CONTACT LENS WEARERS
As the number of patients who wear contact lenses increases,
an awareness has developed that these patients represent a
special subgroup in whom particular care is needed when
prescribing, as they may develop specific additional problems
related to commonly prescribed drugs. A summary of such
agents is given in Table 52.6.
FURTHER READING
Ghate D, Edelhauser HF. Ocular drug delivery. Expert Opinion on Drug
Delivery2006; 3 : 275–87.
Marquis RE, Whitson JT. Management of glaucoma: focus on pharma-
cological therapy. Drugs and Aging2005; 22 : 1–21.
CONTACTLENSWEARERS 429
Table 52.6:Common drug-induced problems in patients with contact lenses
Drug Adverse effects Comment
Oral contraceptives (high oestrogen) Swelling of the corneal surface – poorly Visual acuity deterioration
fitting lenses
Anxiolytics, hypnotics, first-generation Reduced rate of blinking Dry eyes and higher risk of infections
antihistamines (e.g.
diphenhydramine, etc.)
Antihistamines, anticholinergics, Reduced lacrimation Dry eyes – irritation and burning
phenothazines, diuretics and
tricyclic antidepressants
Hydralazine and ephedrine Increased lacrimation
Isotretinoin, aspirin Conjunctival inflammation and irritation
Rifampicin and sulfasalazine Discolour lenses
Case history
A 68-year-old man has hypertension and ischaemic heart
disease. His angina and blood pressure are well controlled
while taking oral therapy with bendroflumethiazide, 2.5 mg
daily, and slow-release diltiazem 120 mg daily. His visual
acuity gradually declines and he is diagnosed as having sim-
ple open-angle glaucoma. His ophthalmologist starts ther-
apy with pilocarpine 2% eye drops, one drop four times a
day, and carteolol drops, two drops twice a day. A week
after starting to see his ophthalmologist he attends his GP’s
surgery complaining of shortness of breath on exertion,
paroxysmal nocturnal dyspnoea and othopnoea. Clinical
examination reveals a regular pulse of 35 beats per minute,
blood pressure of 158/74 mmHg and signs of mild left ven-
tricular failure. His ECG shows sinus bradycardia with no evi-
dence of acute myocardial infarction.
Question
How can you explain this problem and what should your
management be?
Answer
Carteolol is a non-selective β-adrenergic antagonist that can
gain access to the systemic circulation via the nasolachrymal
apparatus thus avoiding heptic first-pass metabolism. It can
thus act (especially in conjunction with a calcium antagonist –
diltiazem in this case) on the cardiac conducting system and
on the working myocardium. Discontinuing the ocular carte-
olol should resolve the problem.
Key points
Drugs used to lower intra-ocular pressure
- Systemic administration of:
- osmotic agents (e.g. mannitol);
- acetazolamide (carbonic anhydrase inhibitor).
- Topical administration of:
- pilocarpine (muscarinic agonist);
- timolol (β-adrenoceptor antagonist);
- dorzolamide (carbonic anhydrase inhibitor);
- latanoprost (PGF 2 αanalogue);
- brimonidine (α 2 -agonist).