Judickaitė, Austėja

Introduction Severe arterial hypertension (AH) in young adults is uncommon yet associated with progressive organ damage. Hypertensive retinopathy indicates systemic microvascular injury and may reveal previously undiagnosed hypertension.[1,2] This case highlights rapid organ damage in a young woman and emphasizes early diagnosis and blood pressure (BP) control. Case Presentation A 27-year-old woman reported episodic blurred vision in the right eye, with visual acuity remaining 1.0 in both eyes. The patient had a two-year history of migraine with visual impairment during severe headache episodes. Ophthalmologic examination revealed bilateral optic disc edema, arteriolar narrowing, venous stasis, macular hard exudates with a partial macular star in the left eye, and serous retinal detachments in both eyes. Optical coherence tomography showed bilateral subretinal fluid and retinal pigment epithelium detachment. Fluorescein angiography demonstrated diffuse vascular leakage and optic disc hyperfluorescence. In the hospital, incidentally measured arterial BP was markedly elevated, reaching 223/150 mmHg. The patient was diagnosed with acute kidney injury, indicated by elevated creatinine and pathological albuminuria. Renal ultrasonography revealed parenchymal thickening and an elevated resistive index. Twenty-four-hour BP monitoring showed uncontrolled BP. Treatment included four antihypertensive drugs and a loop diuretic. AH etiology is unclear. Secondary causes are under investigation, including endocrine, renal, neurologic, and cardiologic evaluation. Discussion This case demonstrates that uncontrolled secondary AH can lead to multi-organ damage in young patients.[1] Retinal vessels are highly sensitive to BP changes, resulting in grade IV hypertensive retinopathy according to the Keith–Wagener–Barker classification, characterized by optic disc edema.[2] Such fundoscopic findings reflect systemic microvascular injury and hypertension-induced organ damage, including acute renal impairment.[2,3] Severe fundoscopic changes may regress with effective BP control.[2] Conclusions Severe hypertension in young adults may remain clinically silent until advanced organ damage occurs, with hypertensive retinopathy as the first or only clinical sign. Therefore, hypertensive disorders should be suspected even in young patients.

Introduction Metallic corneal foreign bodies are common and may lead to serious complications, including corneal ulceration or, rarely, full-thickness perforation. [1] Spontaneous iris prolapse at the perforation site, though uncommon, is vision-threatening. [2] This case illustrates such progression and the value of timely diagnosis and conservative management. Case Presentation A 66-year-old man presented with a one-week history of progressive blurred vision in the right eye after rubbing it. On examination, visual acuity (VA) was 0.03 (0.1 corrected), intraocular pressure 8 mmHg. Ocular ultrasonography showed a superior choroidal detachment with vitreous opacities, while computed tomography was unremarkable. Slit-lamp exam revealed a paracentral corneal opacity with rust deposits from a prior metallic foreign body. Fluorescein pooling and a positive Seidel test indicated a small corneal perforation, with iris tamponade at the wound. The anterior chamber was shallow laterally, the pupil was irregular and drawn to 9 o’clock, but remained reactive. The fundus view was hazy due to vitreous opacities. A therapeutic contact lens was applied, and topical levofloxacin and cyclopentolate were started along with systemic antibiotics and antiinflammatory therapy. After 24 hours, VA improved to 0.1 (0.4 corrected), and ultrasonography showed a flat superior choroidal detachment. The anterior chamber reformed and he was discharged with VA 0.3 (0.7 pinhole), a clear cornea, and the perforation sealed by iris tamponade. The anterior chamber remained shallow but stable, and mild diffuse lens opacities persisted. Discussion Metallic corneal foreign bodies usually resolve after removal, but rare complications like fullthickness perforation can occur. [3] Spontaneous iris prolapse may act as a temporary autologous tamponade, as in our case, allowing conservative management with a therapeutic contact lens. Careful monitoring is essential to ensure healing and prevent secondary complications, such as infection or persistent leakage. [2] Conclusions This case shows that spontaneous iris prolapse does not always require surgical intervention. Conservative management with a healing lens can be effective, but vigilant follow-up is critical to preserve corneal integrity and visual function.

Background. Cardiac surgery with cardiopulmonary bypass (CPB) is associated with microcirculatory changes. Little is known about the effect of CPB on the structural and vascular parameters of the retina. We aimed to investigate changes in these parameters in patients after CPB surgery. Methods. In this prospective observational clinical trial, 44 patients who underwent elective CPB surgery were enrolled. All subjects underwent a complete ophthalmological examination, optical coherence tomography (OCT), and OCT angiography (OCTA) preoperatively and 1 week after surgery. Changes in macular retinal thickness (RT), ganglion cell complex (GCC), vascular density (VD) of the superficial (SCP) and deep (DCP) capillary plexuses, and peripapillary retinal nerve fiber layer (RNFL) were assessed in relation to CPB duration and aortic cross-clamp (ACC) time. Results. A statistically significant decrease in RT (p=0.008) and VD of the SCP (p=0.023) was observed in the central macula postoperatively. There was a statistically significant increase in peripapillary RNFL thickness in all quadrants and in macular GCC thickness in all regions except the superior region of the ganglion cell and inner plexiform layer (GCL+). A positive correlation was found between ACC time and RT, as well as the VD of SCP changes and the VD of DCP in the central macula. Conclusions. CPB surgery induces significant retinal changes, including reduced RT and VD of the SCP in the central macula, along with increased thickness of the peripapillary RNFL and most regions of the macular GCC. Since retinal alterations are associated with ACC time, it is crucial to minimize ACC time to reduce the risk of ophthalmological complications.

Background and Objectives: Despite the growing amount of new research, the pathophysiology of glaucoma remains unclear. The aim of this study was to determine the relationship between intracranial pressure (ICP), ocular blood flow and structural optic nerve parameters. Materials and Methods: A prospective clinical study was conducted involving 24 patients with open-angle glaucoma and 25 healthy controls. Routine clinical examination was performed. Swept-source optical coherence tomography (SS-OCT) and OCT angiography (OCTA) images were taken (DRI-OCT Triton, Topcon). The vessel density (VD) values of the ONH were calculated around the optic nerve head (ONH). An orbital Doppler device (Vittamed 205, Kaunas, Lithuania) was used for non-invasive ICP measurements. Color Doppler imaging (CDI) (Mindray M7, Shenzhen, China) was used for retrobulbar blood flow measurements in the ophthalmic artery (OA), central retinal artery (CRA) and short posterior ciliary arteries (SPCAs). Results: ICP was 8.35 ± 2.8 mmHg in the glaucoma group and 8.45 ± 3.19 mmHg in the control group (p = 0.907). In the glaucoma group, the VD of the superficial vascular plexus in the inferior-nasal (NI) sector of the ONH showed a correlation with ICP (r = 0.451, p = 0.05). In contrast, the control group exhibited weaker correlations. CRA peak systolic velocity (PSV) demonstrated significant moderate correlations with VD in multiple retinal layers, including the avascular retina layer in the temporal (T) sector (r = 0.637, p = 0.001). Conclusions: Lower ICP was significantly associated with the lower VD of the superficial plexus layer in the inferior-nasal sector in the glaucoma group, with the control group exhibiting weaker correlations in all sectors. Further longitudinal studies with larger sample sizes are needed to establish associations between intracranial pressure, ocular blood flow and ONH parameters.

Background and Objectives: Normal-tension glaucoma (NTG) is a subtype of primary open-angle glaucoma characterized by progressive optic nerve damage despite intraocular pressure (IOP) remaining within the normal range. The underlying pathophysiology of NTG remains incompletely understood, and its diagnosis is often delayed due to the lack of a definitive screening tool. This study aimed to evaluate differences in intracranial pressure pulse wave amplitude recorded from closed eyelids between NTG patients and control subjects using a novel non-invasive monitoring technology. Materials and Methods: A cross-sectional observational study was conducted, enrolling NTG patients and age-matched controls. Intracranial pressure pulse wave signals were recorded from closed eyelids using the ’Archimedes’ 02 device, which employs a highly sensitive digital pressure sensor and hydromechanical coupling for signal transmission. The amplitude of recorded intracranial pressure pulse waves was analyzed and compared between groups. Statistical analyses were performed using IBM SPSS Statistics 30.0, with significance set at p < 0.05. Results: A total of 140 participants were enrolled, including 68 NTG patients and 72 controls. After applying exclusion criteria, 63 NTG patients and 68 controls were included in the final analysis. The median intracranial pressure pulse wave amplitude was significantly higher in NTG patients (0.1326 a.u.) than in controls (0.0889 a.u.), with p = 0.01. Conclusions: These findings suggest that intracranial pressure pulse wave monitoring may serve as a potential biomarker for NTG. Further studies are needed to determine the diagnostic accuracy, sensitivity, and specificity of this technology for NTG detection.

Anizokorija yra būklė, kai vyzdžiai tampa skirtingo dydžio. Anizokorijos atsiradimą lemia disfunkcija tarp vyzdžio plečiamojo (lot. in. dilatator papillae) ir vyzdžio su-traukiamojo (lot. ni. sphincter papillae) raumenų veiklos. Raumenų disfunkcija gali atsirasti, kai patys raumenys ir juos inervuojantys nervai yra pažeisti. Galimos vyzdžių asimetrijos priežastys įvairios: nuo pacientui nepavojingos fiziologinės anizokorijos iki įvairių navikinių, infekcinių arba kraujagyslinių patologinių procesų, kuriuos reikia gydyti nedelsiant. Šeimos medicinos gydytojui svarbu pastebėti anizokoriją, išskirti galimas jos priežastis, kad būtų laiku diagnozuojamos gyvybei pavojingos būklės. Šiame straipsnyje apžvelgiamos dažniausios anizokorijos priežastys, jų diferencinė diagnostika bei tolesnio paciento tyrimo rekomendacijos.

Akantamebinis keratitas (AK) yra retas ir sunkus ragenos uždegimas, kurio atvejų skaičius pastaraisiais metais didėja, tolygiai daugėjant kontaktinius lęšius nešiojančių asmenų skaičiui. Sukėlėjai yra laisvai gamtoje gyvenantys pirmuonys akantamebos, aptinkamos ore, dirvožemyje, gėlo vandens šaltiniuose ir jūros vandenyje. Vystymosi metu amebos gali sudaryti cistas ir trofozoitus. Trofozoitai yra aplinkai neatspari, užkrečiama amebos forma. Esant nepalankioms aplinkos sąlygoms, pirmuonis sudaro cistas. Ankstyvuoju periodu liga dažnai klaidingai diagnozuojama ir gydoma kaip kitų sukėlėjų sukeltas keratitas. Diagnostika remiasi klinikiniu ištyrimu, laboratoriniais ir instrumentiniais metodais. Gydymo kursas dažnai būna ilgas ir sudėtingas dėl didelio akantamebų cistų atsparumo vaistams. Infekcija dažniausiai gydoma biguanidų ir aromatinių diamidinų vaistų deriniu. Vėlesnėse stadijose liga gali komplikuotis į visišką regėjimo praradimą ir ragenos transplantacijos būtinybę. Rizikos veiksnių vengimas ir ankstyvas ligos diagnozavimas yra veiksmingiausi kovos su akantamebiniu keratitu metodai.

Anizokorija, arba vyzdžių asimetrija, atspindi vyzdį sutraukiančio raumens (m. sphincter pupillae) arba vyzdį plečiančio raumens (m. dilatator pupillae) pažeidimus, šių raumenų inervacijos sutrikimus arba išorinių farmakologinių veiksnių sukeltas būkles. Viena iš anizokorijos priežasčių yra Adie toninis vyzdys. Adie vyzdys – retas neurologinis sutrikimas, pasireiškiantis nuolatine, dažniausiai vienos pusės, midriaze, vyzdys vangiai reaguoja arba nereaguoja į šviesą, nedaug susitraukia akomoduojant. Ši būklė dažniausiai yra idiopatinė, pasireiškianti 25-45 metų žmonėms, dažniau moterims. Ligai būdingas išsiplėtęs vyzdys, fotofobija. Adie toninio vyzdžio diagnozė nustatoma remiantis klinikiniais požymiais, papildomai gali būti atliekamas skiesto pilokarpino testas. Daugeliui pacientų, turinčių šią patologiją, gydymas nereikalingas. Šiame straipsnyje apžvelgiame Adie vyzdžio epidemiologiją, patogenezę, etiologiją, kliniką, diagnostikos ir gydymo galimybes, sąsajas su COVID-19 bei kitas anizokorijos priežastis.

Introduction: Adie’s pupil is a rare neurological disorder, which is caused by lesions in ciliary ganglion or postganglionic short ciliary nerves, followed by aberrant regeneration. This process causes unilateral or bilateral mydriasis, unresponsiveness to bright or dim light, slow constriction on accommodation. Most cases are idiopathic, affecting 25-45-year-old adults, more frequently women. Case report: 33-year-old female was admitted to the emergency department complaining of a dilated pupil of the right eye. The patient noted that the day before her colleagues noticed that her right pupil was wider than the left pupil. There were no other vision-related symptoms. The patient has been having headaches for a couple of years, which started after pregnancy, sometimes with hyperhidrosis. On ophthalmologic examination, the pupil of the right eye was 2-3 mm wider than the pupil of the left eye with a poor reaction to light. Ductions were full, palpebral fissures were symmetric. There was no nystagmus. The anterior segments were normal. Visual acuity was normal (20/20). Intraocular pressures were 17,3 mmHg OU. Fundoscopy showed normal optic discs. Cerebral and orbital computed tomography (CT) had shown no significant acute changes so the patient was redirected to an outpatient clinic for further ophthalmic examination. Based on the pictures of the patient anisocoria was first noticed a couple months ago. Optical coherence tomography showed no loss of the nerve fiber layer. Orbital ultrasonography of the right eye showed a 2 mm optic nerve drusen. Pharmacological testing with dilute pilocarpine 0.1 % resulted in constriction of the right pupil but there was no change in the left pupil, Adie’s pupil diagnosis was confirmed. Further examination for other causes of Adie’s syndrome included blood tests (CRP, ESR, ANA, ANCA for autoimmune cause), consultation with a neurologist, and examination of cervical blood vessels. Magnetic resonance imaging (MRI) of the brain showed no pathological changes. Conclusions: Adie’s pupil is a relatively rare disorder, diagnosed by clinical manifestations. A positive diluted pilocarpine test (0.06/ 0.1 /0.2 %) may be useful to demonstrate the cholinergic denervation supersensitivity in the tonic pupil. However, the condition frequently remains undiagnosed. CT or MRI tomography may help to rule out other conditions that can cause anisocoria.