Apraclonidine 1% eye drops 0.25ml unit dose preservative free

Posterior capsule opacification (PCO) is a common post-cataract surgery complication treated with Nd:YAG laser posterior capsulotomy, which may cause intraocular pressure (IOP) spikes and threaten vision. Brimonidine and apraclonidine are widely used to prevent such elevations. This prospective, double-masked, randomized clinical trial evaluated the efficacy of topical dexmedetomidine, a novel ophthalmic drop, in preventing IOP rise after Nd:YAG laser treatment. A total of 111 eyes from 89 pseudophakic patients were randomized to receive dexmedetomidine 0.008% or brimonidine 0.2% one h before the procedure. Patients with glaucoma, baseline IOP > 24 mmHg, keratoconus, corneal edema, prior refractive/corneal surgery, or unstable cardiovascular disease were excluded. IOP was measured with air-puff tonometry at baseline, 30 min, 4 h, and 24 h post-laser. Baseline characteristics were comparable. In the dexmedetomidine group, mean IOP values were 16.3 ± 3.6, 14.8 ± 4.7, 17.1 ± 6.2, and 16.7 ± 4.5 mmHg, while in the brimonidine group, they were 16.7 ± 2.9, 13.3 ± 3.9, 13.2 ± 5.5, and 14.2 ± 3.9 mmHg, respectively. At 30 min, brimonidine significantly reduced IOP (p = 0.000), whereas dexmedetomidine did not (p = 0.116). At 4 and 24 h, IOP increased above baseline with dexmedetomidine but decreased with brimonidine (p = 0.001 and p = 0.004). Dexmedetomidine was associated with more IOP spikes > 10 mmHg (9% vs. 2%, p = 0.035) and IOP > 30 mmHg (7% vs. 2%, p = 0.09). No systemic or ocular side effects occurred. Although dexmedetomidine prevented acute IOP surges, its efficacy was inferior to brimonidine. Further studies should explore optimal dosing, formulations, and long-term safety to clarify its prophylactic potential.

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Horner syndrome (HS), a rare complication of endoscopic thyroid surgery (ETS), manifests as ptosis, miosis, and anhidrosis resulting from oculosympathetic pathway disruption. This study explores HS etiology through two case reports and literature analysis. Case 1 involved a 43-year-old female who underwent unilateral thyroidectomy via a bilateral areolar approach for a thyroid oncocytic adenoma. On postoperative day 1, ptosis and miosis were observed, and the patient was diagnosed with HS. Despite initial glucocorticoid and neurotrophic therapy, symptoms resolved spontaneously by 6 months. Case 2 involved a 36-year-old female with papillary thyroid carcinoma treated via ETS with central lymph node dissection. Transient ptosis and miosis occurred postoperatively and resolved completely after a 6-day course of steroid treatment. Both cases highlighted HS as a complication linked to intraoperative cervical sympathetic chain (CSC) injury, likely due to retractor-induced compression, thermal damage from energy devices, or anatomical variations. A literature review identified only nine prior ETS-related HS cases, emphasizing its rarity (incidence: 0.03%-0.48%). Mechanisms include CSC compression caused by hematoma, edema, or inflammation in confined surgical spaces, with most symptoms resolving as these subside. Differential diagnosis requires excluding intracranial, spinal, or vascular pathologies. Pharmacologic tests utilizing drugs such as Apraclonidine, Cocaine, and Hydroxyamphetamine aid in the diagnosis of HS, while short-term use of steroids and neurotrophins may expedite recovery. Persistent HS beyond 1 year diminishes the likelihood of recovery, necessitating surgical correction for ptosis. ETS, favored for cosmetic outcomes, demands meticulous CSC preservation during dissection, particularly near the superior cervical ganglion. Preoperative patient counseling about HS risk is crucial. This study underscores HS as non-life-threatening yet distressing complication, advocating for refined surgical techniques and heightened anatomical awareness to avoid CSC injury during ETS.

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Botulinum toxin (BoNT) is widely used in the management of neurological disorders and in aesthetic medicine. Although generally safe, facial injections may be associated with complications with relevant functional or aesthetic impact. This narrative review aimed to summarize reported facial complications following BoNT injections and to describe available management strategies. A PubMed search up to November 2025 identified 239 articles; after screening and full-text review, 20 studies met the inclusion criteria. Data were synthesized narratively due to the heterogeneity of study designs. Upper eyelid ptosis was the most frequently reported clinically significant complication and was mainly managed with topical alpha-adrenergic agonists. Diplopia was rare but functionally disabling and was treated conservatively with occlusion or prisms or with targeted extraocular BoNT injection in selected cases. Ocular surface changes, facial asymmetry, perioral dysfunction, local reactions, and headache were generally mild and self-limited. Systemic adverse events were uncommon but occasionally required hospital evaluation. Overall, management strategies were predominantly conservative and supported by low-level evidence. Facial BoNT injections are generally safe, but clinically relevant complications can occur. Management is largely conservative, apraclonidine 0.5% is most commonly used for toxin-induced ptosis, and oxymetazoline 0.1% (FDA-approved for acquired blepharoptosis) is an additional option; other events are treated symptomatically. Overall, evidence is limited, supporting the need for prospective studies and standardized management pathways.

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BACKGROUND: The differentiation of Horner syndrome from physiological anisocoria is important yet clinically challenging. We investigated the diagnostic accuracy of pupillometry to discriminate Horner syndrome from physiological anisocoria compared to pharmacological testing with the alpha-2-agonist apraclonidine, which is considered the current gold standard. METHODS: Forty-four adult patients, mostly referred to our neuro-ophthalmology service for evaluation of anisocoria, were included. Automated binocular pupillometry was performed under standardized light conditions before and >30 minutes after instillation of 1% apraclonidine eye drops. A positive apraclonidine test indicating unilateral Horner syndrome was defined as an increase of pupil size in the smaller pupil and decrease of size in the larger pupil. Receiver operator characteristic curves were calculated to find the best pupillometric parameter discriminating Horner syndrome from physiological anisocoria. RESULTS: We found that the parameters measuring the pupillary dilation lag using pupillometry could reliably discriminate Horner syndrome from physiological anisocoria compared to pharmacological testing. Calculating the change of anisocoria at 3-4 seconds after light-off relative to the anisocoria at the end of the light-on period (Δ3-4) may be most suitable to rule out Horner syndrome reaching a sensitivity of 95% and specificity of 68% using a cutoff of 0.35 mm. CONCLUSIONS: Our results indicate that pupillometry is a robust tool to measure the dilation lag in Horner syndrome and, therefore, to distinguish pathological from physiological anisocoria obviating pharmacological testing. The high sensitivity of the test will allow to identify the patients with Horner syndrome requiring further investigation.

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BACKGROUND: Pupillary function is frequently impaired in autonomic disorders, and biomarkers for early diagnosis and disease progression are urgently needed. Pupillometry allows for noninvasive ocular autonomic evaluation. This prospective study technically and clinically validates a handheld monocular pupillometer available for broad application as an autonomic screening tool in autonomic disorders. METHODS: A total of 40 controls and 100 patients with autonomic disorders underwent pupillometry using the PLR-4000(NeurOptics). Pupillary parasympathetic and sympathetic function were assessed by responses to a light stimulus and to 0.5% apraclonidine eye drops, respectively. Test-retest assessments and validations against a binocular device were performed. RESULTS: In healthy controls, the mean light reflex ratio was 42% ± 5.7% and the median response to apraclonidine was -5.0% (-8.8%-2.8%). Monocular and binocular pupillometers presented similar results. Test-retest experiments showed: median light response difference 3.0% (1.0%-4.8%), median % difference in response to apraclonidine 5.2% (2.2%-10.6%). In patients with neurodegenerative disorders (n = 24), autonomic neuropathies (n = 39), and autonomic ganglionopathies (n = 9), pupillary abnormalities were very prevalent (52%, 45%, and 100%, respectively). All patients with intermittent autonomic disorders had normal pupillomotor function. CONCLUSIONS: The presented device provides accurate, reproducible assessments of pupillary autonomic function in healthy controls and patients with autonomic disorders. With normative data provided, it is an easily accessible, well-tolerated tool to quantitatively assess pupillomotor innervation in a broad clinical setting. Further studies are warranted to explore its potential as a noninvasive biomarker, complementing standard autonomic function tests for early detection, monitoring disease progression, and evaluating treatment response in disorders with autonomic failure.

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Blepharoptosis as an Aesthetic Complication: Eyelid ptosis, or blepharoptosis, following esthetic treatment of the upper third with botulinum toxin Type A (BoNT-A) is a complication with a variable incidence depending on the injector's experience. Among unexperienced injectors, it ranges from 2.5% to 5.4% and approximately 0.51% to 1% in experienced injectors. Blepharoptosis is commonly defined as an eyelid located between 1.5 and 2 mm below the scleral-corneal limbus. It occurs because of the local spread of botulinum toxin, affecting the levator palpebrae superioris muscle, one of the principal muscles for elevating the superior eyelid. It typically becomes evident 3-14 days after BoNT-A application and resolves spontaneously after approximately 3 months, once the toxin's effect subsides. Even though it resolves with time, it can cause great distress for the patient and the physician. Treatment Modality: In turn, knowing the anatomy of the face in high detail will help the physician treat and prevent this complication, which can be avoided with correct training and application. Once it has happened, it is important to recognize the severity of the blepharoptosis (which is classified as mild, moderate, or severe), in order to decide whether to use oxymetazoline or apraclonidine eye drops, muscle exercises, vibrating devices, radiofrequency, and the latest option described with pretarsal BoNT-A application. Even though the treatment is challenging, and evidence is scarce, here we present a literature review and some clinical cases of successful treatment with pretarsal BoNT-A in iatrogenic blepharoptosis following esthetic treatment of the upper third. Objective: This review highlights the importance of facial anatomy knowledge to minimize potential complications associated with BoNT-A application. It also describes the clinical classification and management of iatrogenic blepharoptosis based on severity, with special emphasis on the pretarsal BoNT-A application technique. Methods of Literature Search: A literature search was conducted using electronic databases (PubMed, MEDLINE, Embase, and Google Scholar), focusing on upper third anatomy, prevention of iatrogenic blepharoptosis secondary to BoNT-A application, classification, and therapeutic options based on severity. Results: Iatrogenic eyelid ptosis after BoNT-A application results from the neurotoxin spreading to the levator palpebrae superioris muscle. Current therapeutic options include sympathomimetic eye drops, vibration therapy, facial exercises, radiofrequency, and pretarsal BoNT-A application. This review emphasizes anatomical knowledge, risk factors' identification, and anatomical landmarks to minimize complications. The pretarsal treatment technique for iatrogenic ptosis using BoNT-A is also detailed. Limitations: The limitations of this review consist of the number of patients, which is very limited; another limitation is that none of the patients had severe ptosis to prove the treatment. Conclusion: Blepharoptosis following esthetic BoNT-A treatment is a rare complication among trained injectors. Knowledge of therapeutic options, including pretarsal BoNT-A injection techniques, is crucial for managing this complication, which can have significant esthetic and functional impacts.

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Ozone has been used empirically and as an alternative medical modality for more than a century, and recent technological advancements have provided new insights into its therapeutic potential [1]. Ozone therapy, a noninvasive, low-cost treatment with a favorable side-effect profile, has been increasingly utilized in various dermatologic and esthetic indications [2]. The existing literature reports the use of oxygen–ozone mixtures in the management of localized adiposity, cellulite, wrinkles, skin laxity, acne, hyperpigmentation, striae, and telangiectasia [3]. Here, we present the clinical outcomes of intradermal ozone therapy in two patients who developed eyelid ptosis following botulinum toxin injection. For both cases, the ozone gas was generated using a medical-grade ozone generator (HAS Salutem, Cemil Has Medikal, Izmir, Turkey). The device possesses EC certification in accordance with the Medical Device Directive 93/42/EEC and is manufactured under EN ISO 13485:2016 quality management standards. This system allows for precise photometric measurement of ozone concentration to ensure dosage accuracy. The gas was collected in a siliconized syringe immediately prior to injection to ensure concentration stability, and a 30G needle was used for administration. A 36-year-old woman developed left upper eyelid ptosis approximately 1 week after receiving abobotulinum toxin. A nondermatology practitioner presumed an allergic reaction and initiated systemic corticosteroids; however, the patient showed no clinical improvement and presented to our clinic with persistent symptoms. Dermatologic examination revealed left upper eyelid drooping and mild asymmetry of the periorbital muscles (Figure 1a). As treatment, a total of 2.5 mL of ozone at a concentration of 3 gamma was administered intradermally and intramuscularly into the corrugator muscle (body and tail), the upper eyelid, and the periorbital region. Each site received approximately 0.1–0.2 mL, delivered in two sessions spaced 2 days apart. No additional therapy was provided. Five days later, a marked improvement in ptosis was observed (Figure 1b), and no adverse events occurred. A 48-year-old woman presented with left upper eyelid ptosis that developed on the second day following abobotulinum toxin injection. The patient reported taping her eyelid to manage daily activities. Dermatologic examination confirmed left upper eyelid ptosis (Figure 2a). As treatment, a total of 2.5 mL of ozone at a concentration of 3 gamma was administered intradermally and intramuscularly into the corrugator muscle (body and tail), the upper eyelid, and the periorbital region. Each site received approximately 0.1–0.2 mL, delivered in two sessions spaced 2 days apart. No additional treatment was given. By the 2nd day after treatment, a marked improvement in ptosis was observed (Figure 2b), and no adverse events were detected. Ptosis of the upper eyelid may occur after botulinum toxin injections to the glabellar region and its surroundings due to unintended diffusion of the toxin. The toxin can traverse the orbital septum and induce weakness in the levator palpebrae superioris muscle. Upper eyelid ptosis typically appears 7–10 days after injection and may persist for 2–4 weeks or longer. Therapeutic options include topical sympathomimetic agents such as 0.5% apraclonidine or phenylephrine ophthalmic solution, which stimulate Müller's muscle and elevate the eyelid. Muscle activation techniques including targeted exercises, mechanical stimulation, or electrical stimulation may also help shorten the duration of ptosis [4, 5]. Ozone gas (O3), a potent oxidizing agent, possesses anti-inflammatory, antioxidant, and tissue-reparative properties. The literature indicates that ozone is effective against bacteria, viruses, fungi, and protozoa; that short-term, low- to moderate-dose exposure stimulates endogenous antioxidant systems; and that such exposure does not induce tissue injury. Ozone can be administered intravenously, intramuscularly, subcutaneously, intradermally, or locally. When applied locally to the skin, it enhances circulation, improves impaired biological functions, and increases cytokines involved in tissue repair, such as IFN-β and TGF-β [6, 7]. Recent experimental work further supports these pleiotropic effects of ozone. In a stable ozonized glycerin hydrogel, Russo et al. reported not only broad antimicrobial and antibiofilm activity against multidrug-resistant Gram-positive, Gram-negative, and Candida isolates, but also a significant reduction in TNF-α production by LPS-stimulated human peripheral blood mononuclear cells and enhanced migratory/proliferative capacity of dermal fibroblasts and keratinocytes in scratch assays [8]. These findings are consistent with the anti-inflammatory and tissue-regenerative properties postulated to underlie the rapid clinical improvement observed in our patients and provide additional biological plausibility for the use of ozone formulations as adjunctive therapies in cutaneous complications. The rapid clinical improvement observed in our cases (2–5 days) contrasts with the typical natural history of botulinum toxin–induced ptosis, which generally persists for 2–4 weeks. While direct inactivation of the toxin is unlikely given the timing, the rapid response may be attributed to ozone's anti-inflammatory properties [9]. Localized edema and inflammation can exacerbate the mechanical weight on the eyelid, worsening ptosis. By downregulating pro-inflammatory cytokines (TNF-α, IL-12) and reducing local tissue edema, ozone therapy may alleviate this burden, allowing for faster functional recovery of the levator muscle even if the toxin's paralytic effect has not fully resolved. In our cases, intradermal and intramuscular ozone therapy administered to the corrugator muscle, upper eyelid, and periorbital region resulted in rapid and marked improvement in ptosis, without adverse effects. These outcomes suggest that ozone therapy may represent a promising adjunctive option in the management of botulinum toxin–related complications. Although direct evidence for ozone in the treatment of blepharoptosis is limited, indirect support exists in the literature. In a randomized, comparative study involving patients with piriformis syndrome, intramuscular ozone injection produced pain and disability improvements within 1–2 months comparable to lidocaine and more rapid than botulinum toxin; at 3–6 months, however, botulinum toxin was superior. These findings imply that ozone may accelerate short-term clinical improvement through its anti-inflammatory and analgesic effects. Nevertheless, as the study addressed a musculoskeletal condition rather than ptosis, the evidence remains indirect and primarily supports biological plausibility. Controlled studies specifically evaluating ozone for blepharoptosis are required to establish its efficacy [10]. Several limitations must be acknowledged. First, this report is limited to two cases without a control group. Given that botulinum toxin–induced ptosis is a self-limiting condition, spontaneous resolution cannot be definitively excluded, although the speed of recovery observed here is atypical for the natural course. Second, the assessment of ptosis was based on clinical examination and patient satisfaction rather than objective measurements such as Margin Reflex Distance 1 (MRD1). Finally, subjective factors such as compensatory frontalis muscle activation or changes in lighting in photographs could influence the perceived degree of improvement. In conclusion, intradermal and intramuscular ozone therapy represents a promising adjunctive approach in the management of botulinum toxin–induced ptosis. Our observations suggest it may accelerate recovery, possibly through anti-inflammatory mechanisms and reduction of local edema. However, these findings are preliminary and hypothesis-generating. Large-scale, controlled clinical trials with objective outcome measures are necessary to confirm efficacy, safety, and the optimal treatment protocol before it can be recommended as a standard therapy. Muhammed Burak Yücel: conceptualization, data acquisition, clinical management of cases, manuscript drafting, and critical revision. Çağlar Gençtürk: literature review, manuscript editing, clinical interpretation. Selda Yıldırım Gençtürk: supervision, clinical consultation, manuscript revision for important intellectual content. All authors approved the final version of the manuscript and agree to be accountable for all aspects of the work. The authors thank the patients for their cooperation and for providing written consent for the use of their clinical information and images in this publication. No other individuals or institutions contributed to the study. The authors have nothing to report. Both patients provided written informed consent for the off-label use of ozone therapy and for the publication of their clinical details and photographs. The procedures were conducted in accordance with the ethical principles outlined in the Declaration of Helsinki. The authors confirm that the ethical policies of the Journal of Cosmetic Dermatology have been adhered to. According to institutional guidelines, formal ethics committee approval is not required for case reports involving one or two patients, as long as no identifiable personal data beyond clinical images are used. This study complies with the Declaration of Helsinki principles. Written informed consent was obtained from both patients for the publication of their clinical details and accompanying images. The authors declare no conflicts of interest. Data sharing is not applicable, as this article reports individual clinical cases and no datasets were generated or analyzed.

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