A Textbook of Clinical Pharmacology and Therapeutics

to cause pupillary dilatation, namely muscarinic antagonists
(anticholinergics) and sympathomimetics. Short-acting
relatively weak mydriatics, such as tropicamide, facilitate ret-
inalexamination.Cyclopentolateandatropineare preferred
for producing cycloplegia (paralysis of the ciliary muscle) for
refraction in young children. Atropineis also used for the treat-
ment of iridocyclitis mainly to prevent posterior synechiae,
when it is often combined with phenylephrine.
Table 52.2 shows some commonly used agents, their recep-
tor effects, dose schedule and toxicity. Agents that dilate the
pupil may abruptly increase the intra-ocular pressure in
closed-angle glaucoma by causing obstruction to the outflow
tract, and are contraindicated in this condition. Patients
should be asked whether they are driving before having their
pupils dilated and should be warned not to drive afterwards
until their vision has returned to normal.

DRUGS USED TO CONSTRICT THE PUPIL

AND TO TREAT GLAUCOMA

PHYSIOLOGY OF AQUEOUS HUMOUR DYNAMICS

AND REGULATION OF INTRA-OCULAR PRESSURE

Aqueous humour is produced at a rate of 2–2.5 mL per minute

and flows from the posterior chamber through the pupil into the

anterior chamber. Around 80–95% of it exits via the trabecular

meshwork and into the canal of Schlemm and subsequently into

the episcleral venous plexus and eventually into the systemic

circulation. Fluid can also flow via the ciliary muscles into the

suprachoroidal space. The geometry of the anterior chamber dif-

ferentiates the two forms of glaucoma, namely open-angle glau-

coma (the more common form) and angle-closure glaucoma

(closed-angle glaucoma). Open-angle glaucoma is usually

treated medically in the first instance, by reducing aqueous

humour flow and/or production. Closed-angle glaucoma is

treated by iridectomy following urgent medical treatment to

reduce the intra-ocular pressure in preparation for surgery.

PRINCIPLES OF THERAPY FOR GLAUCOMA

Acute glaucoma is a medical emergency. Mannitolcan reduce

the intra-ocular pressure acutely by its osmotic effect. In add-

ition, therapy with a carbonic anhydrase inhibitor (intra-

venous acetazolamide or topical dorzolamide) may be

required. This is then supplemented with either a topical

β-adrenergic antagonist (e.g. timolol) or a cholinergic agonist

(e.g.pilocarpine), or both.

DRUGSUSED TOCONSTRICT THEPUPIL AND TOTREATGLAUCOMA 425

Tears

Conjunctiva

Sclera

Ciliary body

Systemic circulation

Iris

Aqueous humour

Cornea

Figure 52.2:Potential absorption pathways for drugs applied to
the eye.

Table 52.2:Drugs commonly used to dilate the pupil

Drug Receptor Dose, onset of mydriasis Toxicity and other

and schedule comments

Anticholinergics

Tropicamide Single drop of 0.5% solution, Photosensitivity, blurred vision and

maximum onset of effect is systemic absorption can occur

in 20–40 min and lasts 3–6 h

Cyclopentolate All anticholinergics are Single drops of 0.5 or 1.0% As for tropicamide

antagonists at the solution, maximum onset of

M 3 receptor on the effect is in 30–60 min and

ciliary muscle lasts 24 h

Atropine Single drop of 0.5 or 1.0% As for tropicamide

solution, maximum onset of

effect is 30–40 min and

lasts 7–10 days

Sympathomimetics

Phenylephrine One of two drops of 10% Systemic absorption can occur (avoid in

solution, lasts up to 12 h patients with coronary artery disease

or hypertension)