Ординатура / Офтальмология / Английские материалы / Ophthalmic Drugs Diagnostic and Therapeutic Uses 5th edition_Hopkins, Pearson_2007

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Chapter 7

Mydriatics

Mydriatics dilate the pupil to facilitate a more thorough examination of the fundus, lens periphery and vitreous. They are mostly used on elderly patients, as older pupils are usually smaller and lens opacities and abnormal retinal conditions are not uncommon. However, the use of mydriatics can be essential in any age group, especially where the macula or the peripheral areas of the retina need particularly careful observations, for example, suspected macular cyst or hole, location of a penetrating foreign body, intraocular tumours, peripheral detachments. Martin-Doyle (1967) considers the instillation of a mydriatic indispensable for an adequate examination of the macula. Siderov et al (1996) examined patients’ attitudes to pupil dilatation during optometric examination and found that the majority were in favour, although a large proportion suffered adverse effects such as glare and blurring of vision.

IDEAL PROPERTIES OF MYDRIATICS

•Quick in onset.

•Adequate duration.

•Fast recovery after examination.

•Light reflex abolished.

•No cycloplegia.

•Capable of quick reversal in an emergency.

•No rise in intraocular pressure.

•No other pharmacological effect.

•No local toxic reaction.

•No systemic toxic reaction.

•No adverse subjective complaints such as ‘stinging’.

The indications and contraindications for mydriatic examination have been admirably summarized by Havener (1975).

INDICATIONS FOR MYDRIATIC EXAMINATION

Those occasions when there is a special need for a thorough fundus inspection through a dilated pupil, where the latter does not already exist, include the following:

•Recent onset of floating vitreous opacities, especially if accompanied by the symptoms of flashing light.

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•Relatively sudden decrease in visual acuity.

•Unexplained loss of visual field.

•Unexplained ocular pain, unaccompanied by raised intraocular pressure.

•Redness of the eye that cannot be attributed to infection, allergy, or raised intraocular pressure.

•After contusion, to exclude the presence of ocular damage.

•Difficulty in observing the fundus due to reduced transparency of the media.

•Diabetic patients – annually as a general rule.

•Fundus photography, although some cameras are now designed to be non-mydriatic.

•Aberrometry measurements, which currently require a 6-mm pupil diameter, in patients undergoing refractive surgery with a wavefrontbased procedure. It is pertinent to note here that in some patients the use of a mydriatic causes a significant change in the location of the pupil centre (Yang et al 2002).

Note: as well as their diagnostic uses, mydriatics also have therapeutic indications. In the treatment of anterior uveitis, cycloplegics are used as the adjunctive therapy and are sometimes replaced at a later stage, as the condition resolves, with a drug having only a mydriatic effect.

Only some patients need mydriatic examination. If none of the specific ocular signs or symptoms enumerated above is present, or if the patient has a (systemic) disease not known to produce eye manifestations, a reasonable view of the optic disc and retinal vessels through the undilated pupil might be considered an adequate examination. Spontaneously large pupils are commonly found in many young people, conveniently permitting a relatively thorough fundus examination. It is usually with the older age groups, with their smaller pupils, that mydriatics are on occasion necessary. In his typically succinct style, Havener aptly compares ‘the view of a fundus through a small pupil or a dilated pupil with the view of a room as seen through a keyhole or with the door open’.

Adequate dilation of the pupils reveals small details of great diagnostic significance, for example, diabetic microaneurysms, hypertensive arteriolar attenuation, early signs of macular degeneration, small traumatic retinal holes, peripheral retinal lesions. Newell (1969) emphasizes an important clinical principle when he comments that ‘there is more danger of missing significant ocular or systemic disease by failing to dilate than there is of precipitating glaucoma by dilatation’. This ‘approach’ is reflected in Havener’s remark that ‘a physician who dilates many eyes may expect to precipitate not more than one case of acute glaucoma in a lifetime’. It is to be hoped that such views expressed by eminent authorities, taken in conjunction with the precautions listed in the following contraindications, will give optometric students and practitioners a balanced attitude to the use of mydriatics in appropriate cases. Optometrists have a moral and legal duty to refer pathological conditions (ocular or systemic) for medical attention; they will be unable to do this unless they can ‘see’ such conditions in the first instance.

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Figure 7.1 The penlight test for assessment of limbal anterior chamber depth. Grade 4 represents the greatest depth and Grade1 the least depth (adapted from Pearson 2003).

Table 7.1 Grading of anterior chamber based on the flashlight and Van Herick methods, interpretation of results and corresponding decision on the use by the optometrist of a mydriatic

Van Herick et al (1969) and subsequently Polse (1975) and Stone (1979) described how a very narrow slit-lamp microscope beam is directed perpendicularly to the corneal surface at the temporal limbus to form an optic section. Observation is made with the microscope, using a magnification of ×16 to ×20, placed at an angle of 60° to the illumination system. A fixation target is selected such that the patient’s gaze is directed in the primary position. An assessment is made of width of the dark space representing the interval between the iris and the posterior corneal surface, relative to the width of the corneal section. A fraction is recorded in which the numerator is the width of the dark space and the denominator is the width of the optic section (Fig. 7.2).

The nasal depth of the anterior chamber can be similarly assessed. In some cases, the presence of arcus senilis makes it difficult to determine

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Notwithstanding the low prevalence of very narrow anterior chambers, the fear of precipitating acute angle-closure glaucoma has tended to deter non-ophthalmologists from dilating pupils. The incidence of angleclosure glaucoma secondary to pupil dilation has been the subject of a study by Patel et al (1995). Of 4870 subjects whose pupils were dilated, none developed this complication despite the fact that 38 patients were subsequently judged to have occludable angles on the basis of gonioscopic examination. It follows that identification of patients as having a potentially occludable angle means that their pupils should be dilated with caution and not that the angle will occlude as a result of a single dilated examination. Patel et al acknowledged that their subjects were predominantly of either European or African descent and that their findings might not be generalizable to the Asian population, in whom angle-closure glaucoma is reportedly more common.

Patel et al (1995) made the significant comment that ‘the potential risk to the patient of dilated ophthalmoscopic examination is low, and the benefits may include preservation of sight or even life’.

MODE OF ACTION

Because of the presence of the two opponent muscles, the pupil sphincter and dilator muscles, there are two different modes of action of mydriatics: sympathetic and parasympathetic (Table 7.3). The pupil dilator muscle is innervated by the sympathetic nervous system and sympathomimetic drugs will cause a contraction of the dilator muscle causing mydriasis. The parasympathetic system is largely unaffected by such drugs and thus the pupillary light reflex remains active. Sympathomimetic drugs also have little effect on accommodation.

However, the pupil sphincter muscle, which is innervated by the parasympathetic system, can be paralysed by the same class of drugs that causes cycloplegia: the antimuscarinic agents. With this type of drug the pupillary light reflex is reduced or abolished.

Irrespective of the type of mydriatic employed, when a mydriatic is applied unilaterally the light reflex in the other eye is unaffected and the mydriasis in the treated eye is accompanied by a consensual miosis. That this miosis is a result of the light reflex is confirmed by the fact that the consensual miosis is not manifest when the pupil diameters are measured in darkness (Theofilopoulos et al 1988). It is usual practice to dilate both eyes and this effect will have little significance unless the clinician is trying to assess the amount of anisocoria.

ANTIMUSCARINIC MYDRIATICS (ANTICHOLINERGICS)

By using weak concentrations of ‘strong drugs’ (e.g. homatropine) or ‘weak drugs’ (e.g. tropicamide) of the antimuscarinic group, not only can mydriasis be produced with a much less profound cycloplegia, but its attendant incapacitating effect on near vision is considerably reduced, as the pupil sphincter is more susceptible than the ciliary muscle to these substances.

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TROPICAMIDE

Tropicamide is the antimuscarinic mydriatic of choice today. Normally available in 0.5% and 1.0% strengths, the weaker solution is used most often for mydriasis; the 1% strength is used for cycloplegia. Davidson (1976) states that the mydriatic effect is greater than the cycloplegic effect and that this propensity for mydriasis is of clinical value. Tropicamide is quick in onset and short in duration, and the depth of mydriasis is adequate for most examinations because the pupil light reflex is depressed, facilitating indirect ophthalmoscopy and retinal photography. Pollack et al (1981) investigated the dose/response relationships of tropicamide’s mydriasis and cyloplegia under two levels of illumination. They found that the mydriatic effect was independent of dose (range 0.25–1.0%) and level of illumination whereas the cycloplegic effect was greater for the stronger concentrations.

This finding confirms that 0.5% tropicamide should be used for mydriasis and 1% for cycloplegia. Pollack et al studied patients with a range of eye colours but did not collate the findings for different degrees of pigmentation. Hence it is possible that the strength might need to be varied with the level of pigmentation. If necessary, a second drop can be applied 5 min after the first. The mydriasis caused by tropicamide can be reversed, if necessary, with weak solutions of physostigmine.

Tropicamide can cause initial stinging. Few allergic or adverse systemic reactions have been reported but, if the patient is taking any systemic drug with an antimuscarinic action, the effect of tropicamide might be augmented.

OTHER ANTIMUSCARINIC MYDRIATICS

All cycloplegics can be used as mydriatics but the effect is usually too long lasting. The following have been used in the past:

Cyclopentolate The mydriatic concentration of cyclopentolate is 0.1% (compared with 0.5% and 1.0% for cycloplegia). However, this strength is no longer available and if cyclopentolate is used as a mydriatic then significant cycloplegia will accompany its use. Mydriasis commences in about 10 min and is maximal in about 30 min; the effect can last up to 24 hours (Davidson 1976). It produces similar mydriasis but more cycloplegia than homatropine. Cyclopentolate 1% is sometimes used pre-operatively to produce maximal mydriasis.

Homatropine At one time, homatropine was the principal mydriatic and was often used in mixtures such as homatropine and cocaine or homatropine and ephedrine. The mydriatic effect commences in 10–20 min and is maximal in 30–40 min. At 30 min, both light and accommodative reflexes are absent and an examination may be carried out. Recovery takes the same

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Another possible future development is the use of a prodrug to enhance the mydriatic effect and reduce the possibility of side-effects. Miller-Meeks et al (1991) evaluated the mydriatic effects of phenylephrine oxazolidine prodrug by comparing the mydriasis it produced after 30 min with that produced by viscolized solutions of phenylephrine. A 1% solution of the prodrug produced a markedly greater mydriasis than the 10% solution of phenylephrine.

The use of phenylephrine is contraindicated in conditions such as hypertension, coronary disease, hyperthyroidism and diabetes because it might interact with beta-blockers, monoamine oxidase inhibitors and tricyclic antidepressants. Adverse systemic reactions to phneylephrine include cardiac arrythmias and hypertension.

COCAINE

This alkaloid, derived from the leaves of Erythroxylum coca, is a colourless, crystalline substance, the official salt being the hydrochloride; maximum therapeutic dose 15 mg. Solubility of the alkaloid is 1 in 300 in water, and 1 in 10 in castor oil; solubility of the salt is 2 in 1 in water. Cocaine is a powerful local anaesthetic, blocking nerve conduction on topical application to sensory nerve endings, for example those in the corneal epithelium. The ophthalmic use of cocaine has declined very markedly along with most other medical uses because of its toxicity.

HYDROXYAMPHETAMINE HYDROBROMIDE (PAREDRINE, USA)

This white crystalline powder, soluble one-in-one in water, is a sympathomimetic agent with direct and indirect effects on adrenergic alphaand beta-receptors. It can be given in a single dose of up to 60 mg by mouth, 20 mg by intramuscular injection and 10 mg by intravenous injection.

Its main uses in general medicine are as a decongestant in nasal sprays, by intramuscular or intravenous injection to maintain blood pressure in spinal anaesthesia, and for its direct stimulatory effect on the heart in the treatment and prevention of bradycardia due to excessive carotid sinus irritability. When used as a mydriatic in 1–3% eyedrops, full mydriasis occurs in about 30–45 min and lasts 2–3 hours. It is of little clinical interest as it is not commercially available and there are superior drugs.

EPHEDRINE HYDROCHLORIDE

Ephedrine is a colourless crystalline alkaloid obtained from species of Ephedra or prepared synthetically. Both the alkaloid and the official hydrochloride salt, which can occur as a colourless crystalline substance or as white crystalline powder (with a maximum therapeutic dose of 60 mg) are soluble in water (1 in 36 and 1 in 4, respectively).