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USING THE OPHTHALMOSCOPE AND VIEWING THE OPTIC DISC

Kathleen B. Digre, MD

University of Utah

               

 

Ophthalmoscopy:  

The Direct Ophthalmoscope was invented by Jan Purkinje 1823 (from Prague of Czech) and by Herman von Helmholtz 1851 of Germany--Helmholtz is generally given the credit. Initially ophthalmoscopy was performed with external illumination; today we use a hand-held ophthalmoscope with its own light source often powered by batteries. The direct method gives a direct, erect image of a small area of the fundus. The direct ophthalmoscope helps to focus light to the back of the eye in order to view the disc and the vessels.
 

Acquaint yourself with the dials of the ophthalmoscope. 

In the front there is a switch for white light and a green light.  In some ophthalmoscopes, the green lens can be dialed in. Most of the time you will use the white light.   

There is a small and larger light source.  The smaller light is good for small, undilated pupils, but the larger light provides better illumination.   

The green light (or red free filter) is particularly good for looking for drusen or for nerve fiber defects.  It provides 450 nm monochromatic light.   

Some ophthalmoscopes also have a “bulls-eye” with a cross hatch--we use this sometimes to identify where the patient is focusing (e.g.  have the patient look at the light--is the macula centered in the bulls-eye? If not, the patient may have amblyopia or lazy eye).   

Some ophthalmoscopes also have a narrow slit beam which is useful to view a lesion in the retina--if the beam is not distorted, the lesion is flat, if the lesion is elevated the beam will is raised toward the observer.  The slit beam is especially useful for indirect illumination of the disc. 

The “wheel” has lenses with different diopters of power.  The red numbers are negative power (for near-sighted individuals, long eyes, and myopia) and the black or green numbers are positive power (for far-sighted individuals, short eyes, and hyperopia).

How do you use the ophthalmoscope?

First, have the patient in a dimly lit room so that the pupils are enlarged. In general, it is very helpful to dilate the patient.  Mydriatics like phenylephrine and tropicamide are usually short acting.  Historically physicians in general have not dilated pupils because they do not want to precipitate a glaucoma attack.  This is very uncommon and the treatment is to send the patient to the closest ophthalmologist as soon as possible.  Doctors have been resistant to dilate pupils because they may want to “look for a blown pupil with an intracranial mass.”  Since the advent of CT and MR in the 70’s and 80’s as well as treatment of increased intracranial pressure with mannitol or steroids, it would be rare indeed to have to use the pupil alone to follow a patient or treat intracranial pressure.  The overwhelming majority of new patients seen by physicians in an outpatient clinical setting are not candidates for imminent herniation.  Contraindications to dilation consist of known narrow angle glaucoma and impending surgery, or an unstable neurologic condition where watching pupillary change may be necessary.  

Have the patient fixate a distant target while seated (so that you are taller, or at least at the same height).  Align yourself with the patient--your right eye should look into their right eye and your left eye should look into their left eye.  First look for the red reflex of their eye.  Changes in the cornea, lens or vitreous may alter the red reflex.  Focus on the limbus of the cornea.  Continuously peer through the media (cornea, lens, vitreous).  Turn the “wheel” as you draw closer to focus the light--you need to be 1-3 inches in front of the patient's eye.  The view is magnified about 14 times.  Remember when you look through a keyhole, the view is best when the eye is closest to the aperture.  Bring the vessels of the retina into view.  Find the optic disc, macula, identify the central retinal artery and its branches.


The Optic nerve is formed by axons from ganglion cells in the retina.  These axons pass through the lamina cribrosa and form a cable behind the globe that will travel through the orbit, optic canal, and decussate in the chiasm and synapse to the next neuron in the lateral geniculate.  What we see when we peer into the eye with the ophthalmoscope is the optic disc and retina. The diameter of the optic nerve is 1.62mm.  There are about 1 million nerve fibers that form the optic disc. 

Normal Disc appearance is driven by the shape of the globe, the size of the scleral canal, and what is left behind in development. 

 

 

 

Features of the normal optic nerve 

The disc is the slightly oval, somewhat pink structure that dominates what we usually view in the fundus. The lamina cribrosa is a connective tissue “sieve” consisting of a fibrocollagenous weave of holes that “bundles” the million axons as they cross into the retrobulbar optic nerve.  The lamina is deeper and the optic disc is smaller in hyperopic eyes and the disc is broader but shallower in myopic eyes.  The lamina cribrosa clearly can be seen in about 1/3 of eyes. The retrolaminar nerve (behind the lamina cribrosa) is where the axons are myelinated by oligodendrocytes.  Occasionally myelination occurs in the prelaminar disc or retina.   The cup is an apparent space centrally.  The physiologic cup size varies from less that 0.1 to 0.9 of the total disc diameter.  The usual cup to disc ratio is about 0.3.  The larger the cup, the larger the scleral opening at the back of the globe.  In the photograph above the cup-to-disc ratio is about 0.6.  The space between the cup and the edge of the disc is the neuro-retinal rim.  All around the disc you can see the scleral ring.  The papillary area is the disc itself.  The area around the disc is called the peri-papillary disc area.

 

Can you appreciate the nerve fiber layer?

The surface layer is the nerve fiber layer from all over the retina.  We try to examine the nerve fiber layer to determine whether there is any loss.  Its appearance is like fine horsehairs.

 

Twenty-five per cent of normal eyes have an optic crescent usually located temporally.  Most pronounced crescents are seen in association with myopia.    There are a variety of crescents (see figure - varieties of crescents, under disc ectasia).


 

Tilted discs (nasal fundus ectasia) and other disc variants are related to an oblique insertion of the optic nerve to the globe.  In these discs the vessels emerge as from a cornucopia.  Tilted discs are usually tilted inferiorly.  They are associated with myopia and can have choroidal or RPE changes associated with it. 

Fundus Ectasias


                                                        

The vascular supply of the optic nerve disc


 

The prelaminar disc is supplied with blood from the choroidal vessels, which are branches of the ciliary artery, and the very superficial vessels from the Central Retinal Artery.  Lamina cribrosa supply is the short ciliary arteries.  Posteriorly, there are recurrent branches from the ophthalmic artery and pial vessels.   

Venous drainage from the disc is through the central retinal vein and choroid via the vortex veins 

The central retinal artery (CRA) passes through the disc and into the optic nerve about 1 cm behind the globe and enters the eye at the optic nerve head--usually nasal to the exit site of the central retinal vein.  It divides into superior and inferior branches.  It further branches to supply 4 quadrants of the retina.

 

A cilioretinal artery is present in 32% of eyes.  It often looks like a hook.  The cilioretinal artery may provide a small amount of blood supply to the retina when the central retinal artery is occluded.  Occasionally, these vessels will supply whole quadrants (or more); these cilioretinal arteries are frequently indistinguishable from the branches of the CRA. The cilioretinal artery exits the disc separately from the central retinal artery. The importance of the cilioretinal artery is that it can occlude and cause usually a central visual loss or during a central retinal artery occlusion, its presence will spare central vision and the macula.  Occlusion of a cilioretinal artery is prima facie evidence of giant cell arteritis. 



The normal disc has spontaneous venous pulsations.  Look for them on the disc.  When present they are thought to represent that the intracranial pressure is not increased.  While this is in general true, it does not always hold.  If absent, intracranial pressure may or may not be increased. 

The venous return of the eye includes the central retinal vein that drains the retina.  The posterior vortex vein is a large choroidal vessel, which can be apparent from the edge of the optic disc and drains into veins of the orbit.  It is often seen in myopic or blonde eyes because of hypopigmentation of the retinal pigment epithelium.  Both of these circulations drain into the superior orbital vein and into the cavernous sinus.

 

 

Normal Variations of the disc and fundus 

The color of the retina depends on the amount of pigmentation of an individual.  Individuals with little pigment (blond, lightly pigmented Caucasians) have a very light colored fundus (blonde fundus) that allows for viewing sub-retinal elements, like vortex veins.  Whereas in darkly pigmented individuals (African-American), the fundus is typically more heavily pigmented and those sub-retinal elements are not seen.  As people age, more pigmentation is found (tessellated fundus). 

Effect of refraction and shape of the globe: In myopia, the globe is elongated.  The disc may appear larger partly due to refractive error.  Further, optic disc may be larger.  The cup tends to be larger.  There are frequently scleral and pigmentary crescents at the temporal margin of the disc when the pigment epithelium does not reach the edge of the disc.  The disc can be confused with optic atrophy.

In hyperopia, the globe is foreshortened.  The disc may appear smaller, partly due to refractive error.  The cup is usually small or non-existent; there is evidence of smaller cross section of the lamina cribrosa.  These discs, because they are frequently hyperemic and have no cup, can be confused with disc swelling.

                   

THE DISC APPEARANCE IS AFFECTED BY WHAT IS LEFT BEHIND IN 
EMBRYOLOGICAL DEVELOPMENT
 

There are many vascular abnormalities. Bergmeister papilla is the remnant of normal development of tissue around the fetal hyaloid artery.  The hyaloid artery normally regresses by the 7th month of gestation.  The amount of atrophy and regression determines in part the configuration of the optic cup.   Glial tissue can be seen on the disc and may be related to the Bergmeister papilla.

 

 

Myelinated nerve fibers are a developmental anomaly where myelination appears past the lamina cribrosa on nerve fibers of the disc and retina.  It typically has “feathered” edges which follow the nerve fiber layer.  It may be unilateral or bilateral and usually not associated with visual impairment.  Myelinated nerve fibers can simulate papilledema or be mistaken for nerve fiber layer infarct (soft exudates). 

 

IS THE DISC SWOLLEN?

First, what types of findings mimic papilledema? 

Anomalous optic discs, drusen, tilted optic disc, hyperopia, and "little red discs" cause Pseudopapilledema.

 

Optic disc drusen 

Optic disc drusen are an inherited disc anomaly that can look like papilledema.  Distinguishing features from papilledema include: no hyperemia, surface arteries on the disc are not obscured, no physiologic cup, the elevation is confined to the disc and does not “spread to the nerve fiber layer around the disc, and the disc is irregular. They are congenital, refractile bodies that may be buried but tend to mineralize as the individual ages.  Drusen is the German word for a geode, since drusen look like the crystals in a geode.  A single drusen is a druse.


Other causes of anomalous discs:

Hyperopic Discs and little red discs.  Recognize anomalous discs by looking for an absent cup, tortuosity of the blood vessels, too many blood vessels on the disc. 

 

PAPILLEDEMA

True papilledema is disc swelling caused by increased intracranial pressure.  The findings of papilledema include hyperemia that is caused by dilation of the disc capillaries, and swelling of axons in the peripapillary nerve fiber layer which causes blurred disc margin.  “Blurred disc margin” alone can be seen with anomalous elevation, but vessels are not obscured.  Elevation of the disc usually occurs peripherally before centrally and there may be an early appearance of a “red cell” shape or volcano.  Peripapillary retinal nerve fiber layer hemorrhage may be present.  Retinal veins appear dilated, elongated and tortuous.

 

 OTHER CAUSES OF DISC SWELLING

 


 

Anterior ischemic optic neuropathy (or AION) is caused by a loss of an oxygen source for mitochrondrial function due to non-arteritic or arteritic ischemia to the optic nerve. More commonly AION is associated with hypertension and diabetes.  Ischemia blocks axoplasmic flow causing “damming” of axoplasm at the prelaminar region.


 

 

Optic neuritis is painful monocular visual loss due to demyelination, viral and bacterial infections, sarcoid, syphilis, or Lyme disease.  Retrobulbar optic neuritis may cause transient slight swelling.  Most often is identified after the acute attack when optic atrophy appears.

 

OPTIC ATROPHY 

Optic atrophy is a non-specific finding related to damage to the optic nerve. Clinical features of optic atrophy include: presence of relative afferent pupillary defect (RAPD) if there is asymmetry in the neuropathy; visual field defect. 

The normal optic nerve gets its color from small vessels on the disc and from the nerve fiber layer. 

OPTIC PALLOR

When there is damage to the normal optic nerve, it becomes pale.  Pallor really is the “tomb-stone” --what is left behind when the optic nerve is damaged, whatever the process.   The entire optic nerve may be atrophic or only segments may be atrophic.  The disc can be “cupped out” in response to the damage--this just means that there is profound loss of tissue.  The nerve can become gliotic--this means that there may have been ischemia or inflammation that caused the loss of tissue.  Disc features of optic atrophy include change in the optic disc color (pallor), loss of nerve fiber layer (slit, wedge, or generalized drop out), segmental atrophy (temporal or band), and cupping. 

 

Causes of optic atrophy include: 

Acquired optic atrophy can be the result of underlying optic nerve tumor, optic neuritis, and ischemic optic neuropathy.  It may be generalized or altitudinal. 

Congenital optic atrophy can be caused by genetic conditions including a dominant form (presents age 4-8; mild loss), or recessive form (age 1-9--moderate to severe), recessive form with diabetes (severe).  Other conditions in which optic atrophy occurs include spinocerebellar degeneration (Fredreich’s ataxia; mental retardation).  When associated with diabetes and deafness consider Friedreich’s ataxia, Diabetes Insipidus, Usher’s syndrome, Refsum’s syndrome, and Laurence-Moon-Biedel syndromes. 

Lebers hereditary optic neuropathy initially presents with unilateral central visual loss usually associated with modest disc swelling and tortuous small vessels gradually followed by optic atrophy.  Second eye involvement may be immediate or followed by months or years.  This is a group of mitochondrial disorders that may also include other neurological problems. 

Glaucoma is a kind of optic neuropathy associated with progressive cupping of the optic disc due to increased intraocular pressure.  As neurologists we can think of it as papilledema in reverse. 

Toxic optic neuropathy can be due to nutritional, methyl alcohol, chloramphenicol.  Loss of the macular papillary bundle characterizes this neuropathy. 

 

Bibliography 

Brazis PW, Lee AG. Optic disk edema with a macular star.       Mayo-Clin-Proc. 1996 Dec; 71(12): 1162-6 

Brodsky, MC  Congenital anomalies of the optic disc. In: Miller, NR, and Newman NJ Walsh and Hoyt’s Neuroophthalmology.  Baltimore:  Williams and Wilkins, 1998 pp 775-823. 

Brodsky MC, Baker RS, Hamed LM,  Pediatric Neuro-Ophthalmology.  New York:  Springer, 1995. 

Brown G, Tasman W.  Congenital Anomalies of the Optic Disc.  New York: Grune & Stratton, 1983. 

Digre K, Corbett JJ.  Practical Viewing of the Optic Disc.  Boston:  Butterworth (in press) 

Rosen ES, Eustace P, Thompson HS, Cumming WJK  Neuro-ophthalmology.  London:  Mosby, 1998. 

Spalton D, Hitchings R, Hunter P.  Atlas of Clinical Ophthalmology.  Second Edition.  Mosby Year Book.  London, 1994.

  

Acknowledgements:   

Most of the diagrams and photographs except where noted are from Digre, Corbett with permission.  We would like to thank Dr. Todd Troost for his computer rendition of scleral crescent.  Also, Dr. Sohan Hayreh and Michael Schenk for the vascular anatomy illustrations.  My co-author, James J Corbett, MD, Chair Neurology, University of Mississippi.

 

 

 

           

 

 

 

 

 

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                                              Last updated:  10/05/2002                                                          © 2000-2002 John Rose, MD  University of Utah School of Medicine