Differential Diagnoses Symptoms and Other Useful Lists and Tables Signs Case Presentations for Ophthalmologists
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Medical Diary Official Publication for the Federation of Medical Societies of Hong Kong
VOL.12 NO.9 SEPTEMBER 2007 ॷġ෫ġᚂġଉ THE HONG KONG MEDICAL DIARY OFFICIAL PUBLICATION FOR THE FEDERATION OF MEDICAL SOCIETIES OF HONG KONG www.fmshk.org Editorial Editorial Dr. Timothy YY Lai Medical Bulletin Management of Tearing in Adults Dr. Alan CK Ng Dr. Dylan DN Chan Ocular Allergy in Children Dr. Koon-man Lam Neuro-ophthalmology for General Practitioners: A Revision Dr.CarmenKMChan Normal Tension Glaucoma - a Sick Eye in a Sick Body Dr. Dexter YL Leung Retinal Complications of High Myopia Dr. Timothy YY Lai Amblyopia: An overview Dr. Wilson WK Yip Prof. Dorothy SP Fan Surgical Correction for Near Sightedness Dr. Arthur CK Cheng Traditional Chinese Medicine and Ophthalmology Dr. Jane CC Yeung Special Feature Rosiglitazone and Risk of Myocardial Infarction: Clear Danger or Dr. Norman Chan Media Hype? Clinical Quiz Clinical Quiz Dr. Helen KS Tung Society News Medical Diary of September Calendar of Events ISSN 1812 - 1691 ᚂᖒԙষΙড়ᒑȅᩧҕஶቆᜰЖ VOL.12 NO.9 SEPTEMBER 2007 Contents The Federation of Medical Societies of Hong Kong 4/F Duke of Windsor Social Service Building, Contents 15 Hennessy Road, Wanchai, Hong Kong Tel: 2527 8898 Fax: 2865 0345 Editorial President Dr. FONG To-sang, Dawson 方道生醫生 1st Vice- President Editorial 2 Dr. CHAN Chi-kuen 陳志權醫生 2nd Vice- President Dr. Timothy YY Lai Dr. LO Sze-ching, Susanna 盧時楨醫生 Hon. Secretary Dr. LO See-kit, Raymond 勞思傑醫生 Medical Bulletin Deputy Hon. Secretary Dr. CHAN Sai-kwing 陳世炯醫生 Management of Tearing in Adults 4 Hon. Treasurer Mr. LAM Lop-chi, Nelson 林立志先生 Dr.AlanCKNg Deputy Hon. Treasurer Dr. Dylan DN Chan Mr. -
Un-Explained Visual Loss Following Silicone Oil Removal
Roca et al. Int J Retin Vitr (2017) 3:26 DOI 10.1186/s40942-017-0079-6 International Journal of Retina and Vitreous ORIGINAL ARTICLE Open Access Un‑explained visual loss following silicone oil removal: results of the Pan American Collaborative Retina Study (PACORES) Group Jose A. Roca1, Lihteh Wu2* , Maria Berrocal3, Francisco Rodriguez4, Arturo Alezzandrini5, Gustavo Alvira6, Raul Velez‑Montoya7, Hugo Quiroz‑Mercado7, J. Fernando Arevalo8, Martín Serrano9, Luiz H. Lima10, Marta Figueroa11, Michel Farah10 and Giovanna Chico1 Abstract Purpose: To report the incidence and clinical features of patients that experienced un-explained visual loss following silicone oil (SO) removal. Methods: Multicenter retrospective study of patients that underwent SO removal during 2000–2012. Visual loss of 2 lines was considered signifcant. ≥ Results: A total of 324 eyes of 324 patients underwent SO removal during the study period. Forty two (13%) eyes sufered a signifcant visual loss following SO removal. Twenty three (7.1%) of these eyes lost vision secondary to known causes. In the remaining 19 (5.9%) eyes, the loss of vision was not explained by any other pathology. Eleven of these 19 patients (57.9%) were male. The mean age of this group was 49.2 16.4 years. Eyes that had an un-explained visual loss had a mean IOP while the eye was flled with SO of 19.6 6.9 mm± Hg. The length of time that the eye was flled with SO was 14.8 4.4 months. In comparison, eyes that± did not experience visual loss had a mean IOP of 14 7.3 mm Hg (p < 0.0002)± and a mean tamponade duration of 9.3 10.9 months (p < 0.0001). -
Aafp Fmx 2020
10/7/2020 Common Acute Eye Presentations Dr. Ahmed Mian HonBSc, BEd, MD CCFP (EM) Staff ER Consultant Department of Emergency Medicine, Humber River Hospital and University Health Network Medical Director and Chair, Medical Education HRH ED Investigative Coroner, Province of Ontario Faculty DFCM/EM University of Toronto and DFM Queens' University 1 ACTIVITY DISCLAIMER The material presented here is being made available by the American Academy of Family Physicians for educational purposes only. Please note that medical information is constantly changing; the information contained in this activity was accurate at the time of publication. This material is not intended to represent the only, nor necessarily best, methods or procedures appropriate for the medical situations discussed. Rather, it is intended to present an approach, view, statement, or opinion of the faculty, which may be helpful to others who face similar situations. The AAFP disclaims any and all liability for injury or other damages resulting to any individual using this material and for all claims that might arise out of the use of the techniques demonstrated therein by such individuals, whether these claims shall be asserted by a physician or any other person. Physicians may care to check specific details such as drug doses and contraindications, etc., in standard sources prior to clinical application. This material might contain recommendations/guidelines developed by other organizations. Please note that although these guidelines might be included, this does not necessarily imply the endorsement by the AAFP. 2 2 1 10/7/2020 Disclosure It is the policy of the AAFP that all individuals in a position to control content disclose any relationships with commercial interests upon nomination/invitation of participation. -
Pediatric Anisometropia: Case Series and Review
Pediatric Anisometropia: tacles, vision therapy, and occlusion. Case two Case Series and Review is anisometropia caused by organic vision loss from optic neuritis early in life. Case three is John D. Tassinari OD, FAAO, FCOVD an infant with hyperopic anisometropia and Diplomate Binocular Vision esotropia. The esotropia did not respond to Perception and Pediatric Optometry, spectacles and home based vision therapy. American Academy of Optometry Neonatal high bilateral hyperopia that Associate Professor Western converted to anisometropia because of early University of Health Sciences onset cosmetically invisible unilateral esotropia College of Optometry is speculated. Case four describes a boy Pomona, California diagnosed with hyperopic anisometropia at age 11 months coincident with a diagnosis of pseudoesotropia. His compliance with ARTICLE prescribed spectacles was spotty until age three years. An outstanding visual outcome ABSTRACT was achieved by age five years with spectacles Background only (no occlusion therapy). Case five concerns The etiology and natural course and history a boy who acquired hyperopic anisometropia of pediatric anisometropia are incompletely because one eye experienced increasing understood. This article reviews the literature hyperopia during his toddler years. His regarding pediatric anisometropia with much response to treatment, spectacles and part of the review integrated into a case series. time occlusion with home vision therapy, was The review and case reports are intended to outstanding. Case six is an infant diagnosed elevate clinical understanding of pediatric with 2.50 diopters of hyperopic anisometropia anisometropia including and especially at age six months. Monocular home based treatment outcomes. vison developmental activities, not glasses, were prescribed. Her anisometropia vanished Case Reports three months later. -
Pupillary Disorders LAURA J
13 Pupillary Disorders LAURA J. BALCER Pupillary disorders usually fall into one of three major cat- cortex generally do not affect pupillary size or reactivity. egories: (1) abnormally shaped pupils, (2) abnormal pupillary Efferent parasympathetic fibers, arising from the Edinger– reaction to light, or (3) unequally sized pupils (anisocoria). Westphal nucleus, exit the midbrain within the third nerve Occasionally pupillary abnormalities are isolated findings, (efferent arc). Within the subarachnoid portion of the third but in many cases they are manifestations of more serious nerve, pupillary fibers tend to run on the external surface, intracranial pathology. making them more vulnerable to compression or infiltration The pupillary examination is discussed in detail in and less susceptible to vascular insult. Within the anterior Chapter 2. Pupillary neuroanatomy and physiology are cavernous sinus, the third nerve divides into two portions. reviewed here, and then the various pupillary disorders, The pupillary fibers follow the inferior division into the orbit, grouped roughly into one of the three listed categories, are where they then synapse at the ciliary ganglion, which lies discussed. in the posterior part of the orbit between the optic nerve and lateral rectus muscle (Fig. 13.3). The ciliary ganglion issues postganglionic cholinergic short ciliary nerves, which Neuroanatomy and Physiology initially travel to the globe with the nerve to the inferior oblique muscle, then between the sclera and choroid, to The major functions of the pupil are to vary the quantity of innervate the ciliary body and iris sphincter muscle. Fibers light reaching the retina, to minimize the spherical aberra- to the ciliary body outnumber those to the iris sphincter tions of the peripheral cornea and lens, and to increase the muscle by 30 : 1. -
URGENT/EMERGENT When to Refer Financial Disclosure
URGENT/EMERGENT When to Refer Financial Disclosure Speaker, Amy Eston, M.D. has a financial interest/agreement or affiliation with Lansing Ophthalmology, where she is employed as a ophthalmologist. 58 yr old WF with 6 month history of decreased vision left eye. Ache behind the left eye for 2-3 months. Using husband’s contact lens solution made it feel better. Seen by two eye care professionals. Given glasses & told eye exam was normal. No past ocular history Medical history of depression Takes only aspirin and vitamins 20/20 OD 20/30 OS Eye Pressure 15 OD 16 OS – normal Dilated fundus exam & slit lamp were normal Pupillary exam was normal Extraocular movements were full Confrontation visual fields were full No red desaturation Color vision was slightly decreased but the same in both eyes Amsler grid testing was normal OCT disc – OD normal OS slight decreased RNFL OCT of the macula was normal Most common diagnoses: Dry Eye Optic Neuritis Treatment - copious amount of artificial tears. Return to recheck refraction Visual field testing Visual Field testing - Small defect in the right eye Large nasal defect in the left eye Visual Field - Right Hemianopsia. MRI which showed a subacute parietal and occipital lobe infarct. ANISOCORIA Size of the Pupil Constrictor muscles innervated by the Parasympathetic system & Dilating muscles innervated by the Sympathetic system The Sympathetic System Begins in the hypothalamus, travels through the brainstem. Then through the upper chest, up through the neck and to the eye. The Sympathetic System innervates Mueller’s muscle which helps to elevate the upper eyelid. -
Differentiate Red Eye Disorders
Introduction DIFFERENTIATE RED EYE DISORDERS • Needs immediate treatment • Needs treatment within a few days • Does not require treatment Introduction SUBJECTIVE EYE COMPLAINTS • Decreased vision • Pain • Redness Characterize the complaint through history and exam. Introduction TYPES OF RED EYE DISORDERS • Mechanical trauma • Chemical trauma • Inflammation/infection Introduction ETIOLOGIES OF RED EYE 1. Chemical injury 2. Angle-closure glaucoma 3. Ocular foreign body 4. Corneal abrasion 5. Uveitis 6. Conjunctivitis 7. Ocular surface disease 8. Subconjunctival hemorrhage Evaluation RED EYE: POSSIBLE CAUSES • Trauma • Chemicals • Infection • Allergy • Systemic conditions Evaluation RED EYE: CAUSE AND EFFECT Symptom Cause Itching Allergy Burning Lid disorders, dry eye Foreign body sensation Foreign body, corneal abrasion Localized lid tenderness Hordeolum, chalazion Evaluation RED EYE: CAUSE AND EFFECT (Continued) Symptom Cause Deep, intense pain Corneal abrasions, scleritis, iritis, acute glaucoma, sinusitis, etc. Photophobia Corneal abrasions, iritis, acute glaucoma Halo vision Corneal edema (acute glaucoma, uveitis) Evaluation Equipment needed to evaluate red eye Evaluation Refer red eye with vision loss to ophthalmologist for evaluation Evaluation RED EYE DISORDERS: AN ANATOMIC APPROACH • Face • Adnexa – Orbital area – Lids – Ocular movements • Globe – Conjunctiva, sclera – Anterior chamber (using slit lamp if possible) – Intraocular pressure Disorders of the Ocular Adnexa Disorders of the Ocular Adnexa Hordeolum Disorders of the Ocular -
Neuroanatomy Crash Course
Neuroanatomy Crash Course Jens Vikse ∙ Bendik Myhre ∙ Danielle Mellis Nilsson ∙ Karoline Hanevik Illustrated by: Peder Olai Skjeflo Holman Second edition October 2015 The autonomic nervous system ● Division of the autonomic nervous system …………....……………………………..………….…………... 2 ● Effects of parasympathetic and sympathetic stimulation…………………………...……...……………….. 2 ● Parasympathetic ganglia ……………………………………………………………...…………....………….. 4 Cranial nerves ● Cranial nerve reflexes ………………………………………………………………….…………..…………... 7 ● Olfactory nerve (CN I) ………………………………………………………………….…………..…………... 7 ● Optic nerve (CN II) ……………………………………………………………………..…………...………….. 7 ● Pupillary light reflex …………………………………………………………………….…………...………….. 7 ● Visual field defects ……………………………………………...................................…………..………….. 8 ● Eye dynamics …………………………………………………………………………...…………...………….. 8 ● Oculomotor nerve (CN III) ……………………………………………………………...…………..………….. 9 ● Trochlear nerve (CN IV) ………………………………………………………………..…………..………….. 9 ● Trigeminal nerve (CN V) ……………………………………………………................…………..………….. 9 ● Abducens nerve (CN VI) ………………………………………………………………..…………..………….. 9 ● Facial nerve (CN VII) …………………………………………………………………...…………..………….. 10 ● Vestibulocochlear nerve (CN VIII) …………………………………………………….…………...…………. 10 ● Glossopharyngeal nerve (CN IX) …………………………………………….……….…………...………….. 10 ● Vagus nerve (CN X) …………………………………………………………..………..…………...………….. 10 ● Accessory nerve (CN XI) ……………………………………………………...………..…………..………….. 11 ● Hypoglossal nerve (CN XII) …………………………………………………..………..…………...…………. -
Dermatology DDX Deck, 2Nd Edition 65
63. Herpes simplex (cold sores, fever blisters) PREMALIGNANT AND MALIGNANT NON- 64. Varicella (chicken pox) MELANOMA SKIN TUMORS Dermatology DDX Deck, 2nd Edition 65. Herpes zoster (shingles) 126. Basal cell carcinoma 66. Hand, foot, and mouth disease 127. Actinic keratosis TOPICAL THERAPY 128. Squamous cell carcinoma 1. Basic principles of treatment FUNGAL INFECTIONS 129. Bowen disease 2. Topical corticosteroids 67. Candidiasis (moniliasis) 130. Leukoplakia 68. Candidal balanitis 131. Cutaneous T-cell lymphoma ECZEMA 69. Candidiasis (diaper dermatitis) 132. Paget disease of the breast 3. Acute eczematous inflammation 70. Candidiasis of large skin folds (candidal 133. Extramammary Paget disease 4. Rhus dermatitis (poison ivy, poison oak, intertrigo) 134. Cutaneous metastasis poison sumac) 71. Tinea versicolor 5. Subacute eczematous inflammation 72. Tinea of the nails NEVI AND MALIGNANT MELANOMA 6. Chronic eczematous inflammation 73. Angular cheilitis 135. Nevi, melanocytic nevi, moles 7. Lichen simplex chronicus 74. Cutaneous fungal infections (tinea) 136. Atypical mole syndrome (dysplastic nevus 8. Hand eczema 75. Tinea of the foot syndrome) 9. Asteatotic eczema 76. Tinea of the groin 137. Malignant melanoma, lentigo maligna 10. Chapped, fissured feet 77. Tinea of the body 138. Melanoma mimics 11. Allergic contact dermatitis 78. Tinea of the hand 139. Congenital melanocytic nevi 12. Irritant contact dermatitis 79. Tinea incognito 13. Fingertip eczema 80. Tinea of the scalp VASCULAR TUMORS AND MALFORMATIONS 14. Keratolysis exfoliativa 81. Tinea of the beard 140. Hemangiomas of infancy 15. Nummular eczema 141. Vascular malformations 16. Pompholyx EXANTHEMS AND DRUG REACTIONS 142. Cherry angioma 17. Prurigo nodularis 82. Non-specific viral rash 143. Angiokeratoma 18. Stasis dermatitis 83. -
Treatment of Congenital Ptosis
13 Review Article Page 1 of 13 Treatment of congenital ptosis Vladimir Kratky1,2^ 1Department of Ophthalmology, Queen’s University, Kingston, Canada; 21st Medical Faculty, Charles University, Prague, Czech Republic Correspondence to: Vladimir Kratky, BSc, MD, FRCSC, DABO. Associate Professor of Ophthalmology, Director of Ophthalmic Plastic and Orbital Surgery, Oculoplastics Fellowship Director, Queen’s University, Kingston, Canada; 1st Medical Faculty, Charles University, Prague, Czech Republic. Email: [email protected]. Abstract: Congenital ptosis is an abnormally low position of the upper eyelid, with respect to the visual axis in the primary gaze. It can be present at birth or manifest itself during the first year of life and can be bilateral or unilateral. Additionally, it may be an isolated finding or part of a constellation of signs of a specific syndrome or systemic associations. Depending on how much it interferes with the visual axis, it may be considered as a functional or a cosmetic condition. In childhood, functional ptosis can lead to deprivation amblyopia and astigmatism and needs to be treated. However, even mild ptosis with normal vision can lead to psychosocial problems and correction is also advised, albeit on a less urgent basis. Although, patching and glasses can be prescribed to treat the amblyopia, the mainstay of management is surgical. There are several types of surgical procedure available depending on the severity and etiology of the droopy eyelid. The first part of this paper will review the different categories of congenital ptosis, including more common associated syndromes. The latter part will briefly cover the different surgical approaches, with emphasis on how to choose the correct condition. -
Novel Anterior Segment Phenotypes Resulting from Forkhead Gene Alterations: Evidence for Cross-Species Conservation of Function
Novel Anterior Segment Phenotypes Resulting from Forkhead Gene Alterations: Evidence for Cross-Species Conservation of Function Ordan J. Lehmann,1 Stephen Tuft,2 Glen Brice,3 Richard Smith,4 Åsa Blixt,5 Rachel Bell,3 Bengt Johansson,6 Tim Jordan,1 Roger A. Hitchings,2 Peng T. Khaw,2 Simon W. M. John,4 Peter Carlsson,5 and Shomi S. Bhattacharya1 PURPOSE. Mutations in murine and human versions of an ances- cause it may affect the clinical management of certain trally related gene usually result in similar phenotypes. How- glaucoma subtypes and lead to excessive treatment. The ever, interspecies differences exist, and in the case of two FOXC1 and Foxe3 data, taken together with the novel ocular forkhead transcription factor genes (FOXC1 and FOXC2), phenotypes of FOXC2 mutations, highlight the remarkable these differences include corneal or anterior segment pheno- cross-species conservation of function among forkhead genes. types, respectively. This study was undertaken to determine (Invest Ophthalmol Vis Sci. 2003;44:2627–2633) DOI:10.1167/ whether such discrepancies provide an opportunity for iden- iovs.02-0609 tifying novel human–murine ocular phenotypes. METHODS. Four pedigrees with early-onset glaucoma pheno- types secondary to segmental chromosomal duplications or ecognition that mutations in orthologous genes frequently deletions encompassing FOXC1 and 18 individuals from 9 Rcause similar phenotypes has allowed the field of compar- FOXC2 mutation pedigrees underwent detailed ocular pheno- ative genetics to contribute to the understanding of human typing. Subsequently, mice with mutations in Foxc1 or a re- disease. As the human, murine, and Drosophila PAX6 mutants lated forkhead gene, Foxe3, were assessed for features of the (aniridia, Small eye, and eyeless) demonstrate, genotypic con- human phenotypes. -
ANTERIOR CORNEAL MOSAIC*T by A
Br J Ophthalmol: first published as 10.1136/bjo.52.9.659 on 1 September 1968. Downloaded from Brit. J. Ophthal. (1968) 52, 659 ANTERIOR CORNEAL MOSAIC*t BY A. J. BRON Moorfields Eye Hospital, City Road Branch, London THE corneal anatomy has received intensive study in recent years, but an aspect of its structure which is readily observed clinically has received little attention in the literature. In all normal corneae, after the instillation of fluorescein into the conjunctival sac, a striking mosaic pattern may be observed on the surface of the corneal epithelium after massage of the cornea through the lids. This pattern will be referred to as the anterior corneal mosaic. It was first observed by the author in patients whose eyes had been padded for corneal disease. It was noted in some that a mosaic pattern appeared after the instilla- tion of fluorescein. This pattern disappeared in a short period of time, but could readily be re-induced by pressure on the cornea through the lids. It is the purpose of this paper to describe the characteristics of the anterior corneal mosaic and to discuss its significance. This pattern was studied by Fischer (1928), and has since been re-studied by Schweitzer (1967). Methods Induction of the Mosaic A drop of 2 per cent. fluorescein is instilled into the conjunctival sac and the cornea is viewed with the cobalt beam of the slit lamp. If necessary the fluorescein is diluted to produce a bright fluorescence. A thumb is placed on the upper lid of the eye under examination and with the eye in the straight-ahead position, the lid is moved up and down over the cornea with light or moderate pressure applied to the globe.