Schizo Tonometry

Oskar Gareis and Gerhard K. Lang

9.1 Basic Knowledge

Function: The pupil refers to the central opening in the iris. It acts as an aperture to improve the quality of the resulting image by controlling the amount of light that enters the eye.

Pupillary light reflex: This reflex arc consists of an afferent path that detects and transmits the light stimulus and an efferent path that supplies the muscles of the iris (Fig. 9.1).

— Parasympathetic pupillary reflex pathway.

Retina

B Optic nerve C Optic chiasma

D Optical tract

E Lateral geniculate body

F Pretectal nucleus

— Parasympathetic pupillary reflex pathway.

Retina

B Optic nerve C Optic chiasma

D Optical tract

E Lateral geniculate body

F Pretectal nucleus

Pretectal Nucleus

Sphincter pupillae muscle

- Ciliary I

ganglion

Oculomotor H nerve

Edinger- G Westphal nucleus

Visual cortex (area 17)

Afferents

Efferents

Fig. 9.1 See discussion in text.

Sphincter pupillae muscle

- Ciliary I

ganglion

Oculomotor H nerve

Edinger- G Westphal nucleus

Visual cortex (area 17)

Afferents

Efferents

Fig. 9.1 See discussion in text.

Afferent path. This path begins at the light receptors of the retina (Fig. 9.1, A), continues along the optic nerve (B), the optic chiasma (C) where some of the fibers cross to the opposite side. The path continues along the optical tracts (D) until shortly before the lateral geniculate body (E). There the afferent reflex path separates from the visual pathway and continues to the pretectal nuclei (F) and from there to both Edinger-Westphal nuclei (G). Each of the two pretectal nuclei conduct impulses to both Edinger-Westphal nuclei. This bilateral connection has several consequences:

❖ Both pupils will normally be the same size (isocoria) even when one eye is blind. Deviations up to 1 mm are normal

❖ Both pupils will narrow even when only one eye is illuminated (consensual light reflex).

Efferent parasympathetic path. This path begins in the Edinger-Westphal nucleus (G). Its nerve fibers form the parasympathetic part of the oculomotor nerve (H) and travel to the ciliary ganglion (I) in the orbit. Postganglionic nerve fibers pass through the short ciliary nerves to the effector organ, the sphincterpupillae muscle (J).

Perlia's nucleus and the Edinger-Westphal nuclei are also responsible for the near reflex, which consists of accommodation, convergence, and miosis.

Efferent sympathetic nerve supply to the pupil. Three neurons connected by synapses supply the pupil (Fig. 9.2):

❖ The central first neuron begins in the posterior hypothalamus (A), passes the brain stem and the medulla oblongata to the ciliospinal center (Budge's center; B) in the cervical spinal cord (C8 -T2).

❖ The preganglionic second neuron extends from the ciliospinal center through the white rami communicantes and sympathetic trunk (C) to the superior cervical ganglion (D). It is vulnerable to certain lesions such as Pancoast tumors because it is immediately adjacent to the tip of the lung.

❖ The postganglionic third neuron extends from the superior cervical ganglion as a neural plexus along the internal carotid artery, ophthalmic artery, and long ciliary nerves to the effector organ, the dilator pupillae muscle (E).

Normal pupil size: Pupil size ranges from approximately 1 mm (miosis) to approximately 8 mm (mydriasis).

❖ Pupils tend to be wider in teenagers and in darkness. They are also wider with joy, fear, or surprise due to increased sympathetic tone, and when the person inhales deeply.

❖ Pupils tend to be narrower in the newborn due to parasympathetic tone, in the elderly due to decreased mesencephalic inhibition and sympathetic diencephalic activity, in light, during sleep, and when the person is fatigued (due to decreased sympathetic activity).

Nucleus Perlia

9.2 Examination Methods

Complete examination of the pupilincludes testing direct and indirect light reflexes, the swinging flashlight test, testing the near reflex, and morphologic evaluation of the iris. A synopsis of all findings is required to determine whether a disorder is due to ocular or cerebral causes (see 9.4).

9.2.1 Testing the Light Reflex (Table 9.1)

Light reflex is tested in subdued daylight where the pupil is slightly dilated. The patient gazes into the distance to neutralize near-field miosis.

Direct light reflex: The examiner first covers both of the patient's eyes, then uncovers one eye. Normally the pupil will constrict after a latency period of about 0.2 seconds. The other eye is tested in the same manner.

Indirect or consensual light reflex: The examiner separates the patient's eyes by placing his or her hand on the bridge of the patient's nose. This pre-

Table 9.1 Characteristic pupil findings in unilateral lesions of the pupillary reflex pathway

Localization of the lesion (unilateral)

Direct light reflex

Indirect light reflex ipsilateral contralateral

Swinging flashlight test

Findings

Afferent pupillary pathway .. (optic nerve, retina)

Slight lesion

\ Severe lesion

+

++ ++

+

Slight constrictions, quicker dilation

Dilation

Isocoria

Efferent pupil-lary pathway \

Oculomotor lesion

Ciliary ganglion lesion

+

+

Delayed constriction, delayed dilation

^^^^ Anisocoria

NI NI NI

Legend: - = response absent, + = weak response, ++ = strong response

NI NI NI

Legend: - = response absent, + = weak response, ++ = strong response vents incident light from directly striking the eye being examined, which would elicit a direct light reflex. The examiner then illuminates the other eye while observing the reaction of the covered, non-illuminated eye. Normally both pupils will constrict, even in the non-illuminated eye.

Swinging flashlight test: This test is used to diagnose a discrete unilateral or unilaterally more pronounced sensory deficit in the eye (optic nerve and/or retina). Often damage to the optic nerve or retina is only partial, such as in partial atrophy of the optic nerve, maculopathy, or peripheral retinal detachment. In these cases, the remaining healthy portions of the afferent pathway are sufficient to trigger constriction of the pupil during testing of the direct light reflex. This constriction will be less than in the healthy eye but may be difficult to diagnose from discrete pupillary reflex findings alone. Therefore, the reflexive behavior of both eyes should be evaluated in a direct comparison to detect differences in the rapidity of constriction and subsequent dilation. This is done by moving a light source alternately from one eye to the other in what is known as a swinging flashlight test.

Reproducible results can only obtained if the examiner strictly adheres to this test protocol:

❖ The patient focuses on a remote object in a room with subdued light. This neutralizes convergence miosis, and the pupils are slightly dilated, making the pupillary reflex more easily discernible.

❖ The examiner alternately illuminates both eyes with a relatively bright light, taking care to maintain a constant distance, duration ofillumination, and light intensity so that both eyes must adapt to the same conditions.

❖ The examiner evaluates the initial constriction upon illumination and the subsequent dilation of the pupil.

Where the pupil constricts more slowly and dilates more rapidly than in the fellow eye, one refers to a relative afferent pupillary defect. The defect is "relative" because the difference in pupillary reflex only occurs when there is a difference in the sensory defect to the left and right eyes.

9.2.2 Evaluating the Near Reflex

The near reflex triad consists of:

1. Convergence of the visual axes.

2. Accommodation.

3. Constriction of the pupils (miosis).

The near reflex is tested by having the patient focus on a distant object and then on an object in the near field. Usually this is the patient's finger, which is brought to within 10 cm of the eyes. The near reflex is intact if both eyes continuously converge with accommodation and miosis appropriate for the patient's age as the object is moved to within 10 cm of the eyes. The examiner should take care to avoid illuminating the pupil, which will produce a light reflex with miosis.

9.3 Influence of Pharmacologic Agents on the Pupil

Table 9.2 Influence of pharmacologic agents on the pupil

Substance group and individual active ingredients

Mechanism and duration of action

Indication and special considerations

Miotics

Parasympathomimetics

❖ Direct parasympathomimetics

- Act on acetylcholine receptors of the sphincter pupillae muscle (miosis) and the ciliary muscle (increased accommodation)

Glaucoma therapy

- Acetylcholine

- Extremely short duration of action (several minutes)

Intraocular application only (cataract surgery); ineffective as eyedrops (rapid breakdown)

- Pilocarpine

- Effective for 5 - 7 hours

Standard medication in glaucoma therapy

- Aceclidine

- Effective for 5 - 7 hours

- Weaker miotic effect than pilocarpine

Standard medication in glaucoma therapy

- Carbachol

- Effective for 7 - 9 hours

- Stronger miotic effect than pilocarpine

Standard medication in glaucoma therapy

❖ Indirect parasym-pathomimetics

- Act by inhibiting acetyl-choline

Glaucoma therapy Side effects: cataract, iris cysts, may increase risk of retinal detachment; therefore not the medication of first choice in glaucoma therapy

- Physostigmine

- Effective for 2 - 3 days

- Prostigmin

- Effective for 1 day

9.3 Influence of Pharmacologic Agents on the Pupil 225 ' '

Table 9.2 (Continued)

Substance group and individual active ingredients

Mechanism and duration of action

Indication and special considerations

Mydriatics

Parasympatholytics

- Act by blocking acetylcholine receptors of the sphincter pupillae muscle (mydriasis) and the ciliary muscle (accommodation paralysis)

- Tropicamide

- Effective for approximately 4-6 hours (shortest acting mydri-atic)

Used for diagnostic purposes

- Cyclopentolate

- Effective for approximately 12-24 hours

- More cycloplegic than mydriatic

Used diagnostically for objective measurement of refraction Used therapeutically to relax the ciliary body (in iritis)

- Homatropine

- Effective for approximately 1 -2 days

Used therapeutically (in iritis)

- Scopolamine

- Effective for approximately 1 week

Used therapeutically for protracted mydriasis, for example following surgical repair of retinal detachment or in iridocy-clitis

- Atropine

- Effective for less than one week (longest acting mydriatic)

For all therapy requiring protracted mydriasis, for example following surgical repair of retinal detachment and in iridocyclitis

Sympathomimetics

❖ Direct sympathomimetics

- Act on the adrenaline receptors of the dilator pupillae muscle

Primarily for diagnostic purposes

Continued ^

Continued ^

- 226 9 Pupil Table 9.2 (Continued)

Substance group and Mechanism and duration Indication and special individual active ingre- of action considerations dients

Sympathomimetics

- Epinephrine

- Phenylephrine

Indirect sympathomimetics

! Drug-induced mydriasis is contrain-dicated in patients with a shallow anterior chamber due to the risk of acute angle closure glaucoma.

Only slightly effective; rapidly broken down by amino oxidases

Effective for approximately six hours (onset and duration of action identical to tropic-amide; see parasympatholytics) Advantage: does not cause accommodation paralysis

Inhibit reabsorption of norepinephrine

Effective for approximately six hours

Used in the diagnosis of Horner's syndrome and in intraocular application for better mydriasis during surgery

Used for diagnostic purposes due to its short duration of action

For diagnostic purposes

Today used as eyedrops only for diagnostic purposes and in Horner's syndrome

9.4 Pupillary Motor Dysfunction

Pupillary motor dysfunction must be distinguished from a number of differential diagnoses that include not only ocular disorders but neurologic and internal disorders. Diagnosis is difficult because isocoria or anisocoria are unspecific clinical symptoms. Therefore, functional tests are indicated to confirm the diagnosis. The following section uses diagrams of the initially presenting clinical symptoms to illustrate the various types of pupillary dysfunction. The text presents the differential diagnoses with the functional studies used to confirm the respective diagnosis.

Isocoria with constricted or dilated pupils is primarily of interest to the neurologist and less so the ophthalmologist. These disorders are therefore discussed at the end of the section.

9.4.1 Isocoria with Normal Pupil Size

Relative Afferent Pupillary Defect

Causes: Unilateral sensory disorder such as retinal detachment, neuritis of the optic nerve, atrophy of the optic nerve, or retinal vascular occlusion.

Diagnostic considerations:

❖ Direct light reflex is decreased or absent (relative afferent pupillary defect) in the affected eye.

❖ The consensual light reflex in the affected eye is weak or absent but normal in the unaffected eye.

❖ The swinging flashlight test reveals dilation in the affected eye when illuminated (Marcus Gunn pupil) or reduced constriction and earlier dilation in the presence of lesser lesions (afferent pupillary defect).

❖ Unilaterally reduced visual acuity and/or field of vision.

Unilateral blindness (afferent defect) does not produce anisocoria.

Bilateral Afferent Pupillary Defect

Causes: Bilateral sensory disorder such as maculopathy or atrophy of the optic nerve.

Diagnostic considerations:

❖ Delayed direct and consensual light reflexes.

❖ The swinging flashlight test produces identical results in both eyes (where disorder affects both sides equally).

❖ Bilaterally reduced visual acuity and/or field of vision.

Anisocoria with Dilated Pupil in the Affected Eye

Complete Oculomotor Palsy Causes:

❖ Processes in the base of the skull such as tumors, aneurysms, inflammation, or bleeding.

Diagnostic considerations:

❖ Direct and consensual light reflexes without constriction in the affected eye (fixed pupil).

❖ Near reflex miosis is absent.

❖ Impaired motility and double vision.

H Sudden complete oculomotor palsy (loss of motor and parasympathetic function) is a sign of a potentially life-threatening disorder. In unconscious patients, unilateral mydriasis is often the only clinical sign of this.

Tonic Pupil

Causes: Postganglionic damage to the parasympathetic pathway, presumably in the ciliary ganglion, that frequently occurs with diabetes mellitus, alcoholism, viral infection, and trauma.

Diagnostic considerations:

❖ Direct and consensual light reflexes show absent or delayed reaction, possibly with worm-like segmental muscular contractions.

❖ Dilation is also significantly delayed.

❖ Near reflex is slow but clearly present; accommodation with delayed relaxation is present.

❖ Motility is unimpaired.

❖ Pharmacologic testing with 0.1 % pilocarpine.

- Significant miosis in the affected eye (denervation hypersensitivity).

- No change in the pupil of the unaffected eye (too weak).

❖ Adie's tonic pupil syndrome: The tonic pupil is accompanied by absence of the Achilles and patellar tendon reflexes.

H Tonic pupil is a relatively frequent and completely harmless cause of unilateral mydriasis.

Iris Defects Causes:

❖ Trauma (aniridia or sphincter tears).

❖ Secondary to acute angle closure glaucoma.

❖ Synechiae (post-iritis or postoperative).

Diagnostic considerations: Patient history and slit-lamp examination.

Following Eyedrop Application (Unilateral Administration of a Mydriatic)

Simple anisocoria

Causes: Presumably due to asymmetrical supranuclear inhibition of the Edinger-Westphal nucleus.

Diagnostic considerations:

❖ Direct and consensual light reflexes and swinging flashlight test show constant difference in pupil size.

❖ Pharmacologic testing: Cocaine test (4% cocaine eyedrops are applied to both eyes and pupil size is measured after one hour): bilateral pupil dilation indicates an intact neuron chain.

9.4.3 Anisocoria with a Constricted Pupil in the Affected Eye

Horner's Syndrome

Causes: Damage to the sympathetic pathway.

- Encephalitis.

- Diffuse encephalitis.

❖ Peripheral (second neuron):

- Syringomyelia.

- Diffuse encephalitis.

- Rhinopharyngeal tumors.

- Aneurysm.

- Processes in the tip of the lung.

❖ Peripheral in the strict sense (third neuron):

- Vascular processes.

- Internal carotid aneurysm.

Clinical Picture:

❖ Miosis (approximately 1 -2 mm difference) due to failure of the dilator pupillae muscle.

❖ Ptosis (approximately 1 - 2 mm difference) due to failure of the muscle of Müller.

❖ Enophthalmos due to failure of the rudimentary lower eyelid retractors. This makes the lower eyelid project so that the eye appears smaller. This condition only represents a type of pseudoenophthalmos.

❖ Decreased sweat gland secretion (only present in preganglionic disorders as the sweat glands receive their neural supply via the eternal carotid).

Diagnostic considerations:

❖ Direct and consensual light reflexes are intact, which distinguishes this disorder from a parasympathetic lesion); the pupil dilates more slowly (dilation deficit).

❖ Pharmacologic testing with cocaine eyedrops:

- Peripheral Horner's syndrome: On the affected side, there is slight mydriasis (decrease in norepinephrine due to nerve lesion). On the unaffected side, there is significant mydriasis.

- Central Horner's syndrome: On the affected side, the pupil is dilated. On the unaffected side, the pupil is also dilated (the norepinephrine in the synapses is not inhibited).

Following Eyedrop Application (Unilateral Administration of a Miotic as in Glaucoma Therapy)

9.4.4 Isocoria with Constricted Pupils

Argyll-Robertson Pupil

Causes: The precise location of the lesion is not known; presumably the disorder is due to a lesion is in the pretectal region and the Edinger-Westphal nucleus such as tabes dorsalis (Argyll-Robertson phenomenon), encephalitis, diffuse encephalitis, syringomyelia, trauma, bleeding, tumors, and alcoholism.

Diagnostic considerations:

❖ Direct and consensual light reflexes are absent.

❖ Near reflex is intact or there is overcompensation (the Edinger-Westphal nucleus is being controlled via the convergence center).

❖ The pupil is not round, and constriction is not always symmetrical.

❖ There is no reaction to darkness or pharmacologic stimuli.

Bilateral Pupillary Constriction due to Pharmacologic Agents

Causes:

❖ Deep general anesthesia.

❖ Pilocarpine eyedrops.

Toxic Bilateral Pupillary Constriction Causes: Mushroom poisoning.

Inflammatory Bilateral Pupillary Constriction

Causes:

❖ Encephalitis.

9.3.5 Isocoria with Dilated Pupils

Parinaud's Oculoglandular Syndrome

Causes: Tumors such as pineal gland tumors that selectively damage fibers between the pretectal nuclei and the Edinger-Westphal nucleus.

Diagnostic considerations:

❖ Fixed dilated pupils that do not respond to light.

❖ Limited upward gaze (due to damage to the vertical gaze center) and retraction nystagmus.

- 232 9 Pupil Intoxication

Causes: Atropine, spasmolytic agents, anti-parkinson agents, antidepres-sants, botulism (very rare but important), carbon monoxide, cocaine.

Disorders

Migraine. Schizophrenia. Hyperthyreosis. Hysteria. Epileptic seizure.

Increased sympathetic tone (Bumke's anxiety pupils). Coma. Agony.

10.1 Basic Knowledge Definition

Glaucoma is a disorder in which increased intraocular pressure damages the optic nerve. This eventually leads to blindness in the affected eye.

❖ Primary glaucoma refers to glaucoma that is not caused by other ocular disorders.

❖ Secondary glaucoma may occur as the result of another ocular disorder or an undesired side effect of medication or other therapy.

Epidemiology: Glaucoma is the second most frequent cause of blindness in developing countries after diabetes mellitus. Fifteen to twenty per cent of all blind persons lost their eyesight as a result of glaucoma. In Germany, approximately 10% of the population over 40 has increased intraocular pressure. Approximately 10% of patients seen by ophthalmologists suffer from glaucoma. Of the German population, 8 million persons are at risk of developing glaucoma, 800 000 have already developed the disease (i.e., they have glaucoma that has been diagnosed by an ophthalmologist), and 80 000 face the risk of going blind if the glaucoma is not diagnosed and treated in time.

H Early detection of glaucoma is one of the highest priorities for the public health system.

Physiology and pathophysiology of aqueous humor circulation (Fig. 10.1): The average normal intraocular pressure of 15 mm Hg in adults is significantly higher than the average tissue pressure in almost every other organ in the body. Such a high pressure is important for the optical imaging and helps to ensure several things:

❖ Uniformly smooth curvature of the surface of the cornea.

❖ Constant distance between the cornea, lens, and retina.

❖ Uniform alignment of the photoreceptors of the retina and the pigmented epithelium on Bruch's membrane, which is normally taut and smooth.

The aqueous humor is formed by the ciliary processes and secreted into the posterior chamber of the eye (Fig. 10.1 [A]). At a rate of about 2-6^l per

234 10 Glaucoma Physiology of aqueous humor circulation.

234 10 Glaucoma Physiology of aqueous humor circulation.

Open Angle Glaucoma Anatomy
Fig. 10.1 As it flows from the nonpigmented cells of the ciliary epithelia ® to beneath the conjunctiva ©, the aqueous humor overcomes physiologic resistance from two sources: the resistance of the pupil (B)and the resistance of the trabecular meshwork ©•

minute and a total anterior and posterior chamber volume of about 0.2 - 0.4 ml, about 1 - 2% of the aqueous humor is replaced each minute.

The aqueous humor passes through the pupil into the anterior chamber. As the iris lies flat along the anterior surface of the lens, the aqueous humor cannot overcome this pupillary resistance (first physiologic resistance; Fig. 10.1 [B]) until sufficient pressure has built up to lift the iris off the surface of the lens. Therefore, the flow of the aqueous humor from the posterior chamber into the anterior chamber is not continuous but pulsatile.

Any increase in the resistance to pupillary outflow (pupillary block) leads to an increase in the pressure in the posterior chamber; the iris inflates anteriorly on its root like a sail and presses against the trabecular meshwork (Table 10.2). This is the pathogenesis of angle closure glaucoma.

Various factors can increase the resistance to pupillary outflow (Table 10.1 ). The aqueous humor flows out of the angle of the anterior chamber through two channels:

❖ The trabecular meshwork (Fig. 10.1 [C]) receives about 85% of the outflow, which then drains into the canal of Schlemm. From here it is con-

Table 10.1 Factors that increase resistance to pupillary outflow and predispose to angle closure glaucoma

Increased contact between

❖ Small eyes

the margin of the pupil and

❖ Large lens (increased lens volume) due to:

lens with:

- Age (lens volume increases with age by a

factor of six)

- Diabetes mellitus (osmotic swelling of the

lens)

❖ Miosis

- Age (atrophy of the sphincter and dilator

muscles)

- Medications (miotic agents in glaucoma

therapy)

- Iritis (reactive miosis)

- Diabetic iridopathy (thickening of the iris)

❖ Posterior synechiae (adhesions between lens

and iris)

Increased viscosity of the

❖ Inflammation (protein, cells, or fibrin in the

aqueous humor with:

aqueous humor)

❖ Bleeding (erythrocytes in the aqueous humor)

ducted by 20-30 radial collecting channels into the episcleral venous plexus (D).

❖ A uveoscleral vascular system receives about 15% of the outflow, which joins the venous blood (E). The trabecular meshwork (C) is the second source of physiologic resistance.

The trabecular meshwork is a body of loose sponge-like avascular tissue between the scleral spur and Schwalbe's line. Increased resistance in present in open angle glaucoma.

Classification: Glaucoma can be classified according to the specific pathophysiology (Table 10.2).

H The many various types of glaucoma are nearly all attributable to increased resistance to outflow and not to heightened secretion of aqueous humor.

236 10 Glaucoma Table 10.2 Classification of glaucoma

Form of

Incidence

glaucoma

Open angle glaucoma

Primary

Over 90% of all glaucomas

Secondary

Angle closure Primary glaucoma (pupillary block glaucoma)

Secondary

2 -4% of all glaucomas

About 5% of all glaucomas

2-4%ofall glaucomas

Juvenile glaucoma

1% of all glaucomas

Absolute This is not a separate form of glaucoma, rather it describes an glaucoma often painful eye blinded by glaucoma

(gonioscopy)

Outflow impediment

Open

Completely open. Structures appear normal.

In the trabecular meshwork

Open

Completely open. Trabecular meshworks and secondary occluding cells visible.

Erythrocytes, pigment, and inflammatory cells occlude the trabecular meshwork.

Blocked

Occluded. No angle structures visible

Iris tissue occludes the trabecular meshwork.

Blocked

Occluded. No angle structures visible. Occluding structures visible.

Displacement of the trabecular meshwork produces anterior synechiae, scarring, and neovascularization (rubeosis iridis)

Undifferentiated

Open. Occluding embryonic tissue and lack of differentiation visible.

In the trabecular meshwork (which is not fully differentiated and/or is occluded by embryonic tissue)

10.2 Examination Methods

10.2.1 Oblique Illumination of the Anterior Chamber

The anterior chamber is illuminated by a beam of light tangential to the plane of the iris. In eyes with an anterior chamber of normal depth, the iris is uniformly illuminated. This is a sign of a deep anterior chamber with an open angle (see Fig. 1.12).

In eyes with a shallow anterior chamber and an angle that is partially or completely closed, the iris protrudes anteriorly and is not uniformly illuminated (see Fig. 1.12).

10.2.2 Slit-Lamp Examination

The central and peripheral depth of the anterior chamber should be evaluated on the basis of the thickness of the cornea. An anterior chamber that is less than three times as deep as the thickness of the cornea in the center with a peripheral depth less than the thickness of the cornea suggests a narrow angle (Fig. 10.2). Gonioscopy is essential for further evaluation.

H To evaluate the depth of the anterior chamber with a slit-lamp biomicroscope, select a narrow setting for the light beam. The beam should strike the eye at a slight angle to the examiner's line of sight.

10.2.3 Gonioscopy

The angle of the anterior chamber is evaluated with a gonioscope placed directly on the cornea (Fig. 10.3a and b).

— Slit-lamp examination to evaluate the depth of the anterior chamber. -

Fig. 10.2 The depth of the anterior chamber is less than the thickness of the cornea on its periphery. The corneal reflex and iris reflection touch each other (arrow), indicating a shallow anterior chamber. Gonioscopy is indicated.

— Slit-lamp examination to evaluate the depth of the anterior chamber. -

Slit Lamp Acute Congestive Glaucoma
— Gonioscopy and morphology of the angle structures.
Closed Angle Glaucoma Gonioscopy
b

Gonioscopy can differentiate the following conditions:

❖ Open angle: open angle glaucoma.

❖ Occluded angle: angle closure glaucoma.

❖ Angle access is narrowed: configuration with imminent risk angle of an acute closure glaucoma.

❖ Angle is occluded: secondary angle closure glaucoma, for example due to neovascularization in rubeosis iridis.

❖ Angle open but with inflammatory cellular deposits, erythrocytes, or pigment in the trabecular meshwork: secondary open angle glaucoma.

H Gonioscopy is the examination of choice for identifying the respective presenting form of glaucoma.

10.2.4 Measuring Intraocular Pressure

Palpation (Fig. 1.15, p. 15): Comparative palpation of both eyeballs is a preliminary examination that can detect increased intraocular pressure.

❖ If the examiner can indent the eyeball, which fluctuates under palpation, pressure is less than 20 mm Hg.

❖ An eyeball that is not resilient but rock hard is a sign of about 60 - 70 mm Hg of pressure (acute angle closure glaucoma).

Schiotz indentation tonometry (Figs. 10.4a and b): This examination measures the degree to which the cornea can be indented in the supine patient. The lower the intraocular pressure, the deeper the tonometer pin sinks and the greater distance the needle moves.

Indentation tonometry often provides inexact results. For example the rigidity of the sclera is reduced in myopic eyes, which will cause the tonometer pin to sink more deeply for that reason alone. Because of this, indentation tonometry has been largely supplanted by applanation tonometry.

Applanation tonometry: This method is the most common method of measuring intraocular pressure. It permits the examiner to obtain a measurement on a sitting patient within a few seconds (Goldmann's method, see Fig. 10.5 a-c) or on a supine patient (Draeger's method). A flat tonometer tip has a diameter of 3.06 mm for applanation of the cornea over a corresponding area (7.35 mm2). This method eliminates the rigidity of the sclera as a source of error (see also tonometric self-examination).

Intraocular pressure of 22 mm Hg is regarded as suspicious. Caution: Infection is possible in the presence of conjunctivitis.

Pneumatic non-contact tonometry: The electronic tonometer directs a 3 ms blast of air against the cornea. The tonometer records the deflection of the cornea and calculates the intraocular pressure on the basis of this deformation.

Schiotz indentation tonometry.

Schiotz indentation tonometry.

Indentation Tonometry

Fig. 10.4 a The tonometer is placed on the anesthetized cornea. The examiner retracts both eyelids and the patient focuses on his or her thumb with the other eye.

b Detail view of the tonometer pin indenting the cornea. The harder the eyeball, the shallower the indentation and the smaller the movement of the indicator needle.

Fig. 10.4 a The tonometer is placed on the anesthetized cornea. The examiner retracts both eyelids and the patient focuses on his or her thumb with the other eye.

b Detail view of the tonometer pin indenting the cornea. The harder the eyeball, the shallower the indentation and the smaller the movement of the indicator needle.

Advantages:

❖ Does not require the use of a topical anesthetic.

❖ Non-contact measurement eliminates risk of infection (may be used to measure intraocular pressure in the presence of conjunctivitis).

Disadvantages:

❖ Calibration is difficult.

❖ Precise measurements are possible only within low to middle range pressures.

❖ Cannot be used in the presence of corneal scarring.

❖ Examination is unpleasant for the patient.

❖ The instrument is more expensive to purchase than an applanation tonometer.

242 10 Glaucoma Goldmann applanation tonometry.

Cornea Labeled Through Slit Lamp

a Slit-lamp measurement of intraocular pressure: After application of anesthetizing eyedrops containing fluorescein, the tonometer tip is placed on the cornea.

c View through a slit lamp: The pressure reading is taken when the two inner menisci of the fluorescein arcs touch (arrow).

a Slit-lamp measurement of intraocular pressure: After application of anesthetizing eyedrops containing fluorescein, the tonometer tip is placed on the cornea.

b The cornea is applanated (flattened) over an area measuring precisely 7.35 mm2. The external pressure required is directly proportional to intraocular pressure.

c View through a slit lamp: The pressure reading is taken when the two inner menisci of the fluorescein arcs touch (arrow).

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