Ophtha Guideline PDF - Basic Ophthalmology Training

BASIC OPHTHALMOLOGY TRAINING PARTICIPANT MANUAL JULY, 2020 APPROVAL STATEMENT I FOREWORD II ACKNOWLEDGEMENT The Ministry of Health-Ethipoia would like to gratefully acknowledge the group of experts and organizations, mentioned below, who have invested much of their time and energy in the content development, contribution to the review, refinement and finalization of this training resource package. We thank the ALERT Hospital training center for the technical provided to develop and test this training resource package. Name Organization Dr. SOLOMON BURSSA ALERT Dr.MULUADMASU ALERT Dr.AYDA SIRAJ ALERT Dr.BEZA WUBE ALERT Dr. FEKADU KASSAHUN ALERT DAGNEW HAGZOM ALERT ETSEHYWET GEDLU ALERT Mr.YAKOB SEMAN MOH Mr.ABAS HASSAN MOH Dr.ASHANFI BEZA MOH Dr.SMIRAT MOH Mr.MARKOS PAULOS MOH ACRONYMS III ACA The Anterior Chamber Angle ratio ACE angiotensin-converting enzyme AIDS acquired immunodeficiency syndrome AION anterior ischaemic optic neuropathy AKC atopic kerato conjunctivitis AMD age-related macular degeneration ANA antinuclear antibody ANCA anti-neutrophil cytoplasmic antibody BCC basal cell carcinoma BIO binocular indirect ophthalmoscopy BRAO branch retinal artery occlusion BRVO branch retinal vein occlusion BSV binocular single vision CCC continuous curvilinear capsulorrhexis CCT central corneal thickness CDB corneal dystrophy of Bowman’s layer CMV cytomegalovirus CNS central nervous system CNV choroidal neovascularization CRAO central retinal artery occlusion CRVO central retinal vein occlusion CT computed tomography CXR chest X-ray DCR dacryocystorhinostomy DVD dissociated vertical deviation EBV Epstein–Barr virus ELISA enzyme-linked immunosorbent assay EOG electrooculogram FFA fundus fluorescein angiography HIV human immunodeficiency virus HLA human leucocyte antigen HSK herpes simplex keratitis HSV herpes simplex virus HZO herpes zoster ophthalmicus HZV herpes zoster virus ICE iridocorneal endothelial IL interleukin IOL intraocular lens IOP intraocular pressure LASEK laser-assisted subepithelial keratomileusis 4 LASIK laser-assisted stromal in-situ keratomileusis MRA magnetic resonance angiography MRI magnetic resonance imaging NSR neurosensory retina NVD new vessels of the optic disc PAC perennial allergic conjunctivitis PAS peripheral anterior synechiae PCO posterior capsule opacifi cation PCR polymerase chain reaction PDR proliferative diabetic retinopathy PDT photodynamic therapy PHPV persistent hyperplastic primary vitreous POAG primary open-angle glaucoma PORN progressive outer retinal necrosis PRK photorefractive keratectomy PRP pan-retinal photocoagulation PUK peripheral ulcerative keratitis PVD posterior vitreous detachment SAC seasonal allergic conjunctivitis RAPD relative afferent pupillary defect RNFL retinal nerve fi bre layer ROP retinopathy of prematurity RPE retinal pigment epithelium TF Trachomatous follicle TI Trachomatous Inflamation /intense/ RRD rhegmatogenous retinal detachment VDRL Venereal Disease Research Laboratory VEGF vascular endothelial growth factor VKC vernal keratoconjunctivitis VZV varicella zoster virus 5 TABLE OF CONTENTS Contents APPROVAL STATEMENT............................................................................................................ I FOREWORD..................................................................................................................................II ACKNOWLEDGEMENT............................................................................................................. III ACRONYMS................................................................................................................................. 3 TABLE OF CONTENTS................................................................................................................6 LIST OF FIGURES.........................................................................................................................7 INTRODUCTION............................................................................................................................. 8 COURSE SYLLABUS.................................................................................................................... 10 CHAPTER 1: BASIC ANATOMYAND EMBRYOLOGY OF THE EYE.......................... 14 CHAPTER2: BASIC HISTORY AND EXAMINATIONOF THE EYE.................................. 30 CHAPTER 3: DISEASE OF EYELIDS, ORBIT, LACHRYMAL SYSTEM..................... 41 CHAPTER 4: CONJUNCTIVA DISEASE..............................................................................69 CHAPTER 5: DISEASES OF THE SCLERA.........................................................................82 CHAPTER 6: COMMON DISEASES OF THE CORNEA................................................... 87 CHAPTER 7: DISEASE OF THE LENS (CATARACT)....................................................110 CHAPTER 8: GLAUCOMA....................................................................................................120 CHAPTER 9: DISEASE OF THE RETINA andOPTIC NERVE PATHWAY.................129 CHAPTER 10: REFRACTIVE ERROR............................................................................... 144 CHAPTER 11: STRABISMUS..................................................................................................156 CHAPTER 12: OCULAR TRAUMA AND CHEMICAL BURNS..................................... 164 CHAPTER 13: TRACHOMA..................................................................................................181 REFERENCES............................................................................................................................191 GLOSSARY OF TERMS RELATING TO THE EYE..............................................................192 6 LIST OF FIGURES 7 INTRODUCTION Rational: Low vision and blindness are major public health problems worldwide, especially in developing countries where 90% of the blind live. About 75% of the causes of blindness are avoidable and mainly caused by cataract and trachoma1. The prevalence of blindness in Ethiopia is 1.6%, of which 87.4% are due to avoidable causes. To prevent avoidable blindness in developing countries the role of primary eye care services is enormous. Primary eye care comprises a simple but comprehensive set of promotive, preventive and curative actions that can be carried out by suitably trained primary health workers, specialized auxiliary personnel or other interested people. Locally available personnel and training program for primary health care can be used to promote and strengthen the delivery of eye care at the peripheral level. Different countries from resource-limited regions have used different strategies and approaches to make primary eye care accessible at community level. In order to avoid a public health crisis and keep up with increasing vision loss among the population, correctable vision impairments must be eliminated. Vision loss and visual impairment is a major public health problem in the Ethiopia. Avoidable vision impairment occurs too frequently and is the result of a series of outdated assumptions, missed opportunities, and shortfalls in public health policy and health care delivery. As a result, the Ministry of Health, Ethiopia has planned to develop a standard training guide for General practitioners on basic ophthalmic services that can be delivered at primary or general hospital level in the absence of an ophthalmologist. Ethiopia launched VISION 2020 initiative and human resources development was one the areas included in the subsequent national strategic plans for eye care, implementation was a huge challenge. As a result, there were disproportionately small number of ophthalmologists in the country and only few hospitals in the country had trained ophthalmologist in place to give comprehensive eye care service. To make the matter worse, the few available ophthalmologists were concentrated Addis Ababa and other main cities of the country, making equitable access to eye care service impossible. To tackle the challenge, Medical service general directorate of Minster of health working on eye health in the country supported the training of different eye care cadres including that of ophthalmologists and mid-level eye care workers to address the priorities set in the national strategic plan for eye care. In general, through the trained MD with basic ophthalmology training will improve the equity and access to eye care service in the country. 8 Purpose of basic ophthalmologyTraining: The main goal of this initiative is to reduce avoidable visual impairment as health problem and to secure access to basic services in an equitable manner (vulnerable groups and underserved communities) by providing a continuum of high- quality, comprehensive, integrated basic eye care. Core competency Core competencies that the trainees are expected to attain after this training include:  Conducts comprehensive patient evaluation  Makes a clinical diagnosis based on the information gathered from the patient  Plans management together with the patient or guardian and other health professionals using available information  Identifies and manages ophthalmic emergencies and trauma  Refers patients as appropriate 9 COURSE SYLLABUS Course description:This training is designed for health personnel such General practitioners and clinical officers working at primary health facilities. These workers are often the first professional point of contact for patients with eye diseases. The course builds on their existing professional expertise and experience as health workers or trainees. In addition to extending the general skills gained by the participants during their basic health training, the course aims to impart the specific skills required for everyday interventions in patients with eye diseases at the primary care level. What it does not do is attempt to turn participants into mini eye specialists in respect of the specific topics addressed. Empirical evidence shows that adults learn best by tackling situations, problems or tasks which participants accept as interesting and worthwhile. The course is therefore primarily structured as a series of problem-based tasks for small groups. Course goal: The goal of the training is to strengthen the ability of primary-level health workers to successfully manage patients with eye complaints presenting at primary health care facilities. Learning objectives: By the end of this training, the participant will be able to:  Describe the Eye Examination and Diagnosis  The history includes the patient’s chief complaints, medical illnesses, current medications, allergies to medications, family history and eye disease of orbit, adnexa, lachrymal system, eyelid problems, Conjunctiva, cornea, lens, Glaucoma, retina, optic pathway, Strabismus, Refractive Errors Injuries, andtrachoma Training/learning methods  Illustrated lectures and group discussions  Individual and group exercises  Individual reading and reflection  Teach back sessions  Case studies  Guided practice activities  Practical clinical sessions Training materials/aids  Basic ophthalmology training participant manual  Basic ophthalmology training facilitators guide  Basic ophthalmology training PPT slides  LCD projector, flip charts, markers, laptop computers  Short video 10 Participant selection criteria Participants for this course should be MD and HO with: At least 0-2 years of relevant work experience in the primary hospital clinical services. Method of evaluation o Participant evaluation  Formative - Pre-test - Group exercises - Evaluation of participant developed activities and materials  Summative - Knowledge assessment (40 %): Post-course questionnaire - Ethics and Professionalism (60%): Participant’s activity, attendance, behavior and participation throughout the course o Trainer evaluation o Course evaluation  During session participant reaction  Daily Evaluation  Daily trainers’ feedback meeting  End of Course Evaluation Certification criteria  Participants will be certified when they score more than 80% in the summative assessment. Trainers’ selection criteria  Ophthalmologistieswith minimum of twoyears’ service or related professional with significant contribution the training pakagepreparation  Having TOT certificate on Ophthalmology of this course, andinvolved in at least one basic ophthalmology training as Co-trainer, Course Venue  Accredited in-service training centers venue having functional service for the course(video conferences facilities, internet, movable chairs, space for break out, toilet facility …) and practical session facilities. Course Duration  The duration of any teaching course is a trade-off between achieving various objectives and the length of time a professionally active participant can be removed from his or her duties. The period of 30 days required for this course allows for comfortable session lengths with adequate breaks. An additional day should be set aside before it starts to allow for induction of the facilitators who will assist the master trainer. 11 General design of training The task-based learning approach requires a comprehensive task to be subdivided into essential component tasks. In order for it to have a cumulative learning effect the sequence of sub-tasks ought to mirror the order in which issues relating to the main task would normally be tackled. At appropriate junctures, brief tasks that consolidate or synthesize newly acquired knowledge are added. The sequence for most sessions is as follows:  Skill-based learning through clinical practical sessions based on course protocols  A walk through each clinical algorithm  Use of case studies to illustrate the practical Each morning apart forms the first day starts with an interactive plenary session to explain the session contents. Other prerequisite skills such “How to counsel an eye patient” are taught by means of mini-lectures combined with practical sessions involving volunteer patients. In addition, participants gain first-hand experience with actual patients through a clinical attachement to be held in the morning for the remaining days of the training apart from the first day session. Group Work: Except for two initial lectures to introduce the course and display images of the normal and abnormal eye, most learning is done by group work. Tasks are introduced in the plenary session following which participants learn by observing and supporting each other, mainly in groups of three, throughout the problem-solving process. Communication over the remaining days takes place through active participation rather than lectures. Course Composition  20-25 participants  4-6 trainers Clinic visit/ practical attachement/ A half-day clinical attachment is designed to provide participants with relevant practical exercises and the invaluable experience of managing actual patients in a real-life situation. The clinic attachment should ideally be scheduled for the morning oneach days of the training. The clinic attachementis strategically placed on each day of the course programme in order to ensure that participants acquired all the basic knowledge and skills required to manage actual patients. The short morning session prior to the clinic visit serves to brief participants. This briefing covers the objectives, programme, logistics and expected outcome of the visit. After each clinic visit a debriefing session andafternoon lecture allows participants to discuss and reflect on their experience. The final event is the concluding session, which includes course evaluation and issuing of certificates. 12 Monitoring and evaluation Monitoring and evaluation activities are fully integrated into the course programme. Both pre- and postcourse questionnaires are used to assess new knowledge and skill levels gained by participants in the course. Pre-course evaluation takes place on the starting day of the course. Post-course evaluation is scheduled for the final afternoon: this should leave enough time for evaluation and feedback. Trainees are required to fill daily evaluation checklists over the days of the course in order to ensure that the overall training session is to their satisfaction and an end of course evaluation will be filled on the end of the overall training period to assess the course. Both the dialyandend of course evaluation should be used for the improvement of the training during and after its completion. Trainer evaluation should also be filled by participants to assess trainer’s ability in managing the training courses. Which the result of the trainers’ assessment should be used for future adjustement on allocation of trainers. COURSE SCHEDULE 13 CHAPTER 1: BASIC ANATOMY, PHYSIOLOGYAND EMBRYOLOGY OF THE EYE Chapter description: This chapter will provide the anatomy, physiology and embryology of the eye, to permit an understanding of medical conditions affecting these structures also discussed in this chapter. Chapter objective:  To give a clear description on the anatomy, physiology and embryology of the eye.  Explains the external and internal parts of the eye.  Having the basic idea will help to have a better understanding on thepathology of specific part of the eye. Chapter outline This module has the following sessions:  Introduction of anatomy the eye and  Structure of the Eye  Interior of the eyeball  Accessory structures of the eye  Blood supply to the eye  Nerve supply to the eye  Embryology of the eye  Primordia of ocular structures  The Eye at Birth  Summary 14 INTRODUCTION The eye is the organ of sight situated in the orbital cavity. It is almost spherical in shape and is about 2.5 cm in diameter. The volume of an eyeball is approximately 7 cc. The space between the eye and the orbital cavity is occupied by fatty tissue. The bony wall of the orbit and the fat helps to protect the eye from injury. Structurally the two eyes are separate but they function as a pair. It is possible to see with only one eye, but three-dimensional vision is impaired when only one eye is used specially in relation to the judgement of distance. Fig. 1: Structure of the eye Structure of the Eye The eyeball has three layers namely: 1. The outer fibrous layer—Sclera and cornea 2. The middle vascular layer—Iris, ciliary body and choroid 3. The inner nervous tissue layer—Retina. Interior of the Eyeball The structures inside the eyeball are: 1. Aqueous humour 2. Lens 3. Vitreous. Accessory Structures of the Eye 1. Eyebrows 2. Eyelids and eyelashes 3. Lacrimal apparatus 4. Extraocular muscles of the eye. 15 STRUCTURE OF THE EYE 1. The Outer Fibrous Layer 1.1.Sclera: The sclera or white of the eye forms the firm, fibrous outermost layer of the eye. It maintains the shape of the eye and gives attachment to the extraocular muscles. It is about 1 mm thick. The sclera becomes thin (seive-like membrane) at the site where the optic nerve pierces it. It is called Lamina cribrosa. Fig.2: Schematic diagram of three layers of the eyeball 1.2.Cornea: Cornea forms the anterior 1/6 of the eye. The transparent, ellipsoid, anterior part of the eyeball is known as the cornea. It is the main refracting surface of the eye. The dioptric power is + 43 to + 45 D. 1.3.Limbus: The junction of cornea and sclera is known as the limbus. There is a minute arcade of blood vessels about 1 mm broad present at the limbus. 2. The Middle Vascular Layer 2.1.Iris:Iris is a coloured, free, circular diaphragm with an aperture in the centre—the pupil. It divides the anterior segment of the eye into anterior and posterior chambers which contain aqueous humour secreted by the ciliary body. It consists of endothelium, stroma, pigment cells and two groups of plain muscle fibres, one circular (sphincter pupillae) and the other radiating (dilator pupillae). 2.2.Ciliary body:Ciliary body is triangular in shape with base forwards. The iris is attached to the middle of the base. It consists of non-striated muscle fibres (ciliary muscles), stroma and secretory epithelial cells. It consists of two main parts, namely pars plicata and pars plana. 2.3.Choroid:Choroid is a dark brown, highly vascular layer situated between the sclera and retina. It extends from the ora serrata up to the aperture of the optic nerve in the sclera. 3. The Inner Nervous Tissue Layer 16 3.1.Retina:Retina is composed of ten layers of nerve cells and nerve fibres lying on a pigmented epithelial layer. It lines about 3/4 of the eyeball. Macula lutea is a yellow area of the retina situated in posterior part with a central depression called fovea centralis. It is the most sensitive part of retina. Fig.4: (a)The sclera, ciliary body and iris (Cornea has been removed) (b)The lens and suspensory ligament (Iris has been removed) 3.2.Optic disc—Optic disc is a circular, pink coloured disc of 1.5 mm diameter. It has only nerve fibre layer so it does not excite any visual response. It is known as the blind spot. 3.3.The optic nerve—The optic nerve extends from the lamina cribrosa up to the optic chiasma. The total length of the optic nerve is 5 cm. It has four parts namely,Intraocular — 1 mm, Intraorbital — 25 mm, Intraosseous — 4-10 mm, and Intracranial — 10 mm (Duke–Elder). INTERIOR OF THE EYEBALL 1. Aqueous Humour Both anterior and posterior chambers contain a clear aqueous humour fluid secreted into the posterior chamber by the ciliary epithelium. It passes in front of the lens, through the pupil into the anterior chamber and returns to the venous circulation through the canal of Schlemm situated in the angle of anterior chamber. 2. Lens Lens is a transparent, circular, biconvex structure lying immediately behind the pupil. It is suspended from the ciliary body by the suspensory ligament or zonule of Zinn. It is enclosed within a transparent capsule. 3. Vitreous Vitreous is a transparent, colourless, inert gel which fills the posterior 4/5 of the eyeball. It contains few hyalocytes and wandering leucocytes. It consists of 99% water, some salts and mucoproteins. 17 ACCESSORY STRUCTURES OF THE EYE The eye is a delicate organ which is protected by several structures such as eyebrows, eyelids, eyelashes and extraocular muscles. 1. Eyebrows Eyebrows are two arched ridges of the supraorbital margins of the frontal bone. Numerous hair (eyebrows) project obliquely from the surface of the skin. They protect the eyeball from sweat, dust and other foreign bodies. 2. Eyelids and Eyelashes The eyelids are two movable folds of tissue situated above and below the front of each eye. Thereare short curved hair, the eyelashes situated on their free edges. The eyelid consists of:  A thin covering of skin  Three muscles-the orbicularis oculi, levator palpebrae superioris and Müller’s muscles  A sheet of dense connective tissue, the tarsal plate  A lining of the conjunctiva. Fig. 4: Gross anatomy of the eyelid 3. Lacrimal Apparatus Lacrimal apparatus consists of:  Lacrimal gland and its ducts  Accessory lacrimal glands  Lacrimal canaliculi  Lacrimal sac  Nasolacrimal duct 18 The tears are secreted by the lacrimal gland and accessory lacrimal glands. They drain into the conjunctival sac by small ducts. The tears then pass into the lacrimal sac (via the two canaliculi), nasolacrimal duct and finally into the nasal cavity (inferior meatus). Fig.5: Section of the eye and its accessory structures 4. Extraocular Muscles of the Eye The eyeballs are moved by six extrinsic muscles, attached at one end to the eyeball and at the other to the walls of the orbital cavity. There are four straight and two oblique muscles. They consist of striated muscle fibres. Movement of the eyes to look in a particular direction is under voluntary control but co-ordination of movement needed for convergence and accommodation to near or distant vision, is under autonomic control. 19 Fig. 6: The extraocular muscles of the eye  The medial rectus rotates the eyeball inwards.  The lateral rectus rotates the eyeball outwards.  The superior rectus rotates the eyeball upwards.  The inferior rectus rotates the eyeball downwards.  The superior oblique rotates the eyeball so that the cornea turns in a downward and outward directions.  The inferior oblique rotates the eyeball so that the cornea turns upwards and outwards. BLOOD SUPPLY TO THE EYE Arterial Supply The eye is supplied by the short (about 20 in number) and long ciliary (2 in number) arteries and the central retinal artery. These are branches of the ophthalmic artery, which is one of the branch of the internal carotid artery. Venous Drainage Venous drainage is done by the short ciliary veins, anterior ciliary veins, 4 vortex veins and the central retinal vein. These eventually empty into the cavernous sinus. 20 Fig. 7: Blood supply of the eye NERVE SUPPLY TO THE EYE The eye is supplied by three types of nerves, namely motor, sensory and autonomic. 21 Fig. 8:Nerve supply to the eye 1. The Motor Nerves i. The third cranial nerve (oculomotor) ii. The 4th cranial nerve [trochlear]—It supplies the superior oblique muscle. iii. The 6th cranial nerve [abducens]—It supplies the lateral rectus muscle. iv. The 7th cranial nerve [facial]—It supplies the orbicularis oculi muscle. 2. The Sensory Nerve The 5th cranial nerve [trigeminal]—The ophthalmic division supplies the whole eye. 3. The Autonomic Nerves 3.1. The sympathetic nerve supply is through the cervical sympathetic fibres to: i. Iris—Dilator pupillae muscle ii. Ciliary body iii. Müller’s muscle in the lids iv. Lacrimal gland. 3.2. The parasympathetic nerve supply originates from the nuclei in the midbrain. It gives branches to: i. Iris—Sphincter pupillae muscle ii. Ciliary body iii. Lacrimal gland. 22 EYE LIDS Are movable fold of tissue which serves to protect the eyes.spreads the tear film to wet the cornea and conjunctiva. Divided in to six structural layers 1. Skin and subctutaneous tissue.  The thinnest in the body  It is loose and elastic permitting extreme swelling and subsequently return to normal shape and size 2. Orbiculariesocculi(muscles of protraction) o Narrows the palpebral fissure o Lachrimal pump o Involuntary eye lid movement (blink) o Forced eye closure -winking,blephrospasm o Innervation viic.n. 3. Orbital septum  thin sheet of fibrous tissue  fuses with levatorapponeurois  serves as a barrier between orbit and lids 4. Muscles of retraction  Levator muscle  Muller muscle 5. Tarsus - dense firm connective tissue  A skeleton of the lids  Contains meibomian glands 6. Conjunctiva  Forms the posterior layer of the lids  Contains goblet cells ---- secreting mucin  Lacrimal glands---- krause and wolfering 23 PHYSIOLOGY OF THE EYE AQUEOUS HUMOR The eye is a peripheral organ of vision. It subserves its function due to the optically transparent media, particularly the cornea and the lens, which focus the images of the objects on a sensitive layer—the retina. The eye maintains its shape by intraocular pressure. The avascular structures, lens and cornea, receive their nourishment by aqueous humor. The formation and circulation of aqueous humor and the maintenance of intraocular pressure are important aspects of physiology of the eye. Aqueous humor is a clear fluid, filling the anterior and the posterior chambers of the eye. Its refractive index is 1.336 and viscosity 1.025 to 1.040. The osmotic pressure of aqueous humor is slightly higher than plasma. The aqueous contains glucose, urea, proteins, inorganic salts, ascorbic acid, lactic acid and some dissolved oxygen. The walls of capillaries of iris and ciliary body, two layers of ciliary epithelium and walls of retinal capillaries constitute a system of semipermeable membranes, separating blood from the ocular cavity, known as blood-aqueous barrier. Formation of Aqueous Humor For several years’ aqueous humor was considered as a simple filtrate from blood. Owing to a significant difference in the chemical compositions of aqueous and blood such a concept was rejected. Subsequentlya theory of ultrafiltration from the capillaries of ciliary processes was postulated; but it could not explain all the facts regarding the higher concentration of ascorbates. Therefore, a hypothesis of active ciliary secretory process was proposed. It has been found that the rate of transport of sodium by the ciliary epithelium is sufficient to explain the rate at which water enters the ocular cavity. The active transport of sodium by the ciliary epithelium is carried out by a sodium pump demonstrated by Berggren and Cone. Circulation of Aqueous Humor The circulation of aqueous humor is essential forregulation of the intraocular pressure as well asfor metabolic activities of the intraocular structures.Aqueous humor is drained out by tworoutes: (i) trabecular meshwork route and(ii) uveoscleral route. 24 Fig. 9: Drainage of aqueous humor Trabecular Outflow The trabecular route accounts for bulk of aqueousoutflow (75 to 90%). The formed aqueous humoris collected in the posterior chamber, flowsthrough the pupil into the anterior chamber andfinally escapes through the drainage channels atthe angle of the anterior chamber. The aqueousfilters through trabecular meshwork at the angleof the anterior chamber into the canal of Schlemmand from there a number of aqueous veins andefferent channels drain it into the episcleral veinsand intrascleral venous plexus, respectively.Approximately 2 μl (1% of the fluid in the anteriorchamber) of the aqueous humor drains away perminute. The drainage of aqueous humor isinfluenced by the patency of exit channels and the venous pressure just within the sclera. Improper cleavage of the angle of the anterior chamber causes a rise in the intraocular pressure often seen in congenital glaucoma. If the venous pressure is raised the drainage of aqueous humor is embarrassed which can be demonstrated on episcleral vein in the glass rod phenomenon experiment. The episcleral vein at the site of junction with the aqueous vein presents a laminated appearance due to blood and aqueous running side by side. When the vein is compressed by a glass rod, fluid flows from the vessel with higher pressure into the one with lower. If the venous pressure is higher there is blood influx into the aqueous vein, if the pressure in the aqueous vein is higher, aqueous influx is seen in the vein. Uveoscleral Outflow Nearly 10-26% of aqueous outflow occurs through the uveoscleral route. The aqueous passes across the ciliary body into the suprachoroidal space and is drained in the venous circulation. Intraocular Pressure 25 Intraocular pressure (IOP) is the pressure insidethe eyeball. It is determined by the rate of aqueousproduction by the ciliary epithelium and the amount of its drainage through the trabecular meshwork. The gradient of pressure in the ocular capillaries across which the fluid transfer takes place greatly influences the intraocular pressure. Normally there is a balance between the rate of formation of the aqueous humor and its drainage, hence, wide ranging fluctuations do not occur. The intraocular pressure in a human eye usually ranges from 12 to 20 mm Hg. It is most accurately measured by a manometer. However, manometric measurements are not possible in human eyes and, therefore, a measurement of the degree ofindentation of cornea by a standard weight is utilized. Such a method is called indentation tonometry (Schiotz). The variation in the rigidity of sclera induces significant error in such measurements warranting correction. A more dependable method, applanation tonometry, is in wide clinical use. The measurements are usually expressed as mm Hg and the intraocular pressure is referred as ocular tension. The normal mean ocular tension is 15.4 + 2.5 mm Hg by applanation and 16.1 + 2.8 mm Hg by Schiotz tonometer. Usually the intraocular pressure does not vary significantly between the two eyes. A consistent difference of 4 to 6 mm Hg between the two eyes is known as Downey’s sign and is an indication for investigation for glaucoma. What factors regulate the intraocular pressure at its normal level are not known clearly. However, there is evidence to suggest that a center in the hypothalamus exercises a control on the intraocular pressure to maintain its homeostatic equilibrium. The afferent path from the eye to this center is not determined, but the efferent path runs through the sympathetics traveling down the spinal cord relaying in the cervical ganglion and reaching the eye by way of the cervical chain and the ophthalmic artery. Probably, the center is also responsible for the diurnal variations of intraocular pressure which is often seen. The average variation throughout the day is about 2 mm Hg. A rise may occur in the morning hours which is mainly due to the changes in the rate of aqueous humor production. Following factors tend to alter the intraocular pressure. 1. Variation in the Hydrostatic Pressure in the Capillaries A rise in the ciliary capillary pressure often results in a rise in intraocular pressure and vice versa. Vasodilatation does not lead to an increased pressure, a low pressure is a frequent outcome. 2. Variation in the Osmotic Pressure of the Blood A change in the osmotic pressure of the bloodalters the process of diffusion across the capillarywall; hypotonicity induces a rise andhypertonicity a fall in intraocular pressure. 3. An Increase in the Permeability of the Capillaries 26 An increased permeability of the ciliary capillariesin the formation of plasmoidaqueous which induces a rise in the osmoticpressure of the aqueous and thus increasesthe intraocular pressure. The IOP furtheraccentuates if particulate materials block the drainage channels. 4. Change in the Volume of the Eyeball Generally, a small volumetric change in theeyeball is normally compensated by anincreased drainage mechanism. However, bigtumors, intraocular hemorrhages and suddenvasodilatation induce pressure changes dueto indistensibility of the sclera. 5. Obstruction in the Circulation of Aqueous Blockage at the pupil and/or at the angle ofthe anterior chamber results in profound risein intraocular pressure. 6. Alteration in Aqueous Formation Alteration in the secretory activity of the ciliaryepithelium should hypothetically alter theintraocular pressure. Hypersecretion of theaqueous causes a rise and hyposecretion a fallin intraocular pressure.Besides these, changes in the pH of blood,topical and systemic drugs, general anesthesiaand psychological stress are known to alterthe intraocular pressure. METABOLISM OF OCULAR TISSUES The ocular tissues consist of both vascularized and nonvascularizedstructures. Iris, ciliary body, choroid and retina do not differ in general metabolic activity from other tissues of the body. The retina has a very high metabolic rate and it rapidly dies if its blood supply is cut off even for ashort time. The nonvascularized structures of the eye such as cornea and lens derive their energy requirements from phosphorylation of carbohydrates and auto-oxidative system. Cornea requires energy for the maintenance of its transparency. There are possibly three important routes for the transport of metabolites to and from the corneaperilimbal capillaries, aqueous humor and tears. Glucose enters the cornea either by simple diffusion or by active transport through aqueous humor. The atmospheric oxygen presumably dissolved in tears enters the epithelium. 27 EMBRYOLOGY OF THE EYE The central nervous system develops from the neural tube. A thickening appears on either side of the neural tube in its anterior part, known as the optic plate. The optic plate grows towards the surface to form the optic vesicle. The two eyes develop from these optic vesicles and the ectoderm and mesoderm coming in contact with the optic vesicles. The optic vesicle invaginates from in front and below to form the optic cup. The line of invagination remains open for sometime as the embryonic fissure. The hyaloid artery enters through the fissure to provide nutrition to the developing structures. Later it atrophies and disappears. The inner layer of the optic cup forms the inner nine layers of the main retina and the outer layer develops into the pigment epithelium. The neural ectoderm secretes jelly-like structure, the vitreous which fills the cavity. The ciliary body and iris are formed by the anterior portion of the optic cup and mesoderm. The mesoderm around the cup differentiates to form the coats of eye, orbital structures, angle of anterior chamber and main structure of cornea. Meanwhile the surface ectoderm invaginates and later separates to form the lens. The surface ectoderm remains as the corneal and conjunctival epithelium. The mesoderm in front of the cornea grows in folds, unites and separates to form the lids. PRIMORDIA OF OCULAR STRUCTURES Table1: The eye originates from neural ectoderm, surface ectoderm and mesoderm. SURFACE ECTODERM MESODERM NEURAL ECTODERM 1. Conjunctival epithelium 1. Corneal stroma 1. Sensory retina 2. Corneal epithelium 2. Corneal endothelium and 2. Retinal pigment epithelium Descemet’s membrane 3. Pigment epithelium of iris 3. Crystalline lens 3. Iris stroma 4. Ciliary body epithelium 4. Eyelash 4. Choroid 5. Sphincter pupillae 5. Epithelium of 5. Sclera 6. Dilator pupillae — meibomian glands 6. Vitreous 7. Melanocytes — glands of Moll 7. Extraocular muscles 8. Neural part of optic nerve — lacrimal gland 8. Ciliary muscles — accessory lacrimal glands 9. Bony orbit 1. Eyelids—They develop from both surface ectoderm and mesoderm 28 Fig.10: Derivation of various ocular structures 2. Zonules (tertiary vitreous)—They develop from surface ectoderm and mesoderm 3. Bruch’s membrane—It develops from neural ectoderm and mesoderm The Eye at Birth 1. Orbit is more divergent (50°) as compared to an adult (45°). 2. Eyeball is about 70% of adult length. It is fully developed at the age of 8 years. 3. The newborn is hypermetropic by +2.5 D. 4. Cornea is approximately 80% of its adult size, being fully grown at the age of 3 years. 5. Anterior chamber is shallow and the angle is narrow Chapter Summary The eye is vital sensory organ rest in two bony orbits located on either side of the nose, surrounded by fat and connective tissue. Only the anterior aspect is exposed. Each eye is connected to the brain by the optic nerve which traverses the optic foramen at the apex of the orbit. 29 CHAPTER2: BASIC HISTORY AND EXAMINATIONOF THE EYE Chapter Description: At the end of the course the participant will able to understand Basic eye examination helps to assess a patient with eye disease and several separate steps are necessary by using ophthalmic equipment’s which would help the examiner to make appropriate diagnosis based on history and physical examination. Learning Objectives: To be able to:  Take and understand an ophthalmic history and physical examination.  To give a clear idea about the approach to ophthalmic patients and specific examination techniques.  To examine ophthalmic patients and use of certain ophthalmic instruments  Examine the function of the eye (acuity and visual field).  Examine eye movements.  Examine the structure of the eye.  Use the ophthalmoscope. Chapter outline  Introduction  History taking  Testing the vision (V/A, V/F, colourvision)  Intraocular pressure measurement (IOP)  Ocular motility  Pupillary examination  Examine the eyes- slit lamp microscopic examination (SLM)  Fundoscopic examination 30 INTRODUCTION Ophthalmic diagnosis is heavily dependent on a good history and a thorough examination. The majority of ophthalmic diagnoses do not require additional tests. History taking  Components of the History  personal details (name, address, age, sex, occupation)  Chief compliant  History of present illness  Past ocular history  Ocular medications  General medical andsurgical history  Systemic medication  Social andfamily history History of present illness  Time andmanner of onset: Was it sudden or gradual?  Severity: Has problem improved, worsened, or same?  Influences (precipitating conditions)  Constancy and temporal variation  Laterality: Is the problem unilateral or bilateral  Clarification of what the patient means by certain complaints The main purpose of the history is to find out what exactly the patient is complaining. However, it is always helpful to find out some background information about the patient e.g. age, sex, occupation, and literacy. Such information will indicate what vision the patient needs for work and for personal satisfaction. In History taking one has to consider the following  Particular environmental or occupational factors  Patients diet, drinking and smoking habits  General health of the patient like diabetes, hypertension and neurological disease affecting the eye.  Previous eye disease, injuries or treatment  Use of traditional medicine or uses of other treatment.  Family history of similar complaint e.g. myopia and glaucoma. A good history must include details of:  Ocular symptoms, time of onset, eye affected, and associated nonocularsymptoms.  Past ocular history (e.g. poor vision in one eye since birth, recurrenceof previous disease, particularly inflammatory).  Past medical history (e.g. of hypertension which may be associated withsome vascular eye diseases such as central retinal vein occlusion;diabetes which may cause retinopathy 31 and systemic inflammatory diseasesuch as sarcoid which may also cause ocular inflammation).  Drug history, since some drugs such as isoniazid and chloroquine maybe toxic to the eye.  Family history (e.g. of ocular diseases known to be inherited, such asretinitis pigmentosa, or of disease where family history may be a riskfactor, such as glaucoma).  Presence of allergies. Major symptom of eye disease given A. Disturbances of vision The most common visual symptom which can be sudden or gradual  Blurring or reduction of vision  Dazzling/glare/ – difficulty of seeing in bright light, may be caused by opacities in the cornea or lens  Diplopia / double vision/  Decreased peripheral vision – may be caused by various disorders in the retina, optic nerve or visual pathway pathology up to the visual cortex.  Photophobia – is a fear of light It is usually a sign of inflammatory eye disease, especially a corneal ulcer and uveitis. Distortion of shapes usually indicates a disorder of the retina around the macular. Haloes (rainbow) colored rings around the light e.g. Corneal edema, Glaucoma. B. Discomfort or pain in the eye. Usually a symptom of inflammation of the eye or of the structure surrounding the eye.  Discomfort, irritation or grittiness may be related with conjunctival problems  Pain is commonly related to corneal disease and Glaucoma Eyestrain and tiredness of the eyes are common complaint usually associated with extra ocular muscles abnormalities and refractive errors. C. Eye discharge Abnormal ocular secretions:  Lacrimation or tearing is welling up of tears on ocular surface  Epiphora in an actual spilling of tears over margin of eyelids onto the face  Eye discharge can be purulent, mucopurulent, mucoid or watery Testing the Vision The human eye is an extremely complex organ, and there are three ways to test the vision. 1. Visual acuity (V/A)- tests if the patient can see small objects or letters. 2. Visual field (V/F) --tests the overall area of vision for each eye 3. Colour vision – tests if patient can discriminate between different colours. 32 Fig.11: (a)ameasured with snellen chart(b)Visual Acuity Steps 1. patient stands at 6m and cover the left andtest right eye (OD) first 2. Ask the patient to read letters as much as he can in bright light starting from top letters and record the lowest line read 3. If the patient cannot read the top letter (6/60), then ask the patient to count fingers held up in front of the eye. Human finger is about the same size as top letter in chart o Counting finger at 6 m (CF 6m) = 6/60 VA o CF at 1 m distance (CF 1m) = 1/60 VA 4. If the vision is below CF @ 1m, the patient may still able to detect the movement of the hand in front of the eye (HM) 5. If the pt. cannot even see HM, final test is to shine a light in to the eye, and see if s/he can perceive light (LP= lightperception). Record response as LP or NLP. 6. If LP, test if the patient can identify projection of light in four quadrants of patient’s vision. Also check for color perception like Green andRed. 7. Repeat the same procedure to the left eye by covering the right eye. 8. Any patient with defective VA should be tested again through a pinhole. 9. If vision improves with PH, that indicates refractive error and spectacle can correct it Projection of the light from four quadrants of the eyes should be examined to test the peripheral retina and optic nerve function. Intra ocular pressure It should be measured in any patient with suspected glaucoma. Ideally it should be part of routine eye examination in any one over 40 years of age. There are three methods of assessing IOP. 33 1. Digital palpation very simple but not at all accurate Steps Order your patient to look down Place two fingers on the upper eye lid and depressing slowly Assess the consistency of the globe (whether it is firm or hard) and compare with the fellow eye. 2. SchiØtz tonometry – cheap andcommonly used. 3. Applanation tonometry- Expensive andmuch more accurate Goldmann applanation tonometry is the gold standard and should be used in the clinic whenever possible. Outside of the clinic, Tono-Pen tonometry is much more practical. If you suspect a ruptured globe, skip this part of the exam. Visual field testes Visual field is that portion of one’s surroundings that is visible at one time duringcentral vision. It is not a routine test in all patients. It is important to do in any patients with suspected glaucoma, diseases of the optic nerves in visual pathways, and certain retinal diseases. 1. Confrontation test  Simple and no need of special equipment  Will detect serious visual field defects.  Works by comparing the patient’s visual field with the examiner’s Steps  Sit facing the patient at one-meter distance  If the patient’s left eye is being tested, he should cover his right eye and you should cover your left eye.  Patient looks straight into your eye and you look straight into his toomake sure he is fixing your eye.  Then hold your fingers at an angle equidistant between you and the patient and ask him to say visible or not as your fingers move.  If you can see them and the patient cannot, then he has a defect.  Move in different quadrant  Do the same with the other eye. 2. Perimetery It is difficult to test in children, old or non-comprehending people. In all visual field test, each eye is tested separately. The patient must fix his gaze on a target or spot in front of him. The examiner then sees at what angle objects come into the patients range of vision A calibrated black screen / Bjerrum screen/ gives a more accurate result 3. The Goldmann VF test 4. Visual field analyzers à computerized 34 Color vision It is done by using a chart called ’Ishihara chart’ Simple macular test is to ask the patient for red and green color perception These are used particularly to detect colour blindness. Examination of the eye Nearly all parts of the eye are visible with an appropriate optical instrument. Anyone who cares for the patients should know how to examine the eye. Some of ophthalmic diagnostic instruments are very expensive, but a reasonable examination is possible with available simple instruments. There are two important instrument for examination of the eye 1. To examine the front of the eye, this requires both a good light illumination with bright light, torch, magnifying lens(loupe) and slit lamp bio microscopic (SLM) 2. To examine the back of the eye, need ophthalmoscope. Normal eye  Eye lids should open and close properly  Eye lashes should grow forward and out ward  white part of the eye should be white  Cornea should be clear and transparent  Pupil is black and reactive to light Abnormal appearances:  Ptosis (drooping of the eyelids)  Proptosis or exophthalmos (protrusion of the eye)  Enophthalmos (the opposite of proptosis)  Misalignment of the eyes  Redness, other discolorations, opacities, masses  Anisocoria (inequality of the pupil’s size) Trauma: especially require very detailed reports based on thorough Hx andexam. o The date, time, and place of injury? o what happened in patient’s own words? o what safety precautions were taken? o What measures were taken for emergency? o The type and roughly estimated speed of any foreign body? o whether or not the vision has been affected. Ocular motility examination Terminology  Strabismus (squint) – describe a misalignment of the eyes in which both eyes are not directed at the object of regard. 35  Phoria – is a latent tendency toward misalignment of eyes that occur only when binacularity is interrupted.  Tropia – a manifest deviation that is present when both eyes are open  Positions of gaze:  primary position (straightahead)  Secondary positions (straight up, straight down, right gaze, and left gaze)  Tertiary positions (4 oblique positions: up andright, up andleft, down andright, and down andleft)  Cardinal positions (upandright, up andleft, right, left, down andright, down andleft)  Midline positions (straight up anddown from primary position)  Actions of EOMs Types of hetrophoria and hetrotropia Prefix Name of disorder Description Phoria(latent) tropia(manifest) Eso- esophoria esotropia inward deviation Exo- exophoria exotropia outward deviation Hyper- hyperphoria hypertropia upward deviation Hypo- hypophoria hypotropia downward deviation Pupillary examination It can give a great deal of information andis one of the most important parts of eye exam. The pupil reactions: 1. The light reflex- in which pupil reacts(constricts) when light is shone in the eye. A. Direct light reflex B. Consensual light reflex 2. The accommodation or near reflex in which the pupil constricts when the eye looks at near objects. 36 The reflex is divided into two parts: 1. The afferent part: From retina to mid brain 2. The efferent part: from mid brain along oculomotor nerve to pupil constrictor muscle In normal person both pupils are always same size as each other and both always react in the same way as each other.  If pupils are not reacting normally the defect may be in the afferent or efferent part of reflex.  A defect in the efferent part (something wrong with oculomotor n, or sphincter m.) will nearly always cause affected pupil to be dilated.  An afferent pupil defect is a sign of optic nerve disease or extensive retinal disease. Slit-lamp examination Fig. 12: Slit lamp examination  During Examination of the Eye One Has to Comment the Following Things  Lids/lashes/lacrimal system: Normal anatomy and contours? Any lesions?  Conjunctiva/sclera: White and quiet? Injection? Lesions?  Cornea: Clear? Epithelial disruptions? Stromal opacities? Endothelial lesions?  Anterior chamber: Deep? Cell or flare?  Iris: Round pupil? Transillumination defects? Nodules?  Lens: Clear? Nuclear, cortical or sub capsular cataract?  Anterior vitreous: Inflammation? Hemorrhage? Pigmented cells?  If the examiner wears spectacles, he should keep it. Fundoscopic examination Ophthalmoscope is a form of illumination, which allows the examiner to look down the same axis as the rays of light entering the patient’s eye. To see the fundus  Ocular media must be healthy and transparent 37  Dilate the pupil with mydriatic drops  With the ophthalmoscope it appears 15 times larger than its actual size  In myopic patient the magnification is greater, but in hypermetropic patient it is less. How to use ophthalmoscope  Hold closer both to the examiner’s and to the patient's eye  If the patient has spectacles, he has to put it off. Fig.13:Fundus examination Steps  For examination of the right eye, sit or stand at the patient’s right side.  Select ‘’ O’’ on the illuminated lens dial of the ophthalmoscope and start with small aperture.  Take the ophthalmoscope in the right hand and hold it vertically in front of your own right eye with the light beam directed toward the patient and place your right index finger on the edge of the lens dial so that you will be able to change lenses easily if necessary.  Dim room lights and instruct the patient to look straight ahead at a distant object.  Position the ophthalmoscope about 6 inches (15cm) in front and slightly to the right of the patient and direct the light beam into the pupil. A ‘’reflex’’ should appear as you look through the pupil.  Rest the left hand on the patient’s forehead and hold the upper lid of the eye near the eyelashes with the thumb. While the patient holds his fixation on the specified object, keep the ‘’ reflex’’ in view and slowly move toward the patient. The optic disc should come into view when you are about 1and1/2 to 2 inches (3-5cm) from the patient. If it is not focused clearly, rotate lenses into the aperture with your index finger until the optic disc is clearly visible as possible. The hyperopic, or farsighted, eye requires more ‘plus’ 38 (black numbers)sphere for clear focus; the myopic, or near-sighted, eye requires ‘minus’(red numbers) sphere for clear focus.  Now examine the disc for clarity of outline, color, elevating and condition of the vessels. Follow each vessel as far to the periphery as you can. To locate the macula, focus on the disc, then move the light approximately 2 disc diameters temporally. You may also have the patient look at the light of the ophthalmoscope, which will automatically place the macula in full view. Examine for abnormalities in the macula area. The red-free filter facilitates viewing of the center of the macula, or the fovea.  To examine the extreme periphery, instruct the patient to: o look up for examination of the superior retina o look down for examination of the inferior retina o look temporally for examination of the temporal retina o look nasally for examination of the nasal retina. This routine will reveal almost any abnormality that occurs in the fundus.  To examine the left eye, repeat the procedure outlined above except that you hold the ophthalmoscope in the left hand, stand at the patient’s left side and use your left eye. If you don’t get a clear view it is usually for one or two reason 1. If the patient has a refractive error, try dialing up plus or minus lenses in the ophthalmoscope to bring the fundus into focus. Especially in myopic patient. It is difficult to see the fundus clearly so use a strong minus lens in the ophthalmoscope. 2. If the patient has some opacity in the transparent part of the eye i.e. in the cornea, lens or vitreous, this can be detected with plus lens in the ophthalmoscope when the pupil is dilated. Examining the fundus and using the ophthalmoscope  Optic nerve: Cup-to-disc ratio (see Figure below)? Focal thinning? Pallor? Symmetric?  Macula: Foveal light reflex? Drusen, edema or exudates?  Vessels: Contour and size? Intraretinal hemorrhage?  Periphery: Tears or holes? Lesions? Pigmentary changes 39 Fig.14:Normal fundus CHAPTER SUMMARY  The eye is part of the body and is often affected in systemic disease. Always seekassociated features when taking an ophthalmic history.  A good ophthalmic history can initiate a differential diagnosis and influence subsequentclinical examination. 40 CHAPTER 3: DISEASE OF EYELIDS, ORBIT, LACHRYMAL SYSTEM Chapter description:The chapter willsdscribesdiseases of the orbit, adnexa, lachrymal system, eyelid problems will most likely be the commonest eye disorders that physicians encounter. Any health care provider should be able to diagnose and carry out the first line of treatment for uncomplicated cases infectious and allergic of orbit, adnexa. This chapter goes through the commonest of the orbit, adnexa, lachrymal system, and eyelid problems encountered in any health setup. Chapter objective:  Recognize the medical terms used in common eyelid, orbital diseases  Explain the common diseases of the eye and their presentations  Demonstrate the diagnostic procedures of various diseases  Discuss the treatment procedures in eye diseases  Identify and report the complications Chapter Outline:  Introduction  Disorder of Lids Lacrimal Apparatus and Orbit  PhthiriasisPalpebrarum  Summary 41 DISORDERS OF EYELIDS The eyelids are important both in providing physical protection to the eyes and in ensuring a normal tear film and tear drainage. Diseases of the eyelids can be divided into those associated with:  Abnormal lid position;  Inflammation of the lid;  Lid lumps;  Abnormalities of the lashes. Abnormalities of lid position Ptosis Ptosis is an abnormal low position of the upper lid. Normal lid position and thus lid measurements vary slightly according to age, gender, and ethnicity. An appearance of ptosis may be simulated by a number of conditions (pseudoptosis). True ptosis may be congenital (either isolated or syndromic) but is most commonly acquired as an involutional degeneration. However, ptosis may also be the presenting feature of a number of serious conditions. Pathogenesis It may be caused by: 1. Mechanical factors. a. Large lid lesions pulling down the lid. b. Lid oedema. c. Tethering of the lid by conjunctival scarring. d. Structural abnormalities including a disinsertion of the aponeurosis of the levator muscle, usually in elderly patients. 2. Neurological factors. a. Third nerve palsy b. Horner’s syndrome, due to a sympathetic nerve lesion c. Marcus–Gunn jaw-winking syndrome. In this congenital ptosis there is a mis- wiring of the nerve supply to the pterygoid muscle of the jaw and the levator of the eyelid so that the eyelid moves in conjunction with movements of the jaw. 3. Myogenic factors. a. Myasthenia gravis b. Some forms of muscular dystrophy. c. Chronic external ophthalmoplegia. Symptoms Patients present because:  They object to the cosmetic effect;  vision may be impaired; 42  There are symptoms and signs associated with the underlying cause (e.g. asymmetric pupils in Horner’s syndrome, diplopia and reduced eye movements in a third nerve palsy). Signs There is a reduction in size of the interpalpebral aperture. The upper lid margin, which usually overlaps the upper limbus by 1–2imm, may be partially covering the pupil. The function of the levator muscle can be tested by measuring the maximum travel of the upper lid from upgaze to downgaze (normally 15–18imm). Pressure on the brow (frontalis muscle) during this test will prevent its contribution to lid elevation. If myasthenia is suspected the ptosis should be observed during repeated lid movement. Increasing ptosis after repeated elevation and depression of the lid is suggestive of myasthenia. Other underlying signs, for example of Horner’s syndrome or a third nerve palsy, may be present. Fig.15:Left ptosis Management It is important to exclude an underlying cause whose treatment could resolve the problem (e.g. myasthenia gravis). Ptosis otherwise requires surgical correction. In very young children this is usually deferred but may be expedited if pupil cover threatens to induce amblyopia. Trichiasis Trichiasis is a condition where a few cilia are misdirected backwards and they rub against the cornea. Etiology Trichiasis is caused by trachoma, ulcerative blepharitis, ocular burns, membranous conjunctivitis, injury or an operation on the lid margin. It is also seen in congenital distichiasis. 43 Clinical Features Foreign body sensation or irritation, lacrimation, photophobia and pain are common symptoms of trichiasis. The misdirected lashes may rub against the cornea or cause corneal erosions and vascularization. Causes It may occur in isolation or associated with scarring of the lid margin due to trachoma, chronic blepharitis, HZO. Signs  Posterior misdirection of lashes.  Trauma to the corneal epithelium. Other causes of misdirected lashes  Pseudo- trichiasis- secondary to entropion.  Metaplastic lashes-originate from the meibomian gland orfices.  Distichiasis- a partial or complete second row of lashes arise from or slightly behind the meibomain gland orfices. It is uncommon congenital condition. Treatment 1. Epilation with forceps- is simple and effective but recurrences within a fewweeks are common 2. Electrolysis- is useful for a few isolated lashes 3. Cryotherapy-is effective in eliminating many lashes at a time, but has potential complication like skin depigmentation, lid margin notching damage to themeibomain glands. 4. Laser ablation- useful when only a few scattered lashes are required treatment 5. Surgery- the most effective method of treatment in our set up. Phthiriasispalpebrarum is an infestation of the lashes by the pubic crab louse (phthiruspupis) and its ova(nits)?It typically affects children in poor hygienic conditions and casuses chronic itching and irritation. Treatment Removal with forceps Destruction with topical application of yellow mwrcuric oxide 1% if available Health education, improvement of personal hygiene. Madarosisis decrease in number or complete loss of lashes or eye brows due to local, skin or systemic disorders like alopecia or psoriasis or leprosy. Poliosisis a premature localized whitening of lashes and eyebrow hair following chronic blepharitis and sympathetic ileitis or systemic associations 44 ALLERGIC DISORDERS OF LIDS  Acute allergic lid oedema- may be caused by insect bites, and urticaria, rearely caused by drugs. Treatment –antihistamines  Contact dermatitis- common unilateral or bilateral condition caused by sensitivity to topical medication Signs- localized erythema and crusting Treatment - identification and removal of the cause - Mild steroid ointment like hydrocortisone 1%. Infection of the lids Herpes zoster ophthalmicus It is common, unilateral conditions which typically affect elderly patients and patients with immuno-deficincy states. Symptoms Is with pain in the distribution of the first division of the trigeminal nerve. Signs Maculopapular rash on the forehead Development of vesicles, pustules and crusting ulceration Insevere cases periorbitaloedema due to 20 bacterial celulitis. Treatment  Systemic-aciclovir 1g three times daily for 7 days or famciclovir 250 mg once daily for 7 days, or 750mg ones daily for 7 days.  Topical- Acyclovir or penciclovir cream, and steroid-antibiotic combination such as Terracortril three times daily unit the crusts have separated. Herpes simplex Etiology It is caused by herpes simplex virus type I (HSV I). Incidence It occurs in children or young adults usually.  There is recurrence due to febrile cold, pneumonia, physical exhaustion or exposure tosunlight. Types 1. Primary ocular Herpes-There is acute follicular keratoconjunctivitis with regional lymphadenitisand skin involvement. 2. Recurrent herpes- It has following characteristic features:  Epithelial ulcers  Stromal interstitial keratitis 45  Disciform keratitis  Iridocyclitis. Fig. 16: Herpes simplex Symptoms  Vesicles are seen on lips, nose, cornea (Herpes simplex virus type I / HSV I) and genitals (Herpessimplex virus type II / HSV II)  Great irritation, lacrimation and blepharospasm is present. Signs 1. Skin lesion: initially vesicles with superficial crusts are formed. These vesicles heal without scarformation. 2. Severe follicular keratoconjunctivitis is present usually in children. 3. There may be regional lymphadenitis (preauricular lymph nodes). 4. Slit-lamp examination of the cornea shows: a. Superficial punctate keratitis Numerous, white plaques of epithelial cells are present all over the corneal surface. These are of minute pin—head size. They are arranged in rows or groups. There is absence of vascularization and corneal sensation. b. Dendritic ulcer—Erosions coalesce to form typical dendritic figure like liverwort. It ispathognomonic of herpes simplex. c. Confluent ulcer—Large geographical pattern type of ulcers is seen. d. Disciform (deep) keratitis—It involves the stroma forming disc-like opacity. Complications  Chronic epithelial ulcer with recurrence is a common complication.  Corneal opacity is present in deep or stromal keratitis. 46  Iritis and iridocyclitis is often associated with a severe herpetic keratitis.  Hypopyon may be present in severe cases. Diagnosis 1. Immunological tests—By immunofluorescence of epithelial scrapings. 2. Tissue biopsy and tissue culture—Elementary bodies are seen with suitable staining. Fig.17: ( a). Ulcer stained with fluorescein (b). Ulcer stained with rose Bengal day Treatment 1. Antiviral drugs a) Systemic—Oral acyclovir 400 mg twice daily × 7 days. Ideally it should be started prior to the onset of symptoms. It is the method of choice in cases of recurrent herpes labialis. It has low toxicity. b) Topical i. 5-iodo-2-deoxyuridine (IDU)—0.1% eyedrops and 5% eye ointment. It is applied5 times a day and at bedtime for 10-21 days. Treatment should not be prolonged beyond3 weeks since this may lead to corneal toxicity. ii. Acyclovir—3% eye ointment is applied 5 times daily for 10-21 days. iii. Adenine arabinoside (Ara- A) and vidarabine (Vira-A) 3% ointment—It is not effectivein stromal disease. iv. Trifluorothymidine (F3T)—Trifluridine 1% eyedrops are applied 5-9 times daily for14 days. v. Acycloguanosine—It is effective in cases of stromal disease and iritis vi. Bromovinyl—deoxyuridine 1% ointment and 0.1% drops is a new antiviral drug which isas potent as F3T. vii. A very potent new compound 9-guanine (ganciclovir) is under trial. 47 2. Debridement—It may be used for dendritic but not for geographical ulcers. The corneal surfaceis wiped with sterile cellulose sponge 2 mm beyond the edge of the ulcer (as pathology extendsbeyond visible lesion)  This protects healthy epithelium from infection  It eliminates the antigenic stimulus to stromal inflammation. 3. Atropine and warm compresses are useful in controlling iritis. 4. Topical corticosteroidsare only useful in deep or disciform keratitis. Steroids are contraindicatedin epithelial lesions. 5. Full thickness keratoplastyis done in cases of permanent corneal opacity. The eye must bequiet for a year at least. Blepharitis Blepharitis is often used as shorthand for chronic lid margin disease. However, blepharitis refers to any inflammationof the lid and thus includes a wide range of disease, such as preseptalcellulitis, internal and external hordeola, and herpes simplex (HSV) and varicella zoster virus (VZV) infections. The diagnosis of blepharitis therefore lacks precision but is often used given the considerable overlap between the main causes of chronic lid margin inflammation, discussed below. The descriptive terms anterior and posterior blepharitis are sometimes used to indicate the distribution of disease. Unilateral blepharitis (and recurrent chalazia) in an elderly patient should be treated with extreme suspicion since lid tumors (e.g., sebaceous cell carcinoma) may present in this way. Chronic Blepharitsisa very common condition which is usually bilateral and symmetrical. The main types: - 1. Anterior blepharitis  Staphylococcal  Seborrhoeiu - usually associated with seborrhoeic dermatitis, which may involve the scalp, nasolabial folds and retroauricular areas.  Mixed Signs of anterior blepharitis a. The anterior lid margins Variable hyperemia and telangiectasia 48 Tiny localized intrafollicular abscesses In long standing cases the anterior lid margine may become scared and on the lashes. b. The scales In staphylococcal blepharitis are hard and brittle and are centred on the bases of the lashes. Inseborrhoeicblepharits scales are soft and greasy and are located anywhere on the lid margin and on the lashes. c. The lashes Greasy and stuck together in seborrhoeicblepharitis. Trichiasis, madarosis and occasional in poliosis in severe longstanding anterior blepharitis. Complications 1. External hordeolum (stye) 2. Tear film instability 3. Papillary conjunctivitis, interior punctuate epitheliopathy and marginal keratitis. Treatment a. Inform patient the necessity of intensive long term (several weeks) treatment to achieve improvement. b. Lids hygiene _aimed at removing crusts and toxic products c. Antibiotic ointment d. Weak topical steroids e. Tera subesstitut 2. Posterior Blepharitis It may occur in isolation or in association with anterior blepharitis. Two types  Meibomian gland dysfunction with seborrhea- characterized by Excessive meibomian gland secretion.  Meibominitis- characterizes by inflammation and obstruction of the meibomain glands. Signs  Small oily globules capping the meibomain gland orfices  Pressure on the tarsus results in expression of copious amount of meibomian oil  Oily and foamy tear film  Diffuse or localized inflammation around meibomian gland orfices  In sever cases of meibominitis no secreations can be expressed from the glands  Blockage of the main meibomian duct gives risk to secondary cystic dilation (meibomian cysts) 49 Complication 1. Tear film instability 2. Interior punctuate epitheliopathy and mild papillary conjunctivitis Treatment 1. Systemic tetracyclines for 6_12 weeks. To children under 12years of age, to pregnant or breast_feeding women one of the following can be used. a. Tetracycline 250mg four times daily for 1 week and then twice daily or b. Doxycycline 100mg twice daily for one week and then once daily 2. Erythromycin may be used when TTC is contraindicated but its efficacy is not well established. 3. Other measures  Lid hygiene, topical steroids and substitutes  Warm compresses to melt solidified solution and mechanical expression of the meibomain gland may reduce the amount of irritaing lipids within the gland. Benign nodules and cysts of eye lids Chalazion Is a chronic lipogranulomatous inflammatory lesion caused by blockage of gland orfices and stagnation of sebaceous secretions. Fig.18:Chalazion of left upper lid 50 Etiology Chalazion is commonly seen in adults and often occurs in crops. It perhaps develops as a result of infection by an organism of low virulence or by chronic irritation. The entire gland is replaced by a granulation tissue containing giant cells. Clinical Features Chalazion is a painless, round, smooth swelling which can be palpated by passing a finger over the lid. There may be more than one chalazion. On eversion of the lid, the palpebral conjunctiva is red or gray over the chalazion. Spontaneous resolution of a chalazion seldom occurs. It may form a granuloma following its extrusion through the conjunctiva or rarely through the duct of the gland (marginal chalazion). Signs  Pain less, roundish firm lesion in the tarsal plate  Associated blepharitis is common. Treatment a. Steroid injection into the lesion rarely used b. Surgery_cyst is incised and its contents curetted through the tarsal plate c. Systemic tetracycliness may be required as prophylaxis in patients with recurrent chalazia, acnae rosacea or seborrhoeic dermatitis. Internal hordeolumis a small abscess caused by an acute staphylococcal infection on meibomiaglands. Signs Tender, inflamed swelling within the tarsal plate Treatment  It may discharge by itself, incision and  Incision and curettage if residual nodule remain External hordeolum (Sty) Is an acute small staphylococcal abscess of a lash follicle and its associated gland of Zeis or Moll. Signs  Tender inflamed sewlling in the lid margin  More than one lesion can be present  Mild preseptal cellulites may be present Treatment a. May resolve spontaneously b. Hot compress c. Epilation of associtated lash d. Systemic antibiotic if there is preseptal cellulites Molluscumcontagiosum 51 Is uncommon skin infection caused by poxvirus. Immunocompromised patients may have a typical multiple lesion. Signs _ Single or multiple, pale, waxy, umbilicated nodules Treatment – Is by shave excision, couteriztion, cryotherapy or laser. Miscellaneous cysts 1. A cyst of Moll- issmall, round, non-tender, translucent fluid-filled lesion on the another lid margin. 2. Acyst of zeis - is less translucent than cyst of moll.it contains oily secretions. 3. Asebaceous cyst _ arises from an ordinary scbaceousgland, contains cheesy secretions. 4. Milia _ are derived from hail follicles or scbaceous glands. They are tiny, white. round superficial cysts. Ectropion It is a condition in which the lid margin rolls outwards. Types Types 1. Involutional (ectropion (sequele) It results in epiphora and in longstanding cases the tarsal conjunctiva becomes chronically inflamed and thickened. Treatment _ is surgical correction, and method of correction depends on the position of maximal ectropion, horizontal lid laxity, the severity of canthal tendon laxity and cause of ectropion. Surgical methods are a. Cautery punctures b. Medial conjunctivoplasty c. Lazy-Tprocedure d. Horizontal lid shortening Type 2. Cicatrical ectropion - Caused by scaring or contracture of the skin and underlying tissue. Type 3. Paralytic ectropion - caused by a facial never plasy. Type4.Mechanical ectropion- is caused by tumors onor near the lid marigne which mechanically ever the lid. Symptom The most common symptom is epiphora, i.e. constant watering of the eyes. Signs 1. Conjunctiva becomes dry in appearance and thickened in texture. 2. Chronic conjunctivitis may be present due to exposure of the conjunctiva and cornea. 3. Corneal ulcer may develop (exposure keratitis). Treatment 1. Spastic ectropion—The underlying cause of blepharospasm is treated. 52 2. Cicatricial ectropion—The aim of surgery is to free the lid margin from scar tissue and restorethe lid to its normal position and function. i. V-Y operation is done in mild cases. A ‘V’-shaped incision is made in the skin of thelower lid which includes the scar. The skin is excised and the wound is sutured in Y-shapedpattern thus correcting the ectropion. ii. Excision of scar tissue and application of skin graft is useful in cases of extensivescarring. Split skin graft or full-thickness skin grafts are taken from the upper lid, behindthe ear, inner side of upper arm or thigh. 3. Senile ectropion a. Full-thickness shortening of the lid is done by making an inverted house-shaped incision atleast 5 mm away from the punctum and repairing it. This is useful if the ectropion is mostmarked in the middle portion of the lower lid. b. Kuhnt-Szymanowski procedure—It is useful if the ectropion is severe and marked over thelateral half of the lower lid. It is modified by Byron Smith. A skin flap is prepared and a fullthicknessshorting is done at the lateral canthus. The excess skin is removed and tractionsutures applied. 4. Paralytic ectropion—Lateral tarsorrhaphy may be indicated. The palpebral aperture is shortenedby uniting the lid margins at the junction of middle and outer one-third. Entropion This is an inturning, usually of the lower lid. It may occur if the patient looks downwards or be induced by forced lid closure. It is seen most commonly in elderly patients where the orbicularis muscle becomes weakened. It may also be caused by conjunctival scarring distorting the lid (cicatricial entropion). The inturned lashes cause irritation of the eye and may also abrade the cornea. The eye may be red. Short-term treatment includes the application of lubricants to the eye or taping of the lid to overcome the inturning. Permanent treatment requires surgery. It is a condition in which the lid margin rolls inwards. Etiology There are two main types of entropion—spastic and cicatricial. Types 1. Involutional (senile) entropion  Affects mainly the lower lid.  The constant rubbing of the lashes on the cornea- ulcerationtowards the globe. 2. Congenitalentropion It is caused by sever scaring of the palpebral conjunctiva, which pulls the lid margin towards the globe. This can be caused by cicatrizing conjunctivitis, trachoma and chemical burns. 3. Cicatricalentropion It is very rare. It is an in turing of the entire lower eyelid and lashes with absence of the lower lid crease 53 Fig.19:Entropion. Treatment – is surgical depending on the cause and severity of entropion. Ectropion Here there is an eversion of the lid. Usual causes include:  involutional orbicularis muscle laxity;  scarring of the periorbital skin;  seventh nerve palsy. The malposition of the lids everts the puncta and prevents drainage of the tears, leading to mepiphora. It also exposes the conjunctiva. This again results in an irritable eye. Treatment is again surgical. Benign lid lumps and bumps Chalazion This is a common painless condition in which an obstructed meibomian gland causes a granuloma within the tarsal plate. Symptoms are of an unsightly lid swelling which usually resolves within 6 months. If the lesionpersists it can be incised and curetted from the conjunctival surface. An abscess (internal hordeolum) may also form within the meibomian gland, which unlike a chalazion is painful. It may respond to topical antibiotics but incision may be necessary. A stye (external hordeolum) is a painful abscess of an eyelash follicle. Treatment requires the removal of the associated eyelash and application of hot compresses. Most cases are self-limiting. Occasionally systemic antibiotics are required. 54 Molluscum contagiosum This umbilicated lesion found on the lid margin is caused by the pox virus. It causes irritation of the eye. The eye is red and small elevations of lymphoid tissue (follicles) are found on the tarsal conjunctiva. Treatment requires excision of the lesion. CYSTS Various cysts may form on the eyelids. Sebaceous cysts are opaque. They rarely cause symptoms. They can be excised for cosmetic reasons. A cyst of Moll is a small translucent cyst on the lid margin caused by obstruction of a sweat gland. A cyst of Zeis is an opaque cyst on the eyelid margin caused by blockage of an accessory sebaceous gland. These can be excised for cosmetic reasons. Squamous cell papilloma This is a common frond-like lid lesion with a fibrovascular core and thickened squamous epithelium. It is usually asymptomatic but can be excised for cosmetic reasons with cautery to the base. Xanthelasmas These are lipid-containing bilateral lesions which may be associated with hypercholesterolaemia. They are excised for cosmetic reasons. Keratoacanthoma A brownish pink, fast growing lesion with a central crater filled with keratin. Treatment, if required, is by excision. Fig. 20:(a) A squamous cell papilloma; (b) xanthelasma; (c)keratoacanthoma. Naevus (mole) These lesions are derived from naevus cells (altered melanocytes) and can be pigmented or non- pigmented. No treatment is necessary. Malignant Tumours Basal cell carcinoma 55 This is the most common form of malignant tumour. Ten per cent of cases occur in the eyelids and account for 90% of eyelid malignancy. The tumour is:  slow growing;  locally invasive;  non-metastasizing. Patients present with a painless lesion on the eyelid which may be nodular, sclerosing or ulcerative (the so-called rodent ulcer). It may have a typical, pale, pearly margin. A high index of suspicion is required. Treatment: Excision biopsy with a margin of normal tissue surrounding the lesion. Excision may also be controlled with frozen sections when serial histological assessment is used to determine the need for additional tissue removal (Moh’s surgery). This minimizes destruction of normal tissue. - Cryotherapy. - Radiotherapy. The prognosis is usually very good but deep invasion of the tumour can be difficult to treat. Squamous cell carcinoma This is a less common but more malignant tumour which can metastasize to the lymph nodes. It can arise de novo or from pre-malignant lesions. It may present as a hard nodule or a scaly patch. Treatment is by excisional biopsy with a margin of healthy tissue. UV exposure is an important risk factor for both basal cell and squamous cell carcinoma THE ORBIT The bony orbit forms a pyramid comprising a medial wall lying anteroposteriorly, a lateral wall at 450, a roof, and a floor. It has a volume of around 30 mL and contains most of the globe and associated structures: extraocular muscles, optic nerve, cranial nerves, vascular supply, and lacrimal system. Despite the number of different tissues present in the orbit, the expression of diseases due to different pathologies is often similar. Clinical features 1. Soft tissue involvement Lid a) lid and periorbitaloedema b) ptosis c)chemosis and conjunctival injection 2. Proptosis Proptosis, is a protrusion of the eye caused by a space-occupying lesion. It can be measured with an exophthalmometer. A difference of more than 3imm between the two eyes is significant.Various other features give a clue to the pathological process involved 56  If the eye is displaced directly forwards it suggests a lesion that lies within the cone formed by the extraocular muscles (an intra-conal lesion). An example would be an optic nerve sheath meningioma.  If the eye is displaced to one side a lesion outside the muscle cone is likely (an extra- conal lesion). For example, a tumour of the lacrimal gland displaces the globe to the nasal side.  A transient proptosis induced by increasing the cephalic venous pressure (by a Valsalva manoeuvre), is a sign of orbital varices.  The speed of onset of proptosis may also give clues to the aetiology. A slow onset suggests a benign tumour whereas rapid onset is seen in inflammatory disorders, malignant tumours and carotid-cavernous sinus fistula.  The presence of pain may suggest infection (e.g. orbital cellulitis). 3. Exophthalmoses _is a backward displacement of the globe. This may be seen following an orbital fracture when orbital contents are displaced into an adjacent sinus. It is also said to occur in Horner’s syndrome but this is really a pseudo-enophthalmos due to narrowing of the palpebral fissure 4. Ophthalmoplegia 5. Visual dysfunction 6. Dynamic properties  Increasing venous pressure by dependent head position valsalvamanoeuvre or jugular vein compression.  Pulsation  A bruit—is a sign of carotid cavernous 7. Fundus changes ORBITAL DISORDERS Classified as Orbital infections  Thyroid opthalmopathy  Orbital inflammatory diseases  Vascular lesions  Cystic lesions  Tumors  Craniosynostos Preseptal cellulites It is relatively common infection of subcutaneous tissues anterior to the orbital septum. It is much more common than orbital cellulitis, from which it must be differentiated. 57 The main causative organisms are Staphylococci and Streptococci spp. It is generally a much less severe disease, at least in adults and older children Fig.21:Preseptal orbital cellulitis Causes  Infection of adjacent structures (dacryocystitis, hordeolum) or systemic (e.g., upper respiratory tract infection).  Skin Trauma: laceration. Clinical features Fever, malaise, painful, swollen lid/periorbita. Inflamed lids but no proptosis, normal eye movements, normal optic nerve function. Investigation Investigation is not usually necessary unless there is concern over possible orbital or sinus involvement. Treatment Daily review until resolution (admit young or unwell children). Treat with oral antibiotics (e.g., fl oxacillin 500 mg 4x/day for 1 week and metronidazole 400 mg 3x/day for 1 week). Orbital cellulites Bacterial cellulities is a rarely common infection of the soft tissue behind the orbital septum. Infective organisms include Streptococcus pneumoniae, Staphylococcus aureus, Streptococcus pyogenes, and Haemophilus influenza (previously common in younger children, but less likely if Hib vaccinated). Causes Sinus related is most common, mostly secondary to ethmoidal sinusitis (common). Spread from adjacent structures following dacryocystitis, mid-facial and dental Infection Post-traumatic usually within 48 to 72 hours of injury. 58 Post-Surgicalfollowing retinal, lacrimal or orbitial surgery. Clincal features Presentation is with a rapid onset of malaise, fever and orbital signs. Eyelidsswollen, red, warm and tender Proptosis – Mostly lateral and downward Ocular -restricted and painful ocular movement - Signs of optic nevere dysfunction may be present in advanced cases. Investigation Temperature. CBC, blood culture. CT (orbit, sinuses, brain): diffuse orbital infiltrate, proptosis ± sinus opacity. Treatment Admit for intravenous antibiotics (e.g., either fl oxacillin 500–1000 mg 4x/day or cefuroxime 750–1500 mg 3x/day with metronidazole 500 mg3x/day). ENT to assess for sinus drainage (required in up to 90% of adults). Complications Ocular _ exposure keratopathy, IOP, occulusion of CRA or CRV or optic nerve inflammation. Intracranial _ rare but serious, include meningitis, brain abscess and cavernous sinus thrombosis. Subperiorbital abscess _ mostly at the medial wall of the orbit Orbital abscess _ rare in sinus related, but may occur in post traumatic or post-operative cases. Management Hospital admission or referral to ophthalmologist is mandatory. The patient should be evaluated by an ophthalmologist and otolaryngologist. Broads spectrum systemic antibiotic therapy _ should be started parentally without FUNGAL INFECTIONS Mucormycosis (phycomycosis) This is a rare, very aggressive life-threatening fungal infection caused by Mucor species or Rhizopus. Mucormycosis is a disease of the immunosuppressed, most commonly seen in patients who are also acidotic, such as in diabetic ketoacidosis or renal failure. However, the disease also occurs in malignancy and therapeutic immunosuppression. It represents fungalseptic necrosis and infarction of tissues of nasopharynx and orbit. 59 Clinical features Black crusty material in nasopharynx, acute evolving cranial nerve palsies (II, III, IV, V, VI) ± obvious orbital inflammation. slow progress (septic necrosis) Ischemic infaraction blackeschar on the palate, turbinates, nasal septum or skin. Investigation Biopsy: fungal stains show nonseptate branching hyphae. CBC, UA, Glu. Treatment Admit and coordinate care with microbiologist and infectious disease specialist, ENT specialist, ± PCP. Correct underlying disease (e.g., diabetic ketoacidosis) where possible. Intravenous antifungals (as guided by microbiology; e.g., amphotericin B). Early surgical debridement by ENT specialist ± orbital exenteration (for severe or unresponsive disease). ORBITAL ASPERGILLOSIS Aspergillus may occasionally cause an endogenous endophthalmitis similar to Candida. It generally occurs in those with chronic pulmonary disease who are severely immunosuppressed. It is more aggressive than candida infection, with pain and rapid visual loss being marked. Clinical Features Signs  Its clinical course is more (less active) indolent than that of mucormycosis. It is fatal in 80% of cases. Treatment  With requires IV amphotericin B. ORBITAL INFLAMMATORY DISEASE (OID) A number of inflammatory diseases may affect the orbit. These may be purely orbital or related to systemic disease (e.g., thyroid eye disease). The purely orbital diseases may be diffuse (e.g., idiopathic orbital inflammatory disease) or focal (e.g., myositis). 60 IDIOPATHIC ORBITAL INFLAMMATORY DISEASE (PSEUDOTUMOR) This is an uncommon chronic inflammatory process of unknown etiology. It may simulate a neoplastic mass (hence the term pseudotumor), but histology shows a pure inflammatory response without cellular atypia. It is a diagnosis of exclusion and may in fact represent a number of poorly understood entities. It may occur at almost any age. It is usually unilateral. It is unilateral condition, but can be bilateral in about 30% of small children. Clinical features Signs Periorbital swelling, chemosis and conjunctival inflammation Proptosis Opththalmoplegia Optic nerve involvement. Clinical course - is variable Spontaneous remission _ no sequelae Prolonged intermittent episodes _ eventual remission Severe prolonged inflammation _ leading to ptosis and visual impairment. Investigation Orbital imaging: B-scan (low to medium reflectivity, acoustic homogeneity); MRI (hypointense, cf. muscle on T1; hyperintense, cf. muscle on T2; moderate enhancement with gadolinium). Biopsy is required when there is diagnostic doubt. Management 1. Observation _ mild cases 2. Systemic steroid 3. Cytotoxic durgs 4. Radiotherap 5. Dacryoadenitis Lacrimal gland involvement occurs in about 25% patients with OID. Presentation Acute onset of discomfort in the lacrimal gland area followed by swelling, tendeness of the area and reduction of tear sectretion. Treatment Immunosuppression: usually with systemic corticosteroids, although cytotoxics (e.g., cyclophosphamide) and radiotherapy are sometimes used. 61 ORBITAL MYOSITIS In myositis, the inflammatory process is restricted to one or more extraocular muscles, most commonly the superior or lateral rectus. The disease may occur at almost any age and is usually unilateral. Clinical Features Acute pain (especially on movement in the direction of the involved muscle), injection over muscle ± mild proptosis. Investigations Orbital imaging: MRI gives better soft tissue resolution; the whole of the muscle and tendon shows enlargement and inflammation (cf. TED). Treatment No steroidal out- inflammatory agents in mild cases. Systemic steroids in mild and severe cases. TOLOSA-HUNT SYNDROME In this rare condition, there is focal inflammation of the superior orbital fissure ± orbital apex. The disease presents with orbital pain, multiple cranial nerve palsies, and sometimes proptosis. It must be differentiated from other causes of the superior orbital fissure syndrome: carotid- cavernous fistula, cavernous sinus thrombosis, Wegener’s granulomatosis, pituitary apoplexy, sarcoidosis, mucormycosis, and other infections. The condition is very sensitive to steroids. DACRYOADENITIS Lacrimal gland inflammation may be isolated or occur as part of diffuse idiopathic orbital inflammatory disease. It presents with an acutely painful swollen lacrimal gland that is tender to palpation, has reduced tear production, and results in an S-shaped deformity to the lid. The condition must be differentiated from infection and tumors of the lacrimal gland. Isolated dacryoadenitis does not usually require treatment. It is a rare condition caused by non-specific granulomatous inflammation of the cavernous sinus. W

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