Carbon monoxide (CO) toxicity typically presents with drowsiness, headache, and neurological disturbances. Visual field defects involving the optic chiasma are very rarely seen. A case of a 31-year-old female, with a history of heavy smoking and learning disability, presented to the acute medical ward with 3-4 days of frontal headache, neck pain, room spinning sensation, and an episode of loss of consciousness. Neurological examination revealed a bitemporal hemianopia that progressed to a temporal hemianopia over the next day and completely resolved within 48 hours. Blood gas analysis showed a high carboxyhaemoglobin (COHb) level of 9.7%, with normal pH and lactate. The CT brain showed no acute abnormality. Ophthalmology confirmed visual field defects with no diplopia. Neurology advised an MRI to rule out pituitary apoplexy, and the image showed no structural abnormality. The transient visual field changes were consistent with possible CO toxicity-induced hypoxia affecting the optic chiasma or its vascular supply. Symptoms quickly resolved after oxygen therapy and abstinence from smoking. This study highlights the diagnostic challenge of identifying CO toxicity in heavy smokers and their atypical clinical manifestations. It emphasises the need to consider toxic exposure when presenting with fluctuating visual field defects and particularly, when their neuro-imagining is normal. Environmental sources of CO exposure were assessed, and no clear source was identified, with significant tobacco use considered a potential contributing factor.

We report the case of a 77-year-old woman who presented with progressive, painless bilateral visual loss over three weeks. Ophthalmologic evaluation demonstrated bilateral anterior ischemic optic neuropathy and right central retinal artery occlusion. Notably, she lacked classical systemic features of giant cell arteritis (GCA), including headache, scalp tenderness, or jaw claudication. Laboratory evaluation revealed an elevated erythrocyte sedimentation rate (ESR 64 mm/h). Temporal artery ultrasound demonstrated bilateral halo signs, supporting the diagnosis of GCA. High-dose corticosteroid therapy was promptly initiated; however, visual loss remained irreversible. This case highlights the importance of maintaining a high index of suspicion for GCA in elderly patients presenting with unexplained visual symptoms, even in the absence of typical cranial features. Temporal artery ultrasound is a valuable non-invasive diagnostic tool that can facilitate early diagnosis and prompt treatment, potentially preventing irreversible visual complications.

Leber hereditary optic neuropathy (LHON) is a mitochondrial optic neuropathy that typically causes severe bilateral central vision loss. Although several natural-history studies have reported visual outcomes, long-term trajectories beyond 5 years remain incompletely quantified, particularly in Asian cohorts. We performed a single-center retrospective cohort study at a tertiary eye hospital in Japan. Among 174 genetically confirmed LHON patients, we identified 27 patients (53 eyes) who presented within 6 months of onset and were followed continuously for ≥10 years. Best-corrected visual acuity (BCVA, logMAR) was collected from onset to 120 months. Piecewise linear mixed-effects models with patient- and eye-level random effects were fitted over three phases (Acute, < 12 months; Chronic, 12-60 months; Late Chronic, 60-120 months). Kaplan-Meier analyses estimated time to achieving BCVA ≤1.6 and ≤1.3 logMAR. BCVA worsened rapidly after onset, followed by gradual improvement and then an approximately horizontal course. During the Chronic phase, BCVA showed a small but statistically significant improvement (overall -0.030 logMAR/year, 95% confidence interval (CI) -0.045 to -0.015; -0.025 logMAR/year, 95% CI -0.044 to -0.007 in a pre-specified m.11778G > A subgroup). In the Late Chronic phase, estimated slopes were close to zero (+0.003 logMAR/year, 95% CI -0.007 to +0.013 overall), with wide CIs compatible with small long-term improvement or deterioration. By 10 years, the cumulative probabilities of achieving BCVA ≤1.6 and ≤1.3 logMAR were approximately 45% and 26%, respectively. In this Japanese LHON cohort with ≥10 years of continuous follow-up, BCVA showed limited improvement during the early chronic period, and we did not detect a clear directional trend thereafter. Given the modest sample size and selection of long-term attendees, these estimates should be interpreted as descriptive, phase-specific benchmarks rather than definitive evidence of long-term stability or ethnic differences.

Immune-mediated ocular surface disorders represent a group of diseases associated with hypersensitivity reactions. Most of these conditions have a chronic progressive course, which can lead to severe consequences, including loss of visual function. In addition to necessary systemic therapy that depends on the underlying condition, the basic approach to the treatment of immune-mediated ocular surface diseases consists of immunosuppressants and artificial tears. In the acute stage or during exacerbations of severe immune-mediated lesions, the drug of choice is the glucocorticosteroid (GCS) dexamethasone. Fluorometholone and loteprednol considered to be "soft", i.e., low-potency GCSs. Although the use of cyclosporine A, including in the form of a cationic emulsion (Ikervis), is considered ineffective for most forms of dry eye disease, it may be used in a selected group of patients with moderate immune keratoconjunctivitis. In more severe cases, the use of the more potent agent tacrolimus is advisable. As for mandatory tear substitution therapy in this patient population, combined formulations containing hyaluronic acid and the reparative agent dexpanthenol appear promising. The composition of Stillavit Intensive provides reliable hydration of ocular surface tissues due to sodium hyaluronate 1.8 mg, additional anti-inflammatory effects mediated by sodium chondroitin sulfate, and regeneration of the conjunctival and corneal epithelium through D-panthenol 50.0 mg.

The rapid proliferation of anti-obesity medications (AOMs), including glucagon-like peptide-1 receptor agonists (GLP-1 RAs), the dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 agonist tirzepatide, and non-incretin agents, including orlistat, phentermine, and bupropion/naltrexone, has created an underappreciated perioperative patient safety hazard. Existing guidelines have focused narrowly on GLP-1 RAs and aspiration risk, leaving some critical gaps unaddressed: (1) the misidentification trap, whereby drug-induced adverse effects, including acute pancreatitis, bowel obstruction, sudden visual loss, and neuropsychiatric dysfunction, are clinically and radiographically indistinguishable from surgical or anesthetic complications, exposing clinicians to unwarranted blame, and (2) the full perioperative risk profile of non-GLP-1 AOM classes. This narrative review synthesizes the current pharmacovigilance evidence, consensus guidelines, and clinical case data to address these gaps. Non-arteritic anterior ischemic optic neuropathy (NAION) from semaglutide (HR 7.64; World Health Organization safety alert 2025) may be attributed to anesthetic corneal injury, emotional lability may be misinterpreted as emergence delirium, drug-induced pancreatitis from GLP-1 RAs (adjusted HR 9.09 vs. comparator) may be misattributed to the operating surgeon, and bowel obstruction from premature postoperative GLP-1 RA resumption has prompted unnecessary re-laparotomy. Structured preoperative AOM documentation, explicit postoperative hold orders, and the inclusion of drug etiology in postoperative differentials constitute the defensible standard of care in the era of pharmacological obesity management.

Tendons transmit mechanical forces between muscles and bones through their highly aligned, collagen-rich extracellular matrix. When damaged, resident cells help restore this matrix. However, in tendinopathies, this repair response fails, leading to loss of proper tendon function. How altered mechanical states reshape tendon cell and matrix architecture remains poorly understood because existing methods do not readily capture tendon structure across relevant length scales. Here, we combine Fluorescent Labeling of Abundant Reactive Entities (FLARE) with Expansion Microscopy (ExM) to visualize cellular and extracellular structures in native tendon tissue. FLARE-ExM resolves the dense fibrillar matrix across multiple tendon types, including elastic fibers and glycan-rich cellular protrusions. In a tendon resection model, acute loss-of-tension was associated with increased fibril width and expansion of carbohydrate- and protein-rich regions. In ruptured human Achilles tendon, FLARE-ExM revealed extracellular disorganization and disrupted cellular architecture. These results establish FLARE-ExM as a useful approach for studying how mechanical perturbation remodels tendon architecture across physiological and disease contexts.

Microbial keratitis is a significant cause of corneal blindness worldwide. Important but frequently misdiagnosed pathogens include Pythium insidiosum, filamentous fungi, and Acanthamoeba species (spp). Their clinical presentations frequently overlap, and delayed or inappropriate treatment can lead to irreversible vision loss. Therefore, understanding the anatomical basis of infection, natural history, and patterns of spread among these entities is crucial for accurate diagnosis and timely management. Please see StatPearls' companion resource, "Pythium Keratitis," for further information. The cornea, a transparent avascular structure composed of 5 layers: the epithelium, Bowman layer, stroma, Descemet membrane, and endothelium, which function as both a refractive medium and a barrier to infection. Microbial invasion typically begins with epithelial defects resulting from trauma, surgery, or contact lens wear, followed by stromal colonization. Differences in organismal biology determine the route of invasion, tissue response, and clinical evolution (Table 1). Pythium insidiosum keratitis is caused by an aquatic oomycete belonging to the kingdom Straminipila that is found in stagnant water, rice paddies, and moist soil. Infection follows corneal inoculation by contaminated water, vegetation, or soil, particularly in humid, tropical environments. The organism produces slender, aseptate filaments that invade the corneal stroma radially, creating a characteristic reticular or tentacular appearance with limited necrosis but extensive enzymatic degradation. The absence of chitin and ergosterol in its cell wall renders antifungal drugs ineffective. Clinically, the disease progresses rapidly within days, causing severe pain, a grayish, dry-looking stromal infiltrate with tentacular projections, and endothelial plaques (See Image. Pathognomic Features of Pythium insidiosum Keratitis). Notably, the lesion may appear deceptively inactive despite aggressive antifungal therapy, a key diagnostic clue. The natural course is fulminant, often requiring early therapeutic keratoplasty to preserve the globe. Fungal keratitis, caused by Fusarium, Aspergillus, Curvularia, or Candida organisms, is more common and relatively more indolent than Pythium keratitis. Trauma with plant material or contact lenses is a typical cause. Septate hyphae invade the anterior and midstroma, resulting in necrosis and feathery-edged infiltrates with satellite lesions. The infection evolves over days to weeks and typically responds to natamycin or voriconazole. The infiltrate appears soft, raised, or fluffy, with surrounding edema; descemetocele formation or perforation occurs late in the disease course. Proper identification via potassium hydroxide preparation or Calcofluor White staining, which highlights septate branching hyphae, enables timely antifungal therapy and improves outcomes. Acanthamoeba keratitis, a parasitic infection caused by Acanthamoeba castellanii and related species, primarily affects contact lens wearers or those exposed to contaminated tap water. The organism adheres to the corneal epithelium through mannose-binding proteins and invades the stroma along corneal nerves. The hallmark feature is perineural inflammation, producing severe pain disproportionate to clinical findings. The disease course is chronic and relapsing, characterized by punctate epithelial erosions progressing to ring infiltrates over weeks. Confocal microscopy reveals double-walled cysts within the stroma. Because of its indolent course, Acanthamoeba keratitis is often misdiagnosed as herpetic or fungal keratitis, leading to delayed diagnosis and prolonged recovery. Table 2 summarizes the distinguishing characteristics of each organism. The pattern of spread and host inflammatory response further differentiates these infections. Pythium spp spreads centrifugally through stromal lamellae to the Descemet membrane and limbus, provoking an intense neutrophilic reaction and tissue melt. Fungal hyphae, in contrast, cause granulomatous or mixed inflammation, progressing slowly through anterior and midstromal planes. Acanthamoeba spp exhibits unique perineural spread, resulting in radial keratoneuritis and a ring-shaped infiltrate with a lymphocytic host response. Table 3 summarizes the patterns and characteristics of dissemination. Abbreviations: GMS, Grocott-Gomori methenamine silver (stain); PAS, periodic acid Schiff (test); TPK, therapeutic keratoplasty. Diagnostic differentiation among the 3 conditions is notoriously difficult. P insidiosum is often mistaken for filamentous fungal keratitis on smears because of its filamentous morphology. Acanthamoebae cysts may be missed on routine staining unless special techniques such as Calcofluor White or periodic acid-Schiff (PAS) are used. Advanced diagnostic tools such as confocal microscopy, polymerase chain reaction (PCR), and culture on blood agar (for Pythium spp) or nonnutrient agar (for Acanthamoeba spp) enhance specificity. Recently, artificial intelligence (AI)-based diagnostic models using slit-lamp and smartphone images have achieved greater than 90% accuracy in differentiating Pythium keratitis from fungal keratitis, offering promise for point-of-care screening in low-resource regions. In summary, Pythium keratitis is an acute, aggressive, antifungal-resistant infection characterized by a reticular tentacular infiltrate. In contrast, fungal keratitis has a more indolent course, with fluffy, feathery margins that respond to antifungals. Acanthamoeba keratitis is characterized by a chronic, painful, ring-shaped infiltrate and cystic pathology. Recognizing these distinctions, supported by confocal imaging, microbiology, and AI-driven diagnostics, is vital for appropriate management and visual prognosis. Please see StatPearls' companion resource, "Corneal Ulcer," for further information.