This action might not be possible to undo. Are you sure you want to continue?
Marissa N. Valbuena M.D., MHPEd
Associate Professor Department of Ophthalmology and Visual Science College of Medicine University of the Philippines Manila
Authors Preface 1. Anatomy of the Eye Marissa N. Valbuena M.D., MHPEd 2. Physiology of the Eye Richard C. Kho, MD 3. Ocular Symptomatology Marissa N. Valbuena M.D., MHPEd & Arnold T. Salud M.D. 4. Eye Examination Teresita R. Castillo, MD, MHPEd 5. Disturbance in Vision 5.1 Disorders of the Cornea Ruben LimBonSiong, MD 5.2 Cataract Leonardo R. Mangubat, MD 5.3 Disorders of the Retina, Choroid and Vitreous Pearl T. Villalon, MD 5.4 Glaucoma Norman M. Aquino, MD & Marissa N. Valbuena M.D., MHPEd 5.5 Disorders of the Optic Nerve Raul D. Cruz, MD 5.6. Errors of Refraction Juan Ma. Pablo R. Nañagas, MD, MPH, MSNA 6. Red Eye , Tearing and Discharge 6.1 The Red Eye Leo D. P. Cubillan, MD, MS 6.2 Uveitis and Scleritis Teresita R. Castillo, MD, MHPEd 6.2 Tearing Alexander D. Tan, MD iv vi 1 18 33 38
53 67 73 88 98 107
115 120 146
7. Deviation and Displacement of the Eye 7.1 Strabismus Marissa N. Valbuena M.D., MHPEd 7.2 Proptosis Prospero Ma. C. Tuaño, MD 8. Special Topics 8.1 Retinoblastoma Rolando Enrique D. Domingo, MD 8.2 Ocular Manifestations of Systemic Diseases Romulo N. Aguilar, MD, PhD & Teresita R. Castillo, MD, MHPEd 8.3 Eyelid Malposisitons Franklin P. Kleiner, M.D. 8.4 Ocular Trauma and Emergencies Ma. Margarita L. Luna, MD, Marissa N. Valbuena M.D., MHPEd & Paulo Ma. N. Pagkatipunan, MD, MHA 8.5 Ocular Pharmacology Rosie R. Noche, MD
179 187 206 221
Romulo N. Aguilar, MD, PhD Clinical Associate Professor Department of Ophthalmology and Visual Science College of Medicine University of the Philippines Manila Ocular Manifestations of Systemic Diseases Norman M. Aquino, MD Clinical Associate Professor Department of Ophthalmology and Visual Science College of Medicine University of the Philippines Manila Glaaucoma Teresita R. Castillo, MD, MHPEd Clinical Associate Professor Department of Ophthalmology and Visual Science College of Medicine University of the Philippines Manila Eye Examination ; Uveitis and Scleritis ; Ocular Manifestations of Systemic Diseases Leo D. P. Cubillan, MD, MS Clinical Associate Professor Department of Ophthalmology and Visual Science College of Medicine University of the Philippines Manila Red Eye Raul D. Cruz, MD Clinical Associate Professor Department of Ophthalmology and Visual Science College of Medicine University of the Philippines Manila Disorders of the Optic Nerve Rolando Enrique D. Domingo, MD Clinical Associate Professor Department of Ophthalmology and Visual Science College of Medicine University of the Philippines Manila Retinoblastoma
Richard C. Kho, MD Clinical Associate Professor Department of Ophthalmology and Visual Science College of Medicine University of the Philippines Manila Physiology of the Eye Franklin P. Kleiner, MD Clinical Associate Professor Department of Ophthalmology and Visual Science College of Medicine University of the Philippines Manila Eyelid Malpositions Ruben LimBonSiong, MD Clinical Associate Professor Department of Ophthalmology and Visual Science College of Medicine University of the Philippines Manila Disorders of the Cornea Ma. Margarita L. Luna, MD Clinical Associate Professor Department of Ophthalmology and Visual Science College of Medicine University of the Philippines Manila Ocular Trauma and Emergencies Leonardo R. Mangubat, MD Associate Professor Department of Ophthalmology and Visual Science College of Medicine University of the Philippines Manila Cataract Juan Ma. Pablo R. Nañagas, MD, MPH, MSNA Professor Department of Ophthalmology and Visual Science College of Medicine University of the Philippines Manila Errors of Refraction
MD Clinical Associate Professor Department of Ophthalmology and Visual Science College of Medicine University of the Philippines Manila Ocular Trauma and Emergencies Rosie R. Noche. Salud. Villalon. Valbuena. Choroid and Vitreous Arnold T. MHPEd Associate Professor Department of Ophthalmology and Visual Science College of Medicine University of the Philippines Manila Anatomy of the Eye . Glaucoma . Tuaño. C. N. Ocular Trauma and Emergencies Pearl T. MD Clinical Associate Professor Department of Ophthalmology and Visual Science College of Medicine University of the Philippines Manila Tearing v . Tan.Paulo Ma. MD Clinical Associate Professor Department of Ophthalmology and Visual Science College of Medicine University of the Philippines Manila Ocular Symptomatology Alexander D. Strabismus . MD Professor Department of Ophthalmology and Visual Science College of Medicine University of the Philippines Manila Proptosisi Marissa N. Ocular Symptomatology . MD Clinical Associate Professor Department of Ophthalmology and Visual Science College of Medicine University of the Philippines Manila Ocular Pharmacology Prospero Ma. MD Associate Professor Department of Ophthalmology and Visual Science College of Medicine University of the Philippines Manila Disorders of the Retina. Pagkatipunan. MD.
the rest of the module will be problem based.Preface In the Organ System Integration Curriculum of the UP College of Medicine the medical student will have their first exposure to the field of Ophthalmology at Year Level IV. MHPEd July 2005 vi . Valbuena MD. These study materials will supplement the lectures the medical students will receive and will also help them in preparing for the small group discussions. covering the different eye problems that patients may present in the clinic. This series of self-instructional materials is organized in the same manner. Ocular Trauma and Emergencies and Ocular Pharmacology at the end of the series. small group discussions and practicum of skills in history taking and ocular examination. The Sensory Organs – Eye Module is a 4-day rotation consisting of didactic lectures. with additional topics of Ocular Manifestations of Systemic Diseases. Aside from the introductory lectures in Anatomy and Physiology of the Eye and Ocular History and Eye Examinations. Marissa N.
This module is an overview of the anatomy of the eye and the student is advised to read the references listed at the end of the module for more details.D. visual pathway and the central control of ocular movements is essential in understanding the eye diseases and other diseases which have ocular manifestations. Cornea 5. Conjunctiva 2. OBJECTIVES After the completion of this instructional material. Aqueous 8. MHPEd INTRODUCTION An understanding of the anatomy of the eye. Eyebrows 2. Uveal tract – iris. Describe the different parts of the eye and adnexae. 2. Ocular adnexae 1. the student is expected to 1. Lens 7. Orbit B. how patients can be evaluated and examined and how the different eye disorders manifest in patients. ciliary body. Extraocular muscles D. Eyelids 3. choroid 6.. Anterior chamber angle 9.ANATOMY OF THE EYE /1 ANATOMY OF THE EYE Marissa N. Sclera and episclera 4. Describe the functions of the parts of the eye and adnexae. orbit. INTENDED USERS This module was developed to provide the medical student with the background knowledge of the anatomy of the eye and adnexae. Valbuena M. this module will help the student understand how the eye functions. Tenon’s capsule 3. Vitreous C. CONTENT Outline : A. Together with the module on “Physiology of the Eye”. Retina 10. Eyeball 1. Orbital septum 1 .. PREREQUISITE KNOWLEDGE AND PREPARATION The materials discussed in this module is the prerequisite of all the subsequent modules.
Floor : maxillary bone. maxillary bone Fig 1. which serves as a barrier between the eyelid and the orbit. zygomatic bone 4. It is 30 cc in volume in adults and the eye occupies 20 % of the space and the muscles and fat accounts for the rest. Lid retractors 5. lacrimal bone. Orbital Walls 1. It is also related to the frontal sinus above. Orbital apex 2 . Medial wall : ethmoid. maxillary sinus below and the ethmoid and sphenoid sinuses medially. Optic nerve ORBIT The orbit is a pear shaped structure with the optic nerve as its stem. Roof : frontal bone. Orbital walls Orbital Apex The orbital apex is the entry site of all the nerves and blood vessels to the eye and all the extraocular muscles except the inferior oblique Fig 2. Lacrimal Comples E.ANATOMY OF THE EYE /2 4. The orbit is limited anteriorly by the orbital septum. frontal bone. sphenoid bone 2. Lateral wall : sphenoid bone. zygomatic bone 3.
episclera.ANATOMY OF THE EYE /3 Blood Supply A. and develops after the 2nd or 3rd month of life. CONJUNCTIVA The conjunctiva is a thin transparent mucous membrane consisting of 2 parts 1. Central retinal artery 2. limbus and conjunctiva and contribute to the major arterial circle of the iris. The 2 long posterior ciliary arteries anastomose with each other and with the anterior ciliary arteries to form the major arterial circle of the iris. Long posterior ciliary arteries – supplies the ciliary body. The accessory lacrimal glands (glands of Krause and Wolfring) located in the stroma resemble the lacrimal gland in structure and function. TENON’S CAPSULE The Tenon’s capsule is a fibrous membrane covering the globe from the limbus to the optic nerve At the limbus. This provides a direct communication between the skin of the face and the cavernous sinus. The conjunctival arteries are derived from the anterior ciliary and palpebral arteries and anastomose freely. The conjunctiva is innervated by the ophthalmic (first) division of the trigeminal nerve. Bulbar conjuctiva – is loosely attached to the orbital septum in the fornices and is folded many times. The ophthalmic veins communicate with the cavernous sinus. The skin of the periorbital region drain to the angular vein. 2. 4. Conjuctival stroma has an adenoid (superficial) layer and a fibrous (deep) layer. The conjuctival lymphatics with the lymphatics of the eyelids form a rich lymphatic plexus. into which drains the vortex veins. Muscular branches to the muscles – continue to form the anterior ciliary arteries and supply the sclera. Short posterior ciliary arteries – supply choroid and part of the optic nerve 6. The basal epithelial cells are deeper and may contain pigments near the limbus. Lacrimal artery – supplies lacrimal gland and upper eyelid 3. Palpebral conjunctiva – lines the posterior surface of the eyelid and is adherent to the tarsus. The semilunar fold is a thickened fold of bulbar conjunctival at the inner canthus and corresponds to the nictitating membrane of lower animals. Conjunctival epithelium – consists of 2-5 layers of stratified columnar epethelial cells. and to the supraorbital and supratrochlear vein branches of the superior ophthalmic vein. Posteriorly the inner surface of the Tenon’s capsule lies against the sclera and the outer aspect lies in contact with the orbital fat and structures within the extraocular muscle cone. Arterial Supply : Ophthalmic Artery (branch of internal carotid artery) 1. Tenon’s capsule and the episclera are fused together. 2. This allows the eye to move and enlarge the secretory conjunctival surface. The adenoid layer contains lymphoid tissue and ‘follicle-like” structures without germinal centers. 5. The fibrous layer is composed of connective tissue that attaches to the tarsus and is loosely arranged over the globe. 2. EYEBALL 1. The conjunctiva has the following layers: 1. Conjuctival veins follow the arterial pattern. Venous Drainage : Superior and inferior ophthalmic veins. The superficial epithelial cells consists of mucous secreting goblet cells. Medial palpebral arteries to both eyelids B. anterior ciliary veins and the central retinal vein. At the point where Tenon’s capsule is pierced by the tendons 3 . the conjuctiva.
composed of intertwining lamellae of collagen fibrils that run parallel to the surface of the cornea and because of their size and proximity are optically clear. Cell loss occurs with age and injury.6 mm thick. the episclera. upon which the globe rests. 3.75 mm) is slightly bigger than its vertical diameter (10. SCLERA AND EPISCLERA The sclera is the fibrous outer layer of the eye consisting mainly of collagen. Epithelium : 5-6 layers of cells. which contains blood vessels that nourish the sclera. Its horizontal diameter (11. Endothelial repair occurs with cell enlargement and sliding of existing cells with minimal capacity for cell division. Inferiorly.3 mm). continuous with the epithelium of the bulbar conjunctiva 2. These fascial reflections become continuous with the fascia of the muscles and the fused fascia send out expansions to the surrounding structures and to the orbital bones called check ligaments.65 mm) than at the center (0. Stroma : 90 % of corneal thickness. 4. Descemet’s membrane : basal lamina of corneal endothelium 5. the Tenon’s capsule fuse with the fascia of the inferior rectus and inferior oblique to form the suspensory ligament of Lockwood. It is dense and white and continuous with the cornea anteriorly and the optic nerve dural sheath posteriorly.6 mm) There are 5 layers of the cornea : 1. The outer layer of the anterior sclera is covered with a thin layer of fine elastic tissue. it sends out tubular reflections around each of the muscles. The lamellae run within the ground substance of hydarated polyglycans in association with the keratocytes that produce the collagen and ground substance. Endothelium : single layer of cells . a modified portion of the stroma. It is thinnest at the insertion of the recti mucles (0. Cross section of the eye 4. responsible for maintaining the deturgescence of the cornea and failure of function leads to corneal edema. CORNEA The cornea is a transparent tissue inserted to the sclera at the limbus. Fig 3. elsewhere it is 0. Fig 4.ANATOMY OF THE EYE /4 of the extraocular muscles. 3. It is thicker at the periphery (0. Cross section of the cornea 4 .52 mm). Bowman’s membrane : clear acellular layer.
The iris lies in contiguity with the anterior surface of the lens. influencing its pore size 3. A. The ciliary processes are composed mainly of large fenestrated capillaries and veins that drain to the vortex veins. The papillary size is determined by the balance between constriction due to parasympathetic activity via the oculomotor nerve and dilation due to sympathetic activity. The ciliary processes produce the aqueous. The 2 layers of the ciliary epithelium are the internal non pigmented layer (representing the anterior extension of the neuroretina) and the external pigmented layer (representing the RPE). 2. Pars plana – 4 mm . The transparency of the cornea is due to its uniform structure. and deturgescence. The iris capillaries are non fenestrated. UVEAL TRACT The uveal tract is composed of the iris . circular and radial fibers. avascularity. both of which contains aqueous humor. IRIS Is a flat surface with a central opening. 2. The sensory nerves of the cornea is from the ophthalmic division of the trigeminal nerve. flattened posterior zone The ciliary muscle is composed of longitudinal. dividing the anterior chamber from the posterior chamber. Longitudinal fibers : insert to the trabecular meshwork. The superficial cornea gets most of its oxygen from the tears. The pupil controls the light entering the eye. The 2 pigmented posterior layers of the iris represent anterior extensions of the neuroretina and the retinal pigment epithelium (RPE). CILIARY BODY The ciliary body consists of 2 zones 1. Sensory supply is from fibers of the ciliary nerve. Circular fibers: contraction and relaxation of the zonular fibers alters the capsule of the lens thus giving variable focus for far and near objects of fixation. 5 . Pars plicata : 2 mm wide. B. The blood supply of the iris is from the major circle of the iris. Within the stroma of the iris are the sphincter and dilator muscles.ANATOMY OF THE EYE /5 The cornea gets its nutrition from the vessels of the limbus. 6. the aqueous and the tears. the pupil. 1. ciliary processes arise from this zone. Radial fibers The blood supply of the ciliary body is from the major circle of the iris and the nerve supply is from the ciliary nerves. It is the middle vascular layer of the eye and contributes to the blood supply of the retina. the ciliary body and the choroid.
LENS The lens is a biconvex. The lens capsule is a semi-permeable membrane (to water and electrolytes). The internal portion of the choroidal vessels is called the choriocapillaries. the subepithelial lamellar fibers are continuously produced. gradually making the lens larger and less elastic. It is suspended behind the iris by the zonules which connects it with the ciliary body. The choroid nourishes the outer portion of the retina.lar supply of the eye C. 4 mm thick and 9 mm in diameter. A subcapsular epithelium is present anteriorly. located between the retina and the sclera.ANATOMY OF THE EYE /6 Fig 5. avascular clear structure. Anterior to the lens is the aqueous and posterior to it is the vitreous. one in each posterior quadrant. Blood from the choroidal vessels drain via 4 vortex veins. CHOROID The choroid is the posterior portion of the uveal tract. Vascu. Fig 6. The lens nucleus is harder than the cortex. With age. Cross section of the choroid 7. 6 .
Some aqueous passes between the bundles of the ciliary body and through the sclera (uveoscleral pathway). The trabecular meshwork is triangular in cross section with the base directed to the ciliary body. to which the ciliary body and the iris are attached. Fig. pyruvate and lactate and lower concentrations of protein. Its volume is about 230 µL and its rate of production which is subject to diurnal variation is 2.ANATOMY OF THE EYE /7 The lens consists of 65 % water and 35% protein and minerals. 9. the aqueous pass through the pupil to go to the anterior chamber and then to the trabecular meshwork. Its main anatomic features are Schwalbe’s line. The Schwalbe’s line corresponds to the termination of the corneal endothelium. From the posterior chamber. ANTERIOR CHAMBER ANGLE The anterior chamber angle lies at the junction of the periphearal cornea and the root of the iris. pain fibers of nerves in the lens. Its composition is similar to plasma except for higher concentration of ascorbate. urea and glucose. The scleral spur is an inward extension of the sclera between the ciliary body and the Schlemm’s canal. Magnified view of a section of the lens showing lens capsule and epithelium 8.5 µL/ min. to the Schelemm’s canal and into the venous system. AQUEOUS The aqueous is a clear fluid that fills the anterior and posterior chambers of the eye. I is composed of perforated sheets of collagen and elastic tissue with decreasing pore size as the canal of Schlemm is approached. The longitudinal muscles of the ciliary body insert into the trabecular meshwork. Aqueous is produced by the ciliary epithelium. 7. 7 . trabecular meshwork ( which overlies the Schlemms’s canal) and the scleral spur. There are no blood vessels.
In the center of the macula is the fovea. The outer surface of the retina is apposed to the retinal pigment epithelium (RPE). amacrine and horizontal cells 6. inner nuclear layer – cell bodies of the bipolar. external limiting membrane 9. inner plexiform layer – connections of the ganglion cells with the amacrine and bipolar cells 5. It extends anteriorly as the ora serrata. outer plexiform layer – connections of the bipolar and horizontal cells with the photoreceptors 7. the retina and RPE are easily separated to form a subretinal space. Anterior chamber angle 10.1 mm thick at the ora serrata and 0. retinal pigment epithelium (RPE) – The inner layer of the Bruch’s membranes is actually the basement membrane of the RPE The retina is 0. 8 . ganglion cell layer 4. multilayered sheet of neural tissue that lines the inner aspect of the posterior 2/3 of the wall of the eye. Histologically. and the thinnest part of the retina. the fovea is characterized by thinning of the outer nuclear layer and the absence of the other parenchymal layers. clinically seen as a depression and corresponds to the “foveal reflex”.ANATOMY OF THE EYE /8 Fig 8. It corresponds to the retinal avascular zone of fluorescein angiography. and diseases that can lead to accumulation of fluid causes thickening of this area. nerve fiber layer – ganglion cell axons passing to the optic nerve 3. such as occurs in retinal detachment. In the center of the posterior retina is the macula. outer nuclear layer – cell nuclei of photoreceptors 8. Except at the disc and the ora serrata. in which the photoreceptors are all cones. The normally empty extracellular space of the retina is potentially greatest at the macula. internal limiting membrane 2. semi-transparent. All these histologic features provide for fine visual discrimination.56 mm thick at the posterior pole. phototreceptor layer – rod and cones inner and outer segments 10. It is clinically seen as a 3 mm area of yellowish pigmentation (due to xanthophylls pigments) and bounded by the temporal vascular arcades. The foveola is the most central portion of the fovea. The inner layer of the retina is apposed to the vitreous The 10 layers of the retina. RETINA The retina is a thin. from the inner aspect are the following: 1.
The endothelium of the choroidal vessels is fenestrated. which forms the inner blood-retinal barrier. Macula 9 . The outer blood-retinal barrier lies at the level of the RPE.ANATOMY OF THE EYE /9 Fig 9. Fig 10. Layers of the retina The retina receives its blood supply from 1. The retinal blood vessels have a nonfenestrated endothelium. central retinal artery – supply the inner 2/3 of the retina The fovea is supplied entirely by the choriocapillaries and is susceptible to irreparable damage when the macula is detached. choriocapillaries – supply outer third of retina. from outer plexiform layer to RPE 2.
The base of the vitreous maintains a firm attachment through out life with the pars plana epithelium and the retina immediately behing the ora serrata. The hyaloid membrane. The superior oblique is the longest and thinnest of the extraocular muscles. insertion. Diagram of the layers of the retina in the area of the macula 11. 10 . the outer surface of the vitreous is in contact with the posterior lens capsule. It fills the space bounded by the lens. The attachment to the lens capsule and the optic nerve head is firm early in life but soon disappears. The inferior oblique originates from the nasal side of the orbital wall and is the only extraocular muscle that does not originate from the apex of the orbit. action and innervation of the extraocular muscles. retina and optic disc.ANATOMY OF THE EYE /10 Fig 11. avascular body. The vitreous is 99% water. superior and inferior aspect of the eye. retina and optic nerve head. lateral. Collagen and hyaluronic acid makes the vitreous gel like because of their ability to bind large amounts of water. pars plana epithelium. zonules. VITREOUS The vitreous is a clear. comprising 2/3 of the volume and weight of the eye. Histophotograph of the retina at the area of the macula Fig 12. Table 1 below summarizes the origin. EXTRAOCULAR MUSCLES The 4 recti muscles originate from the annulus of Zinn at the apex of the orbit and are named after their insertion at the sclera on the medial.
EYEBROWS The eyebrows are folds of thickened skin covered with hair. OCULAR ADNEXA 1.5 mm from medial limbus 6.7 mm from superior limbus 6. The lateral retus and inferior obliques are also supplied by the branches from the lacrimal artery and infraorbital artery respectively.ANATOMY OF THE EYE /11 Muscle Medial rectus (MR) Lateral rectus (LR) Superior rectus (SR) Inferior rectus (IR) Superior oblique (SO) Inferior oblique (IO) Origin Annulus of Zinn Annulus of Zinn Annulus of Zinn Annulus of Zinn Orbit apex above Annulus of Zinn (functional origin at trochlea) Behind lacrimal fossa Insertion 5. The glabella is the hairless prominence in between the eyebrows. 11 . Extraocular Muscles Fig 13.9 mm from lateral limbus 7.5 mm from inferior limbus Posterior equator at superotemporal quadrant Posterior to the equator in inferotemporal quadrant Direction of pull 90 ° 90° 23° 23° 51° Action from Primary Position Adduction Abduction Elevation Intorsion Adduction Depression Extorsion Adduction Intorsion Depression Abduction Extorsion Elevation Abduction Innervation Cranial Nerve III VI III III IV 51° III Table 1. showing the insertion of the recti muscles to the sclera The blood supply to the extraocular muscles is from the musclular branchs of the ophthalmic artery. Spiral of Tillaux.
open onto hair follicles at the base of eyelashes c. Blinking helps spread the tear film. few hair follicles and no subcutaneous fat. Areolar tissue – under the orbicularis oculi. Fig 14. Palpebral conjunctiva – adheres firmly to tarsal plate Lid Margin – free lid margin is 25-30 mm long and 2 mm wide. 2. 4. elastic. carry tears through the canaliculus to the lacrimal sac. Skin – thin. open in a row near the base of the eyelashes 2. Posterior margin – in close contact with the globe . small elevation with a central opening . Tarsal plates – dense fibrous tissue layer . medial portion of the eyelids 12 . Lacrimal punctum – at the medial end of posterior margin of the lid . It is innervated by the facial nerve. Layers of the eyelids 1. loose. along margins are the small orifices of the meobomian glands (modified sebaceous glands) 3. Glands of Moll – modifies sweat glands . Anterior margin a. keeping the cornea and conjunctiva wet. It is divided by the gray line (mucocutaneous junction) into anterior and posterior margin. 1. main support of the eyelids 5.ANATOMY OF THE EYE /12 2. Glands of Zeis – modified sebaceous glands . EYELIDS The upper and lower lids (palpebrae) are folds of skin that can close to protect the anterior portion of the eye. Eyelashes b. 3. Orbicularis oculi muscle – Circular muscle fibers surround the palpebral fissure which functions to close the eyelids. Lid margin. communicates with the subaponeurotic layer of the scalp.
Lacrimal gland . Canaliculi D.ANATOMY OF THE EYE /13 Fig 15. has orbital portion and palpebral portion B. Cross-section of the eyelids 4. lacrimal nerve (sensory). ORBITAL SEPTUM The orbital septum is the fascia behind the portion of the orbicularis muscle that lies between the orbital rim and the tarsus. Inferior tarsal muscle 6. a branch of the trigeminal first division b. Nasolacrimal duct. Inferior rectus muscle 2. Muller’s muscle (superior tarsal muscle) B. Lymphatics drain into preauricular lymph nodes. have striated and smooth muscle components A. Nerve supply to the lacrimal gland is by a.drains out to the nasal cavity Blood supply of the lacrimal gland is from the lacrimal artery and venous blood drain to ophthalmic vein. Accessory lacrimal glands of Krause and Wolfring – located in the sustantia propria of palpebral conjunctiva C. Lower lid 1. Upper lid 1. LID RETRACTORS The lid retractors are responsible for opening the eyelids. Levator palpebrae superioris 2. great superficial petrosal nerve (secretory) c. Lacrimal sac E. It serves as a barrier between the lid and the orbit 5. LACRIMAL COMPLEX A. sympathetic nerves 13 .
intracranial portion. 1. synapse in the lateral geniculate body on neurons whose axons terminate in the visual cortex of the occipital lobe b. The optic nerve sheath is continuous with the meninges. pupillary fibers – 20% . located within the muscle cone c. do not regenerate if severed.5 mm in diameter b. bypass the geniculate body en route to the pretectal area. 25-30 mm long.10 mm long. intracanalicular portion – 4-9 mm long d. Optic nerve Fibers of the optic nerve consist of a. Lacrimal drainage system OPTIC NERVE The trunk of the optic nerve consists of about 1 million axons arising from the ganglion cells of the retina a. orbital portion – 3 mm in diameter.ANATOMY OF THE EYE /14 Fig .16. The ganglion cells of the retina and their axons are part of the central nervous system and as such. 14 . visual fibers – 80%. and with the opposite optic nerve joins to from optic chiasm Fig 17. intraocular portion – optic nerve head .
ANATOMY OF THE EYE /15
The surface layer of the optic disc receives blood from the branches of the retinal arterioles. The rest of the nerve in front of the lamina cribrosa is from the peripaillary choroidal vessels. At the region of the lamina cribrosa, the blood supply is from the short posterior ciliary arteries. Retrolaminar nerve receive blood from branches of the central retinal artery. The rest of the introrbital portion, intracnalicular and intracranial portions are supplied by pial vessels from branches of ophthalmic artery and other branches of the internal carotid artery.
Fig 18. Cross-section of the optic nerve
Fig. 19 Blood supply of the optic nerve
ANATOMY OF THE EYE /16
SUMMARY An understanding of the anatomy of the eye, ocular adnexae, orbit, visual pathways and the cranial nerves is important in the proper diagnosis of ocular diseases and other disorders with ocular manifestations. REFERENCES 1. Duane, Thomas and Jaeger, Edward . Clinical Ophthalmology, Philadelphia : Harper and Row , latest edition 2. Riordan-Eva, Whitcher, John. Vaughn and Ashbury’s General Ophthalmology , 16th Edition, New York: Lange Medical Books/ McGraw Hill, 2004 3. Scheie, Harold, Albert, Daniel. Textbook of Ophthalmology, Philadelphia : W.B. Saunders Co, latest edition 4. Selected images from the lecture of Leonardo Mangubat, Anatomy of the Eye and Adnexae, SELF-TEST 1. Decrease in aqueous production can best be achieved by destruction of which part of the eye? A. Pars plicata B. Choroid C. Iris D. Pars plana 2. Which one of the following rectus muscle tendons inserts on the sclera farthest from the corneal limbus? A. superior rectus B. inferior rectus C. medial rectus D. lateral rectus 3. The levator palpebrae is innervated by what nerve A. III B. IV C. V D. VII 4. The following structures are part of the medial orbital wall, EXCEPT A. ethmoid bone B. lacrimal bone C. maxillary bone D. sphenoid bone 5.What layer of the retina does the the choriocapillary supply with oxygen? A. ganglion cell layer B. nerve fiber layer C. photoreceptors D. inner nuclear layer
ANATOMY OF THE EYE /17
6.Which of the following statements regarding the cornea is FALSE ? A. The corneal endothelium is important in maintaining corneal dehydration. B. The water content of the cornea is less than that of the sclera. C. Normal central corneal thickness is 1.00 mm D. Corneal diameter is greater horizontally than vertically. 7. Which is not a layer of the eyelid ? A. Skin B. Conjunctiva C. Tenon’s capsule D. Orbicularis muscle E. Tarsus 8.The following structures must maintain their clarity in order good vision EXCEPT A. Cornea B. aqueous C. lens D. vitreous E. choroid 9. The optic nerve consists of axons from what cells in the retina? A. amacrine cells B. bipolar cells C. ganglion cells D. photoreceptor cells 10. Which muscle is an adductor? A. medial rectus B. lateral rectus C. superior oblique D. inferior oblique ANSWERS TO SELF-TEST 1. A 2. A 3. A 4. D 5. C 6. C 7. C 8. E 9. C 10. A .
PHYSIOLOGY OF THE EYE /18
PHYSIOLOGY OF THE EYE Richard C. Kho, M.D.
This self-instructional material (SIM) is designed to help the medical student acquire an overview of the biophysical elements at work within (and outside) the human eye, for the latter to function as a sense organ subserving vision. Understanding basic concepts of light energy, its “transformation” in the human eye, its conversion to nerve impulses and eventual visual perception, is a pre-requisite to effective diagnosis and subsequent management of eye diseases.
Upon completion of this SIM, the student should be able to discuss the following :: 1. The physical properties of light 2. The processes involved as soon as light strikes the human eye 3. The internal bending of light as it focuses on the retina, i.e., optics and refraction in the human eye 4. Retinal processes which transform light energy that result in visual perception 5. Basic neuro-anatomic architecture of the visual pathway, as well as topographical localization of lesions
PREREQUISITE KNOWLEDGE AND PREPARATION
Students should have a working knowledge of the basic anatomy of the human eye. A general knowledge of the neuro-anatomy of the afferent visual pathways would likewise be useful.
This SIM was prepared for the medical student just embarking on the study of the anatomy and physiology of the human eye. It does not aim to supplant ophthalmology textbooks which provide a more detailed discussion of advanced concepts in optics and refraction, retinal physiology, and neuro-ophthalmology.
This module is divided into two parts: PART I: The Eye as an Optical Instrument A. Physical Optics -The physical properties of light B. Geometric Optics -The process in which external light energy is focused on the retina PART II: The Eye as a Sense Organ C. Physiologic Optics -The biochemical and functional processes that occur in the retina to produce visual energy
PHYSIOLOGY OF THE EYE/ 19
D. Psychologic Optics or Neuro-Ophthalmologic Optics -The conduction of visual energy to the occipital visual center PART I: The Eye as an Optical Instrument A. Physical Optics
Light is the basic stimulus for vision. This comprises only a small portion of the electromagnetic spectrum of
Fig 1. The Electromagnetic Spectrum
This small portion, called the visible spectrum, is the ONLY portion of the spectrum that can stimulate the photoreceptors of the human retina. It extends from 380 micra (3800 angstrom units) to 760 micra (7600 angstrom units). Right after the UV spectrum (violet), the wavelength of each color increases as it moves toward the direction of infrared rays (red). There are 3 Important Characteristics of Light: 1) Velocity or Speed -3 X 1010 cm/sec in vacuum; slower in clear air and in denser media. 2) Wavelength -size determines the color; with violet (380µ ) the shortest, and red (760µ ) the longest.
Fig 2. Wavelength
3) Frequency -number of complete cycles moving past a specific point over a given period of time. *Velocity = Wavelength X Frequency
PHYSIOLOGY OF THE EYE/ 20
PART I: The Eye as an Optical Instrument B. Geometric Optics This process, in-between physical optics and physiologic optics, comprise of events that occur from the moment light strikes the eye, and eventually gets focused on the retina. Its principal basis is the transmission and bending of the direction of travel of light rays, i.e., REFRACTION. Refraction of Light As light passes through a transparent solid or liquid media, it slows down depending on the density of the media. The relative unit of measurement of this capacity is called the index of refraction. The Refractive Index (n) is a constant depending on the material; it determines the angle of deviation. air = 1.0 water = 1.33 glass > 1.40 It is simply a relative unit compared to air. As light passes from one medium to another of a different index of refraction and at a certain angle, there is bending of light, i.e. light is Refracted.
Fig 3. Refraction of Light
Prism Any media whose 2 sides are not parallel will refract light rays ---- light is deviated towards the base of the prism. apex
Fig.4 Prismatic Effect on Light
PHYSIOLOGY OF THE EYE/ 21
Basis of Lenses Lenses can be viewed as a certain arrangement of prisms (remember that light is deflected towards the base of the prism). A converging lens (positive lens) can be thought of as two prisms joined at the base, while a diverging lens (negative lens) can be thought of as two prisms joined at the apex.
Fig 5. Converging and Diverging Lenses
Power of the Lens A Diopter is a unit of measurement of lens power. It is a measure of convergence or divergence, and a reciprocal of focal distance. The power of the lens depends on its curvature and the difference in refractive indices. The Eye Can be thought of as a series of lenses whose main goal is to focus light rays from the external world unto the retina: – cornea – aqueous – lens – vitreous The average human eye has a total converging power of about 60 diopters. The main refractive components are as follows: Cornea ~ +40 Diopters Lens ~ +20 Diopters
Emmetropia is a condition wherein parallel light rays fall into a pinpoint focus on the retina.
Fig 6. Emmetropia: Light is focused ON the retina 21
PHYSIOLOGY OF THE EYE/ 22
Ammetropia is a condition wherein parallel light rays DO NOT fall into a pinpoint focus on the retina:
•Myopia •Hyperopia •Astigmatism
Myopia, commonly known as “nearsightedness”, is a condition wherein parallel light rays focus at a point in front of the retina. It can be axial (eyeball longer than average) or refractive (corneal curvature steeper than average).
Fig 7. Myopia: Light is focused IN FRONT OF the retina
To Correct Myopia, one would need a divergent lens (“negative” or biconcave lens to neutralize the convergent effect of the myopic eye) in order to focus light rays on the retina.
Fig 8. A Negative Lens “pushes back” the image unto the retina Hyperopia, commonly known as “farsightedness”, is a condition wherein parallel light rays focus at a point behind the retina. It can be axial (eyeball shorter than average) or refractive (corneal curvature flatter than average).
Fig 9. Hyperopia: Light is focused BEHIND the retina
one image on the retina. Compound Myopic . Fig 10. Simple Myopic .both images at the back of the retina 5. Contact lenses • soft. To correct astigmatism.both images in front of the retina 4.The front curvature of two different balls illustrate the difference in the curvature of spherical corneas (basketball) vs. which in turn increases the lens curvature (lens thickens). Presbyopia With aging (around 40 years old). Compound Hyperopic .one image on the retina. • multifocal 3.one image in front of the retina. 23 . astigmatic corneas (football). One can imagine that the curvature of the eye in astigmatism resembles one side of a football. one image at the back of the retina Correction of Ammetropia: 1. one image behind the retina 3. and thereby increasing its converging power. one would need a convergent lens (“positive” or biconvex lens) in order to focus light rays on the retina. Mixed Astigmatism . parallel light rays focus on 2 separate lines or planes. one would need cylindrical lenses (lenses each with power in two different meridians/axes) spherical astigmatic Fig 11. the brain sends out signals to contract the smooth muscles of the ciliary body. Refractive Surgery • PRK (photorefractive keratectomy) • RK (radial keratotomy) • LASIK (laser-assisted in situ keratomilieusis) Principle of Accommodation To focus on a nearby object. this enables the zonules to loosen up. hard. Spectacles 2. Here. one image in front of the retina 2. rigid gas permeable. One would need “plus lenses” (presbyopic glasses/reading adds) to make up for the lost automatic focusing power of the lens. etc. Simple Hyperopic . there is loss of focusing or accommodative power of the human eye.PHYSIOLOGY OF THE EYE/ 23 To Correct Hyperopia. A Positive Lens “pulls frontward” the image unto the retina Astigmatism is a condition wherein the curvature of the cornea or of the lens is not the same in different meridians. Types of Astigmatism: 1. instead of a basketball (in eyes without astigmatism).
Physiologic Optics The Human Retina is a thin. it must be absorbed by the visual pigments located at the outer segments of the rods and cones. it is split into cis-retinal (cis-retinene) and opsin after passing through a series of orange intermediate compounds (lumirhodopsin.PHYSIOLOGY OF THE EYE/ 24 PART II: The Eye as a Sense Organ C. etc). The young. plus a protein called opsin. a cis-retinal and a trans-retinal structure. the latter has to be converted into the biochemical energy of the visual nerve impulse. metarhodopsin. etc. is split into two to form molecules of Vitamin A in the form of an alcohol. 24 . Iodopsin. Two major events occur with the split of rhodopsin: 1) A sudden reduction of sodium influx through the photoreceptor plasma membrane together with increased permeability of the membrane to calcium ions result in a relative hyperpolarization of the plasma membrane and initiates an electrical/nerve impulse. adult retina contains approximately 120 million rods. These visual pigments (rhodopsin. multilayered sheet of neural tissue that lines the inner aspect of the posterior 2/3 of the wall of the globe. Only the cis-retinal isomer combines with opsin to form rhodopsin.) are lipid-protein complexes of a fat-soluble aldehyde of Vitamin A. semi-transparent. Photochemistry of Vision When light strikes rhodopsin. A molecule of its precursor (beta-carotene) derived from plants. Fig 12. Vitamin A occurs in two forms (isomers). Layers of the Human Retina The human retina is capable of perceiving the following visual senses: •Light sense •Form sense •Color sense Light Sense: The Role of Visual Pigments For the eye to perceive light. and about 6million cones. First. Vitamin A occurs only in animal tissue.
Minimum Visual Angle Experimentally. i. This combination also releases energy which is utilized in the oxidation of retinol (Vit A-alcohol) to retinal (Vit A-aldehyde or retinene). it is the minimum amount of separation between two light sources at a given distance from the eye so that they can still be seen as two. It determines the acuity of vision.. The Photochemistry of Vision Form Sense: Visual Acuity Form sense discriminates between stimuli. Minimum Visual Angle • The big “E” on the Snellen Chart subtends an angle of 5 minutes Fig 15. Simply put. as soon as it is formed combines with opsin to form the stable product rhodopsin. Cis-retinal.e. the smallest detectable line subtends one minute of arc. Fig 13. 25 . Fig 14.PHYSIOLOGY OF THE EYE/ 25 2) The transformation of cis-retinene to trans-retinene releases energy. These two lights subserve an angle at the nodal point of the eye called the minimum visual angle. Trans-retinal is reconverted to cis-retinal by the action of the retinene isomeraze enzyme with energy provided by the DPNH2-DPN dehydrogenase system. to see two stimuli separately as two instead of fusing them into one. The Snellen E and its corresponding visual angles.
Fig 18. Construction of the Snellen Chart for consistency One usually measures visual acuity at 20ft (6m) and is recorded as two numbers: The numerator represents the distance between chart and patient. For example.The Color Spectrum 26 . what a normal (emmetropic) eye can read at 40ft. E FP TOZ LPED PECFD EDFCZP FELOPZD DEFPOTEC Feet 20/200 20/100 20/70 20/50 20/40 20/30 20/25 20/20 Meters 6/60 6/30 6/21 6/15 6/12 6/9 6/7. a visual acuity of 20/40 simply means that the patient’s eye can only read from 20 ft. while the denominator represents the smallest row of letters that the patient’s eye can read. Recording Visual Acuity Using the Snellen Chart Color Sense: A Function of the Cone Photoreceptors White light or sunlight is a composite of different colors corresponding to each wavelength in the visible spectrum.5 6/6 Fig 17 and Table 1.PHYSIOLOGY OF THE EYE/ 26 Testing Visual Acuity using the Snellen Chart •Letters are constructed so that they subtend the same visual angle when viewed at distances of up to 200ft Fig 16.
all photo pigments are present except for a relative deficiency of one color---an “anomaly”. –Deuteranomalous (green anomaly) –Protanomalous (red anomaly) –Trianomalous (blue anomaly) • In Dichromats. all 3 colors are present but has a relative deficiency in one. Neuro-ophthalmic Optics Basic Concepts Monocular vision. recessive pattern of inheritance. both retinas send the same visual impressions to the visual cortex. True color blindness (total absence of one type of photo pigment or color-sensitive cone) is rare. It has a sex-linked. Most of the time. is a less-advanced form of visual function wherein visual impressions from one side cross-over to the contralateral cerebral cortex completely (there is complete decussation). As a result. Fig 19.PHYSIOLOGY OF THE EYE/ 27 Color Blindness “Color blindness” occurs in about 10% of all males and about 1% of all females. Visual Pathway in Monocular Vision In Binocular vision. seen in lower vertebrates. there is total loss of one color pigment –Deuteranopes (no green) –Protanopes (no red) –Trianopes (no blue) Monochromats or Cone Monochromats (atypical) have only one color pigment Achromats or Rod Monochromat (typical) are totally color blind. there is nasal (partial) decussation of fibers from the two sides. • • PART II: The Eye as a Sense Organ D. • In Trichromats. 27 .
.e. the left visual pathway until its termination in the left occipital lobe. From the external world. In addition. all the way to its end terminal. The Afferent Visual Pathway Note that the visual field and the retina are optically inverted. i. Vertically. Visual Pathway in Binocular Vision Stereopsis or depth perception is possible only with binocular vision Neuro-anatomic Pathways These are structures which perceive. the following are its components: • • • • • • • Eye (retina) Optic Nerve (CN II) Chiasm Optic Tract LateralGeniculate Nucleus (LGN) Optic Radiation Striate Cortex Fig 21. 28 . there is direct one-to-one correspondence between visual direction in space and retinal location. the right visual fields (both the right field of right eye and the right field of left eye) are projected to the left hemi-retina of both eyes and. and this logical architecture is the basis for localization of lesions in the visual pathway via visual field testing (perimetry). and process visual information. relay. This retino-topic organization is preserved throughout the entire visual pathway. visual field and retinal projections follow a similar pattern of optical inversion.PHYSIOLOGY OF THE EYE/ 28 Fig 20. retrochiasmally.
Right Superior Homonymous Quadrantanopia (“pie in the sky”) left optic radiation (parietal lobe). E. and eventual diagnosis of many intracranial lesions. A. Location of lesion with corresponding visual field defects left optic nerve – central scotoma/generalized depression of the left eye optic chiasm. G. Fig 22.bitemporal hemianopia left optic chiasm (lateral aspect). B. D. C.left nasal hemianopia left optic tract.Right Homonymous Hemianopia SUMMARY •PART I: The Eye as an Optical Instrument A. localization. Geometric Optics • refractive index (n) • prisms • lenses (converging and diverging) • emmetropia • ammetropia 29 . F.Right Homonymous Hemianopia left optic radiation (temporal lobe).Right Inferior Homonymous Quadrantanopia (“pie on the floor’) left occipital lobe (visual/striate cortex).PHYSIOLOGY OF THE EYE/ 29 Understanding the neuro-anatomy of the visual pathway is the key to effective evaluation. Physical Optics • 3 properties of light: 1) velocity 2) wavelength 3) frequency B.
Hitchings RA. 4) Goldberg S. 6) Selected Images from http://www. 2nd ed. Asbury T. 1994. Clinical Neuroanatomy Made Ridiculously Simple. Appleton and Lange.ph 30 . McGraw-Hill Book Company. 13th ed. London: Wolfe Publishing. 1980. Riordan-Eva P. Psychologic Optics or Neuro-Ophthalmologic Optics • monocular vision • binocular vision • neuroanatomy of the afferent visual pathway o lesions and corresponding visual field defects REFERENCES 1) Espiritu RB.PHYSIOLOGY OF THE EYE/ 30 myopia hyperopia astigmatism simple myopic simple hyperopic compound myopic compound hyperopic mixed astigmatism correction of ammetropia o spectacles o contact lenses o refractive surgery o o o • •PART II: The Eye as a Sense Organ C.com. General ophthalmology. Atlas of Clinical Ophthalmology. Miami: Medmaster Inc. 2) Vaughan D. Ophthalmologic Optics. editors. Technique Of The Neurologic Examination: A Programmed Text. 1979. 3) Spalton DJ. 2001. Physiologic Optics • light sense: role of visual pigments o photochemistry of vision • form sense: visual acuity o minimum visual angle o testing visual acuity with the Snellen Chart • color sense: a function of photoreceptors o color blindness Trichromat Dichromat Monochromat Achromat D.eyecenter. 3rd ed. editors. Hunter PA. Manila: Department of Ophthalmology and Visual SciencesUP-PGH Medical Center. 1992. 5) DeMyer W.
one would need which lens? A. on the retina ___B. orange D.PHYSIOLOGY OF THE EYE/ 31 SELF TEST 1. To correct astigmatism. aqueous 5. behind the retina 6. vitreous D. Match the following refractive states in reference to the location of the image relative to the retina. simple hyperopic C. which of the following colors has the shortest wavelength? A. Which type of astigmatism has both images focused at the back of the retina? A. simple myopic B. myopia 1. to one of lower refractive index? A. in front of the retina ___C. True or False? A diverging (negative) lens can be thought of as 2 prisms with the bases adjacent. diverging (negative) lens B. mixed astigmatism 31 . diverging (negative) lens B. converging (positive) lens D.. slows down B. 4. is dissipated 3. lens B. blue B. compound hyperopic E. ___A. converging (positive) lens D. cylindrical lens C. prisms 7. Which of the following structures accounts for the highest refractive omponent of the human eye? A. prisms 8. one would need which type of lens? A.. speeds up C. hyperopia 2. cornea C. Which of the following happens to the velocity of light as it passes from a medium of higher refractive index. compound myopic D. To correct hyperopia. In the visible spectrum. red 2. cylindrical lens C. green C. stays the same D. emmetropia 3..
Rhodopsin is formed by the combination of which molecules? A. left temporal lobe B. the numerator represents the distance between the chart and the patient.PHYSIOLOGY OF THE EYE/ 32 9. Which of the following lesions would most likely give rise to a left superior homonymous quadrantanopia? A. cylindrical lens C. right parietal lobe ANSWERS TO SELF-TEST 1) 2) 3) 4) 5) A B F B A-2. 10 min D. Which condition is described as having total loss of red color? A. left homonymous hemianopia C. 13. protanomaly C. bitemporal hemianopia D. 20 min 12. opsin and beta-carotene B. left parietal lobe D. A lesion of the optic chiasm would most likely present with which kind of visual field defects? A. deeuteranomaly 14. left superior homonymous quadrantanopia 15. Each arm (1/5 its total height) of the big “E” in the Snellen Chart subtends how much angle? A. 5 min B. cis-retinal isomer and opsin D. B-3. lumirhodopsin and metarhodopsin 11. right temporal lobe C. C-1 6) 7) 8) 9) 10) B C D C C 11) 12) 13) 14) 15) B T A C B 32 . deuteranope D. True or False? In recording visual acuity. converging (positive) lens D. one would need which type of lens to make up for the lost converging power of the human lens? A. diverging (negative) lens B. In presbyopia. 1 min C. beta-carotene and Vit A alcohol C. prisms 10. binasal hemianopia B. protanope B.
rapid or asymptomatic Example of asymptomatic onset is that the blurring of vision was discovered only when patient inadvertently covered one eye.D. INTRODUCTION One should have a good understanding of ocular symptomatology to be able to perform a complete ophthalmic evaluation/ examination. discuss the different ocular symptoms. duration – brief. chronic frequency – continuous.OCULAR SYMPTOMATOLOGY / 33 OCULAR SYMPTOMATOLOGY Marissa N. unilateral or bilateral Determine if forms of treatment have already been initiated/tried. this should be supplemented by small group learning directed to developing their skills in taking ocular history. 2. 4. Valbuena M. If so. MHPEd Arnold T. PREREQUISITE KNOWLEDGE AND PREPARATION The student should have basic knowledge of the anatomy and physiology of the eye and adnexae. the student should be able to 1. INTENDED USERS Although this material was developed to provide the medical students with knowledge on ocular symptomatology. Skills in interviewing a patient will also be helpful. CONTENT Ocular symptoms can be classified into three general types: 1. abnormalities of ocular appearance 3. OBJECTIVES Upon completion of this unit of instruction. to be able to perform a good ocular history. moderate or severe location – focal or diffuse. 2. 5. to what extent have they helped to relieve the symptoms? Are there circumstances that provoke or worsen the condition? Is this the first time these symptoms are experienced? No associated other signs/symptoms? 33 .. intermittent degree – mild. 3. abnormalities of ocular sensation – pain and discomfort These symptoms should always be described according to 1. abnormalities of vision 2. which in turn is necessary to come up with accurate diagnoses.D. onset – gradual. Salud M.
ocular media disturbance (corneal edema. which is worse. the examiner should determine when it occurred. Vision in one eye may have been deteriorating over the years. “maulap ang panningin”. Patients with presbyopia reading material further away from their eyes. becoming noticeable when the patient accidentally covered one eye. retinal abnormalities 5. PHOTOPHOBIA Patients may describe this as “silaw” or “nasisilaw” hyphema. Is the visual loss transient or permanent? Transient loss of vision may be to vascular disorders anywhere from the retina to the occipital cortex. “nawawala ang paningin” or “nabulag” When a patient reports impairment of vision. Visual Loss Patients can describe visual loss as “nanlalabo”. Is the patient’s vision worse or better refraction may have better vision when will read better if they position their Patients with central focal cataracts may in some circumstances ? Patients with error of they squint their eyes. ptosis 3. Actual onset of visual impairment may not coincide with the time given by the patient. ABNORMALITIES OF VISION A. which failed first and how much time has elapsed between the two. Disturbances in peripheral vision may be focal such as scotoma. hemorrhage) 4. whether onset was sudden or gradual. vitreous 34 . refractive error 2. Consider the following as possible causes: 1. GLARE. One should distinguish between decreased central acuity and peripheral vision. If both eyes are involved. have worse vision in bright sunlight. Decline in visual acuity may be due to abnormalities anywhere along the optical and neurologic pathway. Visual Aberrations 1.OCULAR SYMPTOMATOLOGY / 34 1. intracranial visual pathway abnormalities B. or may involve a bigger area as in hemianopsia. Abnormalities in the central nervous visual pathway disturb the visual field more than the central visual acuity. whether one or both eyes were affected. cataract. optic nerve diseases 6. A scotoma is a blind or partially blind area in the visual field while hemianopsia is blindness in one-half of the visual field.
DOUBLE VISION “Nagdadalawa ang paningin” “doble ang paningin”. 3. horizontal. corneal irregularities Binocular diplopia disappears when one eye is covered may be vertical. Glare may also result from uncorrected EOR. hazy ocular media 2. May be caused by migraine. or to certain forms of nystagmus 6.OSCILLOPSIA “Gumagalaw o lumilikot and paningin” Shaking field of vision may be due to harmless lid twitching (myokymia).FLOATING SPOTS “May lumulutang sa harap ng mata” May represent normal vitreous strands due to “normal” vitreous changes. image magnification/ minification. Causes include uncorrected error of refraction. naduduling” Monocular diplopia manifests as a split shadow or ghost image. or inflammatory cells.Or may be secondary to pathologic presence of pigments. 5. The diplopia may be more severe ( 2 images more widely separated) in certain gazes or head position.OCULAR SYMPTOMATOLOGY / 35 Irritative disease of the conjunctiva or cornea specially foreign bodies of the cornea may induce photophobia.FLASHING/FLICKERING LIGHTS Patients may describe this as “may parang kidlat”. VISUAL DISTORTION Manifests as irregular patterns of dimness. media abnormalities such as cataract. wavy or jagged lines. or migrainous scintillations. 4. scratches on spectacle lenses. excessive pupillary dilatation. Acute inflammation of the iris may likewise make the eye sensitive to ordinary light. “biglang may maliwanag” May indicate retinal traction. blood. diagonal or torsional. 35 . lesions involving the macula and optic nerve. optical distortion from strong corrective lenses.
endophthalmitis) non-specific (fatigue from ocular accommodation. Ptosis – drooping of the eyelids. E. “makati” 36 . Eye Pain “Masakit”. 3. “banlag” . Tenderness. exodeviation (outward turning of the eye). Preseptal cellutitis Orbital cellulits “Namamaga ang mata” VS Conjunctivitis “namumula ang mata”. optic neuritis) ocular (may be due to corneal abrasion. binocular fusion. corneal foreign body or any anterior segment inflammation. Eye Irritation Superficial discomfort is usually caused by ocular surface abnormalities 1. hypertropia (upward turning of the eye) or hypotropia (downward turning of the eye) 3. corneal foreign body. periocular (may be tenderness of the lid. “Napipikit”. D. hyperpigmented spots (on the iris/ocular surface) – examples are Nevus of Ota . “mahapdi” Must be characterized in terms of location: 1. “kirat ang mata” Focal growths – in the eyelids or eye surface . “sore eyes” Subconjunctival hemorrhage “dumugo ang mata” Scleritis Iritis Acute glaucoma Pterygium etc Color abnormalities other than redness 1. or referred discomfort from non-ocular tension or fatigue) Deep seated aching. orbital myositis. ABNORMALITIES OF OCULAR SENSATION A. “lumuluwa ang mata” Ocular deviation or misalignlent – “duling”. glaucoma. Herpez zoster may give pain in the eye before any visible involvement of the eye and may persist after the disease has resolved.OCULAR SYMPTOMATOLOGY / 36 2 ABNORMALITIES OF APPEARANCE A. 2. “makirot”. C. soreness or pain on pressure may be due to inflammation of the lids. tear sac. B. Itching – Often a sign of allergic sensitivity. “maga” Exopthalmos – protrusion of the eyeball. Orbital infection can give rise to severe pain. esodeviation (inward turning of the eye). Red Eye Must differentiate between redness of the lids and periocular area (ocular adnexa) from that of the globe. sinuses or temporal artery) retrobulbar (due to orbital inflammation. subepithelial melanosis B. jaundice 2. boring or throbbing pain may be may be due to inflammation of the iris and ciliary body. 4. “bukol”.
OCULAR SYMPTOMATOLOGY / 37 2. “nagluluha” 4. Headaches may not come from the eye. REFERENCE 1. 16th Edition. 37 . “maaligasgas” 3. “Malabo ang mata” 2. Migraine headaches and sinusitis are frequent causes of headache. The doctor should take the history of the patient with any of the following chief complaint : 1. Scheie.B Saunders LEARNING ACTIVITY Students should pair and role play. mild foreign body sensation. “may buhangin”. “mahapdi ang mata” 4. Headache from rise in intracranial pressure is usually severe and associated with nausea and vomiting. 2004 2. “banlag” The “doctor” will write the patient’s history and the partner will comment on the completeness and accuracy of the history. Albert. Whitcher. Harold. Can occur with dry eyes or other types of mild corneal irritation. Riordan-Eva. gritty. John. Characretize discharge as to color. Dryness – Burning. New York: Lange Medical Books/ McGraw Hill. High and low blood pressure may also give rise to headaches around the eyes. consistency. SUMMARY Ocular symptoms consist of abnormalities in vision. Philadelpia : W. Vaughn and Ashbury’s General Ophthalmology . Daniel. amount a Mucoid discharge – allergic b Mucopurulent – bacterial/viral conjunctivitis c Dried matter/crusts on lashes – Blepharitis C. Textbook of Ophthalmology. appearance and sensation. or may be a sign of abnormal lacrimal drainage . The student should ask clarifying questions in order to get sufficient detail to pinpoint the etiology of the ocular disorder. Headache Uncorrected errors of refraction and presbyopia frequently cause headache referred to the eyes or brow and comes with reading and computer work. “may sore eyes” 3. Tearing – may be due to irritation of the ocular surface. Ocular Secretions – “nagmumuta”. One will be the doctor and the other the patient.
The students should likewise familiarize themselves with the basic eye instruments utilized in examining the eye. tonometer and the direct ophthalmoscope. discuss the value and rationale of the various parts of the basic eye examination 2.BASIC EYE EXAMINATION /38 BASIC EYE EXAMINATION Teresita R. An eye examination may also provide the physician with information on the status or condition of certain systemic diseases such as diabetes. this will enable the physician to recognize ocular conditions that may require further referral to an ophthalmologist for definitive management. Specifically. record the results of the eye examination properly and accurately PREREQUISITE KNOWLEDGE AND PREPARATION Students should have a working knowledge of the basic anatomy of the eye and its adnexa. evaluate ocular motility 5. It will explain how to examine the eye and basic visual function. MD. extraocular muscle 38 . INTENDED USERS Although this material was developed to provide the medical student with the principles of each area of the eye examination. penlight. It is advised that this written material be completed first prior to performance of the eye examination on an actual patient. perform direct ophthalmoscopy for a systematic fundus examination 7. Visual acuity. CONTENT All patients should have an eye examination as part of a general physical examination. assess the pupillary reflexes 4. determine intraocular pressure 6. gross examination of the eye and its adnexae. determine a patient’s visual acuity 3. hypertension and thyroid diseases. MHPEd INTRODUCTION This self-instructional material is designed to help the student learn important concepts on proper eye examination. Performing a systematic eye examination will enable the physician to evaluate ocular complaints and subsequently provide immediate emergency care whenever the need arises. OBJECTIVES Upon completion of this unit of instruction. this should be supplemented by small group sessions directed at actual performance of these skills. Castillo. These include distance and near vision eye charts. he/she should be able to 1. Furthermore. The proper method of basic eye examination in an individual is an important skill that every physician should possess. the student should be able to discuss the principles of performing the basic eye examination.
including children because of the importance of early detection of amblyopia. Alternative notations are shown in Table 2. VA = distance from the patient to the chart __ distance at which normal eye can read the given line Example: VA = 20/40 indicates that the patient can recognize at 20 ft. Distance visual acuity is recorded as a ratio or fraction which compares the performance of the patient with an agreed upon standard. Table 1.BASIC EYE EXAMINATION / 39 movements. 2 Pocket Near Vision Chart 39 . Visual acuity of 20/20 represents normal vision. 1 Snellen Letter Fig. Notations used in Recording Visual Acuity VA OD OS OU sc cc ph NV visual acuity (oculus dexter) Right eye (oculus sinister) Left eye (oculus uterique) Both eyes without correction with correction pinhole near vision DISTANCE VISUAL ACUITY Distance visual acuity measurement should be performed in all patients. VISUAL ACUITY TESTING Measurement of the visual acuity provides clinicians with a standard tool for reporting and recording a patient’s vision. Standard notations used for recording of visual acuity are shown in Table 1. a symbol that can be recognized by a person with normal visual acuity at 40 ft. These will be discussed individually. intraocular pressure determination and fundus examination using the direct ophthalmoscope constitute the basic eye examination. Fig. Determination of visual acuity is done prior to any manipulation of the eye to avoid any medico-legal issues that may arise in the future.
Reduce the distance between the patient and the chart until he/she is able to read the 20/200 line. the vision is recorded as 4/60. If the patient can detect hand motion. repeat the test with the patient viewing the test chart through a pinhole occluder and record these results.) at a distance of 6 meters or 20 feet (which is equated with optical infinity). 2. illiterate E.letter. 2. if the patient is able to read the 6/60 (20/200) line at a distance of four meters. Occlude the patient’s right eye and repeat steps 3 and 4. If the patient is unable to see the largest Snellen letter even at a distance of one meter or 3 feet. 6. If the patient has corrective lenses. 5. Record this new distance as the numerator of the acuity designation while retaining the denominator.8 20/20 6/6 1. For example. If the patient’s visual acuity is less than 20/20 in one or both eyes.2 20/70 6/21 0.4 20/40 6/12 0. use a penlight to determine if the direction of the source of the light can be correctly detected by the patient. Ask the patient to read the chart starting at the 20/200 line proceeding to the smallest line which he/she can distinguish more than half of the letters. hold up one hand and ask the patient to count the number of extended fingers. If the patient cannot count fingers.BASIC EYE EXAMINATION / 40 Table 2.5 20/30 6/9 0.3 20/50 6/15 0. Place patient at the designated distance of 20 feet or 6 meters from a well illuminated Snellen Chart. if a patient can count fingers at a distance of ½ meter. the right eye is tested and recorded first. By convention.5 0.7 20/25 6/7. picture charts. number. visual acuity is recorded as CF at ½ meter. The palm of the patient’s hand may also be used to occlude the vision in the right eye. Record your findings as follows: good LPj able to identify light source in all four quadrants 40 . Record the distance at which counting fingers is done accurately. 4. Shine the light on four quadrants. For example. Record the acuity measurement by jotting down the numeric designation of the smallest line that the patient was able to read. proceed as follows: 1. Record a positive response as hand motion designated as HM.0 Visual Acuity is generally tested using the Snellen Chart (Figure 1) . determine whether or not he/she can detect the movement of your hand. Alternative Notations for Recording Visual Acuity English System Notation Metric System Notation Decimal Notation 20/200 6/60 0. 3. Have the patient occlude his left eye using an opaque occluder. 3. 4. If the patient cannot see the largest Snellen letter. ask the patient to wear them during the test. The general steps are as follows: 1.1 20/100 6/30 0.
testing “at near” is done if the patient complaints about their near vision. and from the side. Palpation of the orbital rim and lids may also be indicated based on the patient’s history and symptoms. 6 pt at 35 cm). he should wear them during testing. In some instances. These views would highlight any possible protrusion of the eye ball. If the patient normally wears glasses for reading. both size and distance should be recorded (ex. (looking down over the patients brow while seated). Observe the eyes from the front. Both the approximate type size read and the distance at which the material was held are recorded. Withdrawal or a change in facial expression in response to light or sudden movement indicates the presence of vision. surrounding tissues and palpebral fissure. It is also sometimes done for instances when distance testing is difficult or impossible (at patient’s bedside). NEAR VISUAL ACUITY Near visual acuity testing is routinely done for patients over 35 years of age. If a standard near vision card is not available. Improvement of the patient’s vision using a pinhole would imply that the probably has an error of refraction. The standard near vision chart (Figure 2) is held at a distance of 14 inches or 35 cm. In such instances. If the patient is unable to correctly identify the direction of the source of the light but is able to detect its presence. from above. If the white of the sclera can be seen all around the iris then this could be due to 41 .BASIC EYE EXAMINATION / 41 fair LPj poor LPj able to identify light source from 2-3 quadrants able to identify light source only from one quadrant 5. the examiner should be alert to other signs. this is recorded as No Light Perception (NLP) Differences in acuity can often be due to refractive error. near vision is tested with both eyes open. GROSS EXAMINATION OF THE EYE AND ADNEXAE EXTERNAL INSPECTION With adequate illumination. The presence of redness or any mass should be noted and recorded. the examiner can inspect the lids. any printed material such as a telephone book or a newspaper may be substituted. Otherwise. one will not be able to utilize these standard charts in determining visual acuity. Since letter size designations and test distances vary. The position of the eyes should be examined from in front. Unlike distance vision testing. look at the position of the eyelids relative to the pupil. J5 at 14 inches. If the presence of light can not be detected by the patient. record the patient’s response as light perception (LP). as in infants or toddlers.
Instruct the patient to look up while retracting the lower lid or look down while raising the upper lid to note the presence of redness. The penlight also aids in the inspection of both the cornea and the iris. Duction Test. inspection of the conjunctiva and sclera is done to note the presence of any abnormality. looking straight ahead). instruct the patient to follow your finger or a small target through the six cardinal positions of gaze (Figure 3).BASIC EYE EXAMINATION / 42 exophthalmos or lid retraction. this is referred to as Version Test. The presence of constriction is the normal consensual response. Observe whether the reflection of light is centered in the middle of the pupils. To test the pupillary reaction to light. Consensual Pupillary Reaction. With both eyes open. watching the right pupil for the response. then this could be due to enophthalmos or ptosis. There may well be limitations in certain directions. 3 Six Cardinal Directions of Gaze 42 . first direct the penlight at the patient’s right eye and note if it constricts. direct the penlight at the right eye and watch the left pupil to see if it constricts along with the right pupil. When the EOM movement is tested with both eyes open. To test the consensual pupillary reaction to light. Frequently. Also observe the eye if there is any limitation of movement or nystagmus. Direct Pupillary Reaction. Repeat the procedure on the left eye to test the left pupil. PUPILLARY REACTION TESTING This includes testing the patient’s direct and consensual pupillary reactions to light. On the other hand if the lids are encroaching on the iris and pupil. This will enable the examiner to systematically test each muscle in the primary field of action. pupillary inspection reveals active or prior eye disease with alterations in pupillary shape or size due to damage to the pupillary sphincter or adhesions between the iris and the lens. discharge or any other abnormalities. With the aid of a penlight. keeping it roughly 30 cm from the patient.e. Shine a penlight at the eyes and ask the patient to look at it. a possible isolated weakness or paralysis of a muscle can be detected. Use your finger and move it SLOWLY through the different cardinal positions shown below. Constriction is a normal reaction. Repeat the same examination one eye at a time. Repeat the procedure for the left pupil. Ask the patient to tell you if double vision is noted at any point. Fig. A nerve palsy or muscle weakness can alter the movements of the eyes when going through the six cardinal positions. and double vision associated with looking in that direction. Thus. OCULAR MOTILITY TESTING Examining the eye movements begins by observing the eyes in the primary position (i.
OD – right eye. OS – left eye INTRAOCULAR PRESSURE DETERMINATION This is the pressure that is created within the closed environment of the eye. 4 Common abnormalities in the alignment of the eyes Findings are recorded as follows: SR LR IO MR SO OD OS SR LR IR IR Fig. LR – lateral rectus.BASIC EYE EXAMINATION / 43 Table 3. NORMAL LEFT ESOTROPIA LEFT EXOTROPIA LEFT HYPERTROPIA LEFT HYPOTROPIA Fig. Cardinal Fields of Gaze Right and Up Left and Up Right superior rectus Left superior rectus Left inferior oblique Right inferior oblique Right Left Right lateral rectus Left lateral rectus Left medial rectus Right medial rectus Right and Down Left and Down Right inferior rectus Left inferior rectus Left superior oblique Right superior oblique Common abnormalities in the alignment of the eyes are shown in the figure below. The pressure is governed by a balance between the production of aqueous humor and its drainage. 5 Recording of results of Ocular Motility Testing SR – superior rectus. MR – medial rectus. IR – inferior rectus. The normal flow of aqueous is illustrated in Fig. SO – superior oblique. 43 . IO – inferior oblique. 6 .
The scale on the Schiotz tonometer indicates the amount of actual indentation. A rise in this pressure or a person sensitive to certain pressures can be transmitted to the back of the eye and damage the optic nerve. The instrument indents the cornea in an amount related to the IOP. Furthermore. If the eye is palpated to be hard on palpation. Palpating a “soft” eye would be the same as palpating the tip of the nose.BASIC EYE EXAMINATION / 44 Ciliary body Iris POSTERIOR CHAMBER Lens ANTERIOR CHAMBER Fig. An eye perceived to be softer than these is considered to be “hypotonic”. A nu mber of instruments may be used for this purpose . 7). Schiotz tonometer and non-contact tonometers. but it is important to look at the retina and look for changes due to high pressure. A printed conversion table that comes with the instrument is used to determine the IOP in millimeters of mercury from the indentation scale reading.Schiotz In the absence of any instrument. 44 . Goldman tonometry is most commonly used and is considered the “gold standard”. however. this is reported as “firm” and the patient is suspected to have an elevated IOP. IOP can be estimated by palpation. 6 Normal Aqueous Flow Intraocular pressures (IOP) vary from individual to individual and fluctuate within a normal range. 7 A. One relatively simple method of measuring IOP.Applanation tonometer B. This is called "low pressure glaucoma". or indentation tonometer (Fig. is that it requires special equipment and can only be used by an ophthalmologist. as people with normal pressures may have eyes that are sensitive to "normal range" pressure. is the Schiotz. This with characteristic visual field changes and optic disc cupping is known as Glaucoma.Goldmann Applanation tonometer. and will still produce changes characteristic of glaucoma. however IOPs in the range of 10 to 21 mm Hg are still considered to be within the normal range. Pressures above this are often treated. the instrument can not be used in individuals with corneal abnormalities such as scars. and is generally used for screening purposes. This is done by carefully applying pressure using your forefingers on the upper lid while the patient is looking down. The average IOP in a “normal” population is 15 mm Hg. The Schiotz tonometer with a given weight is placed on the anesthetized cornea. however. Intraocular pressure is measured by tonometry. Its primary disadvantage. the tonopen. A B Fig.
ensure that the ophthalmoscope is working properly: 1. 4. 3. and. Make sure that the light source is the largest circle. Contact lenses worn by either the patient or the examiner may however be left in place.BASIC EYE EXAMINATION / 45 FUNDUS EXAMINATION The fundus can be examined by direct ophthalmoscopy using an ophthalmoscope. The patient’s glasses are removed. hold the direct ophthalmoscope with your right hand and use your right eye to view the patient’s eye. The patient should also be instructed to maintain their gaze throughout the examination. It is essential that every physician learns and gain confidence in using an ophthalmoscope to perform direct ophthalmoscopy. Set the focusing wheel at 0 and select the large. Hold the ophthalmoscope comfortably against the arch of your brow. 2. The patient should be instructed to focus on a distant target. 1. A – direct ophthalmoscope B – indirect ophthalmoscope Table 4. To perform direct ophthalmoscopy. white light. The room should be dimly-lit and the patient comfortably seated. Use your right eye with the ophthalmoscope in your right hand. When you look straight down the patient’s line of sight at the pupil. Begin to look at the right eye about 1 foot from the patient. or on the patient’s forehead or shoulder to keep yourself steady. Adjust the lens setting to 0. The main differences between the direct and indirect ophthalmoscope are listed in Table 4. 5. When examining the patient’s right eye. examiners prefer to remove their own glasses as well. Check the light source. barring large astigmatic refractive errors. you will see the red reflex. 4. A B Fig 8. round. or by indirect (often binocular) methods such as an indirect ophtalmoscope (Figure 8). 2. Use the left hand and left eye to examine the patient’s left eye. 5. follow these steps. 45 . 3. You may place your free hand on the patient’s lid to keep the eye open. List of Differences between the Direct and Indirect Ophthalmoscope Criteria Direct Ophthalmoscope Indirect Ophthalmoscope image upright inverted magnification larger smaller area viewed smaller larger depth absent present Before beginning.
Lesions seen with the ophthalmoscope are measured and described in terms of disc diameters. Some common variations are shown in Figure 11. retinal background and macula. If there is any opacity in the lens or cornea this will appear black or create a silhouette against the red-reflex. Examine the disc as follows: 1. 46 . RED REFLEX Light reflected off the fundus of the patient produces a red reflex when viewed through the ophthalmoscope at a distance of about one foot. Examine the optic disc. when viewed through the ophthalmoscope.normal red reflex B – red reflex obstructed by opacity OPTIC DISC In most cases. 8. Turn the focusing wheel with your index finger to bring the patient’s retina into focus. The optic disc is often used as a “yardstick” of the ocular fundus. the normal optic disc (Fig 10) will appear slightly oval vertically and pink in color. There are numerous variations in the appearance of the disc. A central depression in the surface of the disc is called the “physiologic cup”. 7.BASIC EYE EXAMINATION / 46 6. Look at its margins and note whether they are well defined. 2. 9 A. which lies nasal to the center of the retina. 3. Also note for the presence of any changes such as pigmentation around the disc margins. follow it as it widens to the optic disc. Look at the cup: disc ratio and note whether the cup takes up a large part of the disc. A normal red reflex (Fig. Note for the presence of any hemorrhages within the disc. When a retinal vessel comes into view. 9) is evenly colored and is not interrupted by shadows. Slowly come closer to the patient at an angle of about 15° temporal to the patient’s line of sight. A B Fig. Try to keep the pupil in view at all times. 9. retinal blood vessels. Repeat the same procedure for the left eye.
Figure 12 shows a picture of a normal fundus together with a schematic representation.Retinal and choroidal pigment B Fov Mac Op Fig. 12 RETINAL CIRCULATION The retinal circulation is composed of arteries and veins. the examiner should also note the 47 . The branches of the central retinal artery supplying the four quadrants of the inner retina lie superficially in the nerve fiber layer. visible with the ophthalmoscope.BASIC EYE EXAMINATION / 47 A Fig 11 A. The retinal veins collects at the optic disc and follows a similar system of arrangement. Aside from noting the caliber of the vessels and the light reflexes. Arteries usually appear lighter in color than the veins and have a more prominent light reflex from their surface. The normal artery-to-vein diameter ratio is 2:3.
The examinee should also note the presence of hemorrhages and exudates. exudates hemorrhages A B C D E F Fig 13.BASIC EYE EXAMINATION / 48 arteriovenous crossing patterns. Retinal Changes A – blot hemorrhages B – increased vessel tortuosity C – pigment changes and boat shaped hemorrhage D – boat shaped hemorrhage E – flame shaped hemorrhages F – arterial beading G – pigment changes G 48 .
The retinal pigment epithelium. The foveal reflex should be noted by the examiner. blood and pigment of the choroid contribute to the appearance of the retinal background.5 any other ratio widened present present gray. as follows: STRUCTURE Red Orange Reflex (ROR) Media Optic Disc • disc margins • cup:disc ratio Retinal Vessels • A:V ratio • median light reflex • AV crossing defects • hemorrhages and exudates Retinal background Macula • foveal reflex NORMAL present clear distinct 0.3 – 0. blurred > 0. 14). 12) and appears darker than the surrounding retina.BASIC EYE EXAMINATION /49 RETINAL BACKGROUND The normal retinal background is a uniform red-orange color. pale dull or absent 49 . REPORTING OF FINDINGS Findings on fundus examination are typically reported in a systematic manner. Fig.5 2:3 normal absent absent red orange present ABNORMAL absent hazy indistinct. One condition which changes this color is retinal detachment which produces a dull. This is due to the specialized retinal pigment epithelial cells of the macula that are taller and more heavily pigmented. The central depression of the fovea may act as a convex mirror and produce a light reflection known as the foveal reflex. grayish appearance (Fig. 14 Detached Retina MACULA The normal macula is located temporal to the optic disc (Fig.
3. Louis. 13th ed. 1991. San Francisco: American Academy of Ophthalmology. cornea and iris. General Ophthalmology. disc. Asbury T. 4. Perform tonometry. Berson. good foveal reflex REFERENCES 1. The following is an example of the results of an eye exam: IOP OD = 14 mm OS= 16 mm Funduscopy: OU – (+) ROR. Frank G. D. 1992. Assess the lens for clarity through direct ophthalmoscopy. Manual of Ocular Diagnosis and Therapy. 9. Below is a summary of the steps in performing the basic eye exam: 1. Assess the chamber for clarity and depth.BASIC EYE EXAMINATION / 50 SUMMARY Acquiring the skills to be able to properly perform the basic eye examination will allow physicians to recognize potentially vision threatening conditions early so that such cases are referred to the ophthalmologist for appropriate management.4. 6. Basic Ophthalmology for Medical Students and Primary Care Residents. Brown & Co. Examine the fundus. 7th ed. 3. Newell FW: Ophthalmology: Principles and Concepts. 7. distinct disc borders. CT: Appleton & Lange. 8. 1992. AV= 1:3. Chapter 1. Riordan-Eva P. Norwalk. 50 . (-) hges/exudates. Boston: Little. Vaughn DG. 1993. Chapter 1. Pavan-Langston. 3rd ed. 2. Check the ocular alignment and test the extraocular movements. clear media. 2. 6th ed. Inspect the lids and surrounding tissues. Mosby Co. Palpate the orbit if necessary. Measure the visual acuity of each eye. Inspect the conjunctiva. St. Inspect the pupil and check the pupillary reflexes. 4. “The Eye Examination”. sclera. “Ocular Examination Techniques and Diagnostic Tests”. CD=0. vessels. retinal background and macula. 5.
9 B. R medial rectus B. at 6 meters what a normal person sees at 21 meters B. left hand and use his right eye C. top 4. L medial rectus C. What is the cup:disc ratio for the left eye? 51 . A. these were the disc findings. 7. ending with someone who is nearly blind. right hand and use his left eye B. finger counting _____ D. 0. 0. If a patient’s visual acuity is 6/21. hand motion 2. EXCEPT A. Applanation tonometer B. Use the following choices for your answers to items 4 and 5.BASIC EYE EXAMINATION / 51 SELF–TEST 1. Schiotz tonometer C. Given the following choices. right hand and use his right eye D. L lateral rectus 6. A patient’s left eye constricts upon shining your penlight directly on it. none of the above 5.0 8. She has a problem of the A. perceives light _____ C. the examiner should hold his ophthalmoscope with his A. any one of the above 8-9. If a patient has a corneal leukoma. Snellen chart at 6 meters _____ B. 1. arrange them starting from the procedure that should be done in someone with near normal vision. intact right oculomotor nerve C. side C.5 C. functioning left and right optic nerves B. These findings indicate that the patient has A. digital tonometer D. at 21 meters what a normal person sees at 6 meters 3. left hand and use his left eye. non-functioning right optic nerve D. On funduscopy. the best instrument to use that will give more accurate IOP reading is A. Snellen chart at 1 meter _____ E. _____ A. Proptosis can be seen by looking at a patient from the following positions. Shining a light on the patient’s right eye also causes constriction of the left pupil. In examining a patient’s right eye. R lateral rectus D. 0. The patient in this picture is looking to her left. front D.3 D. this would mean that the person can read A. back B.
8. none of the above ANSWERS TO SELF-TEST 1. 2. provides a larger image than the indirect ophthalomoscope B. it gives the examiner a better view of the peripheral retinal structures D. 7. D -2. 5. The following are characteristics of the Direct Ophthalmoscope EXCEPT A. 9. B – 5. 10. 6. provides an upright image of the retina C. 3. What is the cup:disc ratio for the right eye? 10. C – 3. A – 1.BASIC EYE EXAMINATION / 52 9. E – 4 A A A D C B A B C 52 . 4.
together with the pre corneal tear film is responsible for two-thirds of the total refractive power of the eye thus making it more powerful than the lens. Students are however encouraged to apply knowledge that they will acquire from this SIM to actual and simulated clinical cases during their rotation. This material is intended to serve as supplementary reading for the students as part of the unit on DISTURBANCES IN VISION and focuses primarily on providing the learner the knowledge in understanding how corneal pathologies affect vision and in knowing the common corneal diseases or problems that can affect vision. Of the two. Main Functions of the Cornea 1. RECOMMENDED PREPARATION You are advised to review the anatomy and physiology of the cornea and principles and definitions of basic physical optics before going through this SIM. the learner is expected to: 1. pictures of typical cases will also be presented. namely Ophthalmic Anatomy and Physiology. Transmission of Light: The cornea is a highly transparent tissue and this is largely due to its unique anatomy. the cornea. These students are expected to have completed basic units in ophthalmology.DISORDERS OF THE CORNEA / 53 DISTURBANCE IN VISION DISORDERS OF THE CORNEA Ruben Lim Bon Siong. Discuss the principles on how these corneal diseases are managed. Aside from providing the learner with text on the subject matter. CONTENT The eye is basically an optical instrument wherein light reflected from an object are transmitted and refracted so that the image is focused on the retina. Light is then converted to photo-electrical signals which are transmitted to the occipital cortex and is perceived as vision. INTENDED USERS This SIM was primarily designed for LEARNING UNIT IV students of the UP College of Medicine. The two main refracting components of the eye are the cornea and the lens. Explain how corneal pathologies and diseases affect vision. Discuss the common corneal diseases that affect vision based their basic pathophysiology 3. MD INTRODUCTION This self instructional material is designed for undergraduate medical students (Learning Unit IV of the UP College of Medicine). It is composed of collagen fibrils with uniform diameter and uniform spacing and arrangement. OBJECTIVES After going through this material. Ophthalmic Optics and Objective and Subjective Examination of the Eye. In between the collagen fibrils are the extracellular matrix ground substance composed of proteoglycans (PG) with a constant water content of 78% which is a lot less than the water content of other tissues of the body. It is devoid of blood vessels and has a paucity of cellular elements. Since the diameter of the collagen fibrils and the distance between them is less that ½ the wavelength of 53 . 2. This relative dryness or deturgescence is the one responsible for maintaining the homogeneity of the collagen fibrils.
Scars are usually formed after an inflammatory process when fibrosis sets in. Corneal scars 2. incoming parallel light rays have to be bent or refracted. redness and other symptoms will disappear except for blurring of vision (more so if lesion is overlying or affecting the pupillary area) which is caused by the corneal opacity. Outline: A. melting and sometimes rupture of the cornea. fungi and protozoans. During the active infection. Abnormalities of corneal size/ shape / curvature A. Any disruption of the normal configuration of the collagen fibrils will therefore cause failure in the efficient transmission of light and the cornea will appear hazy or opaque. 2. 54 . corneal opacity is associated with marked eye redness. Disruption in the transmission of light 1. This prevents light to be transmitted properly and is reflected back thus making the cornea appear opaque (Fig 3). are usually required to make an accurate diagnosis. cornea and aqueous humor (Fig 2). The aim is to make the learner appreciate the close relationship between the structure and function of the cornea and to know the common etiologies that can affect each function. tear film. Common Causes of Blurring of Vision due to Corneal Pathology or Diseases Conceptual Framework: The foregoing discussion will be divided into the major headings based on how certain corneal disorders affect the two main functions of the cornea as mentioned above. new and abnormal collagen fibrils and other cellular elements are laid down in a “haphazard” manner causing the disruption of the normal homogenous arrangement of the collagen fibrils. In fibrosis. Disturbance in the refraction of light 1.DISORDERS OF THE CORNEA / 54 visible light. Microbial keratitis: these are infections of the cornea which can be caused by viruses. Invasion of microorganisms into the cornea induces an intense inflammatory response and with the actions of microbial toxins and enzymes causes corneal tissue necrosis. Corneal deposits 4. This is made possible by the smooth anterior shape/curvature of the cornea which is convex (thus light is bent inward or converged) and by the difference in the indices of refraction between air. either due to treatment or the natural course of the disease. Disruption in the Transmission of Light: Corneal Scars Corneal scars are usually tan to white in color and may involve different areas of the cornea and may come in different shapes and sizes depending on the etiology and pathology. So any disturbance in the shape/curvature of the cornea and the indices of refraction of the different structures can cause the failure of the converged light rays to be focused on the retina leading to blurry vision. light is not diffracted and is therefore transmitted (Fig 1). Corneal edema 3. which are not available to the learner. tearing and photophobia (Fig 4). Once healing ensues. bacteria. Refraction of Light: In order for light entering the eye to be focused on the retina. Corneal tumors B. Etiologies: 1. Corneal melt 5. It is not the main aim of this material to make the learner adept in diagnosing these conditions since specialized instruments and tests. Abnormalities of the corneal epithelium and tear film 2.
5. nails. It should be noted that exposure keratopathy can be prevented. This condition can also lead to severe scarring if secondary microbial keratitis occurs. malnutrition. Bilateral inferior corneal scars are usually seen in patients with a history of severe measles occurring in childhood. the direction of the flow of water is reversed and the cornea will retain water and swell like a sponge (corneal decompensation) causing disruption of the normal arrangement of the collagen fibrils. 4. immunodeficiency. Lid margin and lash disorders: Abnormalities of the lid margins may cause misdirection of the eye lashes towards the cornea and the constant and chronic rubbing will lead to surface vascularization and eventual scarring. Patient will usually complain of marked blurring of vision and recurrent eye pain. This condition is bilateral in 80% of cases and more than half has glaucoma. This condition is seen in trichiasis. In alkali burn. The human corneal endothelial layer does not regenerate when lost or injured and decreases in number as a person ages. glass etc) and high velocity projectiles (iron nails due to hammering. lid and orbital deformities. Peters anomaly is part of a spectrum of disorders known as anterior segment dysgenesis and presents as central corneal leukoma with defects in the posterior stroma. vitamin A deficiency and lack of tears. entropion.DISORDERS OF THE CORNEA / 55 2. sequelae of Stevens Johnson Syndrome etc. Failure of the lids to close properly (lagophthalmos) will lead to a condition called exposure keratopathy wherein the exposed cornea (usually the inferior half ) will opacify due to the drying effect (Fig 6). those with CN VII palsies. trachoma. vision will be variably affected either by the opacity itself or the distortion of the shape of the cornea. nocturnal exposure etc. epiblepharon. Corneal lacerations and perforations are usually caused by sharp objects (knife. Most of these injuries have to be managed surgically by doing corneal repair/suturing to close the wound and restore the integrity of the globe (Fig 5). Corneal Edema The corneal endothelium is the single most important structure of the cornea and is the one responsible in active pumping of water away from the cornea to the aqueous humor thereby maintaining corneal clarity. acute proptosis. Depending on the extent of involvement. shattered glass. bullets etc). healing will bring about fibrosis and subsequent corneal scarring along the wound and suture track. 3. 55 . The exposed cornea develops secondary bacterial infection and usually ends in corneal rupture and subsequent scarring. foreign body sensation and tearing. corneal destruction is generally more severe since it causes corneal necrosis and melting due to its ability to penetrate deeply into the cornea. darts. An adequate number must be present throughout life in order for it to function properly. Strands of iris may attach to the posterior border of the leukoma. This usually starts as exposure keratitis in a very sick child compounded by dehydration. Contact burns from molten metal and other heated materials can also cause severe corneal injuries and scarring. When the cell density dips below a critical level. scissors. redness. Similar to skin lacerations. Exposure keratopathy: the cornea is prone to desiccation if left exposed to the environment. Corneal trauma: this includes mechanical and chemical njuries to the cornea and is among the major causes of corneal problems in the Philippines. Acid chemical burns on the cornea causes denaturation and precipitation of the collagen and will lead to scar formation. Affectation may be diffuse or focal depending on extent of involvement. This problem is usually seen in comatose patients. The edematous and markedly thickened cornea will appear hazy or ground glass in appearance. chronic blepharitis. Congenital corneal scars: corneal scars can develop while in utero due to anomalies during embryogenesis. pneumonia. Descemet’s membrane and the corneal endothelium.
thickened cornea with normal corneal diameter and eye pressure and absence of birth trauma should be suspected to have Congenital Hereditary Endothelial Dystrophy (Fig 7). Etiologies: 1. Calcium hydroxyapatite deposits at the Bowman’s layer starting at the 3 and 9 o’clock area and meeting at the center over time forming a white horizontal band across the cornea with a Swiss cheese pattern. (Fig 11) 4. Substances can get trapped within the corneal collagen lamellae or within intracytoplasmic vacuoles or organelles and cause opacities that will lead to blurring of vision. Chromosomal defects cause problems in normal metabolism leading to deposition of substances at different layers of the cornea. 3. Fuchs’ Endothelial Dystrophy. Abnormal 56 . Diagnosis is based on clinical presentation and by histopathology. These patients have an abnormally fast rate of endothelial cell loss as compared to the normal population. 2. This appears as a central golden brown to yellow discoid opacity on the cornea. Each form affects vision differently primarily due to difference in appearance and location. absence of vascularization. absence of any form of inflammation. infection. The invasion of blood vessels into the cornea will lead to leakage of glycoproteins. Corneal Staining: hyphema (blood in the anterior chamber) coupled with high eye pressure will lead to deposition of heme in the corneal stroma. Trauma can be direct in the form of mechanical contact of instrument or lens implants or intraocular structures like vitreous to the corneal endothelium. (Fig 10) 3. is seen usually after age 50. cholesterol and neutral fat into the cornea and to eventual deposition of these substances. The corneal guttata will increase in number and spreads toward the periphery. Lipid Keratopathy: this is usually seen in vascularized corneal scars of various etiologies (trauma. Total endothelial cell density will decrease and corneal decompensation may ensue in due time. the cornea is also like a sieve.DISORDERS OF THE CORNEA / 56 Etiologies: 1. Corneal Deposits Aside from it acting like a sponge. more so in females. Since the cornea is avascular. Congenital or Hereditary: Infants with bilateral diffuse corneal haziness and ground glass appearance. Chronic Increased Eye Pressure (Glaucoma): Abnormally high eye pressure can affect corneal metabolism and damage the corneal endothelium by causing relative hypoxia and hypoglycemia in the anterior chamber of the eye. (Fig 9) 2. the corneal endothelium depends on the aqueous humor for its nutrients and oxygen supply. Metabolic disorders: systemic metabolic disorders can cause alterations in corneal clarity due to abnormal storage of metabolic substances within the epithelium. Post Surgical: Anterior segment intraocular surgery such as cataract extraction can cause trauma to the corneal endothelium. The opacities are usually yellow or cream-colored located at the corneal stromal layer typically associated with a branch or several branches of blood vessels at the core. stroma or endothelium. Corneal Dystrophy: this is a large group of hereditary corneal disorders sharing several common features like bilateral and symmetrical involvement. on the other hand. (Fig 12) 5. and with proven or suspected chromosomal abnormalities. All cases will initially present with central corneal guttata located at the posterior side of the cornea. immune-mediated). Corneal decompensation are seen in both congenital glaucoma in children and chronic glaucoma in adults. It may be indirect like inadvertent introduction of noxious chemicals into the eye (Fig 8). Calcific Band Keratopathy: this is usually seen in eyes with chronic inflammation like anterior uveitis and in patients with high serum calcium and disorders in phosphate metabolism.
Prolonged vitamin A deficiency leads to external eye involvement. Corneal Melt Apart from microbial keratitis. Alkaline solutions rapidly penetrate the corneal stroma destroying the proteoglycan ground substance and collagen fibers. Dermoids are composed of fibrous tissue and hair with sebaceous glands that is covered by conjunctival epithelium. Vision may or may not be affected depending on the location of the lesion whether it will distract the transmission and refraction of light. Examples are systemic mucopolysaccharidoses. tan to fleshy color. Corneal Intraepithelial Neoplasia: suspected to be caused by the human papillomavirus. At greatest risk are the malnourished infants and the baby born to a Vitamin A-deficient mother. If the process is arrested. usually by prompt and appropriate therapy. (Fig 15 R) Strong correlation with UV exposure has been documented. this condition is primarily a conjunctival disorder but due to its intimate relationship with the cornea. It is a wing-shaped or triangular fold of conjunctiva and fibrovascular tissue with its apex invading the superficial cornea.000 new cases of blindness worldwide each year. Severe scarring and corneal vascularization are seen in severe cases. Pterygium is a benign conjunctival lesion that behaves malignantly. metaplastic keratinization of areas of the conjunctiva (Bitot spots). Alkali Chemical Burn: strong alkali raise the pH of tissues and cause saponification of fatty acids in cell membranes and ultimately cellular disruption. Most of these conditions are rare and are autosomal recessive. mucolipidoses. either benign or malignant can occur on the ocular surface involving the cornea and conjunctiva. (Fig 15 C) 3. especially if the infant has another biological stress such as measles or diarrhea. and an array of protein and amino acid metabolic disorders. it will be included here. These lesions are easily diagnosed by their clinical presentation and appearance and is confirmed by histopathology. including xerosis (dryness of the conjunctiva and cornea). then healing and fibrosis will take place leaving the cornea scarred and opacified. Vitamin A Deficiency: this leads to xerophthalmia. corneal ulcers and scars and eventually diffuse corneal necrosis (keratomalacia). chemical burn and autoimmmune diseases. Etiologies: 1.DISORDERS OF THE CORNEA / 57 substances typically accumulate in lysosomes or lysosome-like intracytoplasmic structures as a result of single enzyme defect. (Fig 14) Corneal Tumors New growths. elevated. It affects vision in two ways. it grows progressively towards the center of the cornea 57 . (Fig 13) Etiologies: 1. lesion appears as translucent. hyper and hypolipoproteinemias. Blurring of vision will occur once the growing epithelial sheet reaches the central area. corneal melt or necrosis can be brought about by Vitamin A deficiency. 2. round to oval solid mass embedded in the superficial cornea and sclera. Epibulbar dermoids are located over the central cornea and can severely affect vision. which is responsible for at least 20. Pterygium: Strictly speaking. It also destroys the limbal stem cells preventing normal epithelial healing.000 – 10. Dermoid Choristoma: this congenital lesion typically occurs on the inferotemporal limbus as a smooth. gray or frosted epithelial sheet starting from the limbus and extending onto the cornea with fimbriated or scalloped borders and pseudopodialike extensions. Corneal melting is brought about by a complex interaction and cascade of enzymatic and molecular events involving a myriad of substances and is beyond the scope of this material. (Fig 15 L) 2. sphingolipidoses. One.
the corneal surface epithelium can also be injured. If one or both of these are abnormal. In severe and chronic cases however. When seen under scanning electron microscopy. What will be discussed here are those corneal diseases and disorders that result in severe errors of refraction and therefore severe blurring of vision. Most cases are mild and just cause occasional symptoms. preservatives or both). And two. it is intimately related to the tear film. This condition is also known as keratoconjunctivitis sicca. Stevens-Johnson syndrome (Fig 17). it can cause irregularities on the corneal surface due to microtrauma to the epithelium. smudges and the like will cause degradation in the quality of the image. the surface is thrown into dense microvilli. They will also complain of fluctuating vision due to rapid evaporation and break up of the tear film in between blinking. light rays will converge on different focal plains. As in dry eye syndrome. especially over the central area overlying the pupil can cause blurring of vision. If the radius of curvature increases (flat cornea). the opposite effect will occur which is hyperopia. The lipid prevents rapid tear evaporation and mucin allows molecular interaction between the tear film the corneal surface (surface tension). the tear film has a high index of refraction when compared to air. If the radius of curvature of the cornea decreases (steep cornea). alkali chemical burn. Abnormalities of Corneal Size/Shape/Curvature The total refractive power of the eye is around 60 diopters (D) and cornea and tear film contributes 40 D and the rest by the crystalline lens. it pulls on the peripheral cornea and cause distortion of the shape resulting in astigmatism. 58 . Presence of these superficial punctate lesions make the surface irregular and will thus affect vision. 2. any abnormalities of the tear film and/or the corneal surface epithelium. Additionally. patient will complain of dry eye symptoms. If light rays pass through a cornea with variable radii of curvature. Toxic Keratitis: this pertains to microtrauma to the corneal surface epithelium secondary to contact to chemicals (such as alcohol based products like hair spray) or topical medications (active ingredient. This physical attribute allows further convergence of light rays as it passes from air then through the tear film and the cornea. foreign body sensation. Thus. light rays will converge more. Presence of cracks. (Fig 16) Patient complains of dryness. all three components are affected. burning sensation and blurring of vision. 3. In some patients. Deficiency in Tear Volume: Dry eye syndrome is a common disorder with different etiologies wherein there is decreased tear production. despite adequate tear volume. severe dry eye. Lipid deficiency is caused by blepharitis and meibomian gland dysfunction. hyperopia and astigmatism are collectively known as Errors of Refraction and will be discussed in another SIM. This 40 D is a result of a constant range of radii of curvature and indices of refraction of the cornea as provided by a normal anatomy. The outermost layer of the corneal epithelium per se is not smooth. Disturbance in the Refraction of Light Abnormalities in the Corneal Epithelium and Tear Film The main refractive surface of the eye is the anterior cornea. An important prerequisite for any refractive surface is that it should be smooth. To make the corneal surface a perfect refractive surface. Etiologies: 1. moving the focal plain in front of the retina resulting in myopia. B. aqueous and mucin. Myopia. which coats the anterior surface of the cornea. Mucin deficiency can be caused by vitamin A deficiency. Tear Quality Abnormalities: the tear film is actually a complex structure composed of three main components: lipid.DISORDERS OF THE CORNEA / 58 and covers the pupil area. This is known as astigmatism. and cicatricial pemphigoid.
Dry eye syndrome is treated by using topical lubricating agents and/or by preserving existing natural tears by preventing tear drainage. Corneal transplantation may be the only option. Flattening of one meridian causes a corresponding steepening in the meridian 90 degrees away and vice versa. Patient complains of progressive rapid blurring of vision during adolescent years and then stabilizes when patient has attained full growth. management is geared towards two goals. This effect is seen in pterygium. then the therapy should be directed towards lowering the pressure to appropriate levels. are permanent. The cornea usually appears grossly clear.DISORDERS OF THE CORNEA / 59 Etiologies: 1. If it is due to high eye pressure. you will notice that the image can be distorted by either pulling or pushing the sides of the balloon. management is usually surgical which may range from manual excision to laser removal to corneal transplantation. because by doing so. Principles of Management: Corneal scars. Calcium deposits can be removed by chelation since the location is superficial while deeper ones like lipid and heme cannot be removed. There are no medical therapies available to turn scar tissue to normal corneal tissue. although progression can occur at any time. effect of sutures after cataract surgery. peripheral thinning disorders and others. Corneal distortion due to peripheral scars or lesions: this is to emphasize the fact that you do not need to have direct involvement. In treating corneal melting. but on profile one may see a focal area of bulging. Sometimes corneal grafts are also used to restore corneal clarity. (Fig 19) Corneal edema due to endothelial damage or dysfunction is also permanent because the cells do not regenerate. To improve vision. (Fig 18) Hereditary pattern is not prominent. either improvement of vision or cosmetic or both. 59 . Corneal transplantation is reserved only for those conditions with significant visual loss. as a rule. To improve appearance. Depending on the location. This concept becomes easy to understand if one imagines the cornea as a silver mylar balloon. Corneal transplantation is usually done. With adequate lubrication. It is best appreciated when examined using specialized instruments. Corneal deposits due to systemic metabolic disorders or from corneal dystrophy may recur after a corneal transplant since the underlying condition is not corrected. you change the curvature of the center. It is almost always bilateral but usually asymmetrical. so that the cornea takes on the shape of a cone. Definitive treatment is by doing a corneal transplantation. except in severe cases where an apical scar is visible. size and degree of visual involvement. like a scar. unless it is for an emergency procedure to restore the integrity of the globe. The role of medical therapy is to minimize pain and discomfort and to prevent secondary infections. Corneal masses are usually treated by surgical removal if the indications for surgery are present. the health of the corneal epithelium will be restored. Due to the progressive bulging of the cornea. By looking at your reflection at the flat surface of the balloon. dyed by tattooing or by corneal transplantation. on the center of the cornea to cause disturbance in vision. Surgical management is usually done later to treat sequelae. scars from peripheral corneal perforations. Keratoconus: this is a common disorder where the central or paracentral cornea undergoes progressive thinning and bulging. Always remember that the cornea is one whole integral structure. Etiology is unknown and likely multifactorial. the underlying etiology should immediately be addressed. corneal scars may be covered with cosmetic contact lenses. the cornea becomes abnormally and irregularly steep resulting in very severe myopia and astigmatism. 2.
This is done by employing optical appliances or by surgically altering the cornea so that the shape will be restored to normal. vascularization or can be congenital. and corneal disorders that affect its normal size. lens D. Disorders of the cornea that can disturb the refraction of light includes dry eye disease. Scars are caused by infection. The water content of the normal cornea is: A. incisional or laser refractive procedures. Depending on the indications. 2. all other possible risk factors that may aggravate tear quality should be removed or minimized. (eds) Cornea Vol 1 to 3. trauma. Deposits in the cornea can be caused by metabolic products. (eds) The Cornea 3rd ed. retina 2. 60% B. proteins. shape and curvature. If the normal anatomy of the cornea is altered. iron. exposure. calcium. Corneal edema can be congenital. pterygium and neoplasia can block the transmission of light or alter the shape of the cornea. amyloid and other amorphous substances. tear film B. lipids. Thoft RA. excision of abnormal growths or tissues. Management of these disorders involves the restoration of the cornea’s normal anatomy primarily through corneal tissue transplantation. This principle also holds true in treating toxic keratitis. choices may include glasses and contact lenses. Holland EJ. Disorders that can disrupt the normal transmission of light are corneal scars. or corneal grafting and transplantation. corneal epithelial dysfunction. Mannis MJ. Masses on the cornea like dermoid. corneal melt and corneal tumors.TEST 1. 78% D. There are several options when treating corneal disorders with abnormal shape or curvature in order to improve vision. Corneal melting caused by vitamin A deficiency. it will lead to blurring of vision. corneal edema. Krachmer JH. SELF. chemical burn or autoimmune diseases can lead to permanent corneal scarring. hemoglobin. 90% 60 . Smolin G. Goal is to correct the refractive errors so that the image will be sharply focused on the retina. corneal deposits.DISORDERS OF THE CORNEA / 60 Moreover. SUMMARY The main function of the cornea is to transmit and refract light. cornea C. 67% C. REFERENCES 1. due to surgical and non surgical trauma or due to chronic glaucoma. control or removal of etiologic and contributing factors. surgical interventions to improve corneal shape and curvature and use of optical appliances to enhance the transmission and refraction of light into the eye. The main refractive component of the eye is: A.
lipid C.DISORDERS OF THE CORNEA / 61 3. color of the iris 4. Which statement about the corneal endothelium is FALSE? A. The major causes of corneal scarring in the Philippines is/are: A. The following affects the normal refraction of light into the eye. decreasing tear production D. index of refraction D. Steepening of the cornea caused by keratoconus leads to what form of refractive error? A. Hard contact lenses B. EXCEPT: A. EXCEPT: A. inducing astigmatism by changing the central corneal curvature C. the corneal endothelium is responsible for actively pumping water out of the corneal stroma C. exposure of the cornea due to poor lid closure with secondary bacterial infection D. Stevens Johnson Syndrome D. anterior segment dysgenesis C. increasing central corneal thickness 9. radius of curvature of the cornea C. corneal infection and trauma B. calcium 8. Peripheral corneal lesions can cause blurring of vision by: A. blocking the transmission of light B. iron B. presbyopia C. corneal transplantation C. Which substance is usually deposited at the Bowman’s Layer of the cornea? A. misdirection of eye lashes towards the cornea C. amyloid D. the human corneal endothelium retains its mitotic activity throughout life B. hyperopia and astigmastism D. myopia and astigmatism B. What is the main mechanism of corneal scarring in a patient suffering from measles? A. excimer laser photoablation D. The following are treatments options on the cornea to improve vision. the corneal endothelium can be damaged by intraocular surgery 6. direct invasion of the cornea by measles virus B. trachoma 5. corneal tattoo 61 . monocular diplopia 10. the corneal endothelium is a monolayer of cells lining the posterior surface of the cornea D. deposition of blood in the cornea 7. quality of the corneal surface B.
DISORDERS OF THE CORNEA / 62 Answer to Self Test: 1. D 4. C D B A D Fig. 1 Theory of Corneal Transparency Fig. 10. A 5. 7. 4 (L) Active fungal keratitis (R) Active bacterial keratitis 62 . B 2. 2 Radius of curvature the cornea Fig. A Pictures: 6. 9. 3 (L) Typical appearance of corneal scar (R) Hypertrophic scar Fig. C 3. 8.
5 (L) Corneal perforating injury (R) Sutured corneal perforating injury Fig 6 Exposure keratopathy secondary to lagophthalmos due to CN 7 palsy Fig.DISORDERS OF THE CORNEA / 63 Fig. 7 Congenital hereditary endothelial dystrophy (CHED) Fig. 8 Post cataract extraction corneal edema Fig. 9 Corneal dystrophy (L) Granular Type 3 ( R ) Avelino Stromal 63 .
10 Lipid keratopathy secondary to herpes simples keratitis Fig. 12 Corneal staining secondary to heme deposition Fig. 13 Autoimmune peripheral corneal melting 64 .DISORDERS OF THE CORNEA / 64 Fig. 11 Calcific band keratopathy Fig.
DISORDERS OF THE CORNEA / 65 Fig. 15 (L) Dermoid Choristoma (C) Corneal and conjunctival neoplasia ( R ) Pterygium Fig. 16 Dry eye disease with ocular surface damaged (stained with Rose Bengal dye) Fig. 17 Severe dry eye disease with ocular surface damage due to Stevens-Johnson syndrome 65 . 14 Acute chemical burn Fig.
18 (L) Keratoconus with acute hydrops ( R) Slit lamp view of corneal profile in keratoconus Fig. 66 . Note radial 10-0 nylon sutures. 19 Clear corneal graft.DISORDERS OF THE CORNEA / 66 Fig. Post penetrating keratoplasty (full thickness corneal transplant).
Mangubat. 4. Systemic examinations – general systemic examination is done in cases wherein the clinician suspects the lens problem to be part of the presentation of a systemic condition. Ancillary examinations – special ophthalmological and laboratory examinations are done as aids in the formulation of the complete diagnosis. This material is intended to serve as supplementary reading for the students as part of the unit on Cataract and focuses primarily on providing the medical student with the knowledge and skill in recognizing and assessing patients with cataract. the student is expected to: 1. Visual Acuity testing (with and without correction) c.D. as well as the general eye examination so as to better appreciate this material. 1. 67 . Movement of Extraocular Muscles e. Ocular Examination – basic eye examination comprises of the following parts should be done on each patient. Funduscopic examination 3. History – a comprehensive history is an important component specially the onset and the nature of the chief complaint 2. Intraocular pressure determination d. Pictures of typical cases will also be presented. INTRODUCTION This self-instructional material is designed for undergraduate medical students. Based on information given. 4. RECOMMENDED PREPARATION Students are advised to review the anatomy and physiology of the lens before going through this material. 3. Identify the elements in a patient’s history and eye examination that leads to the formulation of cataract as a diagnosis. M. Students are encouraged to apply knowledge that they will acquire from this material to clinical cases that they will encounter during their rotation in the clinics of the department. OBJECTIVES After going through this material. You are further advised to review the parts of a clinical history. a. be able to analyze and interpret the provided data to make a diagnosis. Diagnosis of Cataract There are four (4) basic elements that one would need to consider to be able to formulate a diagnosis. CONTENT What is Cataract? Cataract is defined as any opacification of the lens causing deterioration of Visual Acuity of < 6/9 or worse. particularly LEARNING UNIT IV students of the UP College of Medicine. Define cataract.CATARACT / 67 DISTURBANCE IN VISION CATARACT Leonardo R. Differentiate the kinds of cataract. Gross eye examination – Biomicroscopic (Slit lamp) examination b. 2.
Other aspects of the patient’s history that should be considered included: a. How long has the problem been existing? The duration of the problem should be extracted from the patient. 5. Slit lamp biomicroscope – Instrument used in the assessment of lenticular findings in the eye. What is the patient’s chief complaint? The most common presenting complaints of patients with cataract include progressive blurring of vision with no other associated symptoms. This will help in eliminating the other differential diagnosis. What is the nature of the work of the patient? Is there any exposure of the patient to intense UV light? c. 2. 1. 3. Family history. 6.CATARACT / 68 1. Tonometer – used to determine the patient’s intraocular pressure. b. EYE EXAMINATION The basic tools that one would require in conducting an examination include the following: a. Penlight – for gross examination of the eye e. Does the patient have any prior consultations / surgeries? It is important to elicit any history of any prior consultations or surgeries. It is important equally important to know from the patient of any previous eye surgeries that may result in cataract. This will help in the determination of the initial onset of the cataract and the medications that may be the cause of the cataract. 4. Most of the onset of the complaints usually starts during the 5th decade of life and are usually progressive. Are there other associated eye problems? There are usually no associated eye problems except if the patient presents with complications like glaucoma or uveitis. Has the patient suffered any systemic illness in the past? Has the patient any history of taking oral medications specially steroids for any systemic illness? 2. Is there a history of any similar illness in the family? Is there any history of any hereditary illness? b. Visual acuity charts – both for distance and near vision c. Medical history. HISTORY The patient’s history guides the clinician in arriving at a complete diagnosis. Personal history. Which eye is involved? Usually both eyes are involved but one eye might have more blurring of vision that the other one. Patient may complain of black spots in the visual field which most of the time are fixed. d. particularly as to the possible etiology of the condition. Direct ophthalmoscope – used for fundus examination 68 . The following are important questions regarding the patient’s current illness that the clinician should ask.
CATARACT / 69 COMMON OCULAR FINDINGS IN CATARACT Typically. 3. Intraocular pressure – Most patients present with normal intraocular pressures. If there is uveitis. the fundus can not be appreciated. 2 Cortical Cataract 69 . and from a white to brunescent lens. the anterior is quiet with no signs of inflammation like cells and flare. Usually. the intraocular pressure may vary. the intraocular pressure is very soft or hypotonic. Gross examination – Patients with cataract present with white pupil (leukocoria). posterior capsule or a combination of the above. They may be found in the cortex. patients exhibit full movement on all directions of gaze. nucleus. Fig 1 shows a typical picture of leukocoria. The opacifications may also vary with location. Slit lamp findings – Patients with cataract present with varying degrees of lenticular opacifications. Visual acuity – Most patients with cataract present with reduction of vision even with correction. if the patient has a relatively poor vision and the lens is very dense. 4. However if complications of cataract set in. However. the patients with cataract present with the following findings: 1. 1. 5. from water clefts to vacuoles. the intraocular is elevated. 6. the fundus findings may vary depending on the posterior segment pathology. the fundus is usually normal. If there is glaucoma. Fig. White pupil (leukocoria) 2. Fig 2-5 shows the different slit lamp findings in cataract. It may vary from a slight haziness of the lens to a dense opacification. Fig. Extraocular muscle movement – Since the extraocular muscles are usually not involved. If the patient has poor vision and the fundus can be appreciated. Funduscopic findings – Patients who have relative good visual acuity.
Ultrasound of the eye In most cases of cataract. 4 Nuclear Cataract Fig. this examination is important to determine the status of the posterior segment of the eye which includes the vitreous and retina. ANCILLARY EXAMINATIONS 1. Diabetes is associated with cataract formation in the younger age group. 3 Posterior Subcapsular Cataract Fig. This is most useful if patient’s cataract is associated with trauma. However. SYSTEMIC EXAMINATIONS Congenital Rubella is associated with development of cataract at birth. 70 . 5. Intumescent Cataract 3. it is normal. 4.CATARACT / 70 Fig.
b. The importance of a comprehensive clinical history and ocular examination are emphasized to be able to diagnose cataract. d. smoking 71 . The rubella virus gains access into the lens. a. 2. you may. Senile / Developmental – This usually starts at age 60 and above. Following this exercise. trauma D. early intervention can be facilitated and permanent visual impairment may be avoided. c. Drugs) – These are cataracts wherein the different drugs / agents affects the enzyme system of the lens epithelial cells causes disruption of the active transport system and protein synthesis. CONCLUSION As medical practitioners. Congenital – This is present at birth or until 1 year of life. SELF-TEST 1. a. It is also important that even with a simple problem of cataract. Congenital Rubella – These are cataracts with history of maternal rubella. It is imperative that immediate referral to an ophthalmologist should be done for further evaluation and possible treatment. it is further recommended that the students be provided clinical sessions to allow them to see actual cases of patients with cataract. b. aging B. diabetes mellitus C. Trauma (Non-perforating. Primary Cataract – These are cataracts with no known etiology.) – These are cataracts wherein the sugar that is entrapped inside the lens is transformed to alcohol resulting in the disruption of the regular lens matrix architecture. One should bear in mind that one should evaluate the patient further for any associated problems with cataract. complications may set in without proper treatment and referral. RECOMMENDED FOLLOW-UP It is recommended that the students be given demonstration sessions on how to properly conduct historytaking and ophthalmological examination of patients. SUMMARY It is the primary objective of this self-instructional material to provide the reader with a guide on how to diagnose patients with cataract.M. Toxic (UV. This results in the removal the normal membrane properties of the lens. in the future encounter patients who will seek consultation for eye problems. By doing so.CATARACT / 71 TYPES OF CATARACT 1. The most common cause of cataract is is A. One should be able to recognize the various ocular signs associated with cataract. Perforating) – These are cataracts that are caused by direct and indirect disruption of the capsules of the lens. Metabolic (D. Secondary Cataract – These are cataracts with known etiologies.
direct ophthalmoscope 3. glaucoma B. In a patient with mild to moderate cataract. The senile type of cataract is usually associated with what ocular disease ? A. utrasonography B. B 4. cataract surgery B. uveitis C. The vision in the affected eye is 20/50. C 72 . diabetic retinopathy D. ultrsonography C. You have a 60 year old patient with cataracts. no associated ocular disease 5. A 2. slit lamp examination C. visual acuity B. A 3. CT scan 4. ophtahlmoscopy with the pupils dilated C. electroretinography D.CATARACT / 72 2. The next step in the management of the patient is to refer the patient for A. The most important examination in assessing the functional severity of the cataract is A. refraction D. fasting blood sugar deternination ANSWERS TO SELF-TEST 1. D 5. the best way to assess the status of the retina is A. Direct ophthalmoscopy showed normal fundus findings. penlight examination with the light directed obliquely to the pupil D.
D. Diagnosis of a Retinal/ Choroidal/ Vitreous Disorder There are four elements necessary to consider the possibility of a retinal disorder. before going through this material. vitreous.VITREOUS & CHOROID / 73 DISTURBANCES IN VISION DISORDERS OF THE RETINA. 3. Photographs representative of various retinal problems will be presented. with typical cases discussed at the end of each clinical section. as well as the optic nerve. History : Good history taking is a must in a situation where loss of vision or changes in vision is the chief complaint. Differentiate the various conditions according to location. In this discussion. Many retinal diseases ( as well as vitreous) have peculiar affectations of vision which may immediately give a clue as to the type of problem. B. RECOMMENDED PREPARATION The student is advised to review the anatomy and physiology of the retina. This is due to the intimate anatomic and physiologic relationship between the two structures. M. To analyze available data and formulate a diagnosis. You are also advised to review the parts of a clinical history and the method of conducting a complete eye examination. VITREOUS AND CHOROID Pearl T. pathophysiology. Gross Eye Examination 2. CONTENT Part I. Extraocular Muscle Movements 73 . It would be ideal if the basic knowledge acquired from this material will serve as a spingboard for further self study and research on the topics covered. Visual Acuity 3. INTRODUCTION This is a self instructional material designed for the undergraduate medical student. Intraocular Pressure Determination 4. to cases that they will encounter in the actual clinical setting of the Department of Ophthalmology and Visual Sciences OBJECTIVES After reading this material. the choroid and the vitreous that lend it susceptible to certain problems. 4. choroid) that cause disturbances in vision.DISORDERS OF THE RETINA. Villalon. To recognize the peculiarities of the human retina. A. and serves as a guide to further reading. It merely provides an overview of diseases of the posterior segment of the eye (retina. one will find frequent reference to the vitreous and the choroid. 2. vitreous and choroid. Identify the various elements in a patient's history and ophthalmologic examination that contribute to the formulation of a working diagnosis of posterior segment l disease. etiology. Students are encouraged to apply knowledge that they will acquire from this material and further readings. Ocular Examination : Basic eye examination should be done on all patients: 1. the medical student in ophthalmology is expected to: 1. appearance of lesions.
HISTORY TAKING IN CASES SUSPECTED OF RETINAL DISORDERS The importance of history taking cannot be overemphasized. brightness visual field loss : central. What is your patient's chief complaint? Patients with retinal problems usually complain of some type of visual disturbance. noted with or without eye and/or head movements. Funduscopy C. The following are important questions to ask patients suspected afflicted with a retinal problem: 1. What other eye problems accompanied the visual disturbance? Pain is rarely present in retinal disorders. therefore leading to the decision to take certain subsequent measures to confirm it. Flashes (photopsias) caused by retinal problems are described as arcuate lightning like streaks of bright light in the periphery. helps in the formulation of a working diagnosis. One must take pains to extract this from the patient who may not volunteer this. contrast. peripheral. Did the visual disturbance come gradually or suddenly? The development of the symptom. 3. either volunteered by the patient.DISORDERS OF THE RETINA. current state. The information also gives the clinician an idea as to possible etiology. for example. This may come in the form of: persistent blurry vision transient blurry vision distorsion or metamorphopsia : change in shape . whether it was a sudden event or a gradually progressive event is very important information. The pain in Diabetic Retinopathy with Neovascular Glaucoma. etc. other patterns difficulty in the dark ( nyctalopia or night blindness) difficulty in bright light ( hemeralopia) floaters* and flashes ( photopsias ) * Floaters are black to gray spots and/or fibers that move about in the field of vision of the patient. treatment response and prognosis. Leukocoria or "white pupil" or a "cat's eye" reflex is a chief complaint usually brought not by the patient himself but by parents of a child. Patients describe them as " gumuguhit sa gilid ".VITREOUS & CHOROID / 74 5. It must be remembered. 4. related diseases like retinal dysplasia. change in size color vision problems : difficulty in identifying colors ( dyschromatopsia). or extracted by the clinician. Coates Disease. Ocular discomfort and/ or redness may accompany intraocular inflammatory conditions with retinal involvement. 2. They seem to float freely and may come in different numbers. D. Systemic Examination : A thorough systemic examination is done in cases where the eye problem is suspected to be part of a systemic condition or distant trauma ( away from the eye). How long has this been going on? 74 . Persistent Hyperplastic Primary Vitreous. is due to the elevated intraocular pressure caused by the glaucoma part of the problem. however. The information gathered. change in shade. thinking that it is not important or relevant. that photopsias may be of optic nerve origin. Ancillary Examinations : Special ophthalmologic and laboratory examinations are done as aids in the formulation of an etiologic diagnosis for patients suspected to have retinal diseases. This is a significant complaint and may be reflective of a serious condition like an intraocular tumor ( ex: retinoblastoma).
Middle East. Ophthalmoscope: used to examine the fundus ( retina and optic disc) 5. What is his sexuality? During history taking keep your mind open to the possibility that the patient may not be volunteering information because he does not think that it is relevant or important. If bilateral. or the patient is deliberately withholding information. to name a few. Do not forget to ask when. oral ulcers. 7.DISORDERS OF THE RETINA. pedal edema. Has he ever had a blood transfusion and when? Has he ever had cobalt therapy ? Is he on any medications for other illnesses? What are these medications ? How long has he been taking these? d) Sexual History: The presence of a history of any sexually transmitted disease should likewise be elicited from the patient. If this is a recurrent affair. boxing. Were there previous consultations and treatments ? When ? What medications were used ? What medications are being used? Did the patient have any eye operation for this or other problems? This information has bearing on the present state of the eye. bungee jumping. OPHTHALMOLOGIC EXAMINATION OF THE PATIENT The basic tools needed for an ophthalmologic examination of the suspected retina patient are 1. joint pains. Slit Lamp : instrument used in the assessment of the ocular media. duration. Gross eye Examination: The ocular adnexae are not affected in retinal disease. Visual Acuity Charts : both for distance and near vision 2. gas injection. etc. Try to get very accurate information about medications. The clinician must be observant of patient responses. 6. For example. interval and treatment as well as treatment responses. then the sequence of events. 5. The pupils must be examined for direct and consensual light reactions. Except in some retinal disorders of inflammatory origin. cryotherapy. Penlight : for gross examination of the eye and adnexae 3. attitude during history taking and find clues that will lead him to conclude these. the retina in high magnification( with special lenses) 1. ask which eye was affected first. there will be no ciliary flush or redness.VITREOUS & CHOROID / 75 The duration of the problem is an important information. intractable fever. Tonometer: used to determine intraocular pressure 4. Which eye is involved? Laterality is just as important as knowing if the same or similar problems have occurred in the fellow eye. It is also important to know if this is the first time or if the problem is recurrent. reactions. other forms of treatment ( lasers . demeanor. if you are seeing a patient who was or is under treatment by someone else.etc). Other aspects of the patient's history that should be considered include: a) Family History : Is there a history of similar illness in the family? Is there any history of any hereditary illness? b) Social History: Does the patient smoke? Does he have pets ? Does he eat raw food? Does he engage in contact sports or other unusual sports like deep sea diving. surgeries. and have been injured in the head and/or eyes? Does he take prohibited drugs or has ever taken any ? What is his occupation? Is there exposure to chemicals or toxic fumes ? Does he travel often and has been to places like Africa. Severe retinal damage as well as some optic nerve diseases can cause abnormal afferent pupillary 75 . history taking of AIDS patients is particularly challenging. China ? c) Medical History: Does he have cardiac disease ? Hypertension? Diabetes Mellitus? Asthma? Hematologic Disease? Cancer ? Pulmonary Tuberculosis ?Other diseases? Accidents that required surgery and/or hospitalization? Any operations and for what? Does he have symptoms like angina. be sure to ask about timing and sequence of events . competitive weight lifting.
the optic nerve head also has typical angiographic fluorescent qualities so that deviations may be interpreted as possibly pathologic and correlated with clinical findings. Retinal detachments usually cause some amount of hypotony due to the accompanying inflammatory changes and involvement of the ciliary body in the detachment.DISORDERS OF THE RETINA. For example retinal edema at the macula can cause metamorphopsia besides actual blurring recorded as loss of lines in the Snellen chart. 76 . as with Visual Acuity. actual blurring. thereby allowing the observer to confirm certain clinical observations. many patients report seeing floaters and light flashes before the onset of "wavy vision". as well as abnormalities in structure and form. there is no set pattern for intraocular pressures in retinal diseases. visual field "cuts".VITREOUS & CHOROID / 76 responses . 6. Intraocular Pressure: Again. The elevated intraocular pressures in end stage Proliferative Diabetic Retinopathy with Neovascular Glaucoma are due to blocking of the drainage angles by neovascular elements of the proliferative disease. This then picked up by a special camera and recorded in film. Funduscopic Findings : These depend on the retinal problem. In retinal detachments. As with the retina and choroid. A "white pupil" in a small child is always an alarming and significant finding. This dye is carried with the circulation and outlines the retinal and choroidal vascular system. Vitreous opacities also cause blurry vision. Problems in the vitreous and anatomic /pathologic vitreoretinal relationships can be determined with this examination. The vitreous always has to be considered in assessing the status of the retina. Visual Acuity: Vision is usually affected in some way in most retinal disorders. 3. ANCILLARY EXAMINATIONS Additional examinations may be necessary to make a diagnosis . Extraocular Muscle Movements: Patients exhibit normal EOMs in retinal disease. Retinal and choroidal diseases have typical fluorescent qualities and manifestations. into the antecubital vein. These will be discussed in a separate section. Fundus Fluorescein Angiography : Fluorescein ngiography is a procedure that involves the injection of a dye. Abnormalities in retinal and choroidal circulation are then highlighted. Macular disease causes blurry central vision while extramacular retinal diseases will cause peripheral visual loss. Typical affectations in vision are seen in specific retinal diseases. 2. The more commonly requested examinations are: 1. 4. Macular diseases usually do not cause pressure changes. 5. Many retinal disorders come with vitreous problems. sodium fluorescein. Slit Lamp Biomicroscopy with special lenses: These depend on the retinal problem and will be discussed in a separate section.
the presence or absence of a retinal detachment can be determined. 77 . A breakdown of the “outer blood-retina barrier” can lead to accumulation of fluid in the subretinal space and the sub RPE space. triglycerides. and . and possibly a diagnosis. The ten layer system is supplied by two different vascular systems. adjacent to the choriocapillaris of the choroid. Any breakdown in the neurons. SYSTEMIC EXAMINATION Many retinal diseases are part of systemic problems like Diabetes Mellitus. are supplied by the retinal vasculature itself. Collagen Disease. in the presence of a very dense cataract. The inner layers. B. knowing the extent of supply of each system. one can then predict the depth of retinal involvement. For example. giving clues as to the type of tumor. keeps the retina “dry” with its “outer blood-retina barrier”. etc.DISORDERS OF THE RETINA. non healing ulcers and wounds in the lower extremities in Diabetes Mellitus. participates in the recycling of retinol. and to the optic nerve and finally into the brain. In the ten layers are three main cell types that relay visual/chemical information through the retina . It is also very useful in assessing the amount of and density of intravitreal material such as blood. Hematologic Disorders . ) and x-rays form an important part of "systemic examination" and must be done when a patient is suspected of having a certain disease. A physiologic “pump” also exists in the human RPE layer and this contributes to keeping fluid away from the retina. the supporting cells and the relay system itself can manifest as visual disorders. BUN. Systemic Lupus Erythematosus and other collagen diseases. Hypertension. Malignant Disease. skin discoloration of the lower extremities. from outside to in. This manifests as retinal edema. disposes of metabolic wastes of the other cells. Part II. Peculiarities of the Retinal Microstructure A. Pulmonary Tuberculosis. It is used to assess the density of tumors. may present typical funduscopic findings. cholesterol. Patients can present with pedal edema. It takes care of most metabolic processes of the outer retinal layers. and is the outermost layer. Certain retinal diseases can be traced to problems of perfusion . The Retinal Pigment Epithelium: The retinal pigment epithelium (RPE) is the first of the ten layers. creatinine.VITREOUS & CHOROID / 77 2. Some of these like Diabetic Retinopathy. and to locate intraocular foreign bodies in trauma cases. Hypertensive Retinopathy. The outer retinal layers derive nutrition from the choriocapillaris of the choroid. The 3 Neuron Relay System: The human retina is a tall structure that has ten layers. Blood chemistry (blood sugar. Ocular Ultrasonography : In the presence of media opacities the ultrasound is a useful tool to evaluate the anatomic relationships in the posterior pole. from the inner nuclear layer inwards.
vitreous liquefaction and anterior displacement can cause undue traction on the vitreous base and may end up in a retinal tear or dialysis. Retinoschisis F. Central Retinal Vein Occlusion. called Zonnula Occludens keeps the RPE layer leakproof from the highly vascular choriocapillaris of the choroid. The Outer Blood-Retina Barrier: This is found in the RPE. to which it is adjacent. E. Maculopathies: Age Related Macular Degeneration. Hypertensive Retinopathy. Juvenile Foveal Retinoschisis. Toxocariasis H. The Inner Blood-Retina Barrier : This is attributed to the tight endothelial cell junctions of the retinal capillaries. The Blood –Retina Barriers: There are two so called blood-retina barriers that keep the retina ‘dry”: D. A. Vitreous Hemorrhage. leading to retinal detachment. Cystoid Macular Edema C. Retinoblastoma E. Retinal Vascular Disease : Diabetic Retinopathy. as well as lipids and proteins from the retinal vascular tree. An additional feature is the presence of a physiologic “pump” that keeps fluid contained outside the retina. This gel is 99% water and only 1% solid. the solid part being collagen fibrils that make up the meshwork. The tight intercellular attachments between RPE cells. the macula. This manifests as retinal edema. Choroid and Vitreous Examples of Retinal and Vitreous Disorders with typical fundus findings will be described briefly in this section. hemorrhages. Tumors: Metastatic Tumors. 1. Macular Holes. The Vitreoretinal Relationship : The globe is filled with a gel called the viteous. Retinal Detachments . Central Serous Chorioretinopathy. Vitreous Opacities / Degeneration: Vitreous Detachment and Syneresis. and the very few cells called hyalocites. causing the formation of a macular hole. along blood vessels and also at the so called vitreous base (where the retina ends peripherally and anteriorly). Please read about details and other retinal and vitreous disorders. Many disorders in vision originate from problems with the vitreoretinal interface. Uveal Effusion : Vogt-Koyanagi-Harada Syndrome H: Infectious Retinopathies : HIV Retinopathy 78 . Synchisis Scintillans. Best’s Vitelliform Macular Degeneration D. Color Blindness. hard exudates. Retinochoroiditis : Toxoplasmosis. Vitritis G. on the macula.VITREOUS & CHOROID / 78 C. Heredodegenerative Diseases of the Retina: Retinitis Pigmentosa. Any disturbance in the integrity of these tight attachments leads to oozing of fluid and/or blood.DISORDERS OF THE RETINA. Melanomas. For example. Another example is undue traction of the vitreous gel and posterior hyaloid of the vitreous. Retinopathy of Prematurity B. The vitreous is firmly attached to the optic nerve. 2. Central Retinal Artery Occlusion. Asteroides Hyalitis. Part III: Diseases of the Retina.
and is closely related to the onset of diabetic nephropathy. soft exudates. moderate. Vision deteriorates when the patient has macular edema.VITREOUS & CHOROID / 79 DIABETIC RETINOPATHY Diabetic Retinopathy is a complication of Diabetes Mellitus and manifests mainly as vascular changes in the retina. neovascular glaucoma. Good blood sugar control has been proven by wide based studies. Panretinal treatment is performed when the disease reaches the proliferative high risk stage. retinal hemorrhages. Non proliferative DM retinopathy Proliferative DM retinopathy proliferative DM retinopathy with vitreoretinal traction 79 . The only proven treatment is laser treatment . with each subdivided further into minor stages: mild. Surgery is also done for non clearing vitreous hemorrhage.DISORDERS OF THE RETINA. dot and blot retinal hemorrhages.. The typical fundus findings in non proliferative DM retinopathy are: microaneurysms. Treatment for vitreoretinal traction comes in the form of vitreoretinal surgery. Diabetic Retinopathy is one such complication. while macular focal and grid laser treatment can be done at any stage if maculopathy causes significant visual loss.severe. and must be maintained to delay the onset of the complications of diabetes mellitus or their progression. macular traction. The hallmark of the proliferative stage is the growth of abnormal new vessels (neovascularization) either on the disc or on the retina. vitreous hemorrhage. vitreoretinal traction and detachment. dense premacular hemorrhage. very severe for the former and early and high risk for the latter. hard exudates. to be a key modifiable factor. There are two stages of diabetic retinopathy : non proliferative and proliferative stages. The onset of the disease is usually after many years of diabetes.
CRVO CENTRAL RETINAL ARTERY OCCLUSION Central Retinal Artery Occlusion or CRAO . Vision is very poor in this situation. others. Treatment comes in the form of laser treatment ( scatter treatment similar to PRP of DM retinopathy) when certain criteria are met. CRAO manifests as sudden painless loss of vision. is one of only two "absolute" emergencies in ophthalmology. and remaining vision just after the episode is usually in the area of count fingers and hand motions. one thinks of systemic vascular diseases such as hypertension . The more severe type is the ischemic type where the fundus is covered with splinter hemorrhages radiating from the optic disc and which appear to be following the disposition of the nerve fiber layer. It does not occur as frequently as CRVO. there are fewer retinal hemorrhages and usually no soft exudates. cardiac valvular disease. but there is definite retinal venous tortuosity and dilation. Vision is much better than in the ischemic type. In the younger individual. A fundus fluorescein angiogram will help confirm the type of CRVO.VITREOUS & CHOROID / 80 CENTRAL RETINAL VEIN OCCLUSION Central Retinal Vein Occlusion or CRVO manifests in two ways or types: ischemic and non ischemic ( also called "stasis") .in the non ischemic type . Retinal veins are tortuous and dilated. CRAO is usually related to systemic vascular disease like hypertension. Some patients report a prodrome of temporary "wipeout" of vision several times in a span of days to weeks before the actual CRAO. diabetes. arteriosclerosis as the cause of the episode. In contrast. peripheral vascular disease.DISORDERS OF THE RETINA. collagen disease. In the elderly. At this time the patient's vision appears white or gray with all details gone temporarily. hematologic disorders. One typically finds soft exudates ( "cottonwool spots") indicating retinal ischemia. arterioscelrosis. arrhythmias. Visual loss is severe. The disc borders are not blurry. The disc may have blurry borders covered with the retinal hemorrhages. Prognosis for visual 80 . etc. Embolic phenomena must also be entertained. This "wipeout" is very brief and lasts for a few seconds. one thinks if other things such as inflammatory disease. CRVO can happen to both elderly and young individuals. hematologic disorders. such as in patients with internal carotid stenosis. collagen disease.
In ARMD. Treatment of the Wet type is thermal laser treatment to the abnormal vascular complex. age is a definite risk factor. if extrafoveal.. lack of vitamin C and other antioxidants. It is more common in the elderly and the incidence rises sharply after the age of 75 years. in people over 50 years of age. Exudative or Hemorrhagic Type. The subfoveal types are treated using a new modality called Photodynamic Therapy(PDT). CRAO AGE RELATED MACULAR DEGENERATION Age Related Macular Degeneration( ARMD) is one of the major causes of central visual loss in the Western world.. undue exposure to UV light. ethnicity. the Dry Type and the Wet . which involves the injection of a photosensitive dye and a special type of laser. There is also atrophy of the retinal pigment epithelium. In the Wet Type a neovascular complex grows under the retina from the choroid. Nothing has been proven about these risk factors but recent studies show that there may be proof of its relationship to smoking. Treatment must be instituted within 5 minutes of the attack and comes in the form of immediate lowering eye pressure to improve intraocular perfusion. cardiovascular disease. Dry ARMD Wet ARMD RETINITIS PIGMENTOSA 81 .DISORDERS OF THE RETINA. This bleeds and causes scarring of the retina. The basic pathology of the Dry type is the accumulation of cellular debris and formation of "drusen" under the retina. Other risk factors implicated are: smoking. The Wet Type comprise only 10% of all ARMD but is resposible for 90% of those with vision of 20/200 and less.VITREOUS & CHOROID / 81 recovery is very poor. There are two types. The Dry type is the more common one and visual loss is not as severe as in the Wet type.
There are several modes of transmission: autosomal recessive. blunt trauma. (ex. with no known demonstrable effect on vision. RP with very little or no pigment is possible ( sine pigmento) and is usually type II. Fundus findings include vitreous cells and opacities. congenital stationary night blindness). Absence of night blindness is possible especially in type II RP. diffuse pigmentation of the retinal pigment epithelium( RPE). blurring of vision in some cases ( with macular involvement. Retinitis pigmentosa Retinal Detachment Retinal Detachments are conditions where the retinal pigment epithelium is separated from the inner retinal layers. RP systemic syndromes. It is characterized by progressive degeneration of the rods and cones. There is no known treatment of Retinitis Pigmentosa. X-linked recessive. progressive contraction of peripheral visual fields.VITREOUS & CHOROID / 82 Retinitis Pigmentosa( RP) is a retinal disorder that belongs to the family of Heredodegenerative Diseases and “ Tapetoretinal Diseases”. and type II in which the cones are affected earlier than the rods. 82 . There are 2 types of RP: type I in which the rods are affected earlier than the cones. RP is a bilateral disease and “unilateral RP” does not exist. Cataract extraction may help improve vision. uveitis.DISORDERS OF THE RETINA. and waxy pallor of optic disc in late stages. with accumulation of fluid in the “subretinal space” (space between RPE and photoreceptor layer). narrowed arteries. Symptoms include night blindness or nyctalopia for most cases of type I . and in most cases is associated with migration of pigment epithelial cells into the retina.000 IU of vitamin A helps slow down deterioration of ERG. and remains so until visual fields are markedly contracted. bone spicule and comma shaped Intraretinal proliferation of pigmented cells. Genetic analysis has shown that the defect in most affected individuals is in the gene that codes for rhodopsin. If findings are unilateral other causes must be ruled out. Patients with the autosomal dominant form may be symptom free till middle age. and development of cataract) . Other causes of night blindness must be ruled out ( ex. autosomal dominant patterns of inheritance. vitamin A deficiency. long standing retinal detachment). The first two have the earliest onset and worst prognosis. Daily doses of 15.
myopic degeneration. In adults. patients experience blurry vision of variable onset depending on cause.DISORDERS OF THE RETINA. neovascularization due to central and branch retinal vein occlusion. Massive vitreous hemorrhage can cause significant loss of vision without the floaters. The principles of retinal reattachment surgery are: finding the break (s). Rhegmatogenous retinal detachments are associated with retinal thinning and peripheral retinal degeneration. Causes of traction detachments are diabetic retinopathy. Management of Traction detachment is surgical as well. Any cause of peripheral neovascularization may cause vitreous hemorrhage. sealing of the retinal breaks with a chorioretinal scar. other abnormalities are 83 . tumors. wavy vision. Causes of exudation are inflammatory disease of the choroid and retina. visual field cuts. Trauma ( including the Battered Child syndrome) should always be ruled out in children. the most frequent cause is diabetic retinopathy. Causes of Non rhegmatogenous detachments are exudation and traction. posterior vitreous detachment. Symptoms of rhegmatogenous retinal detachments are: sudden onset of blurry vision. and vitreoretinal traction during vitreous liquefaction and detachment. or “streaming dark lines”. accelerated hypertension as in ecclampsia. Management of rhegmatogenous retinal detachment is surgical. addressing the primary cause. Occasionally there are reports of light flashes in the peripheral field of vision. trauma. Other causes are retinal break(s) without detachment.VITREOUS & CHOROID / 83 Retinal detachments can be “rhegmatogenous” (with retinal break) or “non rhegmatogenous” ( without a break). other vascular disease like diabetes mellitus. while management of exudative detachment is primarily medical. Retinal detachment Vitreous Hemorrhage Decreased vision and floaters caused by non traumatic vitreous hemorrhages are common causes of emergency consults with the eye doctor. including the chronic stages of pars planitis and other uveitides. with closure of the retinal break. ischemic retinopathies. Symptoms come in the form of sudden onset of blurry vision. Management will be directed at: finding the cause and clearing the blood. rhegmatogenous retinal detachment. subretinal tumors. trauma. In most cases retinal examination will permit adequate assessment of the situation and identification of cause. When vitreous hemorrhage is too dense an ocular ultrasound must be done to determine if retinal detachment. As a rule. flashes and floaters Symptoms of exudative and traction detachments are determined by the cause. frequently with floaters in the form of “many dust like particles” which are dispersed RBC.
In the presence of retinal detachment. 84 . There are two types of Ocular Toxoplasmosis: congenital and acquired. Recurrences of activity are possible and can be found at the edges of scars from previous attacks. The later in pregnancy the infection is acquired by the mother. Scarring of the retina and choroid are prominent in the quiescent phase. tumor. Diagnosis is best made clinically although immunologic examinations are helpful. The use of steroids whether oral.DISORDERS OF THE RETINA. topical or peribulbar are not without hazard. surgical removal of the vitreous hemorrhage with /without laser treatment is considered within the context of management of the secondary retinopathy. the more serious the ocular problem. if no retinal detachment or tumor is detected. The acquired type is via ingestion of the organism in uncooked food or infected fomites. Ocular Toxoplasmosis Ocular toxoplasmosis. Treatment is in the form of oral antibiotics that interfere with the organism’s pathway for protein transcription. Retinochoroidal scars in “quiet” toxoplasmosis “Headlight in the fog” in active toxoplasmosis Vogt-Koyanagi-Harada Syndrome Vogt-Koyanagi Harada Syndrome (VKH) is a rare and unusual form of diffuse granulomatous uveitis. caused by an intraocular obligate parasite is one of the more common forms of posterior uveitis ( inflammation of the uveal tract). The classic finding is retinochoroiditis. and passed on to the unborn child. retina and choroid hence. the break is sealed with laser. If a retinal break without a detachment is found. This allows faster resorption of blood. This is found more in pigmented individuals. The congenital type is acquired by the pregnant immunoincompetent mother. Macular involvement will certainly lead to poor vision. the hemorrhage may be observed for 4-6 months and left to absorb. other disease requiring immediate attention.pyrimethamine. Visual affectation is dependent on the part of the retina affected. The general rule is. vitreoretinal surgery is advised.VITREOUS & CHOROID / 84 present behind the blood. The infection is easily quelled by the patient but the organism finds its way into the eye and causes an inflammatory reaction in the vitreous. clindamycin. bilateral patching. a retinochoroiditis. such as sulfadiazine. If this is a hemorrhage accompanying the traction detachment and/or retinal neovascularization. Immediate management comes in the form of strict bedrest with head elevation ( high back rest).The organism Toxoplasma gondii. is a protozoan that has predilection for the retina.
Later in the course of the disease the patient develops vitiligo ( white patches on the skin) and poliosis (whitening of eyelashes). Fundus fluorescein angiography may help define structures involved. based on clinical presentation and findings. The course is long term and indolent. optic disc edema.. collagen vascular disease. a spinal tap and immunologis tests will help make a diagnosis of VKH. retinal vaso-occlusive disease).VITREOUS & CHOROID / 85 The patient usually complains of sudden onset of blurry vision. perhaps floaters. A high index of suspicion. the eye becomes vulnerable to a number of opportunistic infections and neoplastic conditions. Kaposi’s sarcoma. The manifestations of disease differ with the type of opportunistic infection. Pneumocystis carinii infection.These include CMV retinitis. retinal vasculitis. Diagnosis must exclude other causes of cottonwool spots (diabetic retinopathy. neck stiffness. tinnitus. The final outcome depends on control of the inflammation and scar formation. Candida Retinitis. These localized ischemic areas are located at the posterior pole and may be related to circulating immune complexes. The disease presents as serous retinal detachments with yellowish white patches of edema of the retinal pigment epithelium. The eye disease is managed with intravitreal implants of these medications in addition to the systemic management. photophobia. Vitreoretinal surgery is indicated when there is vitreoretinal traction and non clearing vitreous hemorrhage. The most consistent feature are cottonwool spots (retinal nerve fiber infarcts) which are present at some time during the course of the systemic HIV infection. Vision is relatively good except where the macula has been affected. Toxoplasmosis. In most cases cottonwool spots are asymptomatic and blurry vision comes only if the lesion is at or close to the macula. Management comes in the form of AIDS management such as systemic gancyclovir and foscarnet. 85 . More frequently because of the underlying systemic immunodepression. sometimes with headache.DISORDERS OF THE RETINA. Serous detachments in VKH “Sunset Glow” in VKH HIV Retinopathy The Human Immunodeficiency Syndrome (HIV) may affect the eye directly. Patients are put on systemic steroids and immunosuppressives. There may be a heavy anterior uveitis.
1994 3. Atlas of Clinical Ophthalmology. as many retinal diseases have very typical stories to tell. Latest edition 2. CONCLUSION As medical practitioners we should be aware of the different types of retinal diseases and their manifestations.Texbook of Ophthalmology. Newell.VITREOUS & CHOROID / 86 Cottonwool spots in HIV Retinopathy CMV retinitis in HIV patient SUMMARY It is the primary objective of this material to provide the medical student a guide on how to recognize the retina patient with a good history and thorough eye examination. 2nd ed. This being so. Yanoff.DISORDERS OF THE RETINA.Frank.. REFERENCES 1. especially in systemic diseases. A 50 year old female comes to you with complaint of sudden onset of blurry vision of the right eye since a week prior to consult. Retina and Vitreous. as in diabetic retinopathy. 15th ed. The importance of comprehensive history taking cannot be overemphasized. She reports that she has had diabetes mellitus for the past 15 years and is on insulin. Vol 9.the medical practitioner should realize that many problems of the retina can be traced to systemic diseases or problems of parts of the body distant from the eye. Vision OD: Count Fingers 2 feet OS: 20/20 J1 with correction Intraocular Pressure OU: 15 mm Hg 86 . as in distant trauma. Podos. 2001 4. 1992 EXERCISES Case 1. it is then possible for a systemic disease to be diagnosed because of the typical retinal changes. Tasman. with poor control of blood sugar.. General Ophthalmology. Textbook of Ophthalmology.Riordan-Eva.Asbury. More than this . Jaeger. Vaughan. It is therefore very important for the medical practitioner to recognize these retinal problems so that proper management can be instituted immediately.
Vision OD: 20/20 J1 without correction OS: 20/70 J5 corrected to 20/25 with a refraction of + 1. What is your working diagnosis of the case ? 2. any history of surgery or intake of medications. what will your working diagnosis be? 87 . macula. Is there anything else that you would want to ask the patient? 4. of 1 week duration. no anterior chamber cells . EOMs OU: normal Based on the data given above: 1.DISORDERS OF THE RETINA. normal vessels. What ancillary procedures would you ask for? Case 2. Why? 3. Why ? 3. Several cottonwool spots and blot hemorrhages are also seen all over the fundus.VITREOUS & CHOROID / 87 Slit Lamp findings: OD: clear lens. hypertension. What ancillary procedures will you order for the patient? 4. What else would you want to know during your history taking? 2. clear vitreous Funduscopy OD: negative ROR OS: occasional microaneurysms noted all over the fundus. any other diseases. He denies any history of diabetes.50 D sphere Intraocular Pressure OU: 17 mm Hg. He says that straight lines are distorted and the image size in the affected eye is smaller than the normal eye. with fine white stippling EOMs OU: normal Based on the data given above: 1. If the patient were 70 years old. hazy vitreous with no view of the retina OS: clear lensq . vessels OS: normal disc. lens. vitreous Funduscopy OD: normal disc. anterior chamber. no anterior chamber cells. A 25 year old jeepney driver consults you for sudden blurring of vision of the left eye. Slit Lamp Findings OU: normal cornea. macula is elevated (edematous).
be able to extract a complete history and perform an ocular examination. excellent illumination and a stereoscopic view of the disc. 3. Marissa N. The main disadvantage of the indirect ophthalmoscope is the small image size. and pallor of the neuroretinal rim. The optic disc can be examined clinically with a direct ophthalmoscope. Size of the optic cup in relation to the area of the optic disc. retina and optic nerve before going through this material. Size. As a result.D. discuss the principles of management of glaucoma RECOMMENDED PREPARATION The student is advised to review the anatomy and physiology of the anterior chamber angle. Aquino M. Cup-to-disc diameter ratio and cup-to-disc area ratio.. The direct ophthalmoscope. the medical student in ophthalmology is expected to: 1. CONTENT Glaucoma and The Optic Nerve The assessment of the morphologic features of the optic disc are essential in glaucoma. functional visual field disturbance or visual field loss occur. OBJECTIVES After reading this material. 4. The best method to examine the optic disc is with the posterior fundus lens with a slit lamp. 8. shape. and location of parapapillary chorioretinal atrophy. This leads to the formation of defects within the nerve fiber layer of the retina (RNFL) with subsequent cupping. Configuration and depth of the optic cup. 6. 2. 4. 9. Size and shape of the optic disc. 5. discuss the examinations for glaucoma. and 10. Diffuse and/or focal decrease ot the diameter of the retinal arterioles. although providing high magnification. or excavation. configuration. 3. discuss the pathophysiology of glaucoma 2. He is also advised to review the parts of a clinical history and the method of conducting a complete eye examination. or a posterior fundus lens (with a slit lamp). Presence and location of splinter-shaped hemorrhages. (Table 1). 7. This system provides high magnification. of the optic nerve head. Occurrence.GLAUCOMA / 88 DISTURBANCES IN VISION GLAUCOMA Norman M. MHPEd INTRODUCTION Glaucoma is a neurodegenerative disease characterized by death of retinal ganglion cells and loss of their axons. Table 1: Clinical Evaluation of the Optic Nerve Head 1. Position of the exit of the central retinal vessel trunk on the lamina cribrosa surface. does not provide sufficient stereoscopic detail. given a patient with glaucoma. size. Visibility of the RNFL 88 . an indirect ophthalmoscope. Valbuena M.D.
There are also racial differences in cup-to-disc ratios. genetic predisposition.1. 89 . However.2. The tissue between the cup and the disc margin is the neuroretinal rim (Fig. and course of the disease (Table 2).3 is considered normal. (Fig. Usually.1). It is common practice to grade an optic disc by comparing the diameter of the cup to the diameter of the disc in both the horizontal and vertical meridians. vascular and biochemical insults have been found to play a significant role in the pathogenesis of the disease.Concept of proposed pathogenesis of glaucoma. This is usually expressed as a ratio such as 2/10 or 0. a horizontal cup-to-disc ratio of 3/10 or 0. Fig. In normal patients. European Glaucoma Society The appearance of the optic disc often provides essential information about the existence.2.GLAUCOMA / 89 The optic disc is usually round or slightly oval in shape and contains a central cup.Normal Optic Nerve. Cup-to-disc ratio increases slightly with age. Arrows show borders of optic disc and cup Elevated intraocular pressure was traditionally considered to be solely responsible for the anatomic damage in glaucoma.2) Fig. Inherent structural defects. the stage. this rim has a uniform width and a color that ranges from orange to pink. it has now been shown that there are other factors which play a role in the production of these morphologic changes seen in the glaucomatous optic nerve.
Nerve fiber layer loss Less Specific Signs 1. 4 . Fig. 5). 3). Splinter hemorrhage 6. The optic nerve head then takes on an excavated and undermined appearance that has been likened to a “beanpot” (Fig. This may be difficult to appreciate unless previous clinical records. Splinter hemorrhage usually appears as a linear red streak on or near the disc surface (Fig.Localized loss of neuroretinal rim (notching) 90 . The hemorrhage clears over several weeks but is often followed by localized notching and pallor of the rim with subsequent visual field loss. Localized narrowing of the neuroretinal rim (notching) 2. Progressive enlargement of the cups Focal Signs 1. Vertical elongation of the cup 3. In more advanced glaucoma. Baring of circumlinear vessels 4. Exposed lamina cribrosa 2. If this occurs at either (or both) the superior or inferior pole of the disc. the tissue destruction extends behind the cribriform plate and the lamina bows backward. the cup becomes vertically oval.Enlarged optic cup with narrow neuroretinal rim. Large optic cup 2. Fig. Nasal displacement of vessels 3. Focal enlargement of the cup appears as localized notching or narrowing of the rim (Fig. Cupping to the rim margin 4. It is also useful to compare one eye to the fellow eye as disc asymmetry is unusual in normal individuals. 6). Regional pallor 5. diagrams or photographs are available. 3. Asymmetry of the cups 3. Peripapillary atrophy Generalized enlargement of the cup may be the earliest change detected in glaucoma (Fig. 4).GLAUCOMA / 90 Table 2: Optic Disc Signs of Glaucoma Generalized Signs 1.
The normal visual field extends approximately 60 degrees superior and nasal. 70 degrees inferior. The dimensions of the normal field of vision are defined relative to fixation.7). Fig. and appears as a pattern of striations that radiate toward the optic disc.Splinter Hemorrhage in the disc In the normal eye. 6 . of a cadaver. the nerve fiber layer thins and becomes less visible. Diffuse loss of the nerve fiber layer may be a very important sign of early glaucomatous damage (Fig.GLAUCOMA / 91 Fig.Glaucomatous disc damage: Eye of patient.Nerve fiber bundles The Normal Visual Field With the eye open and looking straight. 7 . the nerve fiber layer can be best visualized with red-free illumination. and 90-100° temporal to fixation 91 . the visual field of that eye is defined as all the space that it can see. and a histologic section showing excavation or cupping of the optic disc F Fig. With the development of glaucoma. 5 .
9). . It may be the only practical method to evaluate patients who are unable to perform well using the more sophisticated 92 . and refraction. Many neurologic and neuro-ophthalmologic conditions also alter the visual field. the “peak” of sensitivity at fixation. He described the variable slope of the island. the fovea. 8).Traquiar’s Island of vision/ Hill of vision The size and contour of a visual field can be influenced by other factors in addition to glaucoma. and the normal blind spot as a “gorge” that drops to sea level at a location approximately 15° to the temporal side of the highest peak. eyelid anatomy. Fig. Fig. There are various ways of testing and mapping out a patient’s visual field. Visual sensitivity is greatest in the center. Testing the Visual Field Visual field testing. These include facial structure.Normal limits of the visual field of the right eye Traquair graphically described the visual field as a three-dimensioned “island of vision surrounded by a sea of blindness” (Fig. and decreases toward the periphery. 8 . the visual field of each eye is plotted as the patient sees it. pupil size. It likewise plays a critical role in monitoring the disease’s progression.GLAUCOMA / 92 (Fig. 9 . The blindspot occupies the area defined by the optic nerve head and is typically located 15 degrees temporal to fixation. clarity of the ocular media. is an important diagnostic tool in glaucoma. or perimetry. The confrontational method of visual field testing will quickly demonstrate gross field defects. By convention.
The patient responds when light is perceived in each test spot. The Goldmann perimeter is an example of a manual kinetic perimeter. Retinal nerve fibers radiate from the optic nerve head and are distributed in an arcuate manner around the foveal region (Fig. is moved from a nonseeing area toward a seeing area. 11). 11 . usually a light of variable size and intensity projected on an evenly illuminated surface. The detection of small field defects in early glaucoma may be missed using this technique. Fig. 10).Static perimetry Static visual field testing involves the use of non-moving test spots.GLAUCOMA / 93 instruments used in perimetry testing.Kinetic perimetry Fig. It describes the contour of the hill of vision (Fig. 12). The location is recorded when the patient sees the object. The process is repeated until a boundary of seeing and non-seeing is determined. Fixed test spots of varying intensity of light are presented for a short period of time. Static testing attempts to find the light sensitivities of the eye at preselected locations in the visual field. It is important to correlate changes in the visual field with changes in the optic disc. The Glaucomatous Visual Field Glaucomatous optic nerve damage produces characteristic changes in the contour and shape of the visual field. Visual field changes seen in glaucoma reflect retinal and optic nerve anatomy. Kinetic visual field testing is performed. Glaucomatous damage at the optic nerve head produces visual field defects in the region subserved by the 93 . with a moving test object. as the name implies. 10 . This boundary line is called an isopter. If an appropriate correlation is not present. The Humphrey Visual Field Analyzer and the Octopus are examples of automated static perimeters. The object. other causes of visual field loss must be considered. Several isopters are usually obtained using test objects of different size and or intensity (Fig.
These defects are produced by damage to the nasal neuroretinal rim. With progression.GLAUCOMA / 94 affected nerve fibers.Distribution of retinal nerve fibers The most common location of glaucomatous visual field defects occurs within an arcuate area commonly referred to as Bjerrum’s area which includes that portion of the arcuate region that extends from the blindspot to the median raphe. 15). the scotoma arches from the blind spot and ends at the nasal raphe. where it extends 10-20 degrees nasally from fixation (Fig. 13 . 13) The arcuate scotoma often begins as a single area of relative loss which become larger. paracentral scotomas become deeper and larger and may gradually coalesce forming an arcuate or Bjerrum scotoma. arcuate defects. nasal steps.Bjerrum’s area 94 . therefore wedge-shaped defects develop. the arcuate scotoma may break through the nasal periphery. Nerve fibers radiate without deviation from the optic nerve. Temporal defects are usually found as a late manifestation of glaucomatous visual field loss. The location. 14). 12 . called a scotoma. becoming wider and closer to fixation on the nasal side (Fig. distribution. 16). size and shape of the resulting visual field defect. deeper and multi-focal (Fig. Fig. A temporal defect is a wedged-shaped defect extending from the periphery toward the central visual field (Fig. Fig. It can occur as an isolated finding in early glaucoma or can be associated with a paracentral or arcuate defect. and temporal defects. Paracentral scotomas may be missed because of their location and small size. A paracentral scotoma is a discrete area of absolute or relative visual loss within 10° of fixation. is therefore determined by the location and extent of the anatomic defect. In its full form. The scotoma can be single or multiple and can occur as an isolated finding or can be associated with other visual field defects. Later in the disease. Typical glaucomatous visual field defects include localized paracentral scotomas. A nasal step is a depression in the superior or inferior nasal field near the horizontal raphe.
or this may be a purely vascular disease. Although intraocular pressure is within the normal range. 95 . 14 . Many patients are asymtopmatic.Temporal wedge defect Summary: The Optic Nerve and The Visual Field The visual field is the functional correlate of the anatomical change brought about by the glaucomatous damage to the optic nerve. Pathogenesis of low tension glaucoma may involve abnormal sensitivity to IOP because of vascular or mechanical abnormalities in the optic nerve head. Diagnosis is established when glaucomatous optic disc or visual field changes are associated with elevated intraocular pressure. Visual field examination. a normal appearing anterior chamber angle by gonioscopy and no other reason for elevated intraocular pressure.Full arcuate scotoma Fig. reduction of intraocular pressure may still be beneficial. 15 . is useful in assessing optic nerve function.GLAUCOMA / 95 Fig. They may have blurring of vision which they attribute to an error of refraction. or perimetry. Focal loss of vision such as in scotoma. 16 . Primary Open Angle Glaucoma The chief pathologic feature of primary open angle glaucoma is a degenerative process in the trabecular meshwork resulting in reduction of aqueous drainage leading to a rise in intraocular pressure. unless severe is rarely noticed by the patient. Normal Tension Glaucoma (Low Tension Glaucoma) Some patients may have glaucomatous optic disc of visual field changes But have IOP consistently below 22 mm Hg. Correlating the information obtained by careful examination of the optic nerve with its function is far superior to using either piece of information alone. Raised intraocular pressure preceded the optic disc and visual field changes by months to years.Beginnings of an arcuate scotoma Fig.
which creates a permanent connection between the posterior and anterior chamber is the definitve treatment. Patients complain of sudden severe blurring of vision. Attacks may resolve spontaneously. Prostaglandin analogs – bimatoprost. Hyperosmotic agents – oral glycerol. alpha adrenergic agonists. redness and blurring of vision. Attack is precipitated by papillary dilatation. which can occur spontaneously.apraclonidine. beta adrenergic blocking agents – timolol. Glaucoma valves D. In many cases. Laser peripheral iridotomy . Suppression of aqueous production 1. Medical Treatment A. Ocular findings include ciliary injection. Intraocular pressure is controlled medically if possible. 1. narrow or closed anterior chamber angle with varying amounts of peripheral anterior syneechia. Treatment of Raised Intraocular Pressure I. the fellow eye should receive a prophylactic laser iridotomy. Cyclodestructive Psocedures 96 . nausea and vomiting. redness and blurring of vision associated with halos around lights. Peripheral iridotomy. latanoprost. Laser trabeculoplasty C. On examination. IV mannitol II. oral acetazolamide B. optic disc and visual field changes. Parasymathomimetic agents – pilicarpine 2. Acute angle closure glaucoma is an emergency.GLAUCOMA / 96 Primary Acute Angle Closure Glaucoma When sufficient iris bombe develops to cause occlusion of the anterior chamber angle by the peripheral iris. with severe pain. Patients maybe asymptomatic or may have recurrent short episodes of unilateral pain. They may have attacks of subacute angle closure.dorzolamide. Facilitation of aqueous outflow. by reduced illuminations in the evenings or due to medications. travaprost C. Chronic Angle Closure Glaucoma Some patients with anatomic predisposition for angle closure do not develop acute rises in intraocular pressure but develop instead progressive peripheral synechia resulting in gradual rise in intraocular pressure. patients have elevated intraocular pressure. a hazy cornea. brimonidine 3. Trabeculectomy 2. Glaucoma Drainage Surgery 1. shallow anterior chamber and an elevated IOP. Surgical and Laser Treatment A. Iridectomy B. carbonic anhydrase inhibitors. Extensive peripheral synechia may require drainage surgery. Reduction of vitreous volume 1. Treatment is directed at reducing IOP. betaxalol. Aqueous outflow is blocked and IOP rises causing severe pain. levobunolol 2.
Riordan-Eva. Schiotz tonometry C. Krupin. C/D ratio 0. 20 year old . Direct ophthalmoscopy D. The following are methods for viewing the optic disc. Blurring of vision 2. T. ANSWERS TO SELF-TEST 1. IOP = 15 mm OU B.. IOP=16 mm OD. SELF-TEST 1. It results from ganglion cell loss with resultant optic nerve damage and functional visual field loss.3 OD. Epstein. B 3. R. Mosby. EXCEPT A. Irregular miotic pupil C. Which of the following findings in your patients will make you suspect that he has glaucoma ? A. any of the above. The typical visual field defect in glaucoma is a/an A. C/D ratio 0. depending on the severity of the disease. you will be able to examine the following EXCEPT A. 0.GLAUCOMA / 97 SUMMARY Glaucoma is an important ocular disorder that can cause preventable blindness. Vaughn and Ashbury’s General Ophthalmology . indirect ophthalmoscopy B. (eds) The Glaucomas. Williams and Wilkins.4 OS. You were assigned to see 4 patients at the OPD. 2004-2005. 2. 60 year old. pallor of the optic nerve 5.. quadrantanopia D. B 2. Chandler and Grant's Glaucoma. Ocular pain E. A 5. B. David L. C/D ratio 0. 60 year old. IOP =12 mm OD. A 97 . EXCEPT A. 1997. C 4. John. New York: Lange Medical Books/ McGraw Hill. Ciliary injection B. Signs of acute angle closure glaucoma include the following. 45 year old . C/D ratio 0. nasal hemianopsia C. Shields. 1996. (ed). Use of posterior fundus lens and slit lamp 3.3 OU. 0. Using the direct ophthalmoscope . arcuate scotoma B. REFERENCES 1. 18 mm OS 4. American Academy of Ophthalmology Basic and Clinical Science Course Glaucoma Section 10. 28 mm OS D. nerve fiber layer D. 3. cup disc ratio C.M.3 OD. Hazy cornea due to bedewing D.5 OU. scotoma B. 2004 4. Ritch. IOP = 22 mm OU C. Whitcher. 16th Edition.8 OS.
social and personal history and other contributory factors will certainly yield valuable information. Review of past medical. the student should be able to 1. Pertinent details such as eye pain. detect abnormalities of the optic nerve 3. intracanalicular and intracranial segments. M. as well as topographical localization of lesions before going through this material. Intracranial diseases frequently cause visual disturbances because of destruction of or pressure upon some portion of the optic pathways. pupillary reactions. INTRODUCTION The optic nerve is part of the brain. CONTENT OPTIC NERVE The optic nerve consists of about 1 million axons originating from the ganglion cells of the retina. visual acuity. HISTORY The most important initial procedure in the evaluation of a patient begins with obtaining a complete and careful history. unilateral or bilateral involvement must not be neglected.DISORDRS OF THE OPTIC NERVE / 98 DISTURBANCE IN VISION DISORDERS OF THE OPTIC NERVE Raul D. The longest division is the intraorbital portion. 2.g. The intraocular portion is commonly referred to as the optic disc (papilla) is visible with an ophthalmoscope. The intracranial portion begins from the optic canal just before the optic nerves converge toward each other to become the optic chiasm. headache. discuss the basic examination of optic nerve function (e. family. OBJECTIVES Upon completion of this unit of instruction. The student is also advised to review the parts of a clinical history and the method of conducting a complete eye examination. visual fields. ophthalmoscopy). Similarly. As it enters the optic canal it is known as the intracanalicular portion. the eye can give important diagnostic clues to central nervous system disorders. The retrobulbar portion starts behind the eyeball and can be further divided into the intraorbital. recognize the signs and symptoms of optic nerve disorders 4.D. Cruz. discuss the common causes of optic disc edema such as papilledema and papillitis RECOMMENDED PREPARATION The student is advised to review the anatomy and physiology of the retina. EXAMINATION 1. The optic nerve can be divided into the intraocular (anterior) and the retrobulbar (posterior) portions. the optic nerve and basic neuroanatomic architecture of the visual pathway. Visual acuity 98 .
The finding is known as a relative afferent papillary defect (RAPD or APD) or Marcus Gunn pupil. an herniation of the temporal lobe compressing the third nerve must be considered. In normal room light. This test is done in a dark room using a bright light stimulus. A miotic pupil associated with ptosis and anhydrosis is known as Horner’s syndrome. reliable and inexpensive method of detecting an optic nerve disorder is performing the swinging light test. Figure 1 Diagram of light reflex pathway A dilated pupil usually indicates a cranial nerve III (efferent limb of the light reflex) lesion. The response in the eye tested (direct light reflex ) and also the response in the opposite eye (consensual light reflex) is measured The pupils should equally constrict briskly both directly and consensually to a light stimulus. Pupils The pupillary light reflex is initiated (afferent limb: cranial nerve II) by light stimulation. Other causes affecting the third nerve should be investigated. It is easily and best tested by the conventional Snellen’s eye chart. The pupillary reaction to light is properly done in a dim room. A normal response shows initial constriction of both pupils. This produces a paradoxical dilation of the abnormal eye. A benign lesion of the ciliary ganglion known as Adie’s pupil (tonic pupil) and instillation of mydriatic drops cause a dilated pupil. The lesion is an interruption of the sympathetic pathways anywhere from the hypothalamus to the dilator muscles of the pupil. A subnormal vision should be properly evaluated. Corrected visual acuity should be 6/6 or better. 99 .DISORDRS OF THE OPTIC NERVE / 99 An absolute requirement in any eye examination is to measure best corrected visual acuity. The response of each pupil to a bright light stimulus is observed. If a history of trauma is elicited. The bright light is rhythmically directed from one eye to the other eye for several times until the examiner is satisfied with the responses. A simple. 2. The patient fixates on a distance object. The pupil normally reacts to light by constricting (efferent limb: cranial nerve III). An abnormal response is a dilation without the initial constriction. the pupil is round about 2-3 mm and equal in size to the fellow eye.
Normal response to swinging light test Figure 3. Confrontation Test 100 . To obtain a more objective detailed quantitative assessment of the visual fields perimetry testing can also be done. RAPD defect in left eye using swinging light test 3. Visual Fields The visual fields measures the area of vision of each eye during central fixation. The method of confrontation compares the examiner’s field of vision and that of the patient. Figure 4. The confrontation test is a simple clinical tool routinely done to check the visual field.DISORDRS OF THE OPTIC NERVE / 100 Figure 2. Any dissimilarity between the examiner’s and the patient’s visual field should be recorded.
CT scan and MRI )are very helpful and can provide useful information. the appearance of the arteries and veins and the presence of hemorrhages and exudates are noted.DISORDRS OF THE OPTIC NERVE / 101 The following terms are used to describe visual field problems 1. 3. Figure 5. Scotoma . The optic disc is usually the initial landmark structure identified by the examiner. In majority of individuals spontaneous venous pulsations are seen and this indicate a normal intracranial pressure. At the center of the optic disc is a pale depression known as the physiologic optic cup where the retinal vessels enter the eye. The normal optic disc is pink in color and its borders should be clear. The artery to vein diameter ratio is 2:3 to 3:4. The presence of optic disc elevation.3 or 0. cup and size.loss of the right half of the visual field in right eye and the left half of the visual field in the left eye.around the center 2. SIGNS AND SYMPTOMS The main complaint of patients with optic nerve disease is poor vision. Ophthalmoscopy Direct ophthalmoscopy is an indispensable diagnostic tool in evaluating the optic nerve. The normal optic cup to disc ratio is 0.4. abnormal papillary responses. distinct and regular. Hemianopia – loss of one half of the visual field Homonymous hemianopia – loss of the right or left half of the visual field in both eyes Bitemporal hemianpia . including RAPD. contrast sensitivity. Eye findings will include subnormal best corrected visual acuity. Quadrantanopia – loss of one-fourth of the visual field 4. and imaging studies (ultrasound. The optic disc is nonseeing and results in the physiological blind spot.area of reduced or absent vision Central – involving fixation Cecocentral – involving fixation and the blind spot Paracentral . visual evoked response. 101 . Normal optic disc 5. Other Tests Ancilliary test such as color vision. Baseline recording of the optic disc should include the color.
Optic nerve disorders result in monocular loss of vision causing various nerve fiber layer abnormalities defects such as central. disorders affecting the visual pathway behind the chiasm results in contralateral defects. Pallor of the optic disc or optic atrophy is the end result of severe damage to the optic nerve. optic radiation and the occipital lobe produce characteristic visual field defects. lateral geniculate body. Degeneration of the nerve axons occurs. ischemia. Complete destruction of the optic chiasm causes bitemporal hemianopia. Fig 7. Fig 6. 8 Optic Atrophy 102 . Visual Pathway with corresponding visual field defects Any injury.DISORDRS OF THE OPTIC NERVE / 102 Visual pathway lesions from the optic nerve. paracentral field defects. Optic disc edema Fig. optic chiasm. Macular sparing is associated with occipital lobe lesions. Partial involvement of the optic radiation results in quadrantanopia. cecocentral. A lesion involving the optic tract produces homonymous hemianopia. On ophthalmoscopy the optic disc margins become blurred and indistinct. trauma or irritation to the optic disc can cause swelling of the axons of the optic nerve. A total involvement of the optic radiation and occipital cortex may produce a homonymous hemianopia. optic tract. This condition leads to loss of vision and carries a poor prognosis. Because of the crossing of the optic nerve fibers in the chiasm. This condition is known as optic disc edema.
The main symptom is a sudden painful loss of vision. Ophthalmoscopy findings show a hyperemic optic disc with blurred disc margins. It may be difficult to differentiate it from papilledema by the ophthalmoscopic appearance alone. 103 . Any increase in intracranial pressure will be transmitted to the subarachnoidal space surrounding the optic nerve. subarachnoid hemorrhage and conditions that obstruct the flow of the cerebrospinal fluid. It is usually unilateral and a relative afferent papillary defect (RAPD or Marcus Gunn pupil) is often easily detected. Papilledema is swelling of the optic disc secondary to increased intracranial pressure. Malignant Hypertension Malignant hypertension occurs in patients with accelerated blood pressure elevation. Visual field examination commonly reveals a central scotoma. meningitis. hydrocephalus. Papilledema The optic nerve is an extension of the brain and surrounded by meninges. Once the diagnosis of papilledema is certain. Visual field examination shows enlargement of the physiologic blind spot. The severity of papilledema is proportional to the increase in intracranial pressure. neuro-imaging studies should be done. Papilledema UNILATERAL OPTIC DISC EDEMA Papillitis Inflammatory swelling or demyelination of the anterior portion of the optic nerve is known as papilltis or anterior optic neuritis. Ophthalmoscopy findings include indistinct disc margins. There is dilation and tortuosity of the veins.DISORDRS OF THE OPTIC NERVE / 103 BILATERAL OPTIC DISC EDEMA 1. In the initial stages visual acuity is normal. Treatment is directed to the cause. The swollen disc obliterates the physiologic cup and displaces the central vessels forward. Fully developed papilledema will show a severely hyperemic disc with hemorrhages. ophthalmoscopic picture is similar to papilledema but result from abnormal arterial changes. trauma. If left untreated the persistent increase in intracranial pressure will eventually lead to optic atrophy and loss of vision 2. True papilledema is almost always bilateral and is associated with headache. nausea and vomiting. This condition is seen in intracranial mass lesions. The Fig 9. nerve fiber layer infarcts (cotton-wool spots) and exudates.
Trauma 8. On the basis of ophthalmological findings alone. Severe hyperopic (far-sighted) eyes have smaller eyeballs than normal. Espiritu RB. Compressive – optic nerve meningiona. Berson. Myelination of the optic disc results in white feathery opacified areas that may surround the optic disc margins. methanol. 1980. isoniazid. the abnormality is called retrobulbar neuritis. 1991 Fajardo RV. Toxic substances – ethambutol. Farris. Myelinated optic disc REFERENCES 1. Corticosteroids given intravenously may shorten the clinical course. Latest edition.DISORDRS OF THE OPTIC NERVE / 104 In numerous instances. JMC Press Inc. Bradley G. Frank. The ophthalmoscopic appearance of the optic disc is normal. 3. 5. Optic disc drusen (hyaline bodies) frequently cause the optic disc borders to be indistinct. 2. 4. a spontaneous resolution occurs even without treatment. These congenital disc disorders are called pseudopapilledema or structural congestion of the optic disc. 10. The common causes of pseudopapilledema are severe hyperopia. 6th edtion. This causes crowding of the optic disc structures resulting in blurring of the optic disc margins. Frank G. chloramphenicol 2. Newell. Vascular –anterior ischemic optic neuropathy 4. 104 . If the posterior portion of the optic nerve is involved. Other causes of optic disc edema include the following 1. orbital tumors 5. Mosby Year Book. American Academy of Ophthalmology. vein occlusion 7. Textbook of Ophthalmology. Metabolic – diabetes mellitus 6. (ed) Basic Ophthalmology for Medical Students and Primary Care Residents. Naval CIN Textbook of Ophthalmology. Nutritional deficiencies of vitamin B 3. optic disc drusen and myelination of the optic disc. Hereditary PSEUDOPAPILLEDEMA Developmental optic disc anomalies may mimic true papilledema. (ed) The Basics of Neuro-Ophthalmology. Fig. they may erroneously lead to a diagnosis of papilledema. Ocular diseasae – uveitis.
retina A RAPD is elicited by doing A. intraorbital C. ophthalmoscopy C. bitemporal The following are causes of optic disc edema EXCEPT A. 10.000. 5. 4. 105 . central retinal vessels D. 7. altitudinal D. a confrontation test D. uveitis 2. macula B. binocular D.DISORDRS OF THE OPTIC NERVE / 105 SELF-TEST 1. retinitis pigmentosa C. VII The visual field defect that includes fixation and the blind spot is a ______ scotoma A. cecocentral C. 1. 6. The optic nerve consists of about _____axons from the ganglion cells of the retina A.000. papillits D. 1. II B. junctional The physiologic blind spot in the visual field represents the A. temporal C. central B. monocular B. V D. 8.000 B. 10.000 D. optic disc C. papilledema B. perimetry B. III C. intraocular B. intracranial The afferent limb of the papillary light reflex is the _____ nerve A.000 C. a swinging light test Optic nerve defects result in _____ loss of vision A. 3.000 The optic disc is the _____ portion of the optic nerve A. intracanalicular D.
7. hyperopia C. neuritis C. cecocentral Paracentral scotoma Swollen disc Indistinct disc margins PAPILLITIS PAPILLEDEMA ASSOCIATED SYMPTOMS BILATERALITY VISUAL ACUITY PUPILS VISUAL FIELDS OPHTHALMOSCOPY Headache. Severe _____ can manifest as pseudopapilledema A. Pallor of the optic disc is also known as optic A. myopia COMPLETE THE TABLE PAPILLEDEMA ASSOCIATED SYMPTOMS BILATERALITY VISUAL ACUITY PUPILS VISUAL FIELDS OPHTHALMOSCOPY ANSWERS 1. nausea vomiting Usually Early. presbyopia B. degeneration B. C A A B B 6. 9. dysplasia D. 5. 2. 4. D A C D C PAPILLITIS Eye pain Rarely Blurring of vision RAPD Central. 3. 8. atrophy 10.DISORDRS OF THE OPTIC NERVE / 106 9. astigmatism D. normal normal Enlargement of Blind spot Swollen disc Indistinct disc margins 106 . 10.
These students are expected to have completed basic units in ophthalmology. Based on information given. the student is expected to: 1. 2. 107 . MHA.ERRORS OF REFRACTION / 107 DISTURBANCE IN VISION ERRORS OF REFRACTION Juan Ma. WHAT IS AMETROPIA OR ERROR OF REFRACTION? This is a condition where the refractive elements of an eye at rest are unable to focus light rays from 6 meters or more onto the retina. RECOMMENDED PREPARATION The student is advised to review the anatomy and physiology of the cornea. Identify the various elements in a patient’s history and ophthalmologic examination that leads to the formulation of a diagnosis. CONTENT PART I. Differentiate the various errors of refraction and related conditions according to type. This material is intended to serve as supplementary reading for the students as part of the unit on the Eye as an Optical Instrument and focuses primarily on providing the medical students with knowledge on how to go about recognizing and assessing patients with errors of refraction. Nañagas MD.. OBJECTIVES After going through this material. Objective and Subjective Examination of the Eye and Common Out-Patient Disorders. namely Ophthalmic anatomy and Physiology. and other refractive elements of the eyeball before going through this material. INTENDED USERS This program was designed primarily for LEARNING UNIT IV student of the UP College of Medicine. lens. 4. as well as the general ophthalmologic examination to better appreciate this material. Aside from providing patients with text on the above-mentioned subject matters.MSNA INTRODUCTION This self-instructional material is designed for undergraduate medical students particularly LEARNING UNIT IV of the UP College of Medicine. Formulate a working definition for error of refraction and other related terms. He is further advised to review the parts of a clinical history. be able to analyze and interpret provided data to formulate diagnosis. diagrams of typical cases will also be presented. It may be caused by abnormalities in length of the eyeball or of the refractive elements of the eye (mainly the cornea and crystalline lens) or both. Students are however encouraged to apply knowledge that they will acquire from this material to clinical cases that they will encounter during their rotation in the clinics of the department. Pablo R. 3.
Are there other associated eye problems? 108 .. DIAGNOSIS OF ERRORS OF REFRACTION There are three basic elements that one would need to consider to be able to formulate a diagnosis of error of refraction. Errors of refraction usually present with a prolonged history of their complaints. 2. Furthermore. Headache especially after prolonged eye use is common with hyperopics and astigmatics but non-specific and will have to be differentiated from other causes. What is your patient’s chief complaint? The most common presenting complaints of patients with errors of refraction include blurring of vision for distance. Ancilliary Examinations – manual or automatic refraction is an examination routinely performed to determine the presence and type of error of refraction. The clinician should ask each and every patient suspected to have an error of refraction the following questions. Answers to the following questions serve as aids in the formulation of a complete diagnosis. Hyperopics (far sighted individuals) may complain of early visual fatigue when performing visual tasks (especially at near). How long has this problems been going on? The duration of the problem should be extracted from the patient. 3. History – a comprehensive history is an important component of a work up for error of refraction. keratometry and corneal topography. Clear near vision but blurred distance vision indicates near sightedness or myopia. Each of these aspects will be discussed subsequently. for near. or both. Which eye is involved? Does the problem involve one eye or both eyes? Significant difference of refraction between the two eyes may be the cause of amblyopia or a lazy eye. Other special examinations may include biometry. the history can provide the clinician with an idea as to the visual needs of the patient and the appropriate treatment modality. The patient’s history guides the clinician in arriving at a complete diagnosis. HISTORY TAKING IN A PATIENT WITH ERROR OF REFRACTION Extracting the history from a patient with probable error of refraction can be very useful. 4. 1. . One should be aware of a condition of middle age called presbyopia where the lens of the eye gradually loses its ability to focus at near objects.ERRORS OF REFRACTION / 108 PART II. 2. 1. Ocular Examination – basic eye examination comprised of the following parts should be done on each patient. Gross eye examination – slit lamp examination Visual acuity testing Intraocular pressure determination Movement of Extraocular muscles Funduscopic Examination 3. Whether it is recurrent or progressive should also be noted. particularly as to the possible type of error of refraction.
6. Snellen charts are commonly used for distance vision testing and Jaeger or Snellen equivalent cards for near vision. Visual Acuity. Has the patient suffered any form of illness in the past particularly diabetes? Is she under any form of medication for any illness? These may affect vision. What is the patient’s occupation? What are the patient’s usual visual tasks? Medical History. As has been mentioned earlier. Is there any history of any hereditary illness like diabetes? Changing blood sugar levels may affect a person’s refraction. Does the patient have any prior consultations? One should be able to determine a patient’s previous correction of his/her error of refraction to help determine the course of the condition. Extraocular Muscle Movement. If the vision improves when the patient looks through the pinhole.ERRORS OF REFRACTION / 109 Elicit from the patient whether or not there is any history of redness. ocular pain. the patient most probably has an error of refraction that can be corrected with lenses. Intraocular Pressure. 2. Most patients would typically present with normal intraocular pressures 3. Some forms of heterophoria or heterotropia are associated with errors of refraction. 109 . trauma or any form of eye surgery in the past. or both. Other aspects of the patient’s history that should be considered include: Family History. Social History. most patients with would present with reduction in vision either for far. the patient with error of refraction will present with the following findings: 1. OPHTHALMOLOGIC EXAMINATION OF THE PATIENT The basic tools that one would require in conducting an examination of the patient with suspected error of refraction include the following: ♦ ♦ ♦ ♦ Visual acuity charts – both for distance and near vision Occluder with pin-hole Penlight – for gross examination of the eye Ophthalmoscope – used for fundus examination COMMON OCULAR FINDINGS IN AMETROPIA Typically. glare or photophobia. 5. near. The extraocular muscles are usually not involved in errors of refraction and a majority of patients will exhibit full movement on all directions of gaze. Is there a history of any similar illness in the family? Genetic factor strongly determine refractive errors of the eye.
a sign of astigmatism. light rays are blocked from the retina B. “against” movement in myopia. light rays from a source more than 6 meters from an eye at rest do not focus on the retina C. REVIEW QUESTIONS: PART I & II 1.ERRORS OF REFRACTION / 110 4. Keratometry The keratometer is an instrument that can measure central anterior corneal curvature. It demonstrates irregularities of curvature like keratoconus. It usually functions as a keratometer as well. The more commonly requested ancillary procedures include: 1. It is also used in fitting contact lenses. 110 . additional examinations may be requested to aid in the diagnosis of some conditions. there is an abnormality in the transparency of the cornea. 2. Corneal Topography It is a sophisticated instrument that produces a color-coded topographic map of the cornea that shows the pattern of the corneal curvature. indicating different refracting powers in the two meridia. In cases where the eyeball is elongated the fundus and optic nerve head may exhibit some changes 5. 3. Biometry This instrument using sound waves provides measurement of the axial length of the eyeball. a determining factor of the refractive condition of the eye. Retinoscopy will reveal the following findings: “With” movement of reflex with the streak is seen in hyperopia and small myopias. a form of correction for errors of refraction. Patients wherein the error of refraction is not severe will present with normal findings. It can be used to check the type and amount of astigmatism. Error of refraction or ametropia refers to a condition where A. measuring corneal curvatures. ANCILLARY EXAMINATIONS Commonly. Funduscopic Findings. Retinoscopy has achieved neutrality in A but still ‘with’ in B.
near vision. C. is usually very subjective C. B. Measurement of refractive errors A. can be performed using automatic refractors 8. No hereditary pattern B.ERRORS OF REFRACTION / 111 2. usually develop hyperopia 9. If the poor vision of a patient improves when viewing the test chart through a pin-hole A. In middle age. Normal or emetropic eyes looking at an object 20 or more feet away A. it is the pupil that is at fault B. cannot be done by machines B. a means to take retinal photographs to determine retinal changes due to errors of refraction 6. is color aberration. Error of refraction has A. gradually lose the ability to focus for near or presbyopia B. may be blurred distance vision. there may be error of refraction C. need to accommodate to focus light on the retina B. low 4. the same as funduscopy B. it is part of the aging process for diabetics B. Retinoscopy is A. Strong genetic influence 5. dark glasses are the cure 7. is nasal scotoma 3. the refractive state of the eye may have been affected by the sugar level C. high C. it is surely diabetic retinopathy D. or both. should be able to see appropriate sized Snellen letters with the eye at rest 10. Intraocular pressure in plain errors of refraction is usually A. In error of refraction a presenting symptom A. usually develop myopia C. need to squint to focus light on the retina C. one may A. keratometry will demonstrate the changes in corneal curvature due to sugar levels 111 . normal B. an objective means of measuring errors of refraction C. If a diabetic consults for sudden blurring of vision after a rise in sugar level A.
ASTIGMATISM In astigmatism the refracting surface (usually the cornea) is toroidal (like the surface of an American football) rather than spherical. In against the rule astigmatism. In with the rule. 112 . the refractive power changes successively from one meridian to the next and each meridian has a uniform type of curve. a correcting plus cylinder is located to or near 180° and the horizontal meridian is steepest. B. It can only focus convergent light rays on the retina. The myopic eye focuses light rays from infinity in front of the retina.ERRORS OF REFRACTION / 112 PART III. the vertical meridian is steepest and a correcting plus cylinder is located at or near axis 90°. In regular astigmatism. CLASSIFICATION OF AMETROPIAS (ERRORS OF REFRACTION AND ASTIGMATISM) Diagrammatic Classification of Ametropias The emmetropic eye focuses light rays from infinity on the retina even at rest or without accommodating. a. With the rule and against the rule astigmatism The term “with the rule” and “against the rule” refer to the position of the principal meridians. and therefore the refracting power of the surface is not the same for all meridians. An object at a finite distance focuses on its retina. The hyperopic eye theoretically focuses light rays from infinity behind the retina.
He may be hyperopic C. A. toric D. old patient had 6/6 vision but difficulty with reading Jaeger 1 print. A patient can read books clearly but cannot read from a whiteboard at 20 feet away. A 24 year old female has been getting headaches after she finishes overtime work at her computer in a bank. He may be myopic D. If the vertical meridian of the cornea is steepest A. it is against the rule’ astigmatism C. PART III 1. Ophthalmologic examination showed: V OU: 20/200 or 6/60 improved to 6/7. He is probably normal B. phthsic 2. it is called ‘natural’ astigmatism EXERCISE Case 1. What type would it be.ERRORS OF REFRACTION / 113 REVIEW QUESTIONS . a 20 yr. A 12 year old boy complains that he cannot see the blackboard from his new seat in class located at the back row. She also says her eyes feel tired. Intraocular pressure: soft OU EOMs: full FOU: normal 1. What examination can measure the error and lead to the prescribed correction? Case 2. A. the patient is A. With the given information would it be safe to say that the patient has an error of refraction? 2.5 with pinhole. it is ‘with the rule’ astigmatism B. myopic C. This is normal 5. the curvature is flatter than usual C. the curvature is the same in all meridians B. 113 . He may be hyperopic D. The mother accompanying the boy wears glasses. hyperopia or myopia? 3. He may be myopic C. On visual acuity testing. He may have compound hyperopic astigmatism 4. the curves of the surface are convex 3. hyperopic B. In astigmatism A. This is presbyopia B. When the image of an object at infinity falls in front of the retina. She is not on any medication and her BP taken at the office was normal. the refracting power of the surface is not the same in all meridians D.
contact lenses. and classification of the different errors were presented. Optics. Referral to an ophthalmologist or optometrist is necessary for proper correction through spectacles. CONCLUSION As medical practitioners. REFERENCES 1. Jaeger 1 with difficulty Intraocular pressure: soft. especially in children. A 4. ANSWERS TO REVIEW QUESTIONS Part I and II Part III 1. Yes 2. Basic examination. you may. or astigmatism? SUMMARY It was the primary objective of this self-instructional material to provide the reader with a guide on how to diagnose patients with error of refraction. What type would it be. It is therefore your role to be able to properly recognize these conditions and differentiate them from permanently disabling visual conditions. Espiritu. can prevent permanent amblyopia if anisometropia (significant difference in amount or kind of refractive error between the two eyes) is present. c1990. Basic and Clinical Science Course. hyperopia. c2001. Romeo. Case 1 1. OU EOMs: Full F OU: Normal 1.ERRORS OF REFRACTION / 114 Ophthalmic examination: V OU: 20/20 or 6/6. California: American Academy of Ophthalmology. One should bear in mind that many who complain of blurring of vision may have an error of refraction. Section 2. With the given information would you say the patient may have an error of refraction? 2. RECOMMENDED FOLLOW UP It is recommended that the students be given demonstration sessions on how to properly conduct history taking and ophthalmologic examination of patients. Yes 2. or refractive laser procedures. D 3. Ophthalmologic Optics. B 2. myopia. retinoscopy or autorefraction Case 2 1. Hypeopia or astigmatism B C B B A 114 . B 6. It is the most common cause of visual disability. B 9. 5. 2. A 8. A 7. symptomatology. in the future encounter patients who will seek consultation for eye problems. Manila: Department of Ophthalmology & Visual Sciences. 2. Early intervention. Refraction and Contract Lenses. Myopia 3. Following this exercise. D 6. 3. B 10. 4. it is further recommended that the students be provided clinical sessions to allow them to see actual cases of patients with errors of refraction. C 5.
the student sgould be able to : 1. illustrate the algorithm on the differential diagnoses of a red eye based on the following signs and symptoms: pain. the student must have previous knowledge of anatomy and physiology of the eye and the methods of history taking and ocular examination. Toxic or Chemical Reaction iv. Dry Eye iii. Viral b. Allergic ii. Dry Eye d. eye discharge and itchiness. Conjunctivitis a. and complication of the common causes of a red eye a. treatment. MPH INTRODUCTION The red eye is one of the most frequent clinical presentations of ocular disorders. enumerate the clinical clues. Microbial Keratitis f. Allergic Conjunctivitis c. etiology / pathogenesis. OBJECTIVES After the completion of this learning material. The medical student will be able to differentiate these disorders from each other by asking certain questions from their patients during history taking and looking for specific signs when performing the ocular examination. diagnostic work-up. Bacterial Conjunctivitis e.THE RED EYE / 115 THE RED EYE Leo Cubillan. The following are the differential diagnoses of a red eye: 1. Non-infectious i. Acute Glaucoma g. MD. Infectious i. signs and symptoms. CONTENT DIFFERENTIAL DIAGNOSES OF A RED EYE Red eye is one of the most common serious eye symptom of patients with eye disease. Red eye is seen as a result of dilation of conjunctival or scleral blood vessels in response to inflammation or infection. 2. Subconjunctival hemorrhage as a result of injury to a conjunctival blood vessel also present as a red eye. Viral Conjunctivitis b. Contact lens use 115 . Bacterial ii. Uveitis RECOMMENDED PREPARATION Before going to this material.
THE RED EYE / 116 v. Infecious i. access to an ophthalmologist may not be easy. eye discharge and itches are used for this algorithm. EYE PAIN 2. Entropion / Trichiasis b. Idiopathic orbital inflammation ALGORITHM FOR RED EYE Ophthalmologist are the experts in the diagnosis and treatment of eye diseases. Lagophthalmos 7. 5. Preseptal and orbital cellulites b. Eye pain may be described as a sharp localized pain. 116 . The primary care physician may still be the best first line medical worker in the identification and initial treatment of eye disease. Recurrent Epithelial Erosion ii. Viral iii. Orbital Disorders a. pain when exposed to bright light or a severe eye pain radiating to the head. 4. Bacterial ii. Acanthamoeba b. Foreign Body Uveitis Episcleritis /Scleritis Acute Glaucoma Keratitis a. Conjunctival Neoplasm vi. 3. This algorithm is presented to aid the primary care physician in the diagnosis of the most common cause eye disease presenting as a red eye. Fungal iv. The symptom of eye pain divides the common differential diagnoses of eye pain into two groups. Non-Infectious i. Foreign Body 6. Eyelid Abnormalities a. In the Philippines. The common symptom of eye pain. however. The first step in the algorithm is to determine whether the patient presenting with a red eye has eye pain or not.
Photophobia is usually described as a dull eye pain when exposed to bright lights. uveitis or eye inflammation. NO EYE PAIN 117 . the next question would be the presence of absence of eye discharge. PHOTOPHOBIA If there is no eye discharge in a patient with eye pain. may be considered. the next question would be the presence or absence of photophobia. This is a pain due to the pupillary constriction of an inflamed iris. If there is eye discharge. In the absence of photophobia. microbial keratitis or infection of the cornea may be considered. The presence of abundant nerve fiber endings in the cornea (CN V) causes in the pain when infection is present. The eye pain in glaucoma is moderate to severe and radiates to the head. If photophobia is present. acute glaucoma may be entertained.THE RED EYE / 117 EYE PAIN WITH DISCHARGE For patients with red eye and eye pain.
VIRAL CONJUNCTIVITIS CLINICAL CLUES 118 . If itchiness is present. If the discharge is watery. viral conjunctivitis is a differential diagnosis.THE RED EYE / 118 Dry eye syndrome may be considered in patients with red eye in the absence of eye pain and eye discharge NO EYE PAIN WITH DISCHARGE Red eye patients with no eye pain but with mucopurulent discharge may have bacterial conjunctivitis. no eye pain and with watery discharge. allergic conjunctivitis may be considered. ITCHY EYE The symptom of itchiness is asked among patients with red eye.
19. Mild steroid drops may be given to help reduce inflammation. The main feature of this disease is the presence of watery discharge in the early part of the course. Spread is with direct contact from eye discharge. COMPLICATION 119 . The most important question in the history that would point to this disease. discharge may become mucopurulent if it worsen or there is a secondary bacterial infection. the discharge is watery. However. 29 and 37. antibiotic eye drops may be given in patients with secondary bacterial infection or as a prophylaxis for bacterial infection. In some cases. There is not treatment needed. TREATMENT Hand washing and avoiding direct contact to eye discharge is the best way to prevent the spread of viral conjunctivitis. SIGNS AND SYMPTOMS Onset of symptoms is acute. It usually starts on one eye and develops to become bilateral after few days. The virus may not be neutralized by alcohol so the best preventive measure is hand washing. is the history of exposure to other patients with sore eyes. DIAGNOSTIC WORK-UP The diagnosis of adenoviral conjunctivitis is mainly clinical based on the history. ETIOLOGY / PATHOGENESIS Epidemic keratoconjunctivitis which is the more common type of the viral conjunctivitis is caused by adenovirus types 8. character of the discharge and the presence of follicular conjunctival reaction seen under the biomicroscope. During the early course of the disease. Duration may be from few days to 2-4 weeks. The severity of symptoms is worse on the first eye.THE RED EYE / 119 Viral conjunctivitis is the most common cause of acute onset of eye redness.
In most patients. In the hayfever type of allergic conjunctivitis. it is mainly a type I hypersensitivity reaction to airborne allergens. On ophthalmic examination. ALLERGIC CONJUNCTIVITIS CLINICAL CLUES Allergic conjunctivitis is a chronic or recurrent eye disease characterized by eye redness. Eye itchiness is the most prominent feature.THE RED EYE / 120 In majority of the patients. The subepithelial opacities may persist for weeks or months but may heal without scars. SIGNS AND SYMPTOMS Eye itchiness is a prominent feature of the disease. In atopic keratoconjunctiviis. ETIOLOGY / PATHOGENESIS The etiology of this disease is immunologic in nature. In atopic keratoconjunctivitis. Often. the patient has a hypersensitive immune system which reacts to many antigens. there is a pale papillary reaction on the upper bulbar conjunctivae. subepithelial opacities may develop in the cornea. In few cases. itchiness and watery or stringy discharge. This may cause blurring of vision. there is a periocular scaly skin with thickening of the eyelids (allergic shiners). there may be an atopic predisposition or the patient has atopy. mucoid and distinctively stringy. the disease resolves without sequelae. 120 . Discharge is watery. it is difficult to identify the specific allergen.
when steroid drops are overused. COMPLICATION In the vernal type of allergic conjunctivitis it often occurs to young children which would last for several years.THE RED EYE / 121 DIAGNOSTIC WORK-UP Conjunctival cytologic studies from conjunctival scraping would show eosinophils. Cold compress and mast cell stabilizers / antihistamine eye drops may help control the symptoms. In theses cases. short term topical steroids are needed. 121 . In moderate to severe cases. TREATMENT Treatment involves removal of environmental triggers. cataract may develop early as a complication of the steroids.
The symptoms are worse with wind and dry climates. SIGNS AND SYMPTOMS Patients usually complain of a sandy and gritty sensation associated with slight eye redness. punctual occlusion may be don. Flourescein dye is instilled into the eye and the surface of the tear film is observed for areas of disruption. In severe cases.THE RED EYE / 122 DRY EYE CLINICAL CLUES Dry eye disease or keratoconjunctivitis sicca is a common ophthalmic condition seen among the elderly. Normal tear break-up time is generally greater than 10 seconds. TREATMENT Treatment is mainly with the use of aqueous tear replacement or artificial tears. It usually presents with foreign body sensation and mild eye redness. DIAGNOSTIC WORK-UP Shirmers testing with or without anesthesia is done to confirm dry eye. Consistent measurements of less than 5 mm of wetting at 5 minutes may indicate a dry eye. Other causes of dry eye include increased tear evaporation in patients with inability to completely close the eyelids and unstable tear film in patients with meibomitis. ETIOLOGY / PATHOGENESIS The main etiology for dry eye is the decreased tear production seen among the elderly. Tear break-up time may also be done. Standardized strips of filter papers are used to absorb tears. 122 .
Oral antibiotics are also administered in patients with hemophilus. DIAGNOSTIC WORK-UP Conjunctival scrapings among children with bacterial conjunctivitis and URTI might reveal gram negative coccobacilli. Bacteria from conjunctival scraping may be cultured on a blood agar plate. it may be associated with upper respiratory tract infection (URTI). bacterial conjunctivitis is unilateral and is acute in onset. Among newborns. the most common etiology is hemophilus influenza. SIGNS AND SYMPTOMS Most often. chlamydia or gonococcal conjunctivitis. 123 . ETIOLOGY / PATHOGENESIS In children with URTI. Among children. Chlamydia or gonococcocus may be the etiologic agent.THE RED EYE / 123 BACTERIAL CONJUNCTIVITIS CLINICAL CLUES Conjunctivitis caused by bacteria is usually seen with mucoid to muco-purulent discharge. There is a mucoid to mucopurulent discharge associated with a red eye but no blurring of vision. TREATMENT Antibiotic eye drops are used for bacterial conjunctivitis.
the patient would present with blurring of vision. COMPLICATION 124 . White lesion is seen on the cornea. fungal etiology may be considered.THE RED EYE / 124 MICROBIAL KERATITIS CLINICAL CLUES Microbial keratitis is an acute infection of the cornea with painful red eye associated with mucoid to muco-purulent eye discharge. TREATMENT Topical antibiotics are the mainstay of treatment. If the lesion is on the central cornea. Mucoid to muco-purulent discharge is seen. In these cases. ETIOLOGY / PATHOGENESIS Pneumococcus. SIGNS AND SYMPTOMS Eye redness is moderate to severe associated with eye pain. pseudomonas is a common and dreaded organism. DIAGNOSTIC WORK-UP Corneal scraping is done to determine the etiologic agent. Sensitivity studies are done to determine the most sensitive antibiotic agent. antibiotic drops are used every 15 min during the first few days of treatment. In some patients with a history of trauma and steroid eye drop use. a gram positive organism is the most common cause of bacterial keratitis. In moderate to severe cases. keratectomy is done. Gram stain is used to initially identify the bacteria but definitive diagnosis is achieved with culture studies in blood agar-plate and blood heart infusion medium. Among contact lens wearers.
the cornea becomes edematous resulting in an iridescent and blurring of vision. Most often this is secondary to angle closure. the most prominent feature is a red painful eye associated with headache. corneal transplantation may be needed to save the eye. In these cases. SIGNS AND SYMPTOMS When the eye pressure is acutely elevated.THE RED EYE / 125 In severe microbial keratitis such as those caused by pseudomonas. the patient would experience sudden onset of eye pain associated with headache. With the elevated eye pressure. 125 . corneal perforation occurs in few days without treatment. There is blurring of vision and occasionally. ACUTE GLAUCOMA CLINICAL CLUES In acute glaucoma. ETIOLOGY / PATHOGENESIS The eye pressure is abnormally elevated (intraocular pressure greater than 23 mmHg) due to an acute obstruction in the outflow mechanism of aqueous humor. Angle closure glaucoma is more prevalent among Asians including Filipinos because genetically shallower irido-corneal angle. The outflow mechanism is located at the area in this angle which when obstructed causes an increase in eye pressure. rainbow haloes are seen (iridescent vision).
laser iridectomy or glaucoma filtering surgery may be done. In severe cases. TREATMENT Acetazolamide or hyperosmotic oral solutions may be used to lower the eye pressure initially. there is damage to the optic nerve causing initial blurring of vision of the peripheral vision which eventually leads to blindness. UVEITIS CLINICAL CLUES Uveitis is an ocular inflammation characterized by eye redness around the cornea associated with sensitivity to bright lights (photophobia) 126 . A gonioscope lens is also used to visualize and evaluate the angle structure. Visual field examination is done to determine the extent of damage to the nerve fiber layer of the optic nerve. Topical ocular hypotensive agents are also used. COMPLICATION When the glaucoma becomes chronic or left untreated.THE RED EYE / 126 DIAGNOSTIC WORK-UP Applanation tonometry is done to measure the eye pressure.
COMPLICATION Moderate to severe uveitis is a blinding disease. Iris adhesion to the lens (posterior synechia) may also be seen. the identification of an associated systemic disease would help in the prognosis and treatment of the disease.THE RED EYE / 127 ETIOLOGY / PATHOGENESIS Almost half of the uveitis are idiopathic in nature. Although most uveitis are idiopathic. SIGNS AND SYMPTOMS Most patients complain of eye redness associated with photophobia. uveitis is associated with systemic disease such as Vogt-Koyanagi-Harada. Bechet’s and collagen vascular disease. Common complications include cataract and secondary glaucoma. In patients with bilateral disease or there is a systemic evidence of inflammation. In some cases. Immunosuppresive agents are also given in moderate to severe cases. TREATMENT Steroid is the mainstay of treatment in patients with uveitis. oral steroids are used. keratic precipitates are seen on the inner surface of the cornea which indicated inflammatory reaction in the anterior chamber of the eye. 127 . DIAGNOSTIC WORK-UP Laboratory work-up is directed to the most likely systemic associated disease. On biomicroscopic examination. Others may be infectious in nature such as those caused by herpes virus and mycobacterium tuberculosis. Periocular steroid injection is recommended for patients with uveitis in the posterior pole. Topical steroid drops are used for uveitis located in the anterior part of the eye.
This condition resolves with rest from contact lens wear. CONTACT LENS RELATED EYE REDNESS Eye redness may be seen among contact lens wearer. CORNEAL ABRASION / FOREIGN BODY 128 . Topical steroids and oral NSAIDs are often prescribed for this condition. Antibiotic eye drops may be given as a prophylaxis for eye infection. This results from over-wear of the contact lenses which causes decrease in oxygen supply to the cornea. Some are associated with collagen vascular diseases.THE RED EYE / 128 OTHERS EPISCLERITIS / SCLERITIS Epislceritis or scleritis. present with a red eye associated with eye pain.
Dry Eye b.THE RED EYE / 129 Corneal abrasion from trauma presents with sudden eye pain and eye redness. Appleton & Lange: Stamford. Vaughan DG. What eye condition would you consider as your initial impression based on the history? a. Topical antibiotics are used with eye patching. Allergic Conjunctivitis e. c2000. E 1. Ophthalmology Review Manual. The patient answered “no” to the first question. Permanent treatment may require cautery of the root of the eye lashes or surgery of the eyelids. Student A asked if the patient experienced eye pain. c1995. a. Viral Conjuncitivitis d. Acute Glaucoma 2. Lippincott Williams and Wilkins: Philadelphia. SELF-TEST 1. What eye condition would you consider as your initial impression. 14th ed. ENTROPION / TRICHIASIS Entropion and trichiasis seen among the elderly presents with eye redness due to misdirected lashing which irritates the cornea. Viral Conjuncitivitis d. Asbury and Riordan-Eva P. A group of medical students were assigned to get the history of medical illness. The patient told Student C that she did not experience eye itchiness. Acute Glaucoma ANSWERS 2. CT. A 43 year old man consulted for sudden eye redness associated with eye pain and rainbow haloes in his vision. PA. Microbial Keratitis c. Chern K and Zeagans M. REFERENCES 1. eds. Student B was able to elicit a history of watery eye discharge. Microbial Keratitis c. C 129 . Allergic Conjunctivitis e. A 20 year old female consulted for eye redness. 2. This resolves in 24 to 48 hours. Dry Eye b. General Ophthalomology. Removal of the misdirected lashes is done as an initial treatment.
130 . Formulate a working definition for uveitis. MHPEd INTRODUCTION This self-instructional material is designed for undergraduate medical students. the term uveitis is reserved for inflammation involving the uveal tract. INTENDED USERS This self-instructional material was designed primarily for LEARNING UNIT IV students for the OSI curriculum of the UP College of Medicine. This material is intended to serve as supplementary reading for the students as part of the unit on THE RED EYE and focuses primarily on providing the medical student with knowledge on how to go about recognizing and assessing patients with uveitis and scleritis. 4. strictly speaking. scleritis and related terms. PART II. Aside from providing the students with text on the above-mentioned subject matter. pictures of typical cases will also be presented. the basic eye examination. CONTENT PART I. WHAT IS UVEITIS? Uveitis is a nonspecific term used to denote intraocular inflammation. DIAGNOSIS OF UVEITIS There are four basic elements that one would need to consider to be able to formulate a diagnosis of uveitis. 2. Identify the various elements in a patient’s history and ophthalmologic examination that leads to the formulation of a diagnosis of uveitis and scleritis. 3. Students are however encouraged to apply knowledge that they will acquire from this material to actual and simulated clinical cases that they will encounter during their rotation in the clinics of the department. Based on information given. that is. Classify the various inflammatory conditions involving the sclera and the uvea according to their location. RECOMMENDED PREPARATION Students are advised to review the anatomy and physiology of the sclera and the uveal tract before going through this material. ocular symptomatology and ocular pharmacology. severity. It is also expected that students already possess basic knowledge on ophthalmic anatomy and physiology. It is a part of a series of modules on THE RED EYE. MD. Castillo. be able to analyze and interpret provide data to make a diagnosis. as well as the general ophthalmologic examination so as to better appreciate this material. pathology and etiology. course. Students are further advised to review the parts of a clinical history.UVEITIS AND SCLERITIS / 130 RED EYE Uveitis and Scleritis Teresita R. Thus. the learner is expected to: 1. Although all layers of the eye may be involved by inflammation. ciliary body and the choroid. OBJECTIVES After going through this material. the iris. students are expected to have completed the materials on the overview of THE RED EYE.
the history can provide the clinician with an idea as to the patient’s possible response to treatment regimen. History – a comprehensive history is the one most important component of the uveitis work-up 2. glare or photophobia. 1. does the patient experience his or her symptoms in both eyes simultaneously or do they occur in one eye at a time? 4. Systemic Examination – general systemic examination is done in cases wherein the clinician suspects the uveitis to be part of the presentation of a systemic problem. Does the patient have any prior consultations? Where medications used? One should be able to determine how a patient responds to specific forms of therapy in the past so as to give the present physician an idea as to the patients’ prognosis. Often. Each of these aspects will be discussed subsequently. that is whether or not they occurred suddenly or progressively over a prolonged period of time. Answers to the following questions serve as aids in the formulation of a complete diagnosis. Ocular Examination – basic eye examination comprised of the following parts should be done on each patient Gross eye examination – slit lamp examination Visual Acuity testing Intraocular pressure determination Movement of Extraocular Muscles Funduscopic Examination 3. Floaters on the other hand refer to black or white floating “objects” that the patients appreciate in their field of vision. How long has this problem been going on? The duration of the problem should be extracted from the patient. it should also be determined whether or not a similar problem has occurred in the past. HISTORY TAKING IN THE UVEITIS PATIENT Extracting a comprehensive history from a uveitis patient can not be overemphasized. In addition to blurring of vision. The following are important questions regarding the patient’s current illness that the clinician should ask each and every patient suspected to have uveitis.UVEITIS AND SCLERITIS / 131 1. ocular pain. What is your patient’s chief complaint? The two most common presenting complaints of patients with uveitis include changes in vision and floaters. 3. trauma or any form of eye surgery in the past. These are often described by patients as “flies” or “insects” which move about in their field of vision. The onset of these changes should likewise be noted. The patient’s history guides the clinician in arriving at a complete diagnosis. the patient consults primarily because of blurring of his vision. Are there other associated eye problems? Elicit from the patient whether or not there is any history of redness. Ancillary Examinations – special ophthalmologic and laboratory examinations are done as aids in the formulation of an etiologic diagnosis for uveitis patients 4. Furthermore. 5. Which eye is involved? Does the problem involve one eye alone or both eyes? If both eyes are involved. 2. Vision changes may come in the form of reduction in vision or distortion in vision. patients may also complain of photophobia or eye pain in high illumination. 131 . particularly as to the possible etiology of the condition. Furthermore.
Since the extraocular muscles are usually not involved in the inflammatory process. and thus present with elevation of their intraocular pressures. Patients wherein the inflammation is confined to the anterior segment would have normal funduscopic findings. Extraocular Muscle Movement. oral ulcers or gastrointestinal problems to name a few should also be made. the patient with uveitis would present with the following findings: 1. Basic instruments for an eye examination. BNear vision chart.UVEITIS AND SCLERITIS / 132 6. A–Snellen Chart. any history of alcohol intake. there are patients with prolonged uveitis who may have developed complications of the disease process. 2. The presence of a history of any sexually transmitted disease should likewise be elicited from the patient. Visual Acuity. In cases however. smoking. F-slit lamp biomicroscope COMMON OCULAR FINDINGS IN UVEITIS Typically. Most patients would typically present with a very soft or hypotonic eyeball as a result of involvement of the reduced aqueous humor production in the ciliary body as part of the inflammatory process. D-tonometer. the patients could present with any of the following: 132 . E-ophthalomoscope. Intraocular Pressure. 4. Funduscopic Findings. Has the patient suffered any form of illness in the past? Inquiry as to the presence of any systemic symptoms such as joint pains. most patients with uveitis would present with reduction in vision. a condition otherwise referred to as secondary glaucoma. • Medical History. wherein the posterior pole is involved. Other aspects of the patient’s history that should be considered include: Family history. 3. drug intake or travel. C-penlight. patients would exhibit full movement on all directions of gaze. Is there a history of any similar illness in the family? Is there any history of any hereditary illness? • Social History. • Sexual History. • OPHTHALMOLOGIC EXAMINATION OF THE PATIENT The basic tools that one would require in conducting an examination in the uveitis patient include the following: • Visual acuity charts – both for distance and near vision • Tonometer – used to determine the patient’s intraocular pressure • Penlight – for gross examination of the eye • Ophthalmoscope – used for fundus examination • Slit Lamp Biomicroscope – instrument used in the assessment of inflammatory findings in the anterior segment of the eye D B E A C F Figure 1. Does the patient have any exposure to pets? Inquire also as to the patient’s diet. On the other hand. As has been mentioned earlier.
Severe periphlebitis Fig. Retinal Detachment – may come in the form of diffuse serous detachment of the retina or as multifocal areas of detachments. Perivascular sheathing Fig. Cystoid macular edema Fig. Patients with uveitis. Granulomatous nodules – represents accumulation of inflammatory cells which may be located along the vitreous base or in the retinal pigment epithelium. Fig.6. 2. 133 . Slit lamp findings. Multifocal detachment of the retina 5. these lesions are typically referred to as retinal scars.UVEITIS AND SCLERITIS / 133 • • • • • Cystoid Macular Edema – presents as either an elevation of the macular area or dull foveal reflex. Vasculitis – generally presents in patients with posterior uveitis and often comes in the form of perivascular sheathing or narrowing or obliteration of the retinal blood vessels. Retinal Pigment Changes – generally represent areas of previously active inflammation. 5. Multiple retinal granulomas Fig. 4. particularly those wherein the primary location of the inflammatory process is in the anterior segment would typically present with the following findings.7. 3. Old syphilitic neuroretinitis Fig.
Fig. A B B Fig.10. 8. Figure 8 shows a typical picture of a patient with perilimbal flush as contrasted to a patient whose eye redness is secondary to conjunctival congestion (Figure 9) wherein redness is more diffuse in nature. an inflammatory membrane may also cover the pupil (Fig 12). Ciliary injection Fig. . Fibrinous membrane in pupillary area Fig. Medium sized KP’s C.UVEITIS AND SCLERITIS / 134 • Ciliary perilimbal flush. nor does it diminish with the use of vasoconstrictors. Different kinds of Keratic Precipitates (KP’s) A. they may also be diffusely distributed in certain forms of uveitis.9. Although more often confined in the inferior portion of the cornea. Patients with anterior uveitis present with constricted irregularly shaped pupils as a result posterior synechiae formation or adhesions between the pupil and the anterior capsule of the lens (Fig 11). Redness occurs as a result of congestion of the deeper ciliary blood vessels. The size of KP’s provides the clinician with a clue as to the pathologic classification of the disease as will be further discussed in a later part. Posterior synechiae following an attack of acute anterior uveitis 134 12. on the other hand. The presence of pigmentation. Fig. Their appearance may also vary as to their size (fine or large) and degree of pigmentation (Figure 10). old pigmented KP’s D. This is characterized as redness of the eye that is more marked in the area around the limbus and decreases towards the fornices of the eyes. would generally indicate that the condition is a chronic one. These are deposits of inflammatory cells on the corneal endothelium. In some instances. This type of redness does not blanch with pressure. Conjunctival congestion • Keratic Precipitates (KP’s). mutton fat KP’s B.11. old KP’s with ground glass appearance C B D B • Pupil abnormalities.
Hypopyon Fig. One may also note the presence of inflammatory cells in the anterior chamber as a result of the inflammation. patients may present with haziness in the anterior chamber due to the leakage of protein from leaking blood vessels. called Busacca nodules (Fig. Nodules may also be present in the iris. either within the stroma. Busacca nodules in iris stroma Fig.15.17. Fundus examination may reveal the presence of cellular aggregates in the periphery of the retina referred to as “snowbanking” (Fig. Snowbanking 135 . They become thinned out and may be referred to as moth-eaten in appearance. 6. Fibrinous exudates in acute anterior uveitis • Iris changes. they accumulate and assume a level in the anterior chamber referred to as hypopyon (Fig. referred to as Koeppe nodules (Fig. The iris undergoes changes as a result of the inflammatory process. Patients with intermediate uveitis or wherein the inflammation involves the ciliary body or peripheral retina may present with haziness of the vitreous (Fig. 13). These nodules represent cellular aggregates of inflammatory cells. Intermediate Uveitis Findings. When there are a large number of cells in the anterior chamber. Fig. Koeppe nodules (located at the pupillary border Fig. Fig. Vitreous haze Fig. As a result of the inflammatory process. Cells may also be observed in the retrolental area which may indicate that the inflammatory process involves the ciliary body as well. 13. 17) and one may note cells behind the lens on slit lamp examination. 16). 14).14. 18. This is referred to as flare.16.UVEITIS AND SCLERITIS / 135 • Signs of Inflammation in the anterior chamber. 15) or in the pupillary margin.
choroidal thickening and retinal detachment upon ultrasonographic examination. Some ophthalmologic conditions may present with typical fluorescein findings. protein deposits Intraocular pressure in uveitis may be A. SYSTEMIC EXAMINATION There are a number of systemic conditions that may present with uveal tract inflammation. low D.g. Ultrasound of the Eye In most cases of uveitis. 4. red blood cells B. diffuse congestion B. These are composed of A. corneal endothelial cells D. optic nerve Eye redness seen in patients with uveitis is best described as A. retinitis and areas of focal retinal detachment. REVIEW QUESTIONS. high C. PARTS I & II 1. e. 136 . photophobia D. Optic disc as well as macular problems may also be encountered in these patients. 2. vitreous condensations or haziness. joint inflammations. perilimbal flush C. blanches with pressure Keratic precipitates is a characteristic finding in uveitis. oral/genital sores. Ultrasonography gives the clinician a picture of the posterior segment. Patients with inflammation of the posterior segment may present with findings compatible with retinal edema. pulmonary involvement.UVEITIS AND SCLERITIS / 136 ANCILLARY EXAMINATIONS for UVEITIS Commonly. Uveitic conditions may present with the presence of a cataractous lens. 5. Examples of such would include various arthritic conditions. It also provides a method for detecting problems in the choroid and the retina. Fluorescein Angiography Fluorescein angiography is a procedure wherein abnormalities in blood flow in the vasculature of the posterior segment of the eye may be detected. any one of the above The most frequent chief complaint of patients with uveitis is A. additional examinations may be requested to aid in the diagnosis of some conditions. floaters C. uveal tract D. 3. These diseases may present with mucocutaenous abnormalities. vitiligo. parasitic conditions and immunologic conditions. blurring of vision B. a view of the posterior portion of the eye is compromised due to the presence of anterior segment pathology. eye redness 2. The more commonly requested ancillary procedures include: 1. erythema nodosum. gastrointestinal pathologies to name a few. inflammatory cells C. cornea C. confined to areas of extraocular muscle insertion D. Uveitis refers to inflammation of A. conjunctiva B. normal B.
choice of treatment regimen for the patient 7. in the formulation of a possible etiologic diagnosis B. constricted and irregularly shaped B. PART III. presence of inflammatory deposits on the corneal endothelium C. pathologic classification (Table 2) as to the severity and course of the disease (Table 3) or as to the etiologic cause (Table 4). abnormal optic disc appearance 10. Flare results from A. CLASSIFICATION OF UVEITIS Uveitis may be classified in a variety of ways.UVEITIS AND SCLERITIS / 137 A comprehensive history should be taken from patients suspected of uveitis. exudates C. Inflammation of the uveal tract leads to the presence of flare. The uveitides may be classified based on the anatomical area or areas involved in the inflammatory process (Table 1). vitreous condensations B. The pupil is often A. deposition of inflammatory cells in the corneal endothelium B. Anatomic Classification of Uveitis Anatomical Classification Anterior Uveitis Anatomic Area Involved Anterior segment structures involved Iritis (iris) Cyclitis (ciliary body) Iridocyclitis (both iris and ciliary body) Pars Planitis Pars plana and peripheral retina involved Posterior Pole Involvement Retinitis (retina) Choroiditis (choroid) Chorioretinitis (both choroid and retina involved with the choroid being more affected) Retinochoroiditis (both choroid and retina involved with the retina being more affected) Panuveitis – all three structures of the uveal tract is involved in the inflammatory process Peripheral or Intermediate Uveitis Posterior Uveitis Diffuse Uveitis 137 . Classifying serves three main purposes namely (1) as a guide for the clinician in requesting for further diagnostic examinations (2) to serve as a guide in managing the patient and (3) for prognostication purposes. anatomic structures involved in the inflammatory process D. retinal detachment C. Pupil abnormalities are frequently seen in patients with anterior segment inflammation. Commonly. normal in appearance 8. signs of vasculitis like perivascular sheathing D. The history aids in all of the following. vitreous hemorrhage 6. Funduscopic changes which is frequently present in patients with posterior uveitis include A. hemorrhages B. leakage of protein from the vascular barriers of the eye 9. Ultrasonography may be used as an ancillary tool in the diagnosis of uveitis. Table 1. choroidal thickening D. dilated C. establishing the chronicity of the disease C. adhesions between the lens and the pupillary border D. eccentric in location D. EXCEPT A. patients who have choroidal involvement would present with which picture on ultrasound A.
Etiologic Classification of Uveitis Bacterial Viral Fungal Parasitic Immunologic Systemic Tuberculosis Leprosy Syphilis Herpes simplex Herpes zoster Cytomegalovirus Histoplasmosis Coccidiomycosis Toxoplasmosis Toxocariasis Onchocerciasis Lens-induced Sympathetic ophthalmia Reiter’s syndrome Rheumatoid arthritis Sarcoidosis Collagen disease Reticulum sarcoma Lymphoma Heterochromic iridocyclitis Pigmentary syndrome Neoplastic Miscellaneous conditions 138 . Pathologic Classification of Uveitis and their Corresponding Features GRANULOMATOUS UVEITIS • • • Insidious in onset Usually involves the entire uveal tract Characterized by: Large greasy keratic precipitates Iris nodules Granulomas in the posterior pole • • • NON-GRANULOMATOUS UVEITIS Acute attacks with remissions and exacerbation Usually involves the anterior segment only Characterized by: Fine or small keratic precipitates Marked inflammation with tendency to hypopyon formation Table 3. Classification as to Severity and Course of the Disease Acute Uveitis Chronic Uveitis Recurrent Uveitis • Inflammation presents as an initial attack • Condition has been going on for less than two months or eight weeks • Characterized by repeated attacks of inflammation wherein the eye persists to have signs of low grade inflammation between bouts of exacerbation disappear between bouts of exacerbation • Condition has been going on for more than two months • Characterized by repeated attacks of inflammation wherein all signs of inflammation • Condition has been going on for more than two months Table 4.UVEITIS AND SCLERITIS / 138 Table 2.
pars planitis C. tuberculosis B. Uveitis may be associated with bacterial infections. histoplasmosis D. of insidious onset B. Eye redness is commonly confined in the interpalpebral area and would blanch with instillation of 10% phenylephrine. The patient’s condition can thus be labeled as A. typhoid C. non-tender nodule A. Acute uveitis B. The condition usually occurs in young adults. sarcoidosis PART IV. The condition is usually bilateral in one third of cases and patients often complain of mild discomfort. 139 . On ophthalmologic examination. PART III 1. Recurrent uveitis C. Anterior uveitis B. SCLERITIS This section will deal with inflammatory conditions that involve the sclera and episcleral tissues. iritis D. with females being more affected by males. Patients with primary inflammation involving the iris and ciliary body are labeled as A. Characteristics of non-granulomatous uveitis A. The patient probably has A. He claims that he has no history of any similar attack in the past. Diffuse uveitis 5. presence of large keratic precipitates D. a patient was found to have inflammatory changes in all parts of the uveal tract. tend to have hypopyon in the anterior chamber 3. feeling of heat or irritation in the involved eye. Posterior uveitis D. EPISCLERITIS This refers to a benign inflammatory disease characterized by edema and cellular infiltration of the episcleral tissue. A patient presents with a history of a 4-week duration of eye redness. Common bacterial infections which may manifest in the eye as uveitis is A. Chronic uveitis 4. A. specifically a slight ache. iridocyclitis 2. nodular episcleritis • usually takes longer to resolve (4-6 weeks) • underlying sclera is often normal • associated with movable. intermediate uveitis B. The condition can further be classified as follows: simple episcleritis • more common • often self-limiting (2-19 days) • may be recurrent • episodes become less frequent after the first 3 to 4 years B. Peripheral or intermediate uveitis C.UVEITIS AND SCLERITIS / 139 REVIEW QUESTIONS. presence of iris nodules C.
SLE. It may also be the presenting symptom of an underlying lethal systemic condition or it may herald the onset of a ‘flare’ of an already diagnosed systemic disease thought to be in remission. peripheral corneal inflammation and glaucoma may occur in a small percentage of cases. parasitic) 6.UVEITIS AND SCLERITIS / 140 Fig. SCLERITIS Scleritis is a severe ocular inflammation which consists of edema and inflammatory cell infiltration of the sclera. although uveitis. jaw and sinuses. B27-associated conditions (spondyloarthropathies. This is however not correlated to the type. 140 . Systemic conditions associated with episcleritis include 1. 1. rosacea. Without treatment it may be progressively destructive. fungal. 19. Simple Episcleritis Fig. miscellaneous conditions ( atopy. Unlike episcleritis. connective tissue diseases ( rheumatoid arthritis. posterior Each of these types will be discussed in detail in the subsequent section. it is associated with the best visual prognosis as ocular complications rarely occur. giant cell arteritis. or less commonly. the result of infection. Classification Scleritis has been classified as follows (Watson and Hayreh) A. Cogan’s syndrome) 5. penetrating eye pain which may radiate to the forehead. infections ( herpes. It is also least associated with a systemic disease. Females outnumber males to a small degree. The condition has been reported to occur bilaterally and is recurrent in about one third of cases. It is of insidious onset and may develop over a 5 to 10 day period. Diffuse anterior scleritis is the most common type of scleritis. Often misdiagnosed as episcleritis. Local trauma can also precipitate the inflammation. vasculitic diseases ( polyarteritis nodosa. B. Wegener’s granulomatosis. patients affected with this condition are usually in their fourth to sixth decades of life. Such redness fails to blanch with instillation of 10% phenylephrine or vasoconstrictors. bacterial. The main symptom of this condition is severe. Nodular Episcleritis Systemic Associations are found in about one third of patients. These changes are often immunologically mediated. relapsing 2. inflammatory bowel disease) 4. Behcet’s disease. anterior • diffuse • nodular • necrotizing with or without inflammation ( scleromalacia perforans) B. gout) Patients with episcleritis generally do not develop ocular complications. 20. There have also been reports on a small number of these patients progressing to scleritis. polychondritis) 3. Redness is gradual in onset and has a characteristic bluish-red tinge which may best be observed under natural light. laterality or chronicity of the disease.
lid retraction and limitation of extraocular movements. covered only the conjunctiva. uveitis. Posterior scleritis has the lowest incidence among these conditions. 3. lid swelling. Fig. Frequently. proptosis. This condition is almost always associated with rheumatoid arthritis. The inflammatory process is localized to a nodule(s) which is immobile. it is intermediate between that of the necrotizing type and posterior scleritis. 22. Necrotizing scleritis with inflammation is the most severe and destructive form. Fig. It may also be associated with anterior scleritis. Fundus examination may reveal disc swelling. It occurs twice as often in females and affects both eyes in about one third of cases. although traumatic perforation can easily occur. pain with eye movements and decreased vision. serous retinal detachment. 23. cataract. Ultrasonography is the key to making a diagnosis of posterior scleritis. It is characterized by the presence of white avascular areas surrounded by swollen inflamed sclera (Fig. Patients with this condition complain of periocular pain. As in the diffuse anterior type it is of insidious onset. It is also the most frequently associated with ocular complications such as peripheral corneal thinning or stromal keratitis. firm and tender to touch. Necrotizing scleritis without inflammation or Scleromalacia perforans is painless condition characterized by the appearance of yellow-gray nodules that gradually develop a necrotic slough or sequestrum without surrounding inflammation of the sclera. 141 . Necrotizing Scleritis without Inflammation (Scleromalacia perforans 5. choroidal folds. More than half of patients with this condition have associated systemic conditions such as rheumatoid arthritis. uveal effusions and macular edema. Associated Diseases Systemic conditions have been associated with approximate 50% of all scleritis cases. The necrotic tissue eventually separates leaving the choroid bare. Wegener’s granulomatosis and relapsing polychondritis. Nodular anterior scleritis occurs less frequently than the diffuse anterior type but is more common than necrotizing scleritis. Other eye symptoms include conjunctival chemosis. patients are older than 50 years and have and increased risk of visual loss. Table 5 shows a listing of these conditions. Spontaneous perforation rarely occurs. 21. In terms of severity of the disease. ).UVEITIS AND SCLERITIS / 141 2. and glaucoma. Anterior Nodular Scleritis Fig. Necrotizing Scleritis with Inflammation 4.
Scleromalacia perforans C. diffuse anterior scleritis D. eye redness C. nodular scleritis C. posterior scleritis 3. diabetes mellitus D. thyroid disease A patient presents with localized eye redness of about five days duration. herpes simplex. diffuse anterior scleritis B. mumps) • bacterial ( tuberculosis. 4. eye discharge 2. allergy B. rheumatoid arthritis (RA) systemic lupus erythematosus B27 spondyloarthropathies inflammatory bowel disease relapsing polychondritis (RP) Hemophilus. you note the presence of a movable. 5. Borellia) • fungal • parasitic Vasculitic diseases • • • • • Miscellaneous • • • • • Wegener’s granulomatosis polyarteritis nodosa Behcet’s disease giant cell arteritis Cogan’s syndrome rosacea gout chemical injury Psoriatic arthropathy Psoriatic rash REVIEW QUESTIONS. Systemic Diseases Associated with Scleritis Connective tissue diseases • • • • • Infectious • viral ( herpes zoster. nodular scleritis The inflammatory condition of the sclera which is associated with blurring of vision. On examination. eye pain D. proptosis and pain on eye movement is A. pseudomonas. rheumatoid arthritis C. 142 . The condition associated with the worst visual prognosis is A.UVEITIS AND SCLERITIS / 142 Table 5. Scleromalacia perforans D. nodules B. diffuse episcleritis B. Your impression would be A. diffuse anterior scleritis D. nodular scleritis B. nodular episcleritis C. non-tender nodule. The main difference in the clinical presentation of scleritis from episcleritis is the presence of A. necrotizing scleritis with inflammation The systemic condition that is more frequently associated with scleritis is A. syphilis. PART IV 1.
Is the disease condition chronic. (+) small pigmented KP’s. formed anterior chamber. the patient noted recurrence of symptoms in the left eye and a week later. Based on the above findings. (+) cells in the retrolental area. (+)flare (-) iris nodules. CD 0. Ophthalmologic examination revealed the following findings: Best corrected vision OD = 6/21 OS = CF at 1 meter Intraocular Pressures OD – soft OS – hypotonic EOM’s OU – full Funduscopy OD – essentially normal funduscopic Findings OS – no ROR noted due to a very hazy media Slit Lamp Findings: OD – clear cornea. (+) lens opacity OS – clear cornea. slightly hazy media.UVEITIS AND SCLERITIS / 143 PRACTICE CASES Case 1. is the disease condition granulomatous or non-granulomatous in nature? 4. He also noted the presence of oral ulcers. recurrent. What parts of the uveal tract is involved in the inflammatory process? Based on this.o. slightly dull foveal reflex Clear cornea. no exudates. no hemorrhages. She denies any other associated symptoms nor any history of a similar episode in the past. History reveals that the patient first experienced eye redness in the left eye about one year prior to consultation that was associated with photophobia and blurring of vision. Based on the given information. moth eaten iris Left Eye 6/30 Soft Full (+)ROR.o. experienced similar symptoms in his right eye. Ophthalmologic Examination at time of consultation revealed the following findings: Visual Acuity IOP EOM”S Funduscopy Right Eye 6/21 Soft Full (+)ROR. no exudates. or acute? 3. (+) vitreous condensation 1. distinct disc borders.(+) flare (-) iris nodules. no cells or flare. normal appearance of the iris. how would you classify the patient’s condition? 2. AV 2:3./M presents with a chief complaint of bilateral blurring of vision. slightly hazy media. (-)cells. what is the anatomic classification of this patient’s uveitis? 3. slightly dull foveal reflex Clear cornea. (+) small pigmented KP’s.3. moth eaten iris Slit Lamp Findings 1. (+) note of perivascular sheathing. (+) perilimbal flush. however. distinct disc borders. Assuming that this patient has normal funduscopic findings in the left eye. no KP’s. how would you classify the patient’s condition on the basis of disease activity? 2. (+) fine non-pigmented keratic precipitates. The rest of the history was unremarkable. (+) note of perivascular sheathing. (+)cells. What ancillary procedure may be requested in this patient to determine the extent of inflammation? 143 . About 1 month prior to consultation. Consult was done at that time and symptoms allegedly resolved with unrecalled topical medication. CD 0. 24 y. What ancillary procedure may be useful in determining the presence or absence of posterior segment inflammation? Case 2. no hemorrhages. 50 y. (+) cells/ (+) flare./F presents with a history of two-month duration of blurring of vision and redness in the left eye.3. AV 2:3.
diabetes mellitus and tuberculosis (grandmother). By doing so. OS – 12 mm Hg Fundus Exam: Normal in both eyes Slit lamp Examination OD – essentially normal findings OS – localized redness temporally with note of corneal edema and infiltration (pls.o female presents with a 6-month history of red. Ophtha Exam revealed the following findings: Visual acuity: OD – 20/20. more vision-threatening condition like uveitis or scleritis. RECOMMENDED FOLLOW-UP It is recommended that the students be given demonstration sessions on how to properly conduct historytaking and ophthalmologic examination of patients. OD – 20/25 Gross Exam: Rosacea facies. One should bear in mind that not all conditions which present with a red eye is “sore eyes” and a patient may actually be suffering from another. Given the patient’s history and eye findings. what are your differential diagnoses for this case? 2.UVEITIS AND SCLERITIS / 144 Case 3. The importance of a comprehensive clinical history can not be overemphasized since the etiologic diagnosis of most of these ocular inflammatory conditions relies on the history. It is therefore your role to be able to properly recognize these patients so that immediate referral to an ophthalmologist for further evaluation and management can be done. She previously had an episode of corneal ulcer in the same eye. Her family history was positive for glaucoma (grandfather). A 43 y. photosensitivity and pneumonia. you may. it is further recommended that the students be provided clinical sessions to allow them to see actual cases of patients with uveitis and scleritis. SUMMARY It was the primary objective of this self-instructional material to provide the reader with a guide on how to diagnose patients with uveitis and scleritis. early intervention can be facilitated and permanent visual impairment may be avoided. refer to picture below) 1. CONCLUSION As medical practitioners. Her past medical history was positive for sinusitis. How would you differentiate one condition from another? PART V. in the future encounter patients who will seek consultation for eye problems. She also had a hysterectomy about 2 years ago. normal pupillary reflexes. Following this exercise. Secondly. rosacea. The rest of her history was unremarkable. 144 .15 mm Hg. painful left eye. normal eyelids EOMs: full on all directions of gaze IOPs: OD. one should be able to recognize the various ocular signs associated with these inflammatory conditions.
S. Ronald E. Baltimore. Robert A. Whitcup. R. D. Uveitis: A Clinical Approach to Diagnosis and Management. Appleton and Lange. 1996. C 7.. Mosby. A 8. 2. and Riordan-Eva. 5. Vaughn. C PART III 1. would support diagnosis of episcleritis 145 . 1983.M. Hayreh SS: Scleritis and episcleritis. non-granulomatous type of uveitis 4. A PART IV 1. A 6. 7. 2. Butterworth Heinemann. D 5. 4th edition. 4. Sainz de la Maza M.. Newell. Clinical Ophthalmology A Systematic Approach. 1992.UVEITIS AND SCLERITIS / 145 REFERENCES 1. D 5. B 3. and Nozik.. B 4. 1. Watson PG. D 2. if nodule is movable. American Academy of Ophthalmology.G. 101(2): 389-96 6. Oxford. and Palestine. Foster CS: Severity of scleritis and episcleritis. 4. Frank G. ciliary body and the posterior segment (retina and/or choroid) – based on anterior and posterior segment findings 2. iris. Smith. C 2. D 3. D 9. 3. Connecticut. since there is no view through the pupil Case 2. ANSWERS TO REVIEW QUESTIONS PARTS I and II 1. 2nd ed. C D B B D ANSWERS TO QUESTIONS FOR CASES Case 1. nodular episcleritis vs. 6th edition. Br J Ophthalmol 1976. Asbury. 1. ultrasound. A. Jack J. P. acute uveitis 2. Williams and Wilkins. Nussenblatt. Ophthalmology 1994 Feb. recurrent uveitis – assuming that the patient was inflammation free during the one year period 3. A 4. if it does not blanch scleritis > also check for tenderness since tenderness would support diagnosis of scleritis > check if nodule present is movable.B. (ed) Basic Ophthalmology for Medical Students and Primary Care Residents. specifically iritis 3. C 10. Frank. General Ophthalmology. 1. 1999. Kanski. 15th ed. Uveitis: Fundamentals and Clinical Practice. Baltimore. 60: 163-192 8. 5. Berson. latest edition. fluorescein angiography Case 3. Textbook of Ophthalmology. 3. T. anterior uveitis. nodular scleritis 2. > may instill vasoconstrictors and if blanches episcleritis. Jabbur NS.
4. Tearing is either due to increased production (lacrimation) or from impaired drainage (epiphora). 5 = valve of Hasner (opening at inferior meatus underneath the inferior turbinate) 146 . and an inner mucinous layer secreted by the goblet cells of the conjunctiva. Physiology of the lacrimal drainage system 3. and epiphora which is overflow of tears due to blockage of the lacrimal drainage system. Tearing is often classified into two entities: lacrimation or excess production of tears. Chronic tearing can be a debilitating complaint which may be a nuisance (constant need to wipe off the tears). ocular adnexae. a middle aqueous layer produced by the lacrimal gland and glands of Krause and Wolfring. 3. The superficial oily layer functions to prevent the evaporation of the aqueous layer. Anatomy of the eye. The mucous layer is important for proper wetting of the cornea. enumerate the common conditions that cause tearing. The lacrimal drainage system begins at the punctum leading to the canaliculus to the lacrimal sac down to the nasolacrimal duct. note 1 = valve of Rosenmuller. The tear film has unique characteristics (Table 1). Basic ocular examination (normal and abnormal findings) INTENDED USERS Year Level IV UPCM Medical Students CONTENT Tearing or ‘watery eyes’ is a common ocular symptom which has numerous causes ( Appendix A). enumerate and describe the different clinical examinations which can help determine the cause of tearing.4. OBJECTIVES Upon completion of this instructional material.TEARING / 146 TEARING Alexander Dy Tan MD INTRODUCTION Tearing is a common symptom of many ocular and sometimes even systemic illnesses. source of embarrassment and discomfort for the patient. See Illustration below. A thorough understanding of the lacrimal apparatus. particularly the lacrimal drainage system 2. The duct opens at the inferior meatus under the inferior turbinate. define the symptom of tearing (differentiate between lacrimation and epiphora) 2. PREREQUISITE KNOWLEDGE AND PREPARATION 1. tear film and lacrimal drainage system is necessary in order to determine the cause of a patient’s tearing. provide basic clinical (diagnosis and management) information regarding the different types of nasolacrimal duct obstruction. It is composed of three layers: an outer oily layer (oily secretions from Meibomian and Zeis glands). The pH of tears averages 7. the student should be able to 1.
Important questions to be asked in a patient’s history include the following: 1. It is very important to get a thorough history and physical examination in order to determine the cause of tearing. evaporation and drainage. Increased Tear Production (Lacrimation) Tearing is more commonly caused by increased production. mucoid or purulent). and medications used in order to figure out when the symptoms started and how they responded to therapy. These situations uncover the presence of dryness or ‘tear instability). eye pain. photophobia. It is important to establish a timeline of consultations. Lacerations may involve the lacrimal gland or any part of the drainage system which can affect the amount of tears present in the tear lake. Certain occupations (i. Exposure to someone with similar ‘red eyes’ may suggest a form of viral conjunctivitis. itchiness. blurring of vision. 147 . etc) will lead to a relative lack of tears. eyelid retraction. 3. carpenters. prolonged reading. Associated symptoms – discharge (water. eye redness. 4. and blurred vision. Patients who complain of ‘foreign body sensation’ can have conditions such as: corneal or conjunctival foreign body. While reading or working with the computer. 2. construction workers etc) are predisposed to foreign bodies in the cornea or conjunctiva. Canalicular lacerations should be suspected when there is a lid margin laceration within 5 mm of the medial commissure. etc. while allergies are often associated with itchiness. Onset and duration of tearing (Worsening during prolonged reading or when exposed to wind may indicate a ‘dry eye’. nasolacrimal duct obstruction is more common in women. History of trauma – to rule out conjunctival or corneal foreign bodies. we tend to blink ‘less often’ resulting in more tear evaporation. redness. corneal abrasions. It is important to ask for: history of trauma.e. foreign body sensation. This may suggest a chronic process or may be a result of patients surgery. Consultations with a doctor and medications used. surgeries. corneal ulcer. Conditions that increase production and impair drainage will result in a surplus of tears in the eye.TEARING / 147 We must keep in mind that the amount of tears in our eye is dictated by three factors: production. while increased evaporation (decreased humidity. history of ocular surgery. use of medication. Tearing in these situations is the body’s attempt to wash out the eye of the ‘irritant’. misdirected lashes. Dry eye more common in the elderly.
A Schirmers strip is folded and placed at the junction of the lateral and middle third of the lower eyelid. etc. Generally. Slit lamp biomicroscopy utilizes a microscope with a light in order to magnify the structures in the eyelids and anterior segment of the eye. sinus disease A thorough ocular examination (visual acuity. lens clarity. and the nasolacrimal duct.TEARING / 148 5. Canalicular stenosis can be confirmed with probing while a lacrimal apparatus irrigation is often necessary in 148 . decreased production of tears may be confirmed by doing the Schirmers test. tonometry and funduscopy) is necessary to determine the cause of a patient’s tearing. Characteristics of the Tear Film Decreased Tear Drainage (Epiphora) Tearing due to blocked tear drainage can be a very bothersome symptom. gross examination. from the punctum to the canaliculus. with the slit beam providing other details as presence of anterior chamber inflammation. Ectropion and entropion may cause ocular irritation resulting in tearing. anterior chamber depth. etc. Tests for patients with Lacrimation Schirmers Test: uses a Whatman filter paper in order to measure the amount of wetting (from tears) in five minutes. Patient is asked to look straight ahead and avoid blinking. Thickness Layers Thickness of the Aqueous Layer Tear Volume Tear Production 7 – 10 um 3 6. removal of foreign bodies for patients with conjunctival or corneal foreign bodies. Punctal stenosis can be visualized directly or with the use of a slit lamp. Chronic epiphora can sometimes lead to infections of the lids and lacrimal sac. A slit lamp may be used in conjunction with a Goldman’s applanation tonometer in order to determine a patient’s intraocular pressure. eyelid surgery for patients with misdirected lashes. Other medical problems particularly allergies. Slit lamp examination may show an abnormal tear meniscus. Examination for patients with lacrimation should focus on the anterior segment examination. Any injury or inflammation involving the lashes.2ul per minute Table 1. patients with mild to moderate dry eye may complain of tearing which is mostly a reflex mechanism to compensate for the ‘lack of tears’. anterior chamber and iris will result in some form of tearing. Patients with Dry Eye can also manifest with tearing. cornea. Any point of the lacrimal drainage system can be blocked. Management will range from antibiotic eyedrops for patients with bacterial infections. Correction of these conditions will result in the resolution of the patients tearing. Schirmers Test with anesthetic is thought to measure basal secretion of tears while the test without anesthetic measures reflex tearing. entropion or ectropion. corneal clarity. Schirmers Test can be done with and without anesthetic (Proparacaine). EOM. Patients frequently carry along boxes of tissue paper in order to constantly wipe off overflowing tears. Management of Lacrimation is generally directed to address the underlying cause of tearing.5um 6 – 8 ul 1. conjunctiva. Note. A Schirmers Test with anesthetic wetting of 5 mm or less in 5 minutes is indicative of dry eye. lacrimal sac.
Persistent cases are managed with therapeutic probing 149 . A dacryocystorhinostomy is performed for adult patients with symptomatic and complete nasolacrimal obstruction. connecting the lacrimal sac to the nasal mucosa. (on left): A Gauge 25 Lacrimal Irrigating Canula is inserted through the punctum (exits at the distal cut end of the canaliculus). Punctal ectropion associated with lid laxity can contribute to decreased outflow of tears. Probing may also be confirmatory for patients with canalicular transactions due to trauma. Diagnosis is usually confirmed by doing a dye disappearance test. while severe cases present with fulminant dacryocystitis. Probing : a fine blunt probe can be inserted through the punctum and canaliculus in order to determine the patency of the upper lacrimal drainage system. About 90% of cases will resolve during the first year of life and spontaneous resolution continues even up to the 2nd year of life. dacryocystitis). The surgery is performed under general anesthesia. Palpation of the lacrimal sac area: applying pressure on a distended lacrimal sac may result in mucoid reflux. or from tumors (lacrimal sac tumors. Diagnostic Tests: 1. from injury (canalicular transections). no abnormal finding which can explain the patients tearing).e. Fluorescein is instilled on the cul de sac of both eyes. Obstructions involving the canaliculi or puncta will not result in distension of the sac since the tears will not be able to reach the sac. Children presents with tearing or chronic eye discharge / recurrent conjunctivitis. The DDT does not distinguish between mechanical blockage and functional blockage. Mucoid reflux upon digital pressure at the lacrimal sac area also confirms the diagnosis. Patients with dacryocystitis often have history of swelling of the medial canthal area which when exacerbated results in: pain swelling and erythema (acute dacryocystitis). 4. Conditions such as Bells palsy or weakness of the CN7 may also cause physiologic pump failure of the lacrimal drainage system. no signs of infection. Retention of dye beyond five minutes in one eye is also indicative of blockage. which confirms the presence of nasolacrimal duct obstruction. Dacryocystitis) is lacrimal sac massage. It involves a fistulizing procedure.e. Patients often have a long standing history of on and off tearing of the involved eye. Pathology is an imperforate membrane at the Valve of Hasner at the inferior meatus. Picture 1. Management of nasolacrimal duct obstruction is surgical. dacryolithiasis).TEARING / 149 order to diagnose nasolacrimal duct obstruction. Asymmetric clearance of the dye within 5 minutes indicates relative block in the side with dye retention. Management of uncomplicated (i. Special Topic: Congenital Nasolacrimal Duct Obstruction: is present in up to 10% of all normal infants. Nasolacrimal duct obstruction should be suspected in patients with tearing who have normal anterior segment examination (i. Lacrimal Apparatus Irrigation: involves the irrigation of normal saline solution through the punctum and canaliculus. confirming presence of canalicular laceration 2. with or without history of infection (mucoid discharge. Primary acquired nasolacrimal duct obstruction is more common in elderly females. Dye disappearance test: assesses the presence or absence of adequate lacrimal drainage. 3. reflux (either thru the upper canaliculus or lower canaliculus) would indicate an obstruction. conjunctivitis. Blockage may be due to scarring from inflammation or topical medicines.
7th edition by Frederick Hampton Roy) I. Duane retraction syndrome 4. Ametropia. Caloric. Central nervous system lesions 2. reserpine. ketamine. naloxone. heparin. bright light 150 . Hypersecretion of tears A. diazepam. Congenital. Primary (disturbance of the lacrimal gland) B. lacrimal and reflex tearing – bilateral lacrimation when syringing the ear with warm or cold water and during Tensilon testing 3.TEARING / 150 (rupturing the membrane at the Valve of Hasner) which is usually performed at 12 months of age. Central 1. etc 8. Exposure to wind. Physical pain 6. phoria and eyestrain and fatigue 2. Picture 2. Acquired with onset in early stage of facial palsy (Bells palsy) or sequela with parasympathetic fibers to the otic ganglion growing back into superficial petrosal nerve c. Patients who have undergone failed probings are managed with bicanalicular intubation with silicone tubes or by performing a dacryocystorhinostomy. Bells palsy 5. Melkersson-Rosenthal syndrome (Melkersson idiopathic fibro edema) 7. often associated with ipsilateral paresis of lateral rectus muscle b. cold. Drugs: atenolol. Voluntary lacrimation. Neurogenic 1. nifedipine. tropia. dexamethasone. Hysteria 5. such as when acting C. Corticomeningeal lesions 3. Marin-Amat Syndrome (inverted Marcus Gunn Jaw winking phenomenon) 6. morphine. Crocodile or alligator tears – unilateral profuse tearing when eating a. Congenital NLDO with dye retention in right eye in dye disappearance test APPENDIX Differential Diagnoses for Tearing (from Ocular Differential Diagnosis. ciprofloxacin. Emotional states 4.
Waardenburg syndrome (lateral displacement of the medial canthi with lateral displacement of puncta and lengthening of the canaliculi 5. Parkinson’s disease 17. Raeder syndrome (paratrigemial paralysis. Inadequacy of physiologic lacrimal pump I. Giant cell arteritis (temporal arteritis) d. Tic douloureux j. cervical sympathetic ganglia. such as vomiting and laughing 18. various senile dementias 20. silver nitrate. Reflex. Rothmund syndrome (telangiectasia-pigmentation-cataract) 25. Absence of atresia of lacrimal drainage apparatus 2. orbit. Sluder syndrome i. triflourothymidine. diencephalic epilepsy syndrome (Penfield syndrome) c.TEARING / 151 9. Punctal eversion G. Gradenigo syndrome (temporal syndrome) 21. Complications from diseases such as pemphigus. Lesions affecting the lids a. sinuses. trichiasis 13. Amniotocele 3. Ophthalmorhinostomatohygrosis syndrome 16. uvea. Thyrotoxicosis (Basedow syndrome) II. Goltz syndrome H. neostigmine. Glaucoma 10. lids. hypothalamus. Obstruction of nasolacrimal drainage system B. Traumatic lesions of the lacrimal drainage system 151 . or the lacrimal nucleus a. Rhabdomyosarcoma 24. Congenital anomalies of the lacrimal apparatus 1. Retroparotid space syndrome (Villaret syndrome) 23. Meningitis f. Hypothalamic tumors e. Inflammation or infection of the conjunctiva. Myasthenia Gravis – afternoon ectropion (Erb-Goldflam syndrome) 15. encephalitis b. fluorouracil. Drugs such as: acyclovir. Bee sting of cornea 2. Inadequacy of lacrimal drainage system A. facial paralysis d. Stevens-Johnson syndrome and lupus C. Tabes 3. etc F. Thermal burns D. Sjogren syndrome 19. entropion/ ectropion c. teeth or ears 12. Horner syndrome 11. Pseudobulbar palsy for Parkinson syndrome h. Stimulation of some cortical areas – thalamus. Dacryocystitis D. cornea. cluster headaches) 22. Fistulas of lacrimal sac and nasolacrimal duct 4. such as in Actinomyces israelii . Symptomatic 1. Morquio-Brailsford syndrome (MPS IV) 14. Page syndrome g. papilloma or dacryolith E. Distended canaliculi with obstruction. ptosis b.
dacryocystography C. slit lamp 7. 4. D 7. 3. radiograph B. lacrimal sac D. 7th edition 2. Jones Test E. valve of Rosenmuller 8. Smith’s Ophthalmic Plasctic and Reconstructive Surgery SELF-TEST For questions 1-5 . probing D. Frederick . A 6. Most common location of blockage in congenital NLDO is at A. valve of Hasner E. Best means of confirming the presence of a canalicular laceration is through A. Hypertrophic rhinitis REFERENCES 1. dye disappearance test D. Nasal disease 1. 3. 2. Ocular Differential Diagnosis. Sinusitis 2. B 4. A 2. In children the easiest way of confirming a nasolacrimal duct obstruction is with the use of: A. A 3. punctum C. Hart (Ed) Adlers Physiology of the Eye . D 8. dacryocystography Answers to Self-test 1. What is the mechanism of tearing in the following conditions? Possible answers are A: increased production B: decreased drainage 1. Nesi et al .TEARING / 152 J. Conjunctivitis Corneal Foreign Body Dacryocystitis Canalicular Stenosis Glaucoma 6. Roy. Tumor obstruction K. B 152 . B 5. dye disappearance test E. 5. canaliculus B. slit lamp examination B. probing C.
their origin. antagonist and yoke. Valbuena M. 153 ..STRABISMUS / 153 DEVIATION OF THE EYE STRABISMUS Marissa N. The eye can usually be moved about 50 degrees in each direction from the primary position.patient clinics. the student must have previous knowledge of anatomy and physiology of the eye and the methods of history taking and ocular examination. insertion. Insertion. and actions. Innervation and Action of Extraocular Muscles There are six extraocular muscles controllong eye movement : the four recti muscles. 3. 2. be able to extract a relevant medical history. The primary position of the eye is defined as being that when the eye is directed straight ahead with the head also straight. actions and innervation of the extraocular muscles. 4. as well as a knowledge of the clinical manifestations of these conditions will help the student in his interactions with the patients. Ocular motility problems are among common conditions the students will encounter in the out . their clinical manifestations and principles of management. Given a patient with ocular motility problem. Given an extraocular muscle. OBJECTIVES After going though this material. Enumerate the extraocular muscles. insertion. A clear understanding of the anatomy and physiology of the extraocular muscles. identify its synergist. the knowledge and skills in history taking and physical examination of patients with motility problems. RECOMMENDED PREPARATION Before going to this material.D. CONTENT ANATOMY AND PHYSIOLOGY OF EXTRAOCULAR MUSCLES Origin. Table I summarizes the origin. the student is expected to: 1. Ordinarily however. College of Medicine are encouraged to go through this material.P. Discuss the most common types of strabismus. and be able to perform a complete ocular examination. innervation. The secondary and tertiary actions are additional effects on the position of the eye in primary position. the superior oblique is innervated by the trochlear nerve (IV) and the remaining muscles are innervated by the oculomotor nerve (III). The primary action of a muscle is the major effect on the position of the eye when the muscle contracts while the eye is in primary position. the eyes move only 15 to 20 degrees from primary position before head movement occurs. the two obliques. MHPEd INTRODUCTION Level IV medical students of the U. The lateral rectus muscle is innervated by the abduscens nerve (VI) .
The Y axis is perpendicular to Listing’s plane.7 mm from superior limbus 6. Axes of Fick. Listing Plane and Median Plane The axes of Fick are X. The high ratio of nerve fibers to eye muscle fibers (1:3 to 1:5) allows more accurate control than is found in skeletal muscles in which the ratio ranges from 1:50 to 1:125. voluntary vertical rotations of the eye occur at this axis . Extraocular Muscles Extraocular muscle is a specialized form of skeletal muscles which incorporates several fiber types.9 mm from lateral limbus 7. Listing’s equatorial plane passes though the center of rotation and includes the X and Z axis. The median plane is a sagittal plane passing antero-posteriorly through the body. involuntary torsional movements occur at this axis .5 mm from inferior limbus Posterior equator at superotemporal quadrant Posterior to the equator in inferotemporal quadrant Direction of pull 90 ° 90° 23° 23° 51° Action from Primary Position Adduction Abduction Elevation Intorsion Adduction Depression Extorsion Adduction Intorsion Depression Abduction Extorsion Elevation Abduction Innervation Cranial Nerve III VI III III IV 51° III Table 1. (Fig. At the other extreme is a muscle type is adopted for participation in extreme gaze. The Z axis is a vertical axis.STRABISMUS / 154 Muscle Medial rectus (MR) Lateral rectus (LR) Superior rectus (SR) Inferior rectus (IR) Superior oblique (SO) Inferior oblique (IO) Origin Annulus of Zinn Annulus of Zinn Annulus of Zinn Annulus of Zinn Orbit apex above Annulus of Zinn (functional rigin at trochlea) Behind lacrimal fossa Insertion 5. 1) The X axis is a transverse axis passing through the center of the eye at the equator . Y and Z.5 mm from medial limbus 6. Fig 1 Axes Of Fick 154 . bisecting the head into symmetric parts. voluntary horizontal movements occur at this axis . Center of Rotation. Motor Physiology A. At one extreme is a slow tonic type resistant to fatigue and active in holding gaze straight ahead.
four oblique positions of gazes : up and right. depression is downward movement of the eye. The obliques are inclined 51 degrees to the visual axis. Positions of Gazes 1. Table 3 shows the agonists with their respective synergists and antagonists.straight ahead 2. giving rise to torsion as their primary action but also some vertical and horizontal rotations as well. down and right. MUSCLE Medial rectus Lateral rectus Superior rectus Inferior rectus Superior oblique Inferior oblique PRIMARY Adduction Abduction Elevation Depression Incycloduction Excycloduction Incycloduction Excycloduction Depression Elevation Adduction Adduction Abduction Abduction SECONDARY TERTIARY Table 2 . while abduction is movement of the eye temporally. Table 2 lists the actions of the extraocular muscles. Action Of Extraocular Muscles From The Primary Position D.straight up. up and left. left gaze 3. Secondary positions . Tertiary positions . the horizontal recti are purely horizontal movers along the Z axis and have only a primary action. The antagonist is the muscle in the same eye as the agonist that acts in the direction opposite to that of the agonist. as the right eye adducts. Monocular eye movements ( Ductions ) Ductions are monocular rotations of the eye. right gaze. Excycloduction (extorsion) is temporal rotation of the superior portion of the vertical corneal meridian. giving rise to torsion and adduction. up and left. Secondary and tertiary actions With the eye in primary position. The vertical recti have a direction of pull that is primarily vertical as their primary action. the right medial rectus receives increased innervation while the right lateral rectus receives decreased innervation. right left. 155 . Sherrington’s law of reciprocal innervation states that and increased innervation and contraction of a given extraocular muscle is accompanied by a reciprocal dectrease in innervation and contraction of its antagonist. For example. down and left 4. but the angle of pull from origin to insertion is 23 degrees inclined to the visual axis.STRABISMUS / 155 B. Cardinal positions . An agonist is the primary muscle that is moving the eye in a given direction. The synergist is the muscle is the same eye as the agonist that acts as the agonist to produce the same movement. straight down. Primary. down and left C.up and right. Eye movements 1. Elevation is upward rotation of the eye. Primary position . down and right. Adduction is movement of the eye nasally. Incycloduction ( intorsion ) is nasal rotation of the superior portion of the vertical corneal meridian.
Fig 2. Versions ( Conjugate binocular eye movements ) Yoke muscles are two muscles (one in each eye) that are prime movers of their respective eyes in a given direction of gaze. as the eyes move to the left gaze. Each extraocular muscle in one eye has a yoke muscle in the other eye. Cardinal Positions And Yoke Muscles 156 . Agonists With Their Respective Synergists And Antagonists 2.STRABISMUS / 156 AGONIST MEDIAL RECTUS SYNERGISTS Superior rectus Inferior rectus Superior oblique Inferior oblique Inferior oblique Medial rectus Superior oblique Medial rectus Inferior rectus Lateral rectus Superior rectus Lateral rectus ANTAGONISTS Lateral rectus Superior oblique Inferior oblique Medial rectus Superior rectus Inferior rectus Inferior rectus Superior oblique Superior rectus Inferior oblique Inferior oblique Superior rectus Superior oblique Inferior rectus LATERAL RECTUS SUPERIOR RECTUS INFERIOR RECTUS SUPERIOR OBLIQUE INFERIOR OBLIQUE Table 3 . Figure 2 shows the six cardinal positions of gaze and the yoke muscles whose primary actions are in that field of gaze. the right medial rectus and the left lateral rectus are simultaneously innervated and contracted. For example.
When the eyes are dissociated or not aligned. It is usually caused by opacities in the media. STRABISMUS Definition of Strabismus Strabismus means ocular misalignment of whatever cause. Each eye must be directed simultaneously to the same object. 157 . the visual line in each eye intersects at the object in space and there is binocular fixation. In a person with normal ocular. Cardinal Positions And Yoke Muscles Hering’s law states that equal and simultaneous innervation flows to the yoke muscles concerned in the desired direction of gaze BINOCULAR VISION The eyes are spaced 50 to 65 mm apart. The visual axis is an imaginary line that connects an object in space with the fovea. simultaneous use of each fovea during the critical time that occurs early in life. Amblyopia is a condition in which there is a unilateral or bilateral decrease in visual acuity that is not fully attributable to organic ocular abnormalities. The slightly different image originating in each eye is fused in the brain as a streoscopic image. high refractive errors. fixation is by one eye only. Normal development of stereoscopic vision requires binocular. If visual lines are not directed at the same fixation point.STRABISMUS / 157 Fig 3. sensory and motor systems. anisometropia (difference in refractive errors of the 2 eyes) or ocular misalignment or strabismus during visual immaturity. Treatment consists of occlusion (patching) of the better eye to force the use of the amblyopic eye and the correction of the underlying cause. The correction of amblyopia depends on the maturity of the visual system at the onset and the duration of the abnormal visual experience. strabismus is present.
2.documented prior to age 6 months 2. Intermittent phoria or tropia . Incomitant . incyclodeviation B. thyroid disease Trauma Previous consultation. Vertical . Visual acuity 158 . 10. 12. Tropia . Alternating .deviation varies with direction of gaze or fixationg eye.excyclodeviation.seizures . 1. 2. According to age of onset: 1.prematurity Developmental history Family history B. According to fixation 1. According to direction of deviation: 1. Types of Strabismus: A. the eyes remain aligned. Ocular examination 1. Chief complaint Age of onset . infantile . so eyes are aligned in all directions of gazes at all distances even after occluding one eye. Comitant . History taking : information should be obtained about the following 1. 3. diabetes. D.there is spontaneous alternation of fixation from one eye to the other. exodeviation 2. Most incomitant strabismus is paralytic. Congenital. treatment .document onset with photographs Direction of deviation Constant or intermittent Magnitude of deviation Associated eye complaints – diplopia.hyperdeviation. hypodeviation 3.latent deviation.STRABISMUS / 158 Orthophoria refers to the ideal condition of ocular balance.deviation does not vary with direction of gaze or fixationg eye. Phoria . 6.patching. 2.esodeviation. glasses. 11. 8. Examination of the Patient A. Monocular . According to variation of deviation with gaze position or fixating eye 1. surgery Maternal and birth history . blurring of vision Antecedent or concurring illness .fusion control present part of the time 3. E.there is preference for fixation with one eye. 7. Acquired C.manifest deviation in which fusion control is not present. According to fusion status (whether the deviation can be controlled by fusuin mechanism. Horizontal . 4. Torsional . 2. controlled by fusion mechanisn so that under binocular condition. 5. 9.
For verbal and cooperative children. a. Tests for ocular alignment A. d. To record relative over or underactions. that is . Note whether the amplitude of eye movements is normal or abnormal in both eyes. Prism Test ( Krimsky Test) This test is usually perfomed in patients unable to fixate with both eyes because of poor vision in one eye or in uncooperative patients. directing the light between the patient’s two eyes. For example. Ask the patient to seat facing you with head straight and eyes directed in primary gaze. Corneal Light Reflex 159 . Place increasing amount of prism on the straight eye until the corneal reflex on the deviating eye is centered. Ask the patient to fixate on a light. The child’s fixation pattern will give a clue as to the comparative vision of the two eyes. designate normal as 0. achild who can alternate fixation in his 2 eyes will probably have equal visual acuity.t record its direction and amplitude in specific field of gaze. c. Children often pose a difficult assessment problem. See Fig. Compare the position of the light reflex and record the estimated degrees of deviation. Note any nystagmus and if presen. 4 . Rate amplitude for all fields of gaze by considering normal amplitudes as 100%. c. Ocular motility examinations The following clinical protocol may be used to assess ocular movements : a. no over or underactions are present. Underactions are rated 1 to -4 while overactions are rated +1 to +4. Use 4 to designate maximum over or underaction. Corneal light reflex test ( Hirschberg method ) a. Ask the patient to follow target as you move it into the six cardinal positions. Hold a penlight in front of the patient’s eyes at a distance of about 2 ft. ( See Fig 5) 15 ° Esotropia 30 Esotropia 45 ° Esotropia Fig. 2. Instruct the patient to look directly at the light. charts using tumbling E or pictures can be used. 4. b. and rate lesser amplitudes accordingly. Sit facing the patient.. with the patient in primary position (straight ahead) b. B. 3. b. c.STRABISMUS / 159 Various tests are available for visual acuity determination . Hold your finger or a small fixation target 10-14 inches in front of the patient. Another child who prefers one eye to fixate probably has a better vision in that eye compared to the fellow eye. Prisms placed on the deviating eye is preferred in patients with incomitant or paralytic deviations. Elevate upper eyelid with your finger of your free hand to observe downgaze.
Continue to place prisms of progressively higher power until no movement is noted in either eye (neutralization). Orient the prism apex towards the direction of the deviation. Alternate cover test (prism and cover test) a. Ophthalmoscopy Abnormalities in the fundus should be noted such as abnormal optic disc. using a near fixation point. facing the patient and at an arm’s length to the patient. Refraction 160 . Choose the strength of the initial prism to approximate the deviation estimated by the Hirschberg’s test. rapidly shift the occluder from one eye to the other several times. Ask the patient to look at a distance fixation and position yourself directly opposite the patient. 5. d. g. Repeat the test for near. B. B. Prism Test Fig. Repeat the distance and near tests using patient’s eyeglasses. c. uncover the eye and observe it for any movement. if applicable. Cover the other eye and observe its fellow for any movement. c.1. With the patient seated upright and looking at a distance fixation point. Krimsky Prism Test 4. The examiner should be seated slightly to the side of midline. macular lesions and retinopathy of prematurity. at an arm’s reach. Note its direction. Figure . not allowing any period of binocularity. The cover-uncover test is done to establish the presence of either a manifest deviation (heterotropia) or a latent deviation (heterophoria). Repeat test for near. d. b. f. e.2. Cover tests The validity of a cover test depends upon the patient’s ability to maintain constant fixation on an accommodative target. 5. Each eye must be able to move adequately when fixating . Cover the fixating eye with an occluder or your hand and observe the other eye for any movement. b. After about one second.STRABISMUS / 160 B. while continuing to shift the cover from one eye to the other. The alternate tests are then performed to measure the deviation. Cover-uncover test a. Place a trial prism over one eye. Uncover the eye and allow about 3 seconds for both eyes to be uncovered.
Overacting Inferior Obliques. Comitant Strabismus 1. Accommodation is however accompanied by convergence of the eyes. Fig. Esotropia of the right eye B. cylopentolate and tropicamide. Cycloplegic agents that can be used include atropine.00 to +10. Convex or plus lenses are prescribed to correct the hyperopia. Aside from the esodeviation. The child has a significant grade of hyperopia ( +3. Sensory Esotropia 161 .STRABISMUS / 161 It is important to know the refractive state of the patient in assessing his ocular deviation. Eyes aligned with eyeglsses 3. Refraction is usually appropriate for the patient’s age. A B Fig 8 Accommodative Esotropia A. Congenital Esotropia or Infantile Esotropia Congenital esotropia is usually noted shortly after birth or up to 6 months of age.00 diopters) . he accommodates. Common Types of Strabismus A. 2. Cycloplegia is an adjunct to refraction in young strabismic patients. Congenital Esotropia Right gaze Primary Gaze Left gaze Figure 7. Elevation of the adducting eye. 6. There may be overaction of the inferior obliques . The child is best treated with surgery before the age of 18 months. Cross fixation (infant uses right eye to look at left visual field and left eye to see right visual field) may be present. Refractive Accommodative Esotropia Refractive accommodative esotropia usually starts at age 2 years. causing elevation of the adducting eye. the patient is usually otherwise normal. The esodeviation is big and constant . In order to see clearly.
Principles in treatment of sensory exotropia is the same as that of sensory esotropia. A B Fig 9. Brown syndrome. Vision is usually good for both eyes. full cycloplegic refraction. Treatment is surgical. He closes one eye when exposed to bright sunlight . It becomes manifests when patient is fatigued. Muscle surgery is indicated to correct significant face turn or a significant deviation on primary gaze. The deviation is bigger when the involved eye is fixating and in the direction of action of involved muscle. tumors.STRABISMUS / 162 An esodeviation occurs in a patient with monocular or binocular condition that prevents good vision ( e. Left eye fixating B. optic mreuropathy. characterized by limited abduction. The globe may retract and the eyelid fissure may narrow on adduction. Sensory Exotropia An eye that does not see well for any reason may turm outward. Usually. 162 . The patient should have a neurologic and systemic evaluation. Examples are Duane syndrome. sleepy or inattentive. Mobius syndrome and congenital fibrosis syndrome. muscle surgery to correct the deviation. Paralytic Strabismus There is limitation of action of involved muscle. The exotropia can later become constant.. Intermittent Exotropia Exotropia is an outward deviation of the eye which usually starts out as intermittent. usually unilateral. anisometropia). cataract.There may also be upshooting or downshooting of the eye. Strabismic Syndromes Motility disorders may demonstrate typical feature of a particular syndrome. Duane syndrome is a congenital motility disorder. retinal scars. B. Treatment consist of the following : attempt to correct the cause of the poor vison. 1. Incomitant Strabismus. 4. The frequency and the duration of deviation may increase as the patient grows older. corneal opacity.Alternating Exotropia A.g. or limited adduction or both. There may be a face turn to allow the patient to use both eyes together. Lateral rectus is the most frequently involved muscle as a result of abduscens nerve palsy. the patient can use either eye for fixation . inflammation . Right eye fixating 5.
Patients complain of diplopia most severe in upgaze. Lid retraction. A measured amount is cut from the muscle which is then sutured back to its original insertion site. Good vision 2. Thyroid disease : Grave’s ophthalmopathy is an autoimmune disaease affecting the extraocular muscles. 2. There is narrowing of palpebral fissures on adduction. Binocularity 3. Esodeviations are treated with antiaccommodative therapy ( plus lenses for hyperopia ) and exodeviations by stimulating accommodation. Patient is orthophoric on primary gaze. Systemic illness associated with strabismus A. if present. Surgery. bilateral... freed from its fascial attachments and then sutured to the eye at a measured distance from the original insertion. Recovery of ocular motor function usually happens within 6 months. A muscle is strengthened by resection. Presenting complaints are ptosis and diplopia from involvement of one or more extraoular muscle. Accurate refractive correction. There is limitation of abduction in both eyes. Limitation of elevation because of inferior rectus restriction is the most common motility findings. Prisms. Good alignment 1. An alternative to patching in certain types of patients may be instilling atropine eye drops to the better eye. exophthalmos and ophthalmoplegia are some of the clinical findings.10 Duane syndrome. Neurologic conditions : Cerebrovascular disorders and CNS space occupying lesions may have strabismus as one of the clinical presentations.STRABISMUS / 163 Left gaze Primary Gaze Left gaze Fig. The abdusens nerve and the lateral rectus is most often affected. Treat amblyopia. Recession in a weakening procedure whereby a muscle is detached from the eye. Diabetes mellitus : Diabetes is a complex metabolic disease involving small vessels and causing widespread damage to tissues. Manipulation of accommodation. Myasthenia gravis is characterized by abnormal fatigability of striated muscles which improves after rest. 4. including the eyes Patients may have acute onset diplopia due to infarction of a cranial nerve and subsequent paresis of an extraocular muscle. D. lacrimal glands and orbital connective tissue. If the occulomotor nerve is involved. 163 . (overcorrect myopia and undercorrect hyperopia) 3. B. Muscles are chosen depending on the type and amount of deviation in the various directions of gaze. the pupil is usually spared. May be useful in patients with acute onset of strabismus and diplopia and those with small deviations. by patching the better eye. C. Principles of Management of a Strabismic Patient Aims of strabismus treatment: 1. orbital fat.
Lange Medical Books : New York . Wilson. Constant strabismus at an early age can result to amblyopia. ed. Strabismus and Amblyupia :.A. One of the eyes maybe misaligned (strabismus). It is important that a physician is able to detect strabismus at early age so that treatment can result in good vision. 1999 4. Muscle recession Fig 12 Muscle resection SUMMARY Under normal binocular viewing conditions. so that only one eye at a time views the object of regard. F. 1996. binocularity and good alignment.STRABISMUS / 164 Fig 11. M. REFERENCES 1. Whitcher. ed Pediatric Ophthalmology and Strabismus. Riordan-Eva. San Francisco : American Academy of Ophthalmology. An instructional module for Level V Medical Students. the eyes are aligned and the image of the object of regard falls simultaneously on the fovea of the two eyes. Del Monte.N. J Vaughan and Sahbury’s General Ophthalmology.F. 164 . Valbuena. any condition which can result to poor vision can lead to strabismus. 2004. M. Practical Ophthalmology . In addition. 3. Indianapolis : American Academy of Ophthalmology. P . 1996. 2.
intermittent exptropia C. accommodative esotropia D. R superior oblique D. 5. comittant C. sensory deprivation 7. inferior oblique C. by observation 165 .STRABISMUS / 165 SELF –TEST 1. Graves ophthalmopathy 2. monocular B. down 6. in B. orbicularis oculi D. L inferior oblique The superior division of the oculomotor nerve supplies the superior rectus and A. exotropic 8. modified Krimsky test Example of incomittant squint is A. surgically D. Accommodative esotropia is best treated A. prism cover test D. hyperopic C. out C. 3. cover uncover test B. 4. Prism measurement of lateral rectus palsy is done with the prism’s base oriented A. The agonist in elevating the right eye is A. optically C. The patient is A. After removing the cover in one eye. esotropic D. incomitant D. When the angle of deviation is greater in one direction of gaze the strabismus is A. up D. superior oblique B. the eye moved inward. levator palpebrae This test will distinguish phoria from tropia A. medically B. congenital esotropia B. R superior rectus C. alternate cover test C. orthophoric B. R inferior oblique B.
B. B 2. A 4. B 9.Choose the correct statement about exotropia. exotropic C. C 166 . hypertropic E. D 8. Intermittent exotropia resolve spontaneously as the child grows older. D 3. hypotropic D. Intermittent exotropes close one eye on exposure to bright sunlight. D. A 10. aligned 10. the eye is A. C. B 6. A. ANSWERS TO SELF-TEST 1. D 5. and the light falls temporal to the pupil. Exotropia is best treated with spectacle correction. esotropic B. When doing the corneal light reflex test. Intermittent exotropes usually have amblyopia. C 7.STRABISMUS / 166 9.
He must be aware that there are other ocular complaints and he must have an overview and understanding of these so that he will be able to correlate and integrate the present subject matter with the rest of the ocular manifestations. He must be familiar with the basic eye examination and the instruments necessary to conduct them. The following is a schematic diagram of the adult orbit viewed from above with the roof removed (Fig. Since Ophthalmology is a subject that will still be included in the medical curriculum of upper year levels. It is part of a curriculum intended to introduce Ophthalmology through a problem-based approach. CONTENT It is essential that the student reviews the anatomy of the orbit before a significant discussion on a bulging eye is started. the medical student is informed of the various complaints that compels a patient to consult an eye specialist. One of them is proptosis or a bulging eye. it should nonetheless be included in the curriculum because it will contribute to a complete understanding to the problems of the eye. he should be able to: 1. the medical student should be able to recognize a bulging eyeball and explain the reasons for its presence. evaluate the bulging eye in terms of measurement. Specifically. Although proptosis is not a common manifestation of eye diseases. PREREQUISITE KNOWLEDGE AND PREPARATION The medical students must have a firm understanding of the anatomy of the eye and its periocular adnexae. Tuaño. 4. recall the relevant anatomy of the adult human orbit 2. differentiate between a true proptosis and a pseudoproptosis. In the real clinical setting there are several ways that the eye will exhibit a disturbance prompting the patient to seek consultation. direction. OBJECTIVES Upon completion of this unit of instruction. MD INTRODUCTION This self-instructional material on Proptosis is designed for level IV medical students. INTENDED USERS This manual will be helpful to level IV medical students as an introduction into the subject of eye diseases. define proptosis and recognize a bulging eye 3. discuss the various clinical examinations that are utilized in the evaluation of proptosis. and dynamics. 167 . 5.1). C.PROPTOSIS / 167 PROPTOSIS Prospero Ma. Instead of traditionally discussing the eye and its diseases. this manual will likely serve to remind the students of the uncommon but significant manifestation of proptosis.
The straight line theoretically lies tangential to the most anterior portion of the globe. The lateral walls. 2 The orbit is described as a 4-sided bony cavity located on both sides of the nose. Oftentimes. which have the same length as the medial walls. such as dysthyroid orbitopathy (Fig. such as visual loss and diplopia.3A Mass in the right orbit Fig. The medial walls are parallel to one another and are separated by the ethmoid sinuses. The normal position of the globe in the orbit is marked by a line drawn from the superior to the inferior orbital margin. The globe. On the other hand. Interestingly. Some physicians use these two terms interchangeably. Fig. The forward displacement of the globe is also termed exophthalmos. rarely do orbital lesions retract the position of the globe. 2). either axial or off-axis.PROPTOSIS / 168 Fig. Whereas there are obviously other manifestations of orbital diseases. Proptosis is the hallmark of orbital diseases. 3B). subtending an angle of 45° from the medial walls. The orbit is shaped like a pyramid whose orbital margin serves as the base and the optic foramen as the apex. The orbital cavity is tightly surrounded by bony walls. The globe is located in the anterior portion of the orbit so that retrobulbar and peribulbar lesions will necessarily disturb the position of the globe. it is an anterior displacement. a hypothetical posterior extension of the lateral walls makes them perpendicular to each other. 1 Fig. it is the protrusion of the eyeball which is most unique to the orbit and most striking to the clinician (Fig.3B Proptosis secondary to dysthyroid orbitopathy 168 . namely the cornea (Fig. occupying one -fifth of the orbital volume. the term proptosis denotes protrusion of the eyeball secondary to an orbital disorder other than dysthyroid orbitopathy. 3A). but most prefer to reserve the term exophthalmos for the description of prominent eyes secondary to endocrine disorders. appears “connected” to the orbital apex by the optic nerve before the nerve enters the optic canal. are directed laterally and outwards. It serves as a socket for the eye ball and a passage for nerves and blood vessels which supply the eyeball and the periocular adnexa.
TRUE PROPTOSIS Vascular – carotico-cavernous fistula Endocrine – thyroid-related eye disease Inflammatory – pseudotumor Neoplasm – lacrimal gland tumor / cavernous hemangioma 169 . On the other hand. the presence of an abnormally small globe in one side may give the impression of a prominent contralateral globe. Examples of each classification are mentioned. First. On the initial encounter with a patient with a bulging eye. a normal-sized but retracted globe (enophthalmos) may put on the appearance of a prominent contralateral eye. Likewise. It is frequently observed among high myopes (near-sighted persons) and among pediatric cases with congenital glaucoma. the first concern of the clinician is to determine whether the prominence of the globe is a true proptosis or a pseudoproptosis. lid changes may lead to asymmetry of the lids.PROPTOSIS / 169 Proptosis may be real or apparent. The causes of true proptosis may be generally classified into the following: vascular. The latter displays a huge globe or a longer axial diameter. Awareness of the spectacle history and/or the performance of a refraction procedure may detect the presence of myopia. or stomach • Myopia •Congenital Glaucoma Table 1 There are three general eye conditions which may assume the image of a pseudoproptosis (Table 1). documentation of a previous ocular trauma or inflammation as well as explicit information regarding past medical histories and treatments. endocrine. lungs. a huge globe may be misinterpreted as a proptosed eye. This situation is caused by an old blow-out fracture or a metastatic tumor to the orbit from a primary scirrhous adenocarcinoma of the breast. Secondly. inflammation and neoplasm. The mnemonic VEIN is recommended as a helpful tool in remembering the causes of real proptosis. a long-standing unilateral lid drooping in Horner’s syndrome may present a contralateral lid retraction (and apparent proptosis) through the principle of Hering’s law. An elevated intraocular pressure in an “expandable” pediatric eyeball. Lastly. may likewise lead to an enlarged globe. Pseudoproptosis Pseudoproptosis Lid fissure asymmetry Unilateral macrophthalmos Contralateral enophthalmos • Ipsilateral Lid Retraction • Contralateral Horner’s Syndrome • Phthisis Bulbi • Old Blow-out Fracture • Scirrhous Adeno CA of breast. The presence of a unilateral lid retraction in dysthyroid orbitopathy may give the impression of an ipsilateral proptosis. One may be able to eliminate the possibilities through the help of an accurate history and ocular examination. as in congenital glaucoma. lungs or stomach.
4). laterally and posteriorly and outside the muscle cone. 5) shows a proptosis which is off-axis. most likely a tumor derived from the lacrimal gland. Above the mirror is a millimeter ruler which the examiner uses to measure the amount of forward globe displacement (Fig. the bases of measurement are the most anterior part of the cornea and the lateral orbital margin. the following evaluation procedure is undertaken to determine the correct etiology of the proptosis. The more common instrument used is the Hertel’s exophthalmometer (Fig. The procedure is repeated on the opposite eye. 5 Lacrimal gland tumor This particular picture (Fig.PROPTOSIS / 170 After determining the presence of a true proptosis. Clinical deduction tells us further that the orbital mass is obviously a lacrimal gland fossa lesion. peripheral surgical space – bounded by the 4 rectus muscles and the periorbita 3. The globe is displaced forward and slightly medially and downward. There are several types. 6) is similar to a millimeter ruler. 170 . DIRECTION The direction of the proptosed globe is predicated on the knowledge of the four surgical spaces within the orbit (Fig. It can be concluded that the orbital mass is located opposite the direction of the proptosis. Similar to the previous model. central surgical space or muscle cone – bounded by the 4 rectus muscles 2. The image of the cornea is reflected on a mirror on the instrument. 1. 8).Unlike the previous. 7). measurement as well as the dynamics and clinical behavior of the proptosis. MEASUREMENT An instrument called an exophthalmometer is used to quantify the amount of proptosis. Tenon’s space – a potential space bounded by the Tenon’s capsule and the outer coat of the eye 4. The clinician describes the direction. places the recessed end of the instrument on the lateral orbital margin and measures the displacement of the globe by reading the millimeter markings on the instrument. 4 Surgical Spaces of the orbit Fig. The examiner stands in front of the patient and places the instrument on the lateral orbital margin. The mass must be located superiorly. subperiosteal space.a potential space bounded by the periorbita and the bony orbital walls Fig. it measures the displacement of the two globes at the same time and thus facilitates the comparison of proptosis between the two eyes. It measures the globe position one at a time. The clinician stands at the side of the patient. A Luedde exophthalmometer (Fig.
171 . intermittency 3.0 – 19. the following characteristics are considered: 1. resiliency 2. In comparison. 9).7 Hertel’s Exopthalmometer Fig. The normal exophthalmometry values among Filipinos have been studied and the following measurements have been derived.PROPTOSIS / 171 Fig. clinical behavior / pulsating proptosis 4. duration 6.0 FILIPINOS CAUCASIANS DYNAMICS In evaluating the dynamics of proptosis.0 – 24. 6 Luedde Exophthalmometer Fig. the examiner stands behind a seated patient and peers over the head of the patient. (Table 2) Table 2 Exophthalmometry (mm) Average Normal Measurement (mm) 13. The examiner stares from and above the head of the patient and observes and compares the degree of protrusion of either cornea (Fig. 9 In order to grossly determine the presence and extent of the proptosis without the benefit of an exophthalmometer.0 Range (mm) 10.8 Fig. clinical course Information regarding these features may provide valuable hint in the identification of the orbital disorder. the values for Caucasians are slightly higher than those for Filipinos.5 16. They will eventually narrow down the choices in the differential diagnosis and provide a working impression from which a plan of work-up and management will begin. From this position behind the patient the examiner lifts both upper lids.5 10.
In the presence of a solid retrobulbar space-occupying lesion. This expansion is caused by bleeding within the lymph channels of the tumor.11 Capillary hemangioma Intermittent proptosis refers to varying degrees of eye protrusion as a function of change in the immediate environment of the patient. The proptosis in a child with capillary hemangioma may increase noticeably fast when he is crying but resolves soon after the effort (Fig. 11). 12 A-C). The lymphangioma is expected to resolve spontaneously within a few months of conservative management (Fig. may produce a sudden exaggerated eye protrusion in the presence of an upper respiratory tract infection. 10 Test for resiliency of the globe INTERMITTENCY Fig. The proptosis exacerbates when he bends forward into a prone position or strains during a Valsalva maneuver. Certain vascular tumors.PROPTOSIS / 172 RESILIENCY It is normal to be able to retrodisplace the globe by applying your thumb over the eyeball. Fig. This is reported as negative resiliency. one can easily push the eyeball posteriorly because of the compressibility of the orbital tissues such as orbital fat. the globe is prevented from being pushed backward towards the orbit. Another instance is an adult patient with a varix or abnormally expansile venous channels. It is more convenient to push the globes simultaneously in order to facilitate comparison of the two orbits. The proptosis is noted to increase in size followed by a spontaneous resolution after the stimulus. leading to the formation of “chocolate cysts”. In the absence of any orbital pathology. like a lymphangioma. Fig. A stimulus may be internal such as a systemic infection or external like a change in head posture or position. 12 A Lymphangioma in a 10-year old child: Fig 12 B Fig 12 C 172 .
a chronic condition spanning years of clinical history before clinical consultation may allude to the possibility of a benign tumor. lymphomas and some metastatic carcinomas. may remain stationary or at the very least. CLINICAL COURSE The clinical course describes the growth characteristics of the tumor. They have an insidious presentation prior to a more rapid progression in the later stages of the disease. Fig 12C exhibits complete resolution of proptosis and periorbital swelling. Some benign tumors. such as cavernous hemangioma and pleomorphic adenoma of the lacrimal gland are slowly progressive. Fig 12B demonstrates spontaneous resolution after 2 weeks. These include orbital disorders like dysthyroid orbitopathy.PROPTOSIS / 173 Fig 12A shows the child upon initial consultation with a proptosed right globe with extensive conjunctival chemosis. The globe exhibits dilated and tortuous episcleral vessels because of intense congestion and “arterialization” of the venous channels of the orbit (Fig 13). Pulsating proptosis may also be exhibited by congenital bony defects in the orbital roof of patients with orbital neurofibromatosis. Fig. characterized by rhythmic pulsations of the globe. On the other hand.13 Arterio-venous fistula with dilated & tortuous episcleral veins (corkscrew vessels) DURATION Fig 14 Orbital cellulitis How long the disease has been going on is a question which leads the clinician to ask about the duration of the orbital disorder. 173 . may occur in cases of caroticocavernous fistulas of high-flow quality. The most common primary benign tumors of the orbit include a cavernous hemangioma and a pleomorphic adenoma of the lacrimal gland. It also provides information on the rate and direction of evolution of the mass from the time it is first noted by the patient up to the time when the clinician starts to observe the disease process. The pulsations reflect the same cadence as the peripheral arterial pulsations. are slowly progressive. An acute onset is accompanied by a short history prior to consultation. It implies a rapidly-evolving disease entity like a malignancy or an inflammatory condition such as an orbital cellulitis or orbital pseudotumor (Fig 14). CLINICAL BEHAVIOR / PULSATING PROPTOSIS Pulsating proptosis. There are subacute orbital conditions which are neither acute nor chronic. Many benign orbital tumors. like neurofibromas and optic nerve gliomas.
16 shows 19-year old female diagnosed with diffuse toxic goiter. On the other hand. then stops and continues regressing till the early teens. The clinical course of orbital cellulitis may be even more rapid and appropriately described as explosive. Fig. The regressing size of the lesion on the left upper lid is noted as the patient grows older. 15 Fig. Fig. besides having a short duration of history. like rhabdomyosarcoma and adenoid cystic carcinoma of the lacrimal gland. This is exemplified by capillary hemangioma which grows rapidly during the first year of life. there are tumors which may spontaneously stop and regress.PROPTOSIS / 174 Most malignant tumors. exhibit rapid progression. 174 . There are two lesions (indicated by the red arrows): one on the left upper lid and another on the scalp.15 depicts a 56-year old male with a cavernous hemangioma which was noted 17 years prior to initial consultation. Her rapid proptosis of less than a month duration has resulted in severe bilateral lagophthalmos and injurious exposure changes to the cornea. Fig. 16 6 months old Fig 17 is a collage of pictures of a female with capillary hemangioma from the time it was detected at 6 months of age up to 10 years old.
in the gross examination.pupil. For instance. Furthermore there are novel maneuvers such as auscultation which elicit bruits over the periocular adnexae. This is indicative of an arteriovenous fistula (Fig. The advent of computerized tomography revolutionized the diagnosis and treatment of orbital diseases because it was able to view and distinguish the soft tissues within the orbit. Venography 2. Further enhancement of the visualization was achieved with magnetic resonance imaging which offered a discriminating picture of the orbital apex. anteriorly-located mass 3. 18 Bilateral lid retraction Fig.Vision. Arteriography 3.pulsation. ophthalmoscopy 5. certain special considerations are emphasized. Computerized tomography (CT scan) 5.PROPTOSIS / 175 CLINICAL EVALUATION The patient with a true proptosis undergoes a thorough clinical evaluation. Auscultation 4. The usefulness of radiography was not evident with the first available machines for plain X-ray film because only the bony walls are readily seen. there is particular attention focused on lid and conjunctival changes. 18). Pupillary reaction is also doubly appraised because of optic nerve dysfunction secondary to compression by a tumor or enlarged extraocular muscles. This is reinforced by a sensitive hand in palpation which elicits a corresponding rhythmic pulsation from the same periorbital area. resiliency. 175 . corneal reflexes 7. Routine Eye Exam . Magnetic resonance imaging (MRI) Radiography is an essential tool among orbital patients. There is an absolute need to visualize the concealed structures of the orbital cavity. Palpation . METHODS OF ORBITAL DIAGNOSIS: CLINICAL 1. Utilizing the same routine eye examination applied to any eye patient. Systemic examination Fig. 19). intraocular pressure. Plain radiography has been relegated to detection of bony abnormalities such as fractures and bony growths. 19 Auscultation of the orbit in dysthyroid orbitopathy METHODS OF ORBITAL EXAMINATION: RADIOGRAPHY 1. Gross Examination . Cranial nerve function . Lid retraction and/or lid lag are almost pathognomonic of dysthyroid orbitopathy (Fig. Plain film 4. Color vision 6.lid and conjunctival abnormalities 2. extraocular muscles.
Other laboratory examinations include visual field tests. Visual field examination – for optic nerve evaluation in dysthyroid orbitopathy. True proptosis. 4. In general. Asbury T. redness and blurring of vision. 3. ed.. The most important value of learning the nature and behavior of proptosis is the knowledge that this manifestation contributes its own share of problems to the well-being of the eye. As such. the management of carotico-cavernous fistulas demands the localization of the fistula through selective angiography before embolization treatment can be planned. CT: Appleton & Lange. ultrasonography. Vaughn DG. the complaint must be evaluated because it is peculiarly an orbital complaint. eds. and optic nerve tumors 3. General Ophthalmology. Tissue biopsy SUMMARY Proptosis is an ocular complaint and manifestation which occurs rather infrequently in comparison with other common complaints such as headache. inflammatory and neoplasm. electrophysiology and selective carotid angiography. namely. They are still both useful but limited in use for particular diseases with vascular dynamics. For instance. 1. direction and dynamics or clinical behavior. Ultrasonography 2. measurement. Other non-radiographic tests are available to augment the information already derived from the previous examinations. ER Jr. Basic and Clinical Science Course Sec 7 Orbit. 1992 176 . Laws. The differential diagnoses of pseudoproptosis include unilateral myopia. Harper & Row. Despite its relative rarity. 13th ed. Electrophysiology – for optic nerve evaluation as well 4. undergoes the further clinical evaluation. Eyelids and Lacrimal System. They are essential in identifying the disease process so that the proper management can be instituted. Jones IS and Jakobiec. Proptosis carries a difficulty of identifying the lesion because the latter exists behind the eyeball where it is “invisible” to routine eye examination. Norwalk. Clinical examination is followed by the use of ancillary procedures such as CT scan or MRI of the skull and orbit. In some cases. American Academy of Ophthalmology. Futura Publishing Co. The Diagnosis and Management of Orbital Tumors. Diseases of the Orbit. It is primarily important to determine if the proptosis is real or apparent. FA. on the other hand. 2. they may be used to monitor the progress of the disease in order to achieve proper timing of intervention. lid fissure asymmetry and contralateral enophthalmos. Riordan-Eva P. the clinical considerations include lesions which are vascular. 2003. the clinician needs to conduct not only the routine eye examination but also other recommended steps in a systematic evaluation of the bulging eye. 1979. Laboratory exams – thyroid function tests 5. AV fistula. REFERENCES 1.PROPTOSIS / 176 Venography and arteriography have remained part of the history of orbital radiography. endocrine. biopsy procedures on accessible tumors.1988.
cavernous hemangioma B. 10 – 11 cc D. The volume of the globe is around: A. The volume of the orbit is approximately 30 cc. 40. ipsilateral Horner’s syndrome B. Pseudoproptosis is evident in the following situation: A. 30. axial myopia D.5 mm C. 50. a fracture of the roof and lateral wall of the orbit B. 9. 10. The axis of the adult bony orbit is directed forward and: A. 14 – 15 cc 3. pseudotumor C. inflammatory pseudotumor D. 6.5 mm B. 2 -3 cc B. thyroid-related eye disease C.0 – 19. an inflammatory pseudotumor 7. the same as Caucasians D. upward D. in the same axis as the globe. rhabdomyosarcoma 8. Enophthalmos after a blunt trauma to the anterior part of the orbit is due to: A.PROPTOSIS / 177 SELF-TEST 1.0 mm D. A proptosis which increases after a Valsalva maneuver is probably due to: A. a thyroid-related eye disease D. The maximum depth of the orbit is approximately : A. a cavernous hemangioma B. medially C. a capillary hemangioma C. 2. Acute proptosis (rapidly-progressive proptosis) of the globe is noted in the following. paresis of all the EOM’s 177 .7 cc C.0 – 14.0 mm 4. rupture of the orbital fat cells D. elevated intracranial pressure 6. The antero-posterior diameter of the globe is around 24 mm. laterally B. a fracture of the floor and medial wall of the orbit C. 20.0 mm B.0 mm C. The normal range of exophthalmometry measurements among Filipinos is: A. except: A. still unknown / unreported 5.
B 7. 2. upwards and laterally 10. 3. A 8. downward and medially B. upwards and medially C. proptosis with palpable lid masses B. One suspects a lacrimal gland tumor if the globe is proptosed forward… A. A B D B C 6. 4. proptosis with positive resiliency D. 5. downwards and laterally D. B 178 . B 9.PROPTOSIS / 178 9. A 10. proptosis with negative resiliency C. CT scan of the orbit is most needed in the following situations: A. pseudoproptosis with palpable lid masses ANSWERS 1.
Domingo M.RETINOBLASTOMA / 179 RETINOBLASTOMA Rolando Enrique D. 4. Identify through history taking and physical examination clues. OBJECTIVES After reading and understanding this module. Its incidence is approximately 1:17000 live births. however some series have reported an increased incidence in the last few decades. It gives an overview of the life threatening eye disease known as retinoblastoma. 2. we see around 100 new patients every year. He must also possess basic skills in medical history taking and comprehensive eye examination. RECOMMENDED PREPARATION The student must have working knowledge of the anatomy of the eye. Knowledge acquired from this material will be useful in clinical practice as well as further training in Ophthalmology.D. Background Retinoblastoma is the most common intraocular malignancy of childhood. Genetics The development of retinoblastoma can be traced to mutations on chromosome 13. INTENDED USERS This module is designed primarily for the undergraduate medical students of the UP College of Medicine rotating in the Department of Ophthalmology and Visual Sciences. Recognize and differentiate conditions which may present with signs and symptoms similar to retinoblastoma. Have a general idea of the therapeutic modalities available to a patient with retinoblastoma. Although it possesses basic information on this disease it is also meant to encourage the student to further reading. II. Develop an appropriate sense of urgency once faced with a patient possibly suffering from retinoblastoma. being a tertiary center. INTRODUCTION This self instructional material is designed for the undergraduate medical student. 179 . In the PGH setting. The retinoblastoma gene is one the best studied genes in the human genome. CONTENT I. 3. the medical student is expected to: 1. or an average of two per week. especially in children. signs and symptoms leading to a diagnosis of retinoblastoma. It is a tumor suppressor gene whose presence (even of a single allele) protects against the development of the tumor.
family history of metabolic disorders. all the retina cells (in fact. This means that one single retina cell suffers a mutation on one allele of the RB gene.RETINOBLASTOMA / 180 Most cases (70%) of retinoblastoma are sporadic mutations. Sporadic cases are unilateral. in Filipino. because only a second hit is needed after birth and all retinal cells are at risk. later. Retinoblastoma is very rarely seen after the age of six. These cases are usually bilateral with multiple tumors on both eyes. Fig. III. Factors such as preterm birth. History In a child suspected to have retinoblastoma it is important to ask about the birth and maternal history. Although the average age for the diagnosis of retinoblastoma is 18 months. Retinoblastoma may occasionally present as strabismus. birth weight. The most common presenting symptom of retinoblastoma is leukocoria (white pupil) also called cat’s eye reflex or matang pusa. patients with sporadic mutations develop tumors later (mean age at diagnosis 24 months) because two hits are needed on a single cell. a complete history is enough to rule out retinoblastoma. childhood blindness and death are important. heritable retinoblastoma behaves as an autosomal dominant trait with marked penetrance. all cells in the body) have one mutation at birth. if it is located in the periphery. Clinically. Occasionally. In this instance the child inherits a normal chromosome 13 from one parent and a mutated chromosome 13 from the affected parent. However. The loss of the tumor suppression from both alleles then allows that particular cell to multiply uncontrollably (Knudson’s Two Hit Hypothesis). buphthalmos or enlargement of the eye. 1 Leukocoria If the tumor is located in the posterior part of the retina then the leukocoria may be constant. Retinal cells are very metabolically active and are constantly exposed to light energy. Children with the heritable variety are diagnosed earlier at a mean age of 12 months. Therefore. See figure 1. then after some time suffers another mutation on the remaining allele. in most instances these children will develop a second mutation in one or more cells producing retinoblastoma. Advanced tumors that 180 . in 30% of cases the condition is heritable. inflammation or mimic infection. However. the cat’s eye reflex might be seen only on certain directions of gaze. This is seen in two thirds of retinoblastoma patients with intraocular tumors.When the tumor grows it may cause glaucoma and. Sometimes tumor cells seed into the anterior chamber and settle inferiorly giving the appearance of pus (hypopion) .
Indirect ophthalmoscopy gives a more panoramic and three dimensional view. See fig. lens or vitreous other than a tumor. Gross examination will usually show a white pupil. Fig.2 Retinoblastoma with extraocular extension IV. Fig. 3.RETINOBLASTOMA / 181 grow beyond the confines of the globe (extraocular extension) present with exophthalmos and an orbital mass (fig. Unilateral visual loss usually goes unnoticed and must be tested in a child. In these cases a systemic and neurologic evaluation of the child should be done to detect signs of metastasis. 181 . At this stage intracranial extension via the optic nerve and hematogenous metastasis is likely. Great care must be taken to ascertain the cause of the leukocoria. A dilated funduscopy will show a yellow. aside from gross picture might also result in extraocular muscle restriction. Physical Examination A complete ocular and physical exam on a child suspected to have retinoblastoma is imperative. white or pink mass. 2). as this may be caused by opacities in the cornea. 3 Intraocular retinoblastoma A firm eye and an eye that is larger than the other are signs of an enlarging tumor. And an extraocular tumor.
5 kg will point us in the right direction. Differential diagnosis There are several conditions that may present with leukocoria other than retinoblastoma. This is an anomaly of embryogenesis which is otherwise benign Coats’ Disease involves telangiectatic changes in the retina of children. An ocular ultrasound (B scan) is readily available in most eye centers and can easily demonstrate the presence of a distinct mass in cases wherein there is doubt (see picture below) especially if there is an opacity in the cornea or lens occluding the view. 182 . sometimes ancillary tests might be useful in the few equivocal cases. although these patients are usually older than those affected with retinoblastoma. retinal detachment and scarring. Fig. Pathologies posterior to the lens may also cause a cat’s eye reflex which may be more difficult to differentiate from retinoblastoma. A history of preterm birth less than 28 weeks gestation and birth weight less than 1. The leukocoria is present at birth and the affected eye is usually smaller (microphthalmia). disorganized and form a mass like structure causing leukocaria. Persistent hyperplastic primary vitreous (PHPV) is another condition which may mimic retinoblastoma. There is a fibrous plaque behind the lens connected through a stalk to the optic disc. Cataracts may be congenital or may develop as the child grows. A careful examination is usually helpful in identifying the lens as the cause of the white reflex. A condition commonly mistaken for retinoblastoma is retinopathy of prematurity or ROP. VI.4 Congenital cataract presenting with leukocoria. If the affected portion of the retina is large enough then it may cause leukocoria.RETINOBLASTOMA / 182 V. Other more unusual diseases such as retinal dysplasia. A distinct retinal mass would not be seen on funduscopy. In advanced ROP the retina may become detached. A white pupil may be due to a corneal scar or an opacity in the lens such as the developmental cataract shown below. parasitic endophthalmitis and tuberculosis may present as retinoblastoma. The blood vessels leak and cause subretinal exudation. In all cases the need for a good history and thorough physical examination can never be overemphasized. Ancillary Tests Although a complete ophthalmologic exam including indirect ophthalmoscopy leads to an accurate diagnosis of retinoblastoma in the great majority of patients.
One particular characteristic of retinoblastomas is that calcification is seen in more than 90% of tumors and the CT scan easily demonstrates this (see picture below). 183 . VII. A deadly characteristic of retinoblastoma is its propensity to invade the optic nerve. Therefore. all other childhood eye pathologies very rarely calcify before the age of seven. 5 Ultrasound photo showing a solid mass at the center. Management Once a patient is diagnosed with retinoblastoma the situation must be treated as urgent.RETINOBLASTOMA / 183 Fig. a child less than six years old with an intraocular mass showing calcifications on CT scan is almost certainly suffering from retinoblastoma. and in the advanced stage spread directly into the brain. However. Fig. Visual loss is something to be considered but the threat to life is of utmost importance because untreated retinoblastoma is almost uniformly fatal. The CT scan is also useful in documenting this and guides the physicians in treatment planning. 5 CT scan showing intraocular tumor with calcification on the left. On the other hand. by far the most useful ancillary procedure in the diagnosis of retinoblastoma is still a CT scan.
Genetic counseling for affected families is also necessary. 6 below may be treated conservatively. These small tumors may be treated with lasers or cryotherapy depending on the size and location. loss of life. Retinoblastoma patients must be closely followed up for signs of recurrence or development of new tumors. A complete history and physical examination will usually lead to an accurate diagnosis which is necessary to start the appropriate treatment. A high index of suspicion is needed when confronted with a child showing leukocoria or other signs and symptoms suggestive of retinoblastoma. Patients with large tumors involving the orbit have the worst prognosis. Small tumors such as that seen in Fig. VIII. a pediatrician and a radiologist. Tumors with extraocular extension have higher rates of metastasis and result in poorer prognosis. Medical therapy is commonly used in combination with radiation treatment. Radiation therapy is also sometimes used. Larger tumors occupying more than half of the eye and with no hope for vision are enucleated. Extraocular extension is an indication for chemotherapy post operatively. 184 . It is imperative for enucleated eyes to undergo histopathologic examination to look for signs of extraocular spread.RETINOBLASTOMA / 184 The management of retinoblastoma is performed by a team primarily consisting of an ophthalmologist. Heritable cases are especially at risk and have been reported to develop other malignancies in later life. The newer chemotherapeutic drugs such as the platinum compounds are increasing the survival rates of these patients. to save an eye with retinoblastoma. Summary Retinoblastoma is a life threatening eye disease in children. Fig. It is important to differentiate it from other benign conditions because delay in treatment may mean not only loss of vision but. either alone or in combination. more importantly. Medium sized tumors may be treated with chemotherapy combined with the previously mentioned modalities. 6 Small intraocular retinoblastoma. They are treated with chemotherapy and more extensive surgery.
the most likely treatment modality is: a. PHPV c. 2nd ed. d. Burnier. Choroidal involvement. CBC and peripheral blood smear b. c.Tumors of the Eye and Ocular Adnexa Armed Forces Institute of Pathology . Retinoblastoma b.RETINOBLASTOMA / 185 REFERENCES 1.. 1979. L. CT scan d.E. 1993. A one year old child is brought to you with a smaller right eye with leukocoria initially noticed one month after birth. Zimmerman. SELF-TEST 1. The most probable diagnosis is: a. Enucleation d. Coats’ disease 3. and Yanoff. Blurring of vision b. Devron . F. M. Coats’ disease 4. Mc Lean. b. MD. Persistent Hyperplastic Primary Vitreous (PHPV) c. 2. Hagerstown. Fine.N. ROP d. DC. B. 185 .S. The most common presentation of retinoblastoma is: a. What examination would be most helpful in definitive diagnosis of this patient? a. Charl . The most pertinent histopathologic finding in an eye enucleated for retinoblastoma is: a. M. On examination the cornea is hazy and the anterior chamber is not very clear. New York. A 3 year old child with leukocoria is presented to you. Clinical Ocular Oncology. Heritable retinoblastoma b. NY. Retinopathy of Prematurity d. Cat’s eye reflex c. A four year old child with left sided leukocoria and exotropia is diagnosed with retinoblastoma. Harper and Rowe. Invasion of the optic nerve beyond the margin of resection. Red eye d.. Chemotherapy c. Tumor seeding in the anterior chamber with glaucoma. Squint 2. Jakobiec. 1989.. External beam radiation. 3. A 6 month old child with bilateral leukocoria since age one month who was kept in an incubator for six weeks after delivery probably has: a. Washington. 6.W..Ocular Histology: A Text and Atlas.A. Mass occupying the entire vitreous cavity. Ultrasound c. Laser treatment b. I. Churchill Livingsotne Inc. Bone scan 5.
b. A six month old child underwent enucleation of the right with intraocular retinoblastoma. B C B c C D C C 186 . Take their children to be seen by an ophthalmologist the soonest time possible after birth. Change their minds and not have any children. 5. d. b. Bring their children to the doctor once they see leukocoria or other signs of retinoblastoma. 8. 2. 8. That they should relax since the tumor was completely removed and no further follow up is needed. 4. 7. To see the pediatric oncologist for post op chemotherapy. On discharge you would advice the parents: a. the other eye is normal. c. d. 3. To bring the patient back every few months to check if there are tumors developing on the remaining eye. Answers 1. To watch closely the enucleated side for recurrence. they should: a. c. A man with bilateral retinoblastoma marries and the couple decide to have children. Not worry because the chance of having children with retinoblastoma is very small. 6.RETINOBLASTOMA / 186 7.
CONTENT The eye provides clues to the diagnosis of many systemic diseases and many important complications of these diseases occur in the eye. Many systemic conditions can present with significant ocular manifestations. treatment and referral to the ophthalmologist. Certain ocular signs and symptoms may signal the presence of serious underlying systemic disorders. MD. certain findings may be highly suggestive of the presence of one or more diseases. MHPEd INTRODUCTION This self-instructional material is designed to help the student learn key concepts concerning eye manifestations of common systemic diseases. PhD Teresita R. It is best that this material be supplemented by clinical exposure to provide the students with actual cases. As such. To recognize characteristic ocular features of systemic diseases. The student should also possess a working knowledge of common ocular signs and symptoms. PREREQUISITE KNOWLEDGE AND PREPARATION Students should have a working knowledge of the basic anatomy of the eye and its adnexa. 187 . Castillo. To determine when it is appropriate to refer a patient to an ophthalmologist for consultation or treatment. While some ocular findings may be non-specific. Aguilar. Evaluation of the ocular fundus is particularly important in the evaluation in systemic disease since it is the only region in the body where one can directly visualize manifestations of macro and microvascular pathology. INTENDED USERS This material was developed to provide the medical student with concepts and information on the various ocular manifestations of systemic diseases that is more commonly encountered by a primary physician. MD. It is advised that written materials regarding the above topics be completed first prior to working on this instructional material. specifically those associated with the following conditions • Diabetes Mellitus • Hypertension • HIV / AIDS • Thyroid Disease • Tuberculosis 2. OBJECTIVES Upon completion of this unit of instruction. data gathered from an eye examination can provide the clinician with clues that may serve as aid in the diagnosis and management of the underlying systemic disease. the student should be able 1. It aims to emphasize the critical role of Primary Care Physicians in preventing visual loss by appropriate recognition.OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES / 187 OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES Romulo N.
neurotrophic keratitis and diabetic retinopathy. uveitis Ischemic optic neuropathy Diplopia. CMV Candidiasis Syphilis Lymphoma Leukemia Metastases Multiple sclerosis Giant cell arteritis Myasthenia gravis Acne rosacea Atopy Ocular manifestation Diabetic retinopathy Thyroid orbitopathy Field loss Hypertensive Retinopathy Retinal Vessel Occlusion Corneal Arcus/ Xanthelasma Lens Dislocation Roth Spots Scleritis Keratitis sicca Uveitis Keratitis sicca Anterior Uveitis Uveitis. diabetic retinopathy is the most common and may lead to permanent loss of vision if not attended to. Optic Neuritis.47% Filipinos suffer from bilateral blindness from vascular diseases including DM Retinopathy and was the 6th leading cause of blindness among Filipinos. VI). IV. and if followed through time. Ophthalmoplegia Infiltrate. Studies have shown that at any one time. The prevalence of diabetic retinopathy has been found to be related to the duration of the systemic condition (Table 2). 1. diabetic optic neuropathy. ptosis Keratitis Keratitis. According to the 1995 Second National Survey of Philippine Blindness.OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES / 188 An outline of the more significant of these diseases along with their ocular presentation is summarized in Table 1. uveitis Infiltrative retinitis Choroidal mass Optic neuritis. Other risk factors which have been identified to be associated with the development of diabetic retinopathy include the following: • Hypertension • Renal status • Onset of puberty 188 . EOM palsies (Cranial Nerves III. Table 1. cataract Cardiovascular Rheumatology Infections Malignancy Neurological Dermatological DIABETES MELLITUS Diabetes (DM) is associated with a number of ocular complications. These include cataracts. glaucoma Retinitis Endophthalmitis Iritis. Overview of Ocular Manifestations of Common Systemic Diseases System/category Endocrine Disease Diabetes mellitus Thyroid eye disease Pituitary lesions Hypertension Retinal Emboli Hyperlipoproteinemia Marfan Syndrome Endocarditis Rheumatoid Arthritis Sjogrens Syndrome Seronegative Spondeloarthropathies Collagen Vascular Disease Juvenile Rheumatoid Arthritis Herpes zoster HIV. 25% of the total diabetic population will have diabetic retinopathy. A review of the important ocular pathology seen in some systemic diseases will subsequently be discussed. 90% will eventually develop the condition. Among these.
the risk of retinopathy increases with the duration of the disease. they produce a special growth chemical (VEGF= vascular endothelial growth factor) responsible for triggering new blood vessel growth and the vessels may eventually close and block.OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES / 189 • Hb A1c level Table 2.15 years. Elevated glucose is thought to damage retinal (and renal) capillaries in the following ways: (1) capillary basement membrane thickening (2) loss of capillary pericytes and (3) breakdown of the blood-retinal barrier. As a result of this process. Almost 100% of Type I patients will develop retinopathy after 15 years of diabetes. Pathogenesis of DM Retinopathy 189 . the blood vessels can leak. Relation of Diabetic Retinopathy to the Duration of the Disease Duration 0 – 5 yrs 10 – 15 yrs 16 – 20 yrs 30+ yrs 0% 25 – 50% 75 – 95% 100% 23 – 43% 60% IDDM NIDDM Although the likelihood of developing retinopathy varies between Type I and Type II diabetes. generally. The more severe form of proliferative diabetic retinopathy does not appear at all until disease duration of at least 10 . Figure 1.
a superficial one in the nerve fiber layer and a deeper on within the inner nuclear layer.OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES / 190 Table presents a summary of the various stages of diabetic retinopathy and its hallmark characteristics. 190 . these hemorrhages appear dot (2) or blot shaped (3). Hemorrhage within the nerve fiber layer tends to be flame shaped. B Figure 3. Intraretinal Hemorrhages may be ‘dot’ or’ blot’ shaped (termed ‘dot/blot hemorrhages’) or flame shaped depending upon their depth within the retina. In the inner layer. They are localized capillary dilatations which are usually saccular (round). Table 3. The capillary network in the posterior retina is found in two layers. They usually appear as small red dots in clusters (A) although they may also be isolated (B). following the divergence of axons (1). Microaneurysms are the earliest clinically visible changes of diabetic retinopathy. Classification of Diabetic Retinopathy DISEASE STAGE Non-proliferative Diabetic Retinopathy Mild Moderate Microaneurysms ohly Microaneurysms Hard exudates Macular edema* Intraretinal hemorrhages Microaneurysms (multiple) Intraretinal hemorrhages (diffuse) IntraRetinal Microvascular Abnormalities (IRMAs) Venous beading Soft exudates Neovascularization of the disc (NVD) Neovascularization of the retina elsewhere (NVE) Fibrovascular scar Tractional Retinal Detachment HALLMARK CHARACTERISTICS Severe Proliferative Diabetic Retinopathy A Figure 2. haemorrhage is aligned at right angles to the retinal surface and is consequently viewed end-on when using an ophthalmoscope.
They may evolve into rings known as circinates and form large confluent plaques. Hard exudates are distinct yellow-white intra-retinal deposits which can vary from small specks to large patches. Figure 6. (IRMA) Intraretinal microvascular abnormalities are areas of capillary dilatation and intraretinal new vessel formation They arise within ischemic retina and when they are present in numbers are a feature of preproliferative retinopathy.OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES / 191 Figure 4. Venous beading is a sign of retinal ischemia. 191 . Figure 7. Figure 5. They are the result of local ischemia which leads to disruption of axoplasmic flow. Cotton-wool spots are grayish-white patches of discoloration in the nerve fiber layer which have indistinct (fluffy) edges.
Severe Non-proliferative diabetic retinopathy with multiple microaneurysms (1). Figure 10. 1 3 2 Figure 11. Neovascularization or new vessel formation occurs as the retina becomes more ischemic. Proliferative Diabetic Retinopathy with new vessels at the disc and retinal periphery. or elsewhere in the periphery of the retina (NVE)-B. These new vessels are fragile and bleed easily. New blood vessels may arise from the optic disc (NVD)-A. 192 . Mild Non Proliferative Diabetic Retinopathy with microaneurysms. 1 2 1 3 2 3 3 1 Figure 9. hence the importance of proliferative retinopathy. Figure 12. hard exudates (2) and intra-retinal hemorrhages (3). Moderate Pre-proliferative Diabetic Retinopathy with typical findings of multiple cotton wool spots (1). soft exudates (2) and diffuse intraretinal hemorrhages (3).OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES / 192 A B Figure 8.
Blood accumulates the retina and the vitreous and is often described as boat-shaped. Only a small amount of bleeding is required since blood dissolved in the vitreous produces a haze effect which impairs vision (and ophthalmic assessment). Diabetic patients who complain of any visual symptoms should be referred immediately to an eye specialist for proper evaluation.OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES / 193 Figure 13. Grid or focal laser photocoagulation should be considered for patients with severe NPDR and/or clinically significant macular edema (CSME). Figure 14. Patients with IDDM (Type 1) should be referred for ophthalmologic consult if the disease is of five years duration already. Vitreous hemorrhage can give rise to profound loss of vision if the macula is obscured. Pregnant women with history of diabetes should likewise be referred to an eye specialist for proper monitoring of her ocular status for the duration of her pregnancy. Patients classified to have mild to moderate NPDR should have regular fundus examination and fluorescein angiography. Complications such as vitreous hemorrhage and traction retinal detachment are managed by the performance of vitreoretinal surgery. Management of the eye condition would depend on the stage of the retinopathy. Subhyaloid hemorrhage refers to accumulation of vitreous blood in areas of localized detachment. This subsequently leads to traction on the retina and loss of vision. Figure 15. All patients diagnosed to have NIDDM (Type 2 Diabetes) should be referred to an ophthalmologist at the time of initial diagnosis. Panretinal photocoagulation is the intervention of choice for patients with proliferative diabetic retinopathy. Diabetic patients without evidence of diabetic retinopathy will benefit from early detection of the condition. Foremost in the management of patients with any stage of diabetic retinopathy would be strict blood sugar control. The primary goal in the treatment of diabetic retinopathy is the prevention of visual loss. Retinal Fibrosis and fibrovascular proliferation occurs as a consequence of bleeding from the new vessels. 1 193 .
Laser Scars secondary to laser treatment. 194 . Figure 17. Panretinal photocoagulation Figure 20. Fundus Photographs (top) with corresponding Fluorescein Angiogram pictures.OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES / 194 Figure 16. Grid Laser Treatment Figure 18. Focal Laser Treatment Figure 19.
Clinically. The overall incidence of hypertensive retinopathy is 15%. Optic disc edema occurs in cases of malignant hypertension. hard exudates. The ocular picture is directly related to status of retinal arteries and the rate of rise and degree of systemic blood pressure. The presence of hard exudates in Henle’s layer of the fovea presents in a star-like configuration.OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES / 195 HYPERTENSIVE RETINOPATHY Systemic arterial hypertension is one of the most common diseases worldwide. Other factors which contribute to this are salt sensitivity. volume depetion and orthostasis. The changes leading to primary systemic arterial hypertension is multifactorial. Retinal manifestations of hypertension include vascular constriction. extensive microvascular changes and retinal edema the above PLUS disc edema 195 . In the elderly. rennin-angiotensin overactivity. leakage and arteriosclerosis. retinal hemorrhages. the “macular star”. This manifests as flame-shaped hemorrhages. Leakage occurs due to abnormal vascular permeability. an increase in basal smooth muscle tone occurs as a result of sympathetic activity. this presents as focal narrowing and straightening of the retinal arterial walls. The Keith Wagener Barker Classification was published in 1939 which classifies the condition to four stages as follows: Table 4. Macular Star – hard exudates in the fovea. Arterial sclerosis occurs in the normal aging population (involutional sclerosis) as well as in long standing hypertension. More than half of the population over 60 years has this condition. medial layer hypertrophy and endothelial hyperplasia. Grading systems for Hypertensive Retinopathy have been presented by various authors. Arteriovenous (AV) crossing changes occurs as the condition progresses. cell membrane changes and progressive architectural alterations in the vessel walls. Vasoconstriction manifests with generalized or focal arteriolar narrowing. Arteriosclerosis occurs as a result of intimal layer hyalinization. exaggerated light reflex and AV crossing changes the above PLUS cotton wool spots. Keith Wagener Barker Classification of Hypertensive Retinopathy STAGE I II III IV CHARACTERISTICS mild to moderate arteriolar narrowing or sclerosis moderate to marked arteriolar narrowing with focal or neneralized narrowing. retinal edema and hard exudates. Figure 21.
Scheie Classification for Grading Hypertensive Retinopathy – Changes due to Hypertension GRADE I II III IV CHARACTERISTICS slight. nerve fiber layer infarcts (1) and blot hemorrhage (2). Table 4. Schiei Classification based on Hypertension: A – Grade I . C 196 . B – Grade II. This classification system takes into consideration two aspects of the condition: changes due to hypertension and changes due to arteriosclerosis. Tables 5 and 6 present these. C – Grade III. retinal arteriolar narrowing. generalized arteriolar attenuation (AV ratio 1:2) obvious arteriolar narrowing with focal areas of attenuation (AV ratio 1:3) the above PLUS exudates and hemorrhages the above PLUS optic disc edema A B 1 1 2 1 1 1 D Figure 22.OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES / 196 A more recent grading system was proposed by Scheie. D – Grade IV showing swollen optic nerve.
OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES / 197 Table 5. central retinal artery occlusion (CRAO) c. central retinal vein occlusion (CRVO) b. Blood Vessel Changes: A – normal. B – Tapering (green arrows) . branch retinal artery occlusion (BRAO) (2) subconjunctival hemorrhage (3) ptosis (4) EOM paresis (5) cortical blindness 197 . branch retinal vein occlusion (BRVO) d. C – Banking (green arrow) Other ocular problems associated with hypertension include the following: (1) Retinal vaso-occlusive diseases a. Arteriolar Reflex Changes: A – normal. B – broad light reflex “copper wiring” C – “silver wire” A B C Figure 24. Scheie Classification for Grading Hypertensive Retinopathy – Changes due to Arteriolar Sclerosis GRADE I II III IV Arteriolar Reflex Changes broadening of the arteriolar light reflex obvious broadening of the arteriolar light reflex copper-wire arterioles silver-wire arterioles Blood Vessel Changes minimal AV crossing changes moderate AV crossing changes marked AV crossing changes severe AV crossing changes A B C Figure 23.
It is found in 100% of HIV infected patients. Individuals at risk of acquiring this infection include the following: People receiving transfusions IV drug users Healthy sex partners of infected patients Babies born of infected mothers Hemophiliacs Prostitutes. sex workers Homosexuals and Bisexuals Health workers Ocular manifestations include the following: dry eye retinal microangiopathy often manifested as cotton-wool spots opportunistic infections commonly presenting as Cytomegalovirus (CMV) retinitis tumors like Kaposi’s sarcoma of the lids or conjunctiva neuro-ophthalmologic lesions Cottonwool spots are the most common finding in these patients. Vaso-occlusive Diseases: A – CRVO. Patients are usually asymptomatic and these lesions may disappear spontaneously. HUMAN IMMUNE DEFICIENCY VIRUS/ACQUIRED IMMUNE DEFICIENCY SYNDROME Infection with the Human immunodeficiency virus ( HIV) causes immune system suppression of patient which subsequently allows opportunistic infections and neoplastic conditions to affect the eye. close follow-up by an ophthalmologist is recommended. It is proposed that this occurs as a result immune complex deposition and/or HIV infection of retinal vascular endothelium. B .CRAO B The primary management of ocular complications associated with hypertension would be adequate blood pressure control. For complications such us vascular occlusions. 198 . Laser treatment is performed whenever indicated.OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES / 198 A Figure 25. Cytomegalovirus (CMV) retinitis affects 40% of patients with AIDS. Its presence signifies severe systemic involvement. Cotton Wool Spots may be associated with retinal hemorrhages and microaneurysms. This condition may however occur in other immunodeficiency states.
Later the muscles become fibrotic. Symptoms associated with thyroid eye disease often present between 20 to 45 years of age. the upper lid margin is at or above the superior limbus. CMV retinitis in a patient with HIV infection THYROID EYE DISEASE (TED) This autoimmune eye condition is known by a variety of names such as Graves' Ophthalmopathy/Orbitopathy and Thyroid-associated Orbitopathy (TAO) and dysthyroid ophthalmopathy. Cottonwool spot in a patient with HIV infection. Although exophthalmometry is useful. TED is the most common cause of unilateral or bilateral proptosis in adults. pressure. Proptosis or exophthalmos can be measured with an exophthalmometer. injection over the recti muscle insertions. or hypotropia. proptosis can be determined by viewing the patient overhead. This may be due to sympathetic overdrive affecting Mullers muscle. itching. proptosis. the ocular involvement may precede or lag after the endocrine manifestations. fibrosis of the muscles elevating the lid. As a result of lid retraction. Symptoms may include excessive redness. tearing. Thyroid eye disease commonly affects the medial rectus and inferior rectus muscles accounting for the appearance of esotropia and hypotropia. Other common signs of TED are lid lag on downgaze. Proptosis is due to inflammation of the extraocular muscles and orbital fat. While most patients with this condition will present with hyperthyroidism and the eye disease simultaneously. In some instances. esotropia and hypotropia. the eye condition may even present in the absence of any evidence of thyroid dysfunction. Initially the muscles are swollen and there may be injection over the recti insertions. Ocular involvement may be unilateral or bilateral. Patients with TED can still develop significant optic nerve compression without marked proptosis. Figure 27. puffiness and pain. In some instances the extraocular muscles may enlarge resulting in diplopia due to limited motility of the eye.OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES / 199 Figure 26. causing anterior protrusion of the globe (and sometimes optic nerve compression) in the relatively confined bony space of the orbit. Digital palpation through the patient’s closed eyelids can be used to estimate orbital compliance. It affects women nine times more often than men. 199 . The most common clinical manifestations of TED are lid retraction (Dalrymple’s sign). Unilateral or bilateral lid retraction is the most common sign of TED. lid lag (Von Graefe’s sign) and retraction together with exophthalmos referred to as “Thyroid Stare” (Kocher’s sign).
Corneal Involvement = Class 5 Figure 33. Extraocular Muscle Involvement = Class 4 Figure 32. perforation Colour vision loss Visual acuity decrease Visual field loss Disc swelling or pallor Signs or symptoms 3 4 5 6 Proptosis Extraocular muscle involvement Corneal involvement Sight loss – optic nerve involved Figure 28. Only signs = Class 1 Figure 29. infiltrate. lid lag Proptosis Epiphora. Classification of thyroid orbitopathy Class 0 1 2 Description No signs or symptoms Only signs Soft tissue involvement Upper lid retraction.OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES / 200 Table 3. conjunctival and lid oedema Orbital fat extrusion Swollen muscles Proptosis moderate or severe Gaze restriction. diplopia Staining with fluorescein Ulceration. Proptosis = Class 3 Figure 31. Soft tissue involvement = Class 2 Figure 30. stare. Sight Loss = Class 6 200 .
More serious complications include diplopia. Radiation is also utilized to reduce swelling of periocular tissue and subsequently decompressing the optic nerve. Otherwise. Ocular involvement is more common in patients with miliary tuberculosis. The disease may however continue to progress even the patient’s thyroid status is controlled. There is no single laboratory examination that will confirm the presence of thyroid eye disease. patients may also benefit from strabismus surgery. Special lenses called prisms may be used to relieve this. Table 3 presents the Werner classification (NOSPECS classification) which is often used by clinicians to follow the course of the condition. early lid or orbital decompression surgery may be necessary. disturbing double vision not relieved by prism glasses and drooping or sagging of tissues around the eyes. Loss of vision usually results from compression of the optic nerve by swollen tissues surrounding the eye. severe protrusion of the eyes. or as a result of hypersensitivity reaction to tuberculoprotein. Treatment of Congestive Phase include local therapy with tear substitutes and lubricants to help to protect the surface of the eye from drying. surgery is usually reserved for stable. Other complications include glaucoma and exposure of the front surface of the eye resulting from the inability to completely close the eyelids. the disease usually attains a stable condition. inactive or Cicatricial Phase of the disease with the following complications: abnormal staring appearance. although. Double vision can be troublesome if it affects straightforward and down-looking positions. Extraocular muscle involvement may be documented using radiologic examinations which will reveal extraocular muscle enlargement.OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES / 201 Less serious complications of TED are exposure keratitis. In some instances. Head elevation particularly while sleeping reduces swelling around the eyes. it may also be seen in patients with no evidence of pulmonary disease. When vision is threatened. Since steroid use may cause a number of undesirable side effects with chronic use. Urgent treatment is required otherwise visual loss can be permanent. TUBERCULOSIS Ocular involvement in tuberculosis can be caused by either direct invasion of organism. As was mentioned earlier. The most common manifestation of TB in the eye is granulomatous uveitis (anterior and/or posterior). they are only given as a temporary measure. the condition is not related to thyroid hormone levels and may present even when the patient is in a euthyroid state. Beyond this time. Steroids are used in selected cases. tearing and foreign body sensation and lid and conjunctival edema / chemosis. Other manifestations are: Phlyctenulosis Vitritis Retinal periphlebitis Choroidal tubercles Panuveitis 201 . It is common for thyroid eye disease to fluctuate within the first few years of the disease. ophthalmoplegia and loss of vision.
Other Manifestations of Ocular TB: (A)-phlyctenulosis (B)-choroidal tubercle (C)-retinal periphlebitis SUMMARY The importance of being able to recognize ocular signs. Schubert H. Gouras P. 1994. in particular diabetic retinopathy is crucial in ultimate outcome of treatment. A B C Figure 34.OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES / 202 The inflammatory condition associated with TB is usually treated with corticosteroids. 2. Federman JL. Yanuzzi LA. It is therefore necessary for the primary care physician to be able to perform a thorough eye examination. particularly that of the fundus. Early diagnosis of the conditions earlier discussed. imperative that patients be treated with anti-Koch’s medication prior to institution of the anti-inflammatory regimen to avoid exacerbation of the systemic infection. Vol 9. Madison Slusher M. ed 2. symptoms and complications of many systemic diseases is a vital part of good medical practice. Additional reading is recommended to supplement the information provided. It is however. 1994. in Podos SM. Kanski JJ: Clinical Ophthalmology: A Systematic Approach. Guyer. 1994. This instructional material is by no means complete. Schachat AP. St Louis: Mosby. Yanoff M (eds): Textbook of Ophthalmology. 202 . 1995. Tuberculous Granulomatous Uveitis: (A) – keratic precipitates (B) Bussacca nodules (C) – Koeppe nodules A B C Figure 35. London: Mosby. Green. SJ (ed): Retina. Oxford: Butterworth-Heinemann. DR. in Ryan. St Louis: Mosby. Murphy RP (eds): Medical Retina. Only conditions that are more commonly encountered in local practice have been emphasized. REFERENCES 1. 4. 3. ed 3. WR: The Retina Atlas. Vrabec TR: Retina and Vitreous.
Coleman AL. Tang RA. In what disease condition is this associated? What are the abnormal findings? 203 . In what disease condition is this associated? What are the abnormal findings? Picture 4.OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES / 203 5. Give a diagnosis. Identify the encircled lesions indicated by arrows. . Picture 2. give the stage of hypertensive retinopathy (give staging for both arteriosclerosis and hypertensive changes) 1 2 Picture 3. Using Scheie Classification. San Francisco: American Academy of Ophthalmology. Skootsky S. Brown J. Newman SA. Wilkins JK. Whitcup SM: Ocular Manifestations of Systemic Disease: A Slide-Script Program. EVALUATION Picture 1. 1996.
look for vitreous hemorrhage B. In the management of diabetic retinopathy. You will order for: A. examine for corneal defects with a biomicroscope D. Because of the expense involved. order ultrasound examination to rule out a retinal detachment C. pulse insulin therapy and regular eye exams 7. On ophthalmoscopy one would commonly expect to find: A. A 68-year-old male has had a history of BPs ranging from 170-200/100-120. A 50-yr old female who has had NIDDM for the last 10 years consults for blurred vision. go on with the MRI C. Panretinal photocoagulation should be considered in background retinopathy D. sudden. solitary whitish lesion with blurred margins on the left fundus.OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES / 204 SELF-TEST 1. You will: A. vitreoretinal surgery and endolaser treatment C. Grave’s ophthalmopathy is the most common cause of proptosis in the adult. an asymptomatic 28 year old GRO was found to have a small. he decided to seek a second opinion from you. painless loss of vision D. order a T3 & T4 determination D. dilated venule D. serum cholesterol D. A 45-year-old male consulted a private MD for a bulging left eye. order a CT scan instead B. Type 2 diabetics of > 5 years duration should be referred to an ophthalmologist 3. Mild nonproliferative diabetic retinopathy is best managed with: A. You would: A. the following will apply: A. good blood sugar control and regular fundus fluorescein angiography D. copper-wire venule C. A 26 year old diabetic should be referred to an ophthalmologist at the time of diagnosis C. fasting blood sugar C. HIV test 204 . order an HIV test 2. the following may be encountered: A. In the progression of this disease. cotton wool spots 4. d. concentrate your examination on the macular area 5. panretinal photocoagulation and strict blood sugar control B. consistently abnormal thyroid hormone levels 6. arteriolar constriction B. “thyroid stare” resulting from the combination of lid lag and lid retraction B. a “frozen” eyeball C. T3 & T4 determination B. Type 1 diabetics of > 2 years duration should be referred to an ophthalmologist B. He was advised to undergo an MRI. On routine ophthalmic examination.
Hypertensive retinopathy grade III D.OCULAR MANIFESTATIONS OF SYSTEMIC DISEASES / 205 8. 7. 10. aggressive oral hypoglycemic therapy for type II diabetics C. 8. Hypertensive retinopathy grade IV 10. NVE and NVD C. The patient has: A. Hypertensive retinopathy grade II C. hard exudates 9. the following should be done: A. Non-proliferative diabetic retinopathy is characterized by the following EXCEPT: A. aggressive insulin therapy for type I diabetics D. microaneurysms B. Routine eye examination of a 57 yr. In order to prevent diabetic retinopathy from becoming the world’s leading cause of blindness. 5. 6. Hypertensive retinopathy grade I B. dot hemorrhages D. 2. regular and proper eye examination for individuals at risk B. 4. 3. 9. C B A D B C D B C A 205 . proper diet and exercise for the elderly population ANSWERS TO SELF-TEST 1. old hypertensive male patient revealed exudates and hemorrhages all over the fundus with distinct disc borders and an AV ratio was 1:3.
INTENDED USERS This material is developed for the use of medical students level IV. 6. INTRODUCTION This self-instruction material is designed to help the student learn the basic concepts of eyelid malpositions. 2. classify of the different types of Ectropion. 5. and Eyelid Retraction. particularly vision. Blepharoptosis or Ptosis. Ptosis and Lid retraction discuss the pathophysiology of the different types of Ectropion. the student should be able to recognize the 4 different eyelid malpositions and know the basic concepts of diagnosis and management. recognize the different eyelid malpositions perform diagnostic maneuvers to evaluate the 4 lid malpositions discuss the theoretical management of each of the 4 lid malpositions. 4. Kleiner. OBJECTIVES Upon completion of this unit of instruction. support and lubrication for the eye to enhance its proper functioning. These will be discussed one by one. 206 . Any abnormality or irregularity of the position of the eyelids can have drastic effects on the eye and its function. M. Ptosis and Lid Retraction.D. Entropion. PREREQUISITE KNOWLEDGE: Students should have a working knowledge of the anatomy of the eye and adnexae. ECTROPION: Definition: ECTROPION is the outward turning of the eyelid margin. Entropion. and know theoretically their pathophysiology and management. They provide protection. And basic eye examination. Entropion.EYELID MALPOSITIONS / 206 Eyelid Malpositions Franklin P. but should b useful to any student of ophthalmology. diagnosis and management. There are 4 basic eyelid malpositions: Ectropion. Ptosis and Lid retraction. their classification. Every student of ophthalmology should be able to recognize eyelid malpositions. The detailed discussion on the management of the different eyelid disorders maybe more appropriate for the level VI and VIII students CONTENT The eyelids are important accessory structures that give support and complement the proper functioning of the eye. 3. Entropion. pathophysiology. define the 4 lid malpositions: Ectropion. They should also know the basic history taking and physical examination. particularly eyelid anatomy. The eyelids are important accessory structures that give support and complement the proper functioning of the eye. Specifically they should be able to: 1.
Paralytic Ectropion 3. But once the patient blinks. Normally. But if very lax. Pull the eyelids downward toward the orbital rim. One can test for eyelid laxity by doing the snap back test. in severe cases with visualization of the palpebral conjunctiva. Cicatricial Ectropion 4. since its normal position is in apposition with the globe.EYELID MALPOSITIONS / 207 Recognition: This can be easily recognized in patients due to the everted position of the lid margin. In the eyelid. Signs and symptoms are tearing due to the interrupted flow of tears from the lateral to the medial canthus. with superficial punctate keratitis and corneal opacification. even without the patient blinking. Senile Involutional Ectropion 2. Sometimes they go back to their original position. Congenital Ectropion 5. However. Mechanical Ectropion SENILE INVOLUTIONAL ECTROPION As we age. if there is laxity in the patient’s eyelids. but will go slowly back up. especially at the canthal tendons. one may even visualize the punctum. Following is its classification or possible causes: 1. The eyelid tends to stretch out and lengthen. the eyelids will snap back to their original position. with a space or gap between the palpebral conjunctiva and the globe. they may stay ectropic. Another test is the eyelid distraction test wherein the eyelid is pulled away from the globe to see how far it can stretch out. excessive eyelid laxity can result in ectropion. and at times even due to an ectropic punctum (see medial ectropion). If the ectropion is carried medially. they will not snap back. Patients who constantly rub their eyes can hasten this process. then let go. Irritation and dryness of the conjunctiva is common. which is normally not visible. there can be reflex tearing due to irritation from dry eye or exposure keratitis. Senile Involutional Ectropion 207 . the eyelid will go back again to its original position. our tissues tend to stretch out and become lax. Stretching of 6mm or more confirms the presence of laxity. In more severe cases. interruption of the tear meniscus and lacrimal pump.
Patient’s eyelids may need to be tape at bed time. tarsorrhaphy may be done (suturing of the eyelids together to effect closure). There are two advantages of this operation over other lid tightening or lid shortening procedures. Surgical treatment. Surgical treatment: But if exposure will be present for a longer period of time. such as a stroke. But in prolonged cases. which involves tightening of the eyelid horizontally by attaching the lateral most portion of the tarsus to the lateral orbital rim. and in worse cases. leaving the laxity of the lateral canthal tendon uncorrected.EYELID MALPOSITIONS / 208 Treatment: Senile involutional ectropion is best treated by a horizontal eyelid tightening procedure. goggles or moist chambers may be sufficient. Senile Involutional Ectropion after Tarsal Strip MEDIAL ECTROPION In the normal eyelid. This procedure involves the excision of a medial spindle of papebral conjunctiva just below the punctum. gels. Other lid shortening procedures such as a wedge resection or Kuhnt Szymanowski shorten the tarsus of the lid. Or a gold weight may be implanted in the upper lid. with the placement of inverting sutures to restore the punctum to its normal position. Conservative treatment: In temporary conditions. this means that it is in an ectropic position. If a patient’s punctum is visible in a normal resting position. In a wedge resection. A medial spindle excision operation is most suitable for this condition. or 7th nerve palsy or paresis. This is because it is turned inward facing the lacrimal lake. The lateral tarsal strip operation is the most popular. In temporary cases such as Bell’s Palsy. lubrication with artificial tears. The second advantage is that the scar is tucked away in the lateral canthus. Punctal plugs may be inserted as well. and there may even be lid notching. this is reversible. in conjunction with a 208 . PARALYTIC ECTROPION When the orbicularis oculi becomes paralyzed in affectations of the 7th nerve. Thus a phimosis or shortening of the length of the palpebral fissure may be induced. ointments. atrophy of the muscle can occur resulting in more permanent laxity of the eyelid. One is that it corrects the laxity at the site of the pathology which is the lateral canthal tendon. the punctum is not visible. there is loss of eyelid tone. the lateral tarsal strip operation. the scar may be more obvious.
and the lashes are turned in. if possible ENTROPION Entropion is the inward turning of the eyelid margin. cicatrical ectropion can occur. healed lacerations. etc. usually in conjunction with some other congenital conditions such as blepharophimosis. Management is excision of the mass. with loss of visualization of the lid margin. rubbing against the globe. lengthening of the anterior lamella by scar excision and z-plasty or multiple z-plasties may be performed. MECHANICAL ECTROPION – This is a form of ectropion caused by a mass or lump in the eyelids. In severe cases. Cicatricial Ectropion Preop After skin graft CONGENITAL ECTROPION – this is a form of cicatricial ectropion. (in that order of preference). usually due to shortage of anterior lamella since birth. chemical burns. there is a balance between the anterior lamella and the posterior lamella. Best donor sites for skin grafts to the upper lid are from the opposite upper lid. Implantation of gold weights in the upper lid allows the eyelid to close due to the weight of gravity. checking while the patient is in upgaze or with the mouth open. There is frequent irritation. CICATRICIAL ECTROPION In the normal eyelid. In moderate to severe cases of cicatricial ectropion. longstanding chronic infections of the lid. For mild conditions. If there is shortening of the anterior lamella. Recognition: The eyelid margin is rotated inwards. supraclavicular area and medial arm. redness and possibly discharge of the eye.EYELID MALPOSITIONS / 209 tarsal strip and a small 3-4 mm lateral tarsorrhapy. weighing down on the eyelid and causing it to become ectropic. Recognition of this condition is done by checking on the tightness of the anterior lamella. thermal burns. Other areas are the preauricular area. corneal abrasion and scarring may occur. Management involves lengthening of the existing anterior lamella. infections or abscesses that healed. Best donor site for skin grafts to the lower lids are from the post auricular area. Some conditions that cause this are: scarring of the eyelid skin due to trauma. 209 . causing decrease in visual acuity. Patient complains of constant irritation and foreign body sensation caused by rubbing of the lashes against the cornea. skin grafts may be necessary.
then the entropion is cicatricial in nature. pemphigoid or Stevens Johnson Syndrome. The detachment or dehiscence of the lower lid retractors contributes to the instability of the lower border of the tarsus. this causes the eyelid to flip inwards. Another condition known as distichiasis may be present. Frequent causes of scarring are chronic infection of the eyelids. detachment or dehiscence of the lower lid retractors. Following is the classification according to different causes: 1. This is why entropion is considered a semi-emergency situation. after returning it to its normal non entropic resting position. systemic diseases such as leprosy. If. however. causing it to rotate inwards permanently. which is the growth of a second row of lashes. which is the inward turning of lashes. 4. This may or may not be in conjunction with a cicatricial entropion. 4. preseptal orbicularis over ridng the pretarsal. This scarring causes a deformity of the tarsus. and when combined with lid laxity and overriding of the orbicularis muscle. Involutional enophthalmos is not always present. and only turns inward when the patient blinks or closes his eyes. usually from the area of the meibomian gland orifices. 210 . involutional enophthalmos. resulting in corneal ulcer with possible rupture of the eye. which involves actual rotation of the lid margin inwards. 2. in the anophthalmic socket . lid laxity 2.. SENILE INVOLUTIONAL ENTROPION Senile involutional entropion is caused by aging and laxity of tissues. 3. inflammatory conditions of the conjunctiva such as pemphigus. then it is senile involutional entropion. One can differentiate the two by the following test: Press on the lower lid to return it to its original non entropic position. There are 4 factors that come into play causing the inward turning of the eyelid margin: 1. trauma. This condition must also be differentiated from trichiasis.chronic irritation from artificial eye use. the eyelid stays in that position. it jumps into an entropic position right away.EYELID MALPOSITIONS / 210 Extreme complications are infection of the cornea. but may play a role if present. 3. If on releasing it. Cicatricial Entropion Senile involutional Entropion Congenital Entropion Acute spastic Entropion CICATRICIAL ENTROPION Cicatricial entropion is caused by scarring of the posterior lamella: conjunctiva and tarsus. to rub on the cornea.
isolation and tightening of the lower lid retractors through a subciliary incision. It does not address lid laxity. but these are only temporary measures which cannot definitively solve the problem. however the condition will return when the lashes grow back in about two weeks. Management of Cicatricial Entropion and trichiasis If trichiasis is present in a short segmental area. This is a telltale sign of chronic entropion. a grafting procedure must be done to replace the severely deformed tarsus. but it does not address lid laxity. It is usually reserved for patients with medical problems or on blood thinning medication that cannot undergo a definitive surgical procedure. Wies procedure – This is a full thickness blepharotomy with everting sutures which adressses overriding of the orbicularis and dehiscence of the lower lid retractors. One may even detect the mildest of entropions with this technique. or more firm tissue such as sclera. If the area of entropion is very short or segmental. The subciliary incision will prevent overriding of the orbicularis. Its presence signify chronicity of the condition. However there is a high recurrence rate. Electrocautery or radiofrequency may be used for this purpose. a lid margin rotation procedure such as a tarsotomy may be done. or even more anteriorly. lashes may be removed selectively by epilation (plucking of lashes). to rotate the lid margin outwards. Management of Involutional Entropion Conservative management: One may use lubricants and ointments to prevent rubbing of the lashes against the cornea. is best managed by surgical correction. We will only include a few more common procedures here. Destruction of follicles of the lashes for trichiasis may also be done. Surgical management: There are numerous procedures for involutional entropion in many textbooks. These may require repeated procedures to attain a satisfactory result. buccal mucosa. to the gray line. Quickert Sutures are full thickness everting sutures that can be placed along the entire length of the eyelid. a wedge resection of the eyelid involving that portion of lashes may be done. In severe cases of deformity of the posterior lamella or tarsus. The normal mucocutaneous junction along the lid margin is posterior to the meibomian glands. making the posterior portion of the lid margin conjunctivalized. will usually require a surgical solution. A number of tissues may be used. being a mechanical problem of the lids. hard palate mucosa or ear cartilage. 211 . Taping of the eyelid in an everted position may help relieve the patient. It is a very simple procedure that can be done in the minor operating room. being caused by a permanent deformity of the tarsus. including conjunctiva. It however does not address lid laxity. In mild to moderate cases of cicatricial entropion. Entropion.EYELID MALPOSITIONS / 211 One should also examine the lid margin under slit lamp for conjunctivalization of the lid margin. Cicatricial Entropion. If the mucocutaneous junction looks like it has advanced to the level of the meibomian glands. or the lash line. this implies that posterior portion of the lid margin is in apposition with the globe. Others have used cryotherapy to destroy the follicles by freezing. This procedure can correct overriding of the orbicularis and dehiscence of the lower lid retractors. Jones procedure – This involves identification.
and orbicularis overriding. the nasal bridge grows higher with age. but may be present in the upper lid as well. surgery involving removal of the excess skin and hypertrophic muscle must be done. In addition. the levator aponeurosis. Remedy for this situation may also involve a Y-V medial canthoplasty. and therefore is the preferred procedure for this condition. Both levator muscle and superior rectus muscle are innervated by the superior branch of the 3rd cranial nerve. The normal position of the upper eyelid is 2 millimeters below the superior limbus. lubricants and periodic follow up will suffice. and within the eyelid its muscle fibers teriminate into a broad tendinous sheet. It is usually caused by a prominent or hypertrophic roll of orbicularis and skin or epicanthal fold which rotates the eyelashes inwards toward the eye. If lash touch to the eyes is mild.EYELID MALPOSITIONS / 212 Tarsal strip with retractor reinsertion – A tarsal strip operation is performed to remedy lid laxity. It is in close association with the superior rectus muscle almost throughout its length. which inserts into the superior portion of the anterior surface of the tarsus. ptosis is present. and recurrence rate low. However in chronic cases such as blepharospasm. PTOSIS (BLEPHAROPTOSIS) Definition – Blepharoptosis is drooping of the eyelids below the normal position. or those that do not resolve in early childhood and become persistent. concomitantly with everting eyelid sutures. or in conditions such as blepharospasm. The success rate for this procedure is quite high. lid retractors are identified and reattached to tarsus through a subciliary incision. lid retractor dehishcence. SPASTIC ENTROPION This type of entropion may occur due to constant squeezing of the eyelids and spasm of the orbicularis such as in irritative conditions of the eye with constant foreign body sensation. It is held up and supported by the Whitnall’s ligament. causing the patient to squeeze his eyelids frequently. If the eyelid position is any lower than this. botulinum toxin may be used. an epicanthal fold in the lower lid (epicanthus inversus) may be present. and the palpebral conjunctiva below it. In due time as the face of the child matures. and the medial eyelid skin retracts and the entropion resolves spontaneously. It can be recognized by the vertical orientation of its muscle 212 . and its function is to open the eyelid. closely associated with the levator muscle is the Mullers muscle. This is a lid retractor innervated by sympathetic nerves. Also. A short review of the anatomy and physiology of the eyelid retractors and protractors and other pertinent eyelid structures: The levator muscle originates from the annulus of Zinn. Relief of the spasm by relieving the irritative condition will usually resolve this type of entropion. This is commonly referred to as just plain Ptosis (drooping). In moderate to severe cases. This addresses 3 factors: lid laxity. slightly above the superior rectus muscle. Its function is also to open the eyelid. It is more frequently found in the lower lid. In some cases. This muscle originates from the underside of the belly of the levator muscle and inserts on the superior tarsal border. It lies between the levator muscle above it. CONGENITAL ENTROPION Congenital entropion is present in newborn children and may be present up to early childhood.
the pretarsal. when the patient’s ptotic eyelid is paradoxically higher than the opposite eyelid. This is commonly seen in congenital ptosis. the ptotic eyelid is usually lower than the opposite side. or muscles of the extremities. 4. or in the case of complete 3rd nerve palsy. and is responsible for eyelid closure. Levator function may be good or normal. If both levator muscle and superior rectus muscle are affected by a paralysis or paresis of the superior branch of the 3rd cranial nerve. sphincter muscle which lies just beneath the skin of the eyelids. Other cases of pseudoptosis may occur in the presence of dermatochalasis. Congenital –This is a ptosis that is present at birth. acetylcholine. Confirmation is by tensilon test. This can be easily identified in downgaze. such as extraocular muscles manifesting as diplopia. Mechanical – caused by the weighing down of the upper lid by a mass or growth 6. Myogenic –caused by atrophy or weakening of the muscle. When asking the patient to look downwards. but usually only as a last resort. According to Time of Onset 1. Neurogenic – caused by a paralysis or paresis of the third cranial nerve. with full blown ptosis and fatigue in the afternoons. after medical treatment has been tried. and overlies the tarsus of the upper and lower lids. Myasthenia gravis – gradual weakening of muscles due to malfunction of the neuromuscular junction. When a hypotropia is present. Eyelid height may be normal on waking in the morning but may begin to droop as the day progresses. where overhanging skin from the upper eyelid may simulate a ptosis. According to Etiology 1. This comprises a vast majority of acquired ptosis. they become replaced with fibrous or fatty tissue. along the superior tarsal border. This is commonly manifested by a comparatively higher lid crease than the opposite side. Classification of Ptosis I. The protractor of the eyelid is the orbicularis muscle or orbicularis oculi muscle. As the child gets older. The pretarsal forms the innermost circle. II. The periorbital portion is responsible for forceful and voluntary closure. 213 . This may be isolated to the levator. the eyelid may follow the eye that is turned downward. It is characterized by a variable type of ptosis. with the eye usually taking a downward and outward position.Enophthalmos may also simulate a ptosis.caused by a detachment of the aponeurosis from the tarsus. Medical management with mesthinon is the indicated treatment. 3. we call this double elevator palsy. The eyelid does not open well due to lack of muscle fibers. Acquired – This is a ptosis that is acquired after birth. due to the levator detachment from the tarsus. which overlies the orbital rim and bone. This can be identified in downgaze. 2. 7. which restores function to the ptotic lid. which is responsible for eyelid closure. Pseudoptosis – hypotropia . The preseptal forms the middle circle and overlies the septum. It is a circular.EYELID MALPOSITIONS / 213 fibers. The orbicularis muscle is innervated by the 7th cranial nerve. It has three parts. The tarsal and preseptal portions are responsible for involuntary blinking and reflex closure. Surgical intervention may be contemplated. and the superior palpebral arcade of blood vessels which travels on top of it. preseptal and preorbital portions. This type of ptosis is more commonly associated with a strong levator muscle whose aponeurosis has detached from its tarsal attachment. More commonly this type of ptosis is associated with a weak muscle and no lid crease. When the muscle does not develop properly or muscle fibers die. Origin is from the medical canthal tendon. involving fatigue in the production and sensitivity of the neurotransmitter. 2. Traumatic – caused by trauma 5. This is a medical condition that may involve weakness of other muscles. mimicking a ptosis. It is the antagonist of the levator muscle. The outermost circle is the preiorbital portion. extraocular muscle involvement will be manifested. Aponeurotic. the nonfunctional or atrophic muscles become replaced with fibrous or fatty tissue. and it does not close well due to the rigidity of the fibrous tissue.
A difference of 4mm means a 4 mm ptosis. and a 4mm ptosis 6 mm below the limbus. In bilateral ptosis cases. comparing the two eyelids is not practical. one can judge the level of ptosis by observing the level of the eyelid. With the patient looking straight ahead. This technique is not very useful in patients where the lower eyelid is retracted downwards. In these cases. In cases of unilateral ptosis. Mild – 2 mm. a 2 mm ptosis would be 4mm below the limbus.EYELID MALPOSITIONS / 214 Congenital Ptosis Acquired Ptosis III. Normal palpebral fissure height is 10 mm. This may result in misinterpretations. record and compare. According to severity or degree 1. a difference of 3 mm means a 3 mm ptosis. measure the palpebral fissure height of each side. a 3 mm ptosis would be 5 mm below the limbus. Severe – 4 mm MRD -1 Measuring the severity or degree of ptosis: Palpebral fissure technique: One should have ready a penlight and a mm ruler. MRD+1 2. Measuring Eyelid Height 214 . Moderate – 3 mm MRD 0 3. a difference of 2 mm between the 2 eyelids means a 2 mm ptosis. Since the normal position of the eyelid is 2 mm below the limbus. or asymmetric on either side.
In measuring the levator function. According to strength of levator function 1. Patient is instructed to move only the eyes and not the head. Fair 5-7 mm 3. then the corneal light reflex would be in the center. The position of the eyelid is noted and coincided with the 0 of the ruler. IV. Good 8-10 mm 4.EYELID MALPOSITIONS / 215 MRD or marginal reflex distance method: The marginal reflex distance is defined as the distance between the lid margin and the central corneal reflex. The measurement is expressed in +mm if the eyelid margin is above the reflex or –mm if the lid margin is below the light reflex. Examiner then asks the patient to look down as far as he can. Levator function is then similarly measured on the opposite eyelid. The maximum excursion of the eyelid is noted and measured. Poor 0-4 mm 2. This is taken by shining a light onto both corneas. thus 5 mm from the superior limbus. An eyelid with a 2 mm or mild ptosis would have an MRD of +1 or 1 mm above the reflex. and extra caution should be exerted in interpretation of these cases. Excellent 13-15 mm Technique of measuring levator function: One should have ready a mm ruler. Very Good 11-12 mm 5. One may use the above table to interpret levator function. using his thumb to neutralize the motion of the eyebrow. A normal eyelid situated 1-2 mm below the superior limbus would have an MRD of +3 to +4. or 1 mm below the level of the light reflex. Measuring Levator Function 215 . If one would assume that the normal vertical corneal diameter is 10mm. The MRD technique may be subject to misinterpretation in cases of hypertropia or hypotropia. and measuring the distance between the upper lid margin and the corneal light reflex. An eyelid with a 3 mm or moderate ptosis would have an MRD of 0 or with the lid margin right at the level of the reflex. Examination can be repeated several times to determine accuracy of the measurement. The examiner lays one hand on the patients forehead. the patient should be seated in front of the examiner looking straight ahead. Patient is then asked to look up as high as he can. An eyelid with a 4 mm or severe ptosis would have an MRD of -1.
One should feel the forceful closure of the eyelid against the fingers. Most patients will have the eye in an upward position. Corneal sensation – In a patient undergoing ptosis surgery. including gross exam.In addition to the routine basic eye examination. and one can gauge the strength of the orbicularis muscle. The strip with the corner cut off is traditionally placed in the Right eye. Bells phenomenon – The Bells phenomenon is the reflex action of the eyes to turn upwards when the eyes are closed as in sleeping. This is done by asking the patient to squeeze his eyelids forcibly. one must check the amount of tears absorbed by the Schirmer’s strip. we must have adequate tear production to ensure proper lubrication of the corneal surface. and measure using a mm ruler. 2. because this will serve as the alarm system that will warn the individual that his cornea is in danger of exposure or drying. One would not want to expose a patient with dry eye to a ptosis operation which would cause further exposure and drying of the cornea. A 216 . or during actual sleeping. This can be taken by asking the patient to close his eyes as if sleeping. Dry eye is suspected if the result is less than 2mm of tears in repeated examinations. One may see if there is any superficial punctate keratitis present due to dry eye. The eyes of the patient may remain open. Orbicularis tone – this needs to be checked in a patient where the eyelids will be raised. and funduscopy. Now using the thumb and forefinger. This will surely be aggravated if performed in a patient with poor bells phenomenon. place the tip in each inferior fornix until some dye has come off onto the conjunctiva. Tear production – Again in a procedure that will raise the eyelids. or closed. to check if the patient has enough muscle tone to cause adequate closure of the eyelids. one must think twice or thrice before proceeding with a ptosis procedure that will raise the eyelid. with the strip hangin out. whichever is more comfortable. and observe for 5 minutes. Put the folded end of the Schirmer’s strip in each lower eyelid. Instill a drop of fluorescein in each eye. and cause exposure. tonometry. Test for degree of ptosis – measure palpebral fissures (previously described) -Marginal Reflex Distance (previously described) 2. one should check the following: 1. This can be done by performing the Schirmer’s test.EYELID MALPOSITIONS / 216 A complete Eye Examination for ptosis should start with the basic eye examination. EOM. This protects the eyelids in the sleeping position and should be present in all patients where ptosis surgery is contemplated. After 5 minutes. 3. corneal sensation is important. visual acuity. Examine the cornea under the slit lamp with blue light. If not present. then gently lift the upper lid with your fingers and note the position of the eyeball. or using a fluoresein strip. 4. Test for levator function (previously described) Other tests: 1. This is the bells phenomenon. Another test would be the fluorescein dye test. try to forcibly open the patient’s eyes.
One may use the twisted tip of a piece of tissue paper. Suture sling. Operation can be performed under local anesthesia without sedation. where the superior border of tarsus and mullers muscle are clamped. It is best used for the majority of fair to excellent function ptosis of any degree. The procedure is meant to be a temporary one. and can be performed on one or both eyelids. Procedure is usually done under general anesthesia. Patient requires lubrication at bedtime to prevent exposure. Levator Resection –This is the most common procedure used for ptosis repair. Ask the patient to grade on a scale of 1 to 10 how much of the cotton wisp did he feel against his eye. and the eyelid generally does not close completely at night. allowing for adjustment of height and contour intraoperatively. This technique is best used for a narrow spectrum of ptosis patients that fit the following criteria: 1. The eyelid is suspended by the sling to the desired height. Other materials used are goretex and silicone. and would require a fascia lata sling in the future. This procedure is best performed in young children or infants or adults who refuse to undergo fascia lata harvesting. Fasanella Servat procedure – this is a tarsomullerectomy approached from the conjunctival side. Fascia Lata Sling – This procedure involves harvesting long thin strips of fascia lata from the thigh. This procedure is best for patients with poor function ptosis 5 years or older (due to the length of the leg) Levator Resection Fascia Lata Sling Preop Post op Pre op Post OP 4. very good or excellent function ptosis 3. Mild ptosis – 2 mm ptosis only 2. This is usually approached through an external lid crease incision. due to possible reaction to the material. or similar material – Prolene sutures or Supramid sutures may be used to suspend the eyelid similar to fascia lata. The levator muscle is identified. attaching it to tarsus and fashioning a sling attached to the frontalis muscle. isolated and reattached to tarsus in a higher position. formed lid crease. 217 .EYELID MALPOSITIONS / 217 patient with poor corneal sensation will be predisposed to exaggerated drying and exposure of the cornea. 3. SURGERY FOR PTOSIS Repair of the ptosis is accomplished through a number of surgical procedures: 1. and can be raised by raising the eyebrow. 2. excise and sutured. or a cotton wisp to touch the cornea on each side. This is performed with the patient seated and instructed to look upwards. Some amount of lagophthalmos results. if he should undergo ptosis surgery.
EYELID MALPOSITIONS / 218
LID RETRACTION Definition: Lid retraction is the abnormal displacement of the eyelid toward the orbital rim, resulting in exposure of the sclera above or below the limbus. Upper lid retraction may result in retraction of the eyelid above the superior limbus, while lower lid retraction results in retraction of the eyelid below the inferior limbus. Sclera which is visible below the limbus is termed as scleral show. Etiology: 1. Thyroid Ophthalmopathy – The most common cause of lid retraction is thyroid ophthalmopathy or Graves Ophthalmopathy. In the acute stage, lid retraction may be due to inflammatory changes in the eyelid and eyelid muscles, particularly the eyelid retractors. Stimulation of the Mullers muscle by circulating catecholamines may cause it to contract resulting in lid retraction. Enlargement and hypertrophy of the levator muscle may cause further lid retraction. In the chronic stage, fibrosis and scarring of the muscles and septum may set in, causing permanency of the lid retraction. Lid retraction is frequently accompanied by proptosis, and this may further contribute to the appearance of a retracted lid, however these 2 conditions should be differentiated from each other. A lateral flare may frequently accompany the lid retraction of thyroid ophthalmopathy. 2. Anterior Lamellar shortening – This may be caused by cicatricial changes of the skin, such as in trauma or burns, or excessive removal of skin during blepharoplasty. This can frequently result in lid retraction or scleral show. 3. Post muscle surgery – Patients having undergone recession of the rectus muscles may occasionally develop a lid retraction. 4. Idiopathic- In some cases, no known cause can be identified.
Lid Retraction in Thyroid Ophthalmopathy
Idiopathic Lid Retraction
Measurement of lid retraction – One must have ready a mm ruler. With the patient looking straight forward, the position of the lid may be measured above or below the limbus.
EYELID MALPOSITIONS / 219
Treatment of Lid retraction: 1. Conservative treatment: All cases of lid retraction must be worked up for etiology. Thyroid ophthalmopathy must be ruled out by requesting for the pertinent laboratory examinations: T3, T4,TsH. An orbital CT scan, axial and coronal views will help to determine the presence of thyroid induced hypertrophy of muscles. In mild cases of lid retraction, the eye may be at risk of exposure. Topical lubricants may be given. Taping of the lids may be done at night. 2. Surgical Management: In more severe cases, tarsorrhapy may be indicated to protect the globe and prevent exposure. Definitive surgical treatment of the lid retraction should only be undertaken if the patient is euthyroid for at least 6 months. Upper lid retraction may be treated by recession of the levator mullers muscle complex. This can be approached from an external lid crease incision, or from a transconjunctival approach. In severe cases, a spacer graft may be placed to maximize recession of the levator / mullers muscle complex. Spacer grafts that have been more commonly used are sclera and fascia. For lower lid retraction, spacer grafts are commonly used. Sclera, fascia and hard palate mucosa, and ear and nasal cartilage have been used. For retraction caused by anterior lamellar defects or cicatrisation, z plasties, and skin flaps and skin grafts are used to lengthen the anterior lamella. See section on cicatricial ectropion. REFERENCES 1. Kersten RC (editor) et al Basic and Clinical Science Course 2003-2004 Section 7 Orbit Eyelids and Lacrimal System, American Academy of Ophthalmology, San Francisco, USA, 2003 2. Beard C, Ptosis , 3rd edition, CV Mosby, St. Louis, 1981 3. Hatt M, Ophthalmic Plastic and Reconstructive Surgery , Georg Thieme Verlag, Stutttgart, 1986 4. Collin, JRO, A Manual of Systematic Eyelid Surgery, Churchiull Livingstone, 1983 5. McCord Jr. CD, Chapter 5 Surgery of the Eyelids, Duane’s Clinical Ophthalmology Volume 5, TD Duane, ed, Harper and Row, 1984 6. Kersten RC, Kleiner, FP, Kulwin DR Tarsotomy for the treatment of cicatricial entropion with trichiasis, Arch Ophthalmol 1992: 110:714-717. SELF TEST 1. The following are the factors that contribute to involutional entropion EXCEPT: A. Lid laxity B. Detachment of lower lid retractors C. Overriding of pretarsal over preseptal orbicularis D. Enophthalmos 2. Cicatricial entropion is more commonly caused by: A. Scarring of the posterior lamella B. Scarring of the anterior lamella C. Scarring of the lid margin D. Acute blepharoconjunctivitis
EYELID MALPOSITIONS / 220
3. Entropion is a semi emergency because: A. It may cause irritation of the eye B. Lashes may cause corneal abrasion C. This may eventually lead to rupture of the globe D. All of the above 4. Senile involutional ectropion is commonly caused by: A. Eyelid inflammation B. canthal tendon laxity C. tarsal shortening D. mass on the eyelid 5. Cicatricial ectropion can be treated by: A. skin grafts B. skin flaps C. Z plasty D. all of the above True or False 6. One should always check for presence of Bells Phenomenon prior to doing ptosis surgery. 7. A patient with poor function ptosis is a good candidate for Fasanella Servat. 8. The reason one must neutralize the eyebrow when checking for levator function is so that it does not affect raising of the eyelid. 9. The marginal reflex distance is an efficient way to test for the levator function. 10. The most common cause of lid retraction is thyroid ophthalmopathy. ANSWERS 1. 2. 3. 4. 5. C A D B D 6. 7. 8. 9. 10. T F T F T
OCULAR TRAUMA AND EMERGENCIES /221
OCULAR TRAUMA AND EMERGENCIES Ma. Margarita L. Luna, MD Marissa N. Valbuena MD, MHPEd Paolo Ma. Pagkatipunan MD, MHA
INTRODUCTION Ocular trauma is a common cause of unilateral blindness in children and young adults. Domestic accidents, violent assaults, fire-cracker injuries, work and sports related injuries and vehicular accidents are among the common circumstances in which trauma occurs. Central retinal artery occlusion and acute angle closure glaucoma are urgent non-traumatic eye conditions which needs prompt diagnosis and management. OBJECTIVES At the completion of this study material, the student should be able to 1. given a trauma patient, be able to extract a relevant medical history, and be able to perform the necessary ocular examination. 2. to recognize the condition which needs prompt referral to the ophthalmologist. 3. discuss the principles of management of the common ocular emergencies. RECOMMENDED PREPARATION Before going to this material, the student must have previous knowledge of anatomy and physiology of the eye and the skills of history taking and ocular examination. INTENDED USERS This SIM is intended to provide an overview to LU IV students. LU V to VII students who have exposure to actual patients during their duty in the eye ward and emergency room will benefit from this module. CONTENT I. EVALUATION OF THE EYE TRAUMA PATIENT A. History 1. Details of the event: place and time, interval from injury (minutes, hours, days), accidental or intentional, work-related 2. Past ocular and medical history 3. Prior treatment 4. Accompanying symptoms: pain, loss of vision diplopia irritation foreign body sensation other organ-system involvement 5. Specific injury: mechanism or type of injury (blunt vs. penetrating), nature of injury Chemical injury: acid or base Foreign body injury: metal, organic material, glass Blunt trauma
OCULAR TRAUMA AND EMERGENCIES /222
Thermal burn Animal bites B. Ocular Examination IMMEDIATE MANAGEMENT OF OCULAR TRAUMA IF THERE IS OBVIOUS RUPTURE OF THE GLOBE, AVOID FURTHER MANIPULATION OF THE GLOBE. Unnecessary manipulation by a non-ophthalmologist while attempting to do a complete ocular examination may cause further damage to the eye. All topical anesthetics, dyes and other medications placed in an injured eye must be sterile. An eye shield should be taped over the eye and systemic broad-spectrum antibiotics started. 1. Approach to the Patient 2. Gross External Examination performed prior to visual acuity testing if with history of chemical injury; do copious washing with clean water Face and lids – observe for lacerations, contusion-hematoma Conjunctiva – observe for subconjunctival hemorrhage, lacerations 3. Visual acuity 4. Pupils check for relative afferent pupillary defect peaked pupil fixed, dilated unreactive pupil 5. Extraocular motility diplopia inability to look opposite the orbital fracture :suspect trapped muscles 6. Visual fields confrontation test
OCULAR TRAUMA AND EMERGENCIES /223
Amsler grid (for macular edema)
7. Anterior segment examination a. Conjunctiva – subconjunctival hemorrhage, lacerations, congestion b. Cornea Lacerations Edema
Abrasions Ulcerations c. Anterior chamber Hyphema – blood in the anterior chamber shallow anterior chamber
Note how the slit beams of the cornea and the iris are almost touching each other. The slit beams should be far apart if the anterior chamber is deep.
d. Iris – iridodonesis, iridodialysis e. Lens Phacodonesis lens rupture
OCULAR TRAUMA AND EMERGENCIES /224
dislocation Choroid and Sclera – perforation / rupture, avulsion
8. Intraocular pressure – defer finger/palpation tonometry if with penetrating or perforating injury 9. Vitreous and retina Do a dilated funduscopic examination hemorrhage
retinal detachment, macular edema, foreign body 10. Optic nerve congestion, edema, hemorrhage, avulsion Special studies – ERG (Electroretinogram) and VEP (Visual Evoked Potential) II. MOST URGENT OCULAR CONDITONS 1. Chemical burns 2. Central retinal artery occlusion 3. Acute angle closure glaucoma CHEMICAL BURNS - most urgent - usually work-related or with assault, household cleaning agents A. Types of Chemical Burns 1. Alkali – lye (NaOH); caustic potash (KOH); fresh lime [Ca(OH)2] found in plaster, cement, mortar, whitewash; ammonia (NH4) found in household cleaners, fertilizers, magnesium hydroxide (sparklers), and refrigerant
OCULAR TRAUMA AND EMERGENCIES /225
more extensive corneal damage due to protein denaturation rapid penetration, often less than one minute damage is related more to the degree of alkalinity (pH) rather than tothe actual cation permanent injury is determined by the nature and concentration of the chemical as well as by the time lapsed before irrigation 2. Acid – battery acid, industrial cleaner (H2SO4), laboratory glacial acetic acid or HCl, fruit and vegetable preservatives, bleach, refrigerant (H2SO3), industrial solvents, mineral refining agents, gas alkylation agents, silicone production agents, glass etching agents (HFl) less damaging to the cornea because less progressive and less penetrating cause maximum damage within the first few minutes to hours precipitate tissue proteins that rapidly set up barriers against deep penetration by the chemical damage localized to the area of contact* *with the exception of burns from hydrofluoric acid or from acids containing heavy metals, which tend to penetrate the cornea and anterior chamber resulting in intraocular scarring and membrane formation Anterior segment burns due to tear gas and mace should be managed as alkali burns. Ocular injury from sparklers and flares containing magnesium hydroxide should also be managed as chemical rather than as thermal burns.
B. Treatment 1. Immediate Treatment a. Topical anesthetic immediately instilled b. Lids are held apart, with retractors if necessary c.Immediate lavage with at least 2000 mL of normal saline 0.9% over a minimum period of 1 hour d. Direct pressure on the globe during lavage should be avoided if laceration of the globe is suspected e.Apply topical anesthetic every 20 minutes f. Conjunctival fornices and palpebral conjunctiva should be swept with sterile cotton-tipped applicators to remove any foreign matter g. Eversion of the eyelids should be done to remove any retained particulate matter such as lime or cement
Mydriatic-cycloplegics such as Atropine 1% should be instilled to dilate the pupil and prevent posterior synechiae and reduce painful iridociliary spasm b. Paracetamol 500 mg one tablet per orem every 3 to 4 hours b. By an internist.7). History pertinent medical history (vaso-occlusive diseases) may be preceded by transient ischemic attacks of visual blurring or blackout in embolic or inflammatory vasculitic disease most common cause is embolization. Antibiotic drops such as Ciprofloxacin. Meperidine 50 to 100 mg intramuscularly 4. Ofloxacin. because toxic chemicals are aspirated or swallowed during the initial injury b. Visual acuity 2.OCULAR TRAUMA AND EMERGENCIES /226 h.3 and 7. If burn is mild. Patient should be checked every 5 minutes to make sure that the pH is not changing again in the direction of alkalinity or acidity. By an otolaryngologist. to rule out concomitant burns of the respiratory or upper gastrointestinal tract c. 2. Admit patient b. Tobramycin. septic and non-septic fibrin. Emergency complete physical examination a. Medications a. Irrigation should be continued until pH paper reveals that the conjunctiva’s pH is close to normal (pH between 7. and platelet thrombi atheromas. calcium deposits of diseased heart valves. and platelet thrombi B. Funduscopy Retina at the posterior pole becomes milky white and swollen “Cherry-red spot” at the fovea is seen if cilioretinal artery is intac Hemorrhage is minimal 226 . continue medications and follow-up on an outpatient basis CENTRAL RETINAL ARTERY OCCLUSION (CRAO) A. Ocular findings 1. Painless loss of vision to 20/400 (unless the patient retains central vision via a cilioretinal artery supplying the papillomacular nerve fibers) 3. Analgesics a. or Polymyxin-Bacitracin c. with emboli arising from fatty material of atheromas. septic and non-septic fibrin. Acute obstruction of the airway due to laryngeal edema may occur 5.Carbonic anhydrase inhibitors for increased IOP 3. Vision with no light perception suggests choroidal ischemia due to ophthalmic artery occlusion in addition to CRAO 4. calcium deposits of diseased heart valves. Patching of the burned eye once stable a.
followed by 5 seconds of release b.OCULAR TRAUMA AND EMERGENCIES /227 Cherry red spot at the macula Pale . halos. The aim is to mechanically collapse the arterial lumen and cause prompt changes in arterial flow. Digital massage. Sublingual isosorbide dinitrate 10 mg to dilate peripheral blood vessels and decrease resistance e. Treatment – should be carried out immediately for anyone presenting within 24 hours of visual loss due to CRAO 1.Carbonic anhydrase inhibitors – acetazolamide d.Intravenous methylprednisolone for possible arteritis f. c. or ocular massage using a three-mirror contact lens for approximately 10 seconds. 95% oxygen-5% carbon dioxide mixture to dilate retinal vessels g. nausea and vomiting B. edematous retina. History a. Ocular findings Red eye (ciliary injection) Hazy or steamy cornea Moderately dilated and unreactive pupil Increased intraocular pressure (IOP) Shallow anterior chamber Ciliary injection. acute retrobulbar hemorrhage or ocular hypotension for acute glaucoma 3. Non-specific methods to increase blood flow and dislodge emboli a. Sudden onst of severe blurring of vison followed by excruciating pain. C. Correction of specific precipitating event – orbital decompression for 2. Paracentesis of aqueous humor to decrease IOP acutely ACUTE ANGLE CLOSURE GLAUCOMA A. hazy cornea. to obtain central retinal artery pulsation or cessation of flow. middilated pupil 227 .
Determine if there are associated ocular injury. Is there Significant tissue loss ? 4.OCULAR TRAUMA AND EMERGENCIES /228 C. levator muscle. REFER to an ophthalmologist 2. Antibiotics. If there are. dexon or vicryl 6-0 silk for skin 5. Prophylactic laser iridotomy of the fellow eye LACERATIONS OF THE EYELIDS 1. Consider what special structures w/in the area of laceration may be injured. anti-tetanus. Lacerations not involving the lid margins 5-0 chromic. Contact lens over wear 3. Reducce IOP Oral acetazolamide IV and oral hyperosmotic agents (mannitol and glycerine respectively) Topical beta blockers Pilocarpine 2-4% I drop every15 minutes for 1 hour 2. Ex canaliculi. 3. UV burn from welding Abraded portion of the ccornea stains with green fluorescein dye 228 . REFER to an ophthalmologist Cosmetic & functional success depends on exact re-approximation 6. Treatment 1. Fingernail or any object to the eye 2. cold compresses CORNEAL ABRASION Causes 1. lacrimal gland. Lacerations involving lid margins. Laser peripheral iridotomy 3.
Antibiotic drops Metallic foreign body on the corneal limbus at 5 o’clock position Will there be a scar after the removal of the foreign body ? Yes. Deeper FB .G25 needle under slit lamp. extra or intra. use of moist cotton swab 2. Lid swelling 5. Are there other FB present.ocular? 3. Epithelial defect Management 1. Cycloplegic drops 4.increased risk of infectious keratitis Examination 1.irrigation. CONTUSION OF THE EYEBALL Hyphema – blood in the anterior chamber 229 . Is infection present? Management 1. Metallic .rust ring 2. How deep did the FB penetrate? 2. Blurring of vision 6. Superficial FB . remove rust ring 3. Pain 2. Eye patch CORNEAL FOREIGN BOBIES Characteristic of FOREIGN BODY 1.OCULAR TRAUMA AND EMERGENCIES /229 Signs & Symptoms 1. Vegetable . Antibiotic drops 3. Photophobia 3. if Bowman’s and stroma injured. Tearing 4. Removal of occult foreign body 2.
OCULAR TRAUMA AND EMERGENCIES /230 Commotio retinae – retinal edema Retinal detachment 230 .
OCULAR TRAUMA AND EMERGENCIES /231 231 .
Diplopia can be due to direct neuromuscular damage. axial and coronal views 2. swelling of the orbital content or entrapment of the inferior rectus and inferior oblique within the fracture. Management 1. CT scan. . compressive forces can fracture the thin medial and inferior walls with prolapse and possible entrapment of soft tissues. Surgical repair SUMMARY All physicians.OCULAR TRAUMA AND EMERGENCIES /232 ORBITAL FRACTURE Usually occurs with facial trauma and may be associated with intraocular injury. When orbital entrance receives a blow. He should be skilled in rendering immediate treatment and should prevent 232 .Enopthalmos may develop. Antibioltics and anti-inflammatory drugs 3. especially those working in the emergency rooms should be familiar with the treatment of the injured eye and its adnexae.
Blepharitis E. Blurring of vision 2. Chemical burn D. P. you note that the patient has a mid-dilated pupil with a firm eyeball. Hazy cornea due to bedewing D. Whitcher. Vaughn and Ashbury’s General Ophthalmology . D. extraocular muscle movement test D. Based on this. Butterworth H. Corneal abrasion B. Internal hordeolum B. endophthalmitis and orbital rim fracture B. 589-708 4. 2004 SELF-TEST 1. your primary consideration would be A. chemical burn and central retinal artery occlusion D. 5th Edition 2003 2.J. (Ed) Issues in Ocular Trauma. J. scleral laceration and commotion retinae 5. The following conditions require IMMEDIATE intervention or treatment: A. 2002 3. Nasolacrimal duct obstruction 3.M. Einemann. canalicular transaction and intraocular foreign body C. Ocular pain E. (Ed). hyphema and central retinal vein occlusion E. Which of the following red eye conditions would require early recognition due to their potentially vision threatening nature A. L. palpation tonometry E. direct funduscopy 233 . Parver.J. REFERENCES 1. and Pieramice D. Riordan-Eva. Lippincott Williams and Wilkins. Acute angle closure glaucoma 4. Kanski . Contact lens overwear C. He should likewise be familiar with the common non-traumatic emergencies like central retinal artery occlusion and acute angle closure glaucoma. Signs of acute angle closure glaucoma include the following. Bacterial conjunctivitis D. EXCEPT A. Ciliary injection B. Viral conjunctivitis C. Ophthalmology Clinics of North America. 16th Edition. Pavan-Longston. Clinical Ophthalmology.. Most cases require referral to the ophthalmologist for definitive treatment. This step in the ocular examination may be deferred if globe rupture is suspected: A. gross examination C. Manual of Ocular Diagnosis and Therapy. A patient presents with a one day history of severe eye pain and marked blurring of vision.A Systemic Approach. Irregular miotic pupil C. visual acuity B.P. J.OCULAR TRAUMA AND EMERGENCIES /233 further injuries to the patient. 8 (4) December 1995. Upon doing your ophthalmologic examination. New York: Lange Medical Books/ McGraw Hill.
What clinical finding is not seen in a patient with orbital floor fracture? A. diplopia C. 8. flashlight test using a slit beam D. What examination will help confirm this diagnosis? A. 3. direct funduscopy 9. mydriatic-cycloplegic eyedrops E. A patient’s eye was hit by a tennis ball. Which of the following tests will not be useful in confirming your diagnosis of commotio retinae? A. hypertension D. 9. artificial lubricants Answers to Self –Test 1. confrontation test D. Retinal artery occlusion is NOT commonly associated with: A. A patient who figured in a vehicular accident was referred from another hospital with a diagnosis of traumatic optic neuropathy. hypesthesia D. emboli from atheromas B. temporal arteritis 10. 2. Amsler grid test C.OCULAR TRAUMA AND EMERGENCIES /234 6. 6. extraocular muscle movement test E. determination of conjunctival pH D. 7. 4. Hirschberg light reflex test B. swinging flashlight test C. retrobulbar hemorrhage C. Hirschberg light reflex test B. The following measure is part of the long-term management of chemical burns: A. lid elevation test 7. sweeping conjunctival fornices with cotton-tipped applicators C. B C D C D B E D C 10. copious irrigation with NSS B. exophthalmos 8. limited extraocular muscle movements E. E 234 . 5. thyroid exophthalmos E. ecchymosis B.
3. He should be able to recognize the common ocular signs and symptoms and correlate these with the corresponding anatomic and physiologic changes in the eye and related structures. Systemic Medications Used for Ophthalmic Conditions: Glaucoma Medications Systemic Anti-inflammatory Agents 235 . Routes of administration II. their fate in the human body and their known side-effects.Ocular Diagnostic Drugs (uses) Fluorescein dye Anesthetics Mydriatics Cholinergic Blocking agents Adrenergic stimulating drugs III. OBJECTIVES At 1. It refers to drugs utilized for the diagnosis and treatment of ocular diseases. the medical student should be able to Discuss the various ways in which drugs act on the body. INTRODUCTION In clinical practice. he should be able to do a thorough history taking and basic eye examination.D. M. an ophthalmologist listens to the patients reason for consulting then examines the patient thoroughly.A working diagnosis is formulated and finally decides on the management. Discuss the implications of systemically administered drugs to ocular function.OCULAR PHARMACOLOGY / 235 OCULAR PHARMACOLOGY Rosie Reyes-Noche. To evaluate the patient with eye problem. eye discharge. eye displacement. CONTENT I. Topical Ocular Therapeutic Drugs ( Indications/Mechanism of Action/Side Effects) Decongestants Anti-inflammatory Agents Antibiotics IOP lowering Agents: Beta-Adrenergic Blockers Cholinergic Stimulating Drugs Adrenergic Stimulating Drugs Prostaglandin Analogs IV. He should be aware of common eye conditions causing the following : Vision changes eye redness. Ocular Pharmacology deals with the basic properties of drugs. eye pain. 2. with specific emphasis on drugs used in the eye. tearing. He should be able to decide whether the eye condition is urgent and considered as an ocular emergency and make the necessary referrals. . the end of this unit of instruction. PRE-REQUISITE KNOWLEDGE & PREPARATION The student should have an overview of the normal anatomy and physiology of the eye. eye deviation.. their action. Discuss the diagnostic and therapeutic uses of drugs on the eye.
Tetracaine HCl 0.) : injection in the muscle 3. Subconjunctival Injection Made under the conjunctiva to gain access to the deep structures of the eye by absorption into the blood stream by way of the episcleral and conjunctival blood vessels. Examples 1. Ointments 4. Gels B.): injection under the skin C. Subcutaneous (S.OCULAR PHARMACOLOGY / 236 Systemic Antibiotics V. Removal of foreign body/sutures 2.retrobulbar injections A. Oxybupavacaine 0. FLUORESCEIN DYE Water soluble non-toxic dye. Solutions 3. Injected intravenously for angiography of retina B.) : by mouth 2.O. Proparacaine HCl 0. Retrobulbar Injection Made directly through the skin of the lower lid with the point of the needle emerging behind the eyeball PART II. Diagnosis of corneal abrasion 2. subconjunctival injections . TOPICAL ANESTHETICS Uses: 1. topical B.5% 2.0% 4. yellow at neutral pH.) : injection into the vein 4. Applanation tonometry for glaucoma 4. Topical : Placed directly into the eye. Tear layer evaluation in dry eye or Contact lens fitting 3. Ocular Side Effects Of Systemic Drugs PART I.C.V. Intravenous (I. fluoresces with cobalt blue stimulation Uses: 1. OCULAR DIAGNOSTIC DRUGS A. Diagnosis of aqueous leak post surgery 5.4% 236 . There are 4 forms of topical eye medications 1. D.5% 3. systemic C. Lidocaine 1.M. ROUTES OF DRUG ADMINISTRATION A. Applanation tonometry They are mildly toxic to the cornea and when used in excess can retard healing. Systemic : Delivery of the drug to the affected area by way of the bloodstream 1. Suspensions 2. Intramuscular (I. Oral (P.
ANTI-INFLAMMATORY AGENTS 1. Tetrahydrozoline HCl 0.01% 2. Mechanism of action: Vasoconstrictors Side-effects: Angle closure in narrow angles and keratitis sicca (dry eye syndrome) Examples : 1. Epinephrine eye drops 2. Direct acting cholinergic blocking agents (Parasympathomimetic) : Pilocarpine Hcl eye drops 1%. MYDRIATICS AND CYCLOPLEGICS These are drugs which produces pupillary dilatation and are used to allow adequate examination of the fundus and to reduce the incidence of posterior synechiae formation in uveitis.Used in glaucoma patients after laser trabeculoplasty Examples: 1. Naphazoline HCl 0.05% B. Sympathomimetic : Phenylephrine 2. B. Stimulates the ciliary muscle and subsequently increases outflow. Anti-cholinesterase Isofluorophate( DFP) Echothiopate iodide (Phospholine iodide) Domecanium bromide (Humorsol) Physostigmine salicylate (Eserine) Neostigmine bromide E. They are used to paralyze accommodation in cycloplegic refraction and are used in iritis. Used primarily in acute angle closure glaucoma 2. Tropicamide 0. Dipivefrine(Dipivalyl epinephrine) 3. PART III. Adrenergic Stimulating Drugs Its use in ophthalmology is for vasoconstriction and ocular pressure reduction. They are also used pre-operatively in cataract surgery.. Apraclonidine eye drops .2% and 4%. Antazoline HCl 0. Parasympatholytics: A. Topical Ocular Therapeutic Drugs A. DECONGESTANT Indications:For short term relief of eye redness and eye irritation.OCULAR PHARMACOLOGY / 237 C. Cyclopentolate 1% C.5% 2. cyclitis and diffuse uveitis 1.005%-0. CHOLINERGIC BLOCKING AGENTS Causes pupillary constriction or miosis 1. Non-steroidal Anti-inflammatory Agents (NSAID) 237 .5% D.04%(Visine/EyeMo) 3. Atropine 1%. The stronger mydriatics also paralyzes the ciliary body and are known as cycloplegics.
Bacitracin 5.03% (Ocufen) 5.OCULAR PHARMACOLOGY / 238 Indications: 1. fibroplatic proliferation. stinging. 8. 6. Transient stinging and burning on instillation 2. Quinolones. 9.0% (Indocin) 3. 3. Ketorolac 0. steroid induced glaucoma 2. 7. produce miosis and cause the breakdown of the blood-aqueous barrier. Used for prevention of intra-operative miosis 2. Aminoglycosides. Penicillins 3. Uveitis / Scleritis Mechanism of action : Anti-prostaglandin. 2. Allergic reactions Examples : 1. Erythromycin. prostaglandins increase vascular permeability. cataracts 3. Examples: 1. 4. severe allergic reactions Mechanism of Action: Suppress inflammatory response by inhibiting edema. deposition of collagen. In the eye. Fluorometholone C. Vernal keratoconjunctivitis 4. cellular infiltration. ANTIBIOTICS Indications : For external eye infections Mechanism of action: Bactericidal or bacteriostatic by inhibition of protein/mucopeptide/ cell wall synthesis Side-Effects:local conjunctival irritation. Diclofenac 0. Sulfonamides. capillary dilatation. Flurbiprofen 0. Ocular irritation 3. Dexamethsone 3. activation of infections and in some cases corneal perforation. Corticosteroids Indications : post-operative inflammations. Prednisone/ Prednisolone 2. Side-Effects 1. anterior uveitis. Side effects: 1.1% (Voltaren/Naclof) 2. burning. Tetracyclines 238 . Cephalosporins. Post-operative and traumatic inflammation control. sensitization Examples : 1. scar formation. Suprofen 1% (Profenal) 4.5% (Toradol) 2. Chloramphenicol. allergic reactions. Indomethacin 1.
Carbonic Anhydrase inhibitors Indications : acute angle closure glaucoma Mechanism of Action: Decrease aqueous production Side-Effects: GIT discomfort. stinging. headache. Epinephrine 2. Accommodation spasm resulting to pain and blurred vision 3. Increase permeability of blood-aqueous barrier leading to greater inflammation 2.004% ( Travatan) PART IV.allergy Examples : 1. mental confusion. Timolol Maleate 0. Examples: 1. dryness. transient myopia. Apraclonidine 4. GLAUCOMA MEDICATIONS 1. Levobunolol Hcl 0. Constriction of visual fields Example : Pilocarpine 3. Dipivalyl epinephrine 3. discomfort. Latanoporst 50 mcg/ml(Xalatan ) 2.03% ( Lumigan ) 3.25. Adrenergic Stimulating Drugs Indications : for vasoconstriction and reduction of intra-ocular pressure Mechanism of Action : Increase aqueous outflow.50% 3. Bimatoprost 0. ocular hypertension Mechanism of Action : Decrease IOP by increasing uveo-scleral outflow Side-effects : Increase iris pigmentation. Travoprost 0. Cholinergic Stimulating Drugs Indication : for acute angle closure glaucoma Mech. itching.50% 2. decrease aqueous secretion Side-Effects : Burning.3% 2. agranulocytosis Example : Acetazolamide(Diamox ) 250 mg. lengthening of eyelashes. Metipranolol Hcl 0. paresthesia.OCULAR PHARMACOLOGY / 239 D. Betaxolol Hcl 0. Beta adrenergic Blocking Agents Indications: Open angle glaucoma Mechanism of Action: Reduce IOP by suppressing aqueous production Side Effects:Transient ocular burning. anemia. Contracts ciliary muscles leading to increase aqueous outflow Side-effects 1. Prostaglandin Analogs Indications :Primary open angle glaucoma.of Action: Relief of pupillary block by constricting the pupil and tautening the iris IOP is reduced when the root of the iris pulls away from the trabecular meshwork and angle opens./tab 239 . and hyperemia Examples :: 1. dizziness . IOP LOWERING AGENTS 1. Systemic Drugs s Used For Ophthalmic Conditions A.25 –0.50% 4.0.pain.
bacterial endophthalmitis. allergic reactions. buffalo hump. infections of the adnexae and orbit Mechanism of action : Bactericidal or bacteriostatic Side-Effects : Renal toxicity. SYSTEMIC ANTI-INFLAMMATORY AGENTS 1. Posterior subcapsular cataract 240 . systemic (moon facies. optic neuritis.avoid glycerol in diabetics Examples 1. Glycerol 50% oral solution 2. Erythromycin 8. Aminoglycosides 2.OCULAR PHARMACOLOGY / 240 2.and PGE 2 Side-effect . Mechanism of action : prevent synthesis and release of PGE 1. Optic neuropathy EXAMPLES OF DRUGS Disulfiram (for alcoholism) Hexachlorophene(antiseptic) Vincristin/Busulfan (anti-cancer) Chloroquine/ hydrochloroquine (for arthritis) Practolol (for hypertension) Glucocorticoids (for inflammation) 2. Osmotic Agents Indications: Acute angle closure glaucoma Mech. Aspirin 2. Chloramphenicol 7. :Gastric irritation. Retinal degeneration 3. NSAID: Indications : ocular inflammation where steroids are contraindicated. Conjunctival fibrosis 4. Mannitol 20% IV solution B. OCULAR SIDE-EFFECTS OF SYSTEMIC DRUGS A. Sulfonamides 4. Tetracycline 6. Indomethacin water content 2. hyperacidity Examples : 1. Corticosteroids Indication : posterior uveitis. Cephalosporins 5. vomiting or diarrhea Examples : 1. hepatic toxicity .acne) C SYSTEMIC ANTIBIOTICS Indications : Severe intra-ocular infections . sympathetic ophthalmia Mechanism of Action : anti-inflammatory Side-Effects: Suppress resistance to invasion of micro-organism. Clindamycin PART V.of Action : Increase serum osmolarity to reduce intra-ocular(vitreous) Side-Effects=caution in CHF. nausea. Penicillin 3. IRREVERSIBLE SIDE EFFECTS SIDE EFFECTS 1.
Retinal degeneration 241 . REVERSIBLE SIDE EFFECTS SIDE EFFECTS 1.OCULAR PHARMACOLOGY / 241 5. Mydriasis and Cycloplegia 11. Blepharoconjunctivitis 2. Ocular hypertension 12. Lens deposit 5. Myopia 9. Altered colored perception and visual hallucinations 7. Pigment epitheliopathy 6. Corneal epithelial deposits and retinal deposits: 4. Oculogyric crisis 14. Retinal degeneration B. Pseudotumor cerebri Quinine (for muscle spasms) Chlorpromazine (for psychiatric disorders) EXAMPLES OF DRUGS Retinoic acid( for acne) Tetracycline/Vit A (for acne) Hexachlorophene(antiseptic) Minocycline ( anti-infective) Glucocorticoids Chloroquine/ hydroxychloroquine Tamoxifen/Tilorone ( for cancer) Amidarone ( for cardiac arythmia) D-penicillamine D-penicillamine (for arthritis) Digitalis/Digoxin/Lanatoside C (for cardiac arythmias) Diazepam/Phenobarbital/Phenytoin (anti-convulsant) Carbonic anhydrase inhibitors (for glaucoma) Sulfonamides (anti-infective) Bromocriptine (for Parkinsonism) Chloramphenicol (for infection) Ethambutol Diethylcarbamazine Suramin anti-histamines anti-Parkinson anti-muscarins ( for peptic ulcer) Glucocorticoids Methoxsalen ( for psoriasis) MAO inhibitors( for psychiatric disorders) Thioridazine ( for psychiatric disorders) Chlorpromazine ( for psychiatric disorders) 3. Myasthenia 6. Optic neuropathy 10. Corneal and Lens deposits 15. Lens opacification 13. Nystagmus 8.
Vale and Cox . anti-viral D. 2. O’Connor Davies. Ethambutol C. 4th ed. used in uveal inflammation D. use of autonomic agents for the production of miosis. Bartlett and Jaanus . mydriasis and cycloplegia and the use of local anesthetics and dyes.OCULAR PHARMACOLOGY / 242 SUMMARY This course presents an overview of the clinical pharmacology of the ocular diagnostic and therapeutic agents. topical eye ointments 2. Drugs and the Eye . Corticosteroids B. ketamine C. antibiotics B. all of the above 4. systemic oral D.Clinical Ocular Pharmacology 2nd ed. Acute catarrhal conjunctivitis is treated with. A.evaluation of therapeutic response. The pharmacology and toxicology of the ocular anti-allergic. Ephedrine B. Trichloroethylene D. The principles of drug administration. and ocular & systemic adverse reactions is also included. REFERENCES 1. Specific topics include clinical pharmacokinetics of the eye. The drug most likely to increase intra-ocular pressure A. 3. One of the following drug may cause optic neuritis: A. 3rd ed. alcohol 5. anti-inflammatory C. topical eye drops B. The Action and Uses of Ophthalmic Drug. Vit A D. dilates the pupil B. paralyzes accommodation C. peri-ocular injections C.Hopkins & Pearson . SELF-TEST 1. anti-inflammatory and anti-infective agents as well as drugs used in the treatment of glaucoma is presented. Eye medications are usually given as: A. Proparacaine 242 . Mydriatics and cycloplegics are drugs that A. anti-fungal 3.
A 2. Corticosteroids: A. may be used to deliver antibiotics intra-ocularly in severe endophthalmitis D. topical antibiotic C. A 5. slows epithelialization B. Oral antibiotic B. diagnosis of corneal abrasion B. D 243 . Pilocarpine D. applanation tonometry for glaucoma D. The following drug reduce(s) aqueous production: A. D 8. B 6.OCULAR PHARMACOLOGY / 243 6. topical anti-inflammatory 9 Local injections: A. oral anti-inflammatory D. Metipranolol B. delays wound healing D. In a case of bacterial endophthalmitis. D 7. D 4. stabilizes lysosomal membrane C. injected IV for retinal angiography C. all of the above 10 Fluorescein dye is used in ophthalmology for the following: A. Betaxolol C. D 10. may provide repository for drugs for days or weeks C. All of the above 7. A 3. A 9. all of the above Answers To Self Test 1. the drug of choice is A. will deliver drugs that penetrate the cornea poorly B. all of the above 8.