Dr. Pugazhendhi is currently working as a Postdoctoral Medical Fellow at the Department of Ophthalmology, Stanford University School of Medicine. She received her Doctor of Medicine at PSG Institute of Medical Sciences & Research, India. Her primary research interest is on studying optic disc drusen, optic neuropathies and related neuro-ophthalmic diseases. Current research areas include: 1) Analyzing Optical Coherence Tomography (OCT) and Optical Coherence Tomography Angiography (OCTA) imaging in the understanding and management of optic disc drusen and optic neuropathies, in order to identify biomarkers that can help in prediction and treatment of disease; 2) 3D visualization and OCT reconstruction of the optic nerve head to understand the structure-function relationship of the optic nerve head disorders; 3) Whole Exome Sequencing in Autosomal Dominant Hereditary Optic Disc Drusen patients to identify predictors of disease inheritance; 4) Investigating cellular function analysis of optic disc drusen and optic neuropathy patients using human skin fibroblasts. Her future goal is to be a physician-scientist and to deliver evidence-based medicine through interdisciplinary research and clinical expertise to address the needs of patients.
Postdoctoral Research Fellow, Byers Eye Institute, Stanford University School of Medicine
Research Fellowship (Cornea), Pacific ClearVision Institute, Eugene, Oregon
MD, PSG Institute of Medical Sciences & Research, India (2019)
Yaping Liao, Postdoctoral Faculty Sponsor
Current Research and Scholarly Interests
-Optical Coherence Tomography (OCT) and Optical Coherence Tomography Angiography (OCTA) imaging and image analysis of neuro-ophthalmic diseases.
-3D visualization and OCT reconstruction of the optic nerve head disorders
-Whole Exome Sequencing in Autosomal Dominant Optic Disc Drusen patients
-Human skin fibroblasts study to investigate cellular function in neuro-ophthalmic diseases
- Multimodal Ophthalmic Imaging of Nonarteritic Anterior Ischemic Optic Neuropathy With and Without Optic Disc Drusen. Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society 2021
Comparison of outcomes of 25-gauge vs 27-gauge micro-incision vitrectomy surgery for visually significant macular membranes and full-thickness macular holes
ASSOC RESEARCH VISION OPHTHALMOLOGY INC. 2020
View details for Web of Science ID 000554528303166
- Sixth Nerve Palsy due to Metastasis of Thyroid Carcinoma in a patient on Alternative Medicine Acta Scientific Clinical Case Reports 2020; 1 (6): 08-10
25 vs. 27-gauge micro-incision vitrectomy surgery for visually significant macular membranes and full-thickness macular holes: a retrospective study.
International journal of retina and vitreous
2020; 6 (1): 56
To evaluate visual and safety outcomes for 25-gauge (25G) and 27-gauge (27G) micro-incision vitrectomy platforms (MIVS) for the treatment of epiretinal membrane and full-thickness macular holes.Retrospective analysis of all patients who underwent internal limiting membrane (ILM) peel surgery from January 2017 through December 2018. 207 cases met the eligibility criteria for inclusion. Primary endpoint was post-operative Best-Corrected Distance Visual Acuity (BCVA) at 6 months.For all patients combined, mean logMAR BCVA improved from 0.57 (± 0.40) to 0.37 (± 0.36) post-operatively (p < 0.001). For 25G ERMs, logMAR BCVA improved from 0.51 (± 0.28) to 0.30 (± 0.25) post-operatively (p < 0.001). For 27G ERMs, logMAR BCVA improved from 0.33 (± 0.28) to 0.28 (± 0.27) post- operatively (p = 0.15). For 25G FTMHs, logMAR BCVA improved from 0.87 (± 0.48) to 0.51 (± 0.44) post-operatively (p < 0.001). For 27G FTMHs, logMAR BCVA changed from 0.89 (± 0.47) to 0.96 (± 0.60).Final visual outcomes improved for both 25G and 27G ERM groups and the 25G FTMH group. Both 25G and 27G were safe and well tolerated MIVS platforms for the treatment of ERM and FTMH.
View details for DOI 10.1186/s40942-020-00259-4
View details for PubMedID 33292716
View details for PubMedCentralID PMC7670804
Pathogenesis and Prevention of Worsening Axial Elongation in Pathological Myopia
2020; 14: 853-873
This review discusses the etiology and pathogenesis of myopia, prevention of disease progression and worsening axial elongation, and emerging myopia treatment modalities.Pediatric myopia is a public health concern that impacts young children worldwide and is associated with numerous future ocular diseases such as cataract, glaucoma, retinal detachment and other chorioretinal abnormalities. While the exact mechanism of myopia of the human eye remains obscure, several studies have reported on the role of environmental and genetic factors in the disease development.A review of literature was conducted. PubMed and Medline were searched for combinations and derivatives of the keywords including, but not limited to, "pediatric myopia", "axial elongation", "scleral remodeling" or "atropine." The PubMed and Medline database search were performed for randomized control trials, systematic reviews and meta-analyses using the same keyword combinations.Studies have reported that detection of genetic correlations and modification of environmental influences may have a significant impact in myopia progression, axial elongation and future myopic ocular complications. The conventional pharmacotherapy of pediatric myopia addresses the improvement in visual acuity and prevention of amblyopia but does not affect axial elongation or myopia progression. Several studies have published varying treatments, including optical, pharmacological and surgical management, which show great promise for a more precise control of myopia and preservation of ocular health.Understanding the role of factors influencing the onset and progression of pediatric myopia will facilitate the development of successful treatments, reduction of disease burden, arrest of progression and improvement in future of the management of myopia.
View details for DOI 10.2147/OPTH.S241435
View details for Web of Science ID 000520510500001
View details for PubMedID 32256044
View details for PubMedCentralID PMC7092688
Double-Needle Yamane Repositioning of a Previous Yamane Fixation
CASE REPORTS IN OPHTHALMOLOGY
2019; 10 (3): 431-437
We describe a case of anteriorly dislocated, Yamane-fixated secondary intraocular lens (IOLs) with pigmentary dispersion syndrome. The patient presented with significant visual impairment and elevated intraocular pressure despite being maximally treated with all topical antihypertensive medications. The iris-IOL touch was confirmed by ultrasound biomicroscopy, and fundus examination revealed evidence of pigment granules on the optic disc. The previous Yamane-fixated secondary IOL was repositioned using a double-needle adaptation of Yamane technique and Kim's modification of scleral-fixated IOLs. To our knowledge, this is the first ever documented case of double-needle Yamane technique of a previous Yamane-fixated eye. In cases of inadequate capsular support, the development of new surgical techniques for the fixation of IOL continues to improve the safety and efficacy of these complicated surgeries.
View details for DOI 10.1159/000504563
View details for Web of Science ID 000507329000021
View details for PubMedID 31966035
View details for PubMedCentralID PMC6959107
Maxillary Zoster and Neurotrophic Keratitis following Trigeminal Block
CASE REPORTS IN OPHTHALMOLOGY
2019; 10 (1): 61-66
Herpes zoster ophthalmicus is commonly used to describe viral reactivation from the trigeminal ganglia with ocular involvement. The ophthalmic branch is the most commonly involved, whereas the maxillary and mandibular dermatomes are less commonly affected. Neurotrophic ulcer may occur secondary to intentional or inadvertent damage to the trigeminal nucleus, root, ganglion, or any segment of the ophthalmic branch of this cranial nerve. We report a case of reactivated maxillary herpes zoster combined with neurotrophic keratitis due to percutaneous 2nd and 3rd branch of trigeminal nerve block with alcohol to treat trigeminal neuralgia. A 57-year-old female came to the ophthalmology department complaining of decreased visual acuity and skin vesicle over the right lower lid and cheek. She had undergone right trigeminal nerve block for treatment of trigeminal neuralgia. Clinical examination revealed neurotrophic keratitis and maxillary herpes zoster. She was treated with oral and topical antivirals and vigorous lubrication with eye drops. Her neurotrophic keratitis showed a slow recovery. Although a few cases of herpes zoster following nerve block have been described, it would appear that a case of simultaneous maxillary herpes zoster and neurotrophic keratitis following trigeminal block has not yet been documented. It is possible that trigeminal nerve block may cause reactivation of latent virus and refractory neurotrophic keratitis.
View details for DOI 10.1159/000496683
View details for Web of Science ID 000467640500010
View details for PubMedID 31097946
View details for PubMedCentralID PMC6489053
Is the main lacrimal gland indispensable? Contributions of the corneal and conjunctival epithelia
SURVEY OF OPHTHALMOLOGY
2016; 61 (5): 616-627
The ocular surface system is responsible for ensuring that the precorneal tear film is sufficient in both quality and quantity to preserve optimal vision. Tear secretion is a complex, multifactorial process, and dysfunction of any component of the ocular surface system can result in tear film instability and hyperosmolarity with resultant dry eye disease. The tear film is primarily composed of lipids, aqueous, and mucins, with aqueous accounting for most of its thickness. The aqueous is produced by the main lacrimal gland, accessory lacrimal glands, and corneal and conjunctival epithelia. Although the main lacrimal gland has long been considered an indispensable source of the aqueous component of tears, there is evidence that adequate tear secretion can exist in the absence of the main lacrimal gland. We review and discuss the basics of tear secretion, the tear secretory capacity of the ocular surface, and emerging treatments for dry eye disease.
View details for DOI 10.1016/j.survophthal.2016.02.006
View details for Web of Science ID 000383217000006
View details for PubMedID 26968256