors related to the onset time of complications in these cases.

Amantadine therapy for Parkinson’s Disease: In Vivo Confocal Microscopy corneal findings, case report and revision of literature

BackgroundTo report a case of a patient showing bilateral corneal opacities after amantadine chronic treatment for Parkinson’s Disease (PD) and corneal edema associated with intra-epithelial and -endothelial depositions. After amantadine discontinuation a complete clinical remission with only a partial ultrastructural corneal recovery was reported.Case presentationWe describe a 78-year-old man with non-medical-responding bilateral corneal edema in treatment with systemic Amantadine for PD. In vivo confocal Microscopy (IVCM) analysis revealed hyperreflective particles at the epithelial level and expanded hyperreflective keratocyte and a disarrangement of stromal lamellae; endothelial cells showed hyperreflective intracellular inclusions in central and in peripheral areas with central polymegatism and pleomorphism. After 1 and 6 months the amantadine discontinuation, the absence of bilateral corneal edema and opacities were noted at the slit lamp examination, associated with the disappearance of epithelial and stromal abnormalities, but the persistence of endothelial hyperreflective deposits with a pleomorphism and polymegatism worsening at the IVCM exam.ConclusionThe evaluation of a patient’s cornea 6 months after the discontinuation of systemic amantadine therapy showed a clinical complete remission, with a complete resolution of the bilateral corneal oedema. On the other hand, ultrastructurally, amantadine toxicity is a completely reversible phenomenon at the epithelial level; conversely IVCM showed persistent endothelial degradation.

Neonatal Onset Aicardi-Goutières Syndrome with Congenital Corneal Edema, Expanding the Phenotype

Background: Type I interferonopathy is a group of autoinflammatory disorders associated with enhanced type I interferon levels, due to upregulation of activation mechanisms or downregulation of negative feedback. Aicardi-Goutières syndrome (AGS) is one of these conditions, characterized by encephalopathy that usually manifests in late infancy. A rarer presentation that mimics congenital trans-placentally acquired infection or a 'pseudo-TORCH' subtype has been described. Clinical Description: A boy of 36-week gestational age with intrauterine growth restriction, nuchal transparency and a normal antenatal microarray assay, was delivered by cesarean section for oligohydramnios and fetal distress. The baby cried at birth, but developed mild respiratory distress and was neurologically depressed. A congenital infection was considered in view of being hypoplastic small for date with microcephaly, encephalopathy, intracerebral calcifications, multiple congenital heart lesions, and hepatosplenomegaly. Bilateral corneal edema was noted. Management: Supportive treatment was initiated. Mother-baby serology for congenital infections was negative. Various differential diagnoses for pseudo ToRCH presentations were considered and genetic testing planned. Exome sequencing identified a homozygous, single base pair insertion (c. 56_57insG variant) in exon 2 of TREX1 gene on chromosome 3, previously reported in AGS. The baby did not survive, Conclusion: This paper describes the clinical approach that was used to establish diagnosis in a neonate with “pseudo ToRCH” phenotype. It also expands the clinical phenotype of AGS by reporting a hitherto undescribed ocular finding of congenital corneal edema.

Whole exome sequencing identified FAM149A as a plausible causative gene for congenital hereditary endothelial dystrophy, affecting Nrf2-Antioxidant signaling upon oxidative stress

BackgroundCongenital hereditary endothelial dystrophy (CHED) is a rare genetic disease of the corneal endothelium with a very early onset of bilateral corneal edema due to degeneration and dysfunction of the corneal endothelium. Currently SLC4A11 is the only established causative gene for CHED, but not all these reported CHED patients could be explained by SLC4A11 deficiency, indicating that the genetic predisposition of CHED still requires further exploration. MethodsTrio-based whole-exome sequencing was performed on a CHED patient and his unaffected parents. The GATK2 and an in-house bioinformatics pipeline were applied for variant analyses, following the 2015 American College of Medical Genetics and Genomics (ACMG) guidelines. Potential pathogenic variants were further validated by Sanger sequencing. The expression profiles of FAM149A in cell line, murine tissues or human corneal endothelia were determined by RT-qPCR. Small interfering RNA was used to knock down the expression of FAM149A in vitro. Cell viability was detected by a CCK-8 assay. ROS and 8-OHdG were examined by fluorometric analysis. The nuclear translocation of NRF2 was determined by western blotting. ResultsWe identified a homozygous mutation (NM_015398.3: c.991A > G; p.R331G) in the FAM149A gene that related to the phenotype of CHED. FAM149A was found to be highly expressed in corneal endothelium, and up-regulated upon oxidative stress. Further functional investigations demonstrated that deficiency in FAM149A impaired Nrf2-antioxidant signaling, rendering cells more vulnerable to oxidative stress. Consistently, the expression of FAM149A was significantly reduced in patients with corneal endothelium dysfunction. ConclusionThis study demonstrated, for the first time, FAM149A as a plausible causative gene for CHED etiology, offering new insight for future investigation targeting CHED.

Visceral Leishmaniasis in Dogs

Background: Canine visceral leishmaniasis (CVL) is a zoonosis of variable clinical presentation, either in systemic or cutaneous form. Clinical signs include anorexia, ophthalmopathies, and chronic kidney disease. In the state of Santa Catarina, the foci are concentrated in the capital and its adjacencies, in the east side of the state. The objective of this study is to outline the first three reported cases of CVL in the municipality of Curitibanos, since there are no reports to date in the region of the mountainous plateau, in the middle west of Santa Catarina.Cases: All dogs were treated at the Veterinary Clinic School of the Federal University of Santa Catarina, Campus Curitibanos. The animals, two males and one female, belonged to the same tutor, resided in Curitibanos, and were attended between 2016 and 2020. In the first case, attended in 2016, the complaint was of eye and skin changes about three months ago. The animal lived in an urban environment and came from Uruguaiana, Rio Grande do Sul. On physical examination, the animal presented skin peeling, wet and crusty lesions, bloody discharge in the ears and nasal hyperkeratosis, as well as signs suggestive of uveitis. In this case, euthanasia was carried out. The second case had complaints of respiratory, eye changes, hyporexia, and polydipsia. The dog was prostrate, dehydrated, with lymphadenomegaly and respiratory disorders, compatible with bacterial pneumonia. Bilateral corneal edema confirmed uveitis. Upon return, the animal remained dehydrated with enlarged lymph nodes. In the aspiration of the lymph nodes, suggestive forms of Leishmania sp. were observed. The recommended confirmatory tests were performed, leading to a definitive diagnosis of CVL. The patient was treated with miltefosine, but later died. The third case was attended for general evaluation after a positive diagnosis for CVL during an epidemiological survey of the second case. The animal was alert, tachycardic, and tachypneic with hyperemic mucous membranes. Miltefosine-based treatment and permanent use of deltamethrin-impregnated collar were prescribed and ovariohysterectomy was carried out. The patient is clinically well. In the search for vectors, in no place or moment of search, referring to the cases, vectors for CVL were found.Discussion: It is suggested that patients 2 and 3 are autochthonous cases, whose transmission form has not been fully elucidated, and vector transmission cannot be ruled out, as well as other less common forms of transmission. For case 1, it is suggested that it is an allochthone case, probably imported from the Uruguaiana region, where the disease is endemic. The conduct of a positive result for CVL is euthanasia, with the exception of dogs that have guardians who wish to perform treatment, but not always possible due to the high cost of miltefosine, the only drug approved for dog therapy in Brazil. In the first case, the owner opted for euthanasia, since in 2016 there was no possibility of treatment. For the last two cases, a treatment cycle was performed as recommended by the guidelines. Regarding the municipality of Curitibanos, in the first case diagnosed in 2016, the animal came from Uruguaiana. In conclusion, this study aimed to report the clinical and epidemiological characteristics related to the first three patients with CVL reported in Curitibanos.

Mirtazapine - an underrated drug for L-dopa induced dyskinesias

Background: A52 year old female who was diagnosed as Young Onset Parkinson's Disease (YOPD) at the age of 31 years, developed severe L-dopa induced dyskinesias. She had been taking Amantadine 200 mg/day since the past 12 years, later the dose had been increased to 300mg/day. After three months, the patient complained of visual symptoms, and had developed a painless, progressive and bilateral corneal edema. The patient could not afford DBS as an alternative to these medications. Ultimately, Amantidine was stopped, and post cessation of the drug, the dyskinesias worsened.

Severe Corneal Edema in a Dog Naturally Infected by Leishmania spp.

Background: Visceral leishmaniasis (VL) is an infectious disease caused by the protozoan Leishmania infantum that is transmitted to dogs and humans by sandflies. The incidence of eye injuries in VL is high. They occur in 20 to 81% of infected dogs and include blepharitis, granulomatous conjunctivitis, scleritis, keratitis, anterior uveitis, keratoconjunctivitis sicca, and secondary glaucoma. However, some dogs present only the clinical signs of eye damage. The main objective of this manuscript is to report a case of anterior uveitis with severe corneal edema in a dog with VL that underwent clinical and surgical ophthalmic treatments after miltefosine therapy.Case: An 8-month-old, intact male Labrador Retriever with brown fur presented with pruritus, diffuse desquamation, and conjunctival hyperemia on physical evaluation. On the basis of an ophthalmic examination, nodular conjunctivitis and uveitis were diagnosed in both eyes. Moreover, laboratory examination results showed hyperproteinemia, increased serum alkaline phosphatase activity, and positive reactions to immunochromatographic tests for VL. Clinical treatment was instituted from the moment of diagnosis, when miltefosine and allopurinol were prescribed. At the end of treatment, based on laboratory examination results, only allopurinol was prescribed at a lower dose than initially prescribed for treatment continuation. Topical medications (prednisolone eye drops and sodium hyaluronate) were recommended for the ophthalmic changes. One week after the start of topical treatment, the dog showed an improvement in eye inflammation but still had bilateral corneal edema. A hyperosmotic agent was prescribed to improve edema, and a surgical procedure was recommended if there was no improvement. The physician opted for the surgical procedure in one of the eyes that had not shown significant improvement after the clinical treatment.Discussion: VL is a zoonosis, and the domestic dog is the main reservoir. These animals often have dermatological conditions, and the ophthalmic changes observed can be unilateral or bilateral, with more than one change in the same eye. Lymphoplasmacytic or granulomatous anterior uveitis is the most prevalent change, as the uvea and conjunctiva are important lymphoid areas of the eye; this also explains the high incidence of uveitis and conjunctivitis in dogs with VL. In uveitis, corneal edema is driven by endothelial cell damage induced by prostaglandins, which interfere with the function of the endothelial pump and interrupt the normal dehydrated state of the cornea. Severe corneal edema can result in the formation of fluid-filled multifocal bubbles in the corneal stroma—a condition called bullous keratopathy. These bubbles accumulate under or inside the corneal epithelium, and they can burst spontaneously, leading to corneal erosions or ulcerations. Drug therapy with hyperosmotic agents could, in principle, reduce the formation of bubbles. Surgical options to decrease edema and blistering include a permanent conjunctival graft or thermokeratoplasty. Thermokeratoplasty induces the formation of superficial scars in the corneal stroma, applying multiple cauterization foci to the stroma exposed in the areas of bullous keratopathy and epithelial ulceration. In conclusion, the surgical therapeutic choice results in better visual quality in patients who do not respond well to clinical treatment.

Uveítis bilateral en un equino: Reporte de un caso

Among the main causes of damages to equideoculture are the various diseases, among them ocular diseases, especially keratitis and uveitis. These have an inflammatory origin and are associated with the main cases of blindness in horses. Uveitis is by definition the inflammation of the uveal tract of the eye. The inflammation may involve iris and ciliary body (anterior uveitis) or the choroid and retina (posterior uveitis). In horses is more common to the occurrence of inflammation in all structures (panuveitis). The objective of this study was to report the clinical case of bilateral uveitis in an equine at the Clínica de Equídeos of Centro de Desenvolvimento da Pecuária (CDP) at Universidade Federal da Bahia (UFBA), located in the city of Santo Amaro-BA. In the present case, a Mangalarga Marchador equine had bilateral blindness for approximately 90 days, without previous history of trauma or other conditions in the eyeball. In ophthalmic examination, the animal had bilateral epiphora and chemosis, vitreous opacity with presence of central superficial corneal ulcer and bilateral corneal edema. Reduction of pupillary reflex was also observed, but still present. Eyelid reflex present and threat reflex absent bilaterally, besides Schirmer lachrymal test with a result higher than 35 mm/min and bilateral positive fluorescein test. The animal presented negative serology for Leptospira spp. Due to the history and clinical signs the animal was diagnosed with primary uveitis. After treatment for 30 consecutive days, including the use of antimicrobials and systemic anti-inflammatories associated with the use of topical treatment with antibiotic and lubricant eyelids, the animal presented a marked evolution, with an evident improvement in visual acuity, which was identified after physical and ophthalmologic examination.

Bilateral simultaneous acute angle closure in an adult Nepalese woman

Purpose: To report a case of bilateral simultaneous angle closure in an adult Nepalese woman without any known secondary cause.
 Methods: Observational case report.
 Results: A 50-year-old Nepalese woman presented with decreased vision, pain, redness, and watering in both eyes with associated coloured haloes, nausea, and vomiting for 10 days. At presentation, her visual acuity was 20/400 in the right eye and hand motions close to face with accurate projection of rays in the left eye. Intraocular pressure was 38 mmHg in the right eye and 48 mmHg in the left eye without any antiglaucoma medications. A slit-lamp examination revealed bilateral circum-corneal conjunctival congestion, corneal edema, and shallow anterior chambers. Both pupils were mid-dilated and non-reactive to light. Gonioscopy showed closed angles in all four quadrants bilaterally. Posterior segment examination revealed normal optic disc with cup-disc-ratio of 0.3 in the right eye, and blurring of disc margin with cup-disc-ratio of 0.3 in the left eye. The patient was started on systemic acetazolamide 250 mg 4 times a day, topical brimonidine 0.2% and timolol 0.5% 2 times a day, and topical dexamethasone 6 times a day in both eyes, following which IOP reduced to 11 and 12 mmHg, respectively, the corneal edema subsided, but the anterior chamber remained shallow. Laser peripheral iridotomy was performed in the right eye and surgical peripheral iridectomy was performed in the left eye. After two weeks, vision improved to 20/30 in both eyes with normal intraocular pressure off antiglaucoma medications. Anterior chambers deepened significantly with clear corneas bilaterally. Gonioscopy at this stage showed essentially open angles with appositional closure in superior and temporal quadrants in the right eye and open angles in all four quadrants in the left eye. Posterior segment evaluation revealed normal optic disc in both eyes.
 Conclusions: Bilateral simultaneous acute angle closure is a rare presentation with very few reported secondary causes. We report a case of bilateral simultaneous angle closure in an adult Nepalese woman without any known secondary cause. The case was successfully managed with laser peripheral iridotomy in the right eye and surgical peripheral iridectomy in the left eye.

Nonsurgical treatment involving a contact lens and hyperosmotic solution for acute bullous keratopathy in a cat

A 4-year-old castrated male Korean domestic shorthair cat was referred with bilateral corneal edema. Focal and generalized acute bullous keratopathy in the oculus dexter and oculus sinister, respectively, were diagnosed by ophthalmologic examinations. Intensive topical treatment was administered to both eyes. A therapeutic soft contact lens was inserted in the oculus sinister as a corneal bandage instead of surgical treatment. The patient achieved complete recovery at 44 days after treatment. A therapeutic soft contact lens and an intensive regimen involving a topical hyperosmotic solution successfully treated acute bullous keratopathy in a feline patient.

Decompression retinopathy following nonpenetrating deep sclerectomy for primary congenital glaucoma

BackgroundTo describe a unique case of decompression retinopathy manifesting as pre-macular subhyaloid hemorrhage that occurs in a nine-day old child after undergoing a non-penetrating deep sclerectomy for primary congenital glaucoma.Case presentationWe report a single case of a 9-day-old boy who was referred to our department of ophthalmology for bilateral buphtalmia and corneal edema. He presented marked elevation of the intraocular pressure in both eyes (22 mmHg and 26 mmHg, in the right eye and left eye respectively) associated with significant optic nerve cupping.Non-penetrating deep sclerectomy was performed for each eye, with effective reduction of the intraocular pressure during the first week postoperatively (11 mmHg and 7 mmHg in the right eye and left eye respectively). The right eye presented an isolated subhyaloid hemorrhage located in the pre-macular area, persisting 3 weeks after the initial surgery and requiring pars-plana vitrectomy to clear the visual axis. This uncommon complication was identified as decompression retinopathy.The intraocular pressure remained controlled in the normal range three years after initial surgery in both eyes, with reversal of optic disc cupping.ConclusionsDecompression retinopathy is a potential complication after non-penetrating deep sclerectomy in primary congenital glaucoma, requiring prompt treatment strategy to prevent potential organic amblyopia.

Clinical and genetic investigation of amantadine-associated corneal edema.

PurposeAmantadine use has been temporally associated with bilateral corneal edema in a series of cases; however, its pathophysiological mechanisms have yet to be elucidated. We sought to rule out subclinical Fuchs dystrophy as a contributor, characterize its pattern of corneal edema, and describe the long-term outcome of concurrent topical steroids while resuming amantadine.Patient and methodsAfter a 44-year-old woman presented with new acute onset bilateral corneal edema, amantadine was discontinued, with clinical improvement. However, neurological decompensation required restarting amantadine, which she did concurrently with topical loteprednol. To determine whether subclinical Fuchs dystrophy might be present, triplet-primed polymerase chain reaction was conducted to measure copy number of the CTG18.1 trinucleotide repeat in TCF4. Specular microscopy and Scheimpflug imaging were conducted and followed for 32 months to assess for resolution and stability. Literature review was conducted to assess for consistency of the clinical phenotype.ResultsCorneal edema resolved clinically 4 weeks after discontinuation of amantadine. Serial Scheimpflug imaging demonstrated resolution of posterior and central corneal edema and specular microscopy revealed intracellular opacities with loss of endothelial cell density. Despite resuming amantadine, Scheimpflug imaging and specular microscopy measurements remained stable at 32 months. Triplet-primed PCR of CTG18.1 in TCF4 revealed no trinucleotide repeat expansion.ConclusionsAmantadine-associated corneal edema is characteristically posterior and central and appears unlikely to represent early or subclinical decompensation of Fuchs dystrophy. We describe the unique outcome of continued corneal clearance after restarting amantadine concurrently with steroids, a pattern that has persisted over 32 months to date.

Reversible cataract after exposure to distilled water: a case report

BackgroundTo report a case of a reversible cataract after intracameral infusion of distilled water during full-thickness astigmatic keratotomy.Case presentationA 20-year-old male whose bilateral anterior chambers were exposed to distilled water during astigmatic keratotomy developed bilateral corneal edema, inflammation of the anterior chambers, and an anterior subcapsular cataract in the right eye. After 1 month of topical administration of 0.1% prednisolone acetate and 5% NaCl, the bilateral inflammation of the cornea and anterior chambers cleared; endothelial cell density decreased by 41.1% in the right eye and 12.7% in the left eye. The cataract in the right eye decreased centripetally. Small incision lenticule extraction surgery was performed at 2 months after the astigmatic keratotomy; the patient’s uncorrected distance visual acuity 3 months later was 20/25 in both eyes.ConclusionsThis case suggests that a cataract that develops as a result of instantaneous intracameral exposure to distilled water is reversible.

Radiographic, Ultrasonographic and Postmortem Magnetic Resonance Imaging Features of Meningoencephalocele in a Calf with Tibial Hemimelia Syndrome

1. Abstract A 1-day-old, calf was presented for inability to stand and for evaluation of congenital anatomical and postural abnormalities. Physical examination revealed hypertrichosis, bilateral corneal edema, shortened hind limbs, an abdominal hernia and a fluctuant soft tissue swelling on the caudodorsal aspect of the head. Radiographs revealed a lucent line in the skull underlying an extracranial soft tissue swelling. Focal ultrasound (US) revealed an anechoic cystic structure contiguous with an intracranial fluid-filled cavity. Immediate postmortem magnetic resonance imaging (MRI) showed cranioschisis with two herniated meningeal sacs and focal parieto-occipital porencephaly. At necropsy, multiple intracranial, skeletal and abdominal defects were noted consistent with tibial hemimelia syndrome. Histopathology confirmed a meningoencephalocele that couldn’t be differentiated from a meningocele with US nor MRI. 2. Keywords: Bovine; Congenital Anomaly; Magnetic Resonance Imaging (MRI); Meningoencephalocele; Tibial Hemimelia Syndrome

Ultramarathon-Induced Bilateral Corneal Edema: A Case Report and a Review of the Literature.

Ultramarathon-associated corneal edema is a rare phenomenon. We report a case of a patient who presented with bilateral corneal edema following an ultramarathon. The corneal edema resolved without sequelae 48 h later. The authors hypothesize that the additive effect of enhanced glycolysis, an increased lactate level in the aqueous humor, and oxidative stress alters the normal endothelial regulation of the cornea and leads to corneal edema.