effects side ocular induced-Drug • 7 t Pa r

­production. This is the only autonomic drug that has been reported to cause decreased tear lysozymes. Mydriasis and paraly­ sis of accommodation are intended ocular effects resulting from topical ophthalmic application of hyoscine but may also occur from oral administration. This drug may elevate the intraocu­ lar pressure in open-angle glaucoma and can precipitate angleclosure glaucoma. Allergic reactions are not uncommon after topical ocular application. Transient impairment of ocular accommodation, including blurred vision and mydriasis, has also been reported following the application of transdermal hyoscine patches. Several case reports of unilateral dilated pupils with associated blurred vision and angle-closure glaucoma have been published, and inadvertent finger-to-eye contamination has been shown to be the cause.

Systemic side effects from topical ophthalmic use of hyoscine have been reported infrequently and are similar to those seen secondary to topical ophthalmic atropine. Toxic psychosis, how­ ever, especially in the elderly or visually impaired, has been reported in the literature and to the ­ational Registry.

References and Further Reading

Firth AY. Visual side-effects from transdermal scopolamine (hyoscine). Dev Med Child Neurol 48: 137–138, 2006.

Fraunfelder FT. Transdermal scopolamine precipitating narrow-angle ­glaucoma. N Engl J Med 307: 1079, 1982.

Gleiter CN, et al. Transdermal scopolamine and basal acid secretion. N Engl J Med 311: 1378, 1984.

Goldfrank L, et al. Anticholinergic poisoning. J Toxicol Clin Toxicol 19: 17, 1982.

Kortabarria RP, Duran JA, Chaco JR. Toxic psychosis following cycloplegic eyedrops. DICP. Ann Pharmacother 24: 708–709, 1990.

Lin YC. Anisocoria from trandermal scopolamine. Paediatr Anaesth 11: 626–627, 2001.

MacEwan GW, et al. Psychosis due to transdermally administered scopolamine. Can Med Assoc J 133: 431, 1985.

McBride WG, Vardy PN, French J. Effects of scopolamine hydrobromide on the development of the chick and rabbit embryo. Aust I Biol Sci 35: 173, 1982.

Namborg-Petersen B, Nielsen MM, Thordal C. Toxic effect of scopolamine eye drops in children. Acta Ophthalmol 62: 485, 1984.

Namill MB, Suelflow JA, Smith JA. Transdermal scopolamine delivery system (Transderm-V) and acute angle-closure glaucoma. Ann Ophthalmol 15: 1011, 1983.

Oliva GA, Bucci MP, Fioravanti R. Impairment of saccadic eye movements by scopolamine treatment. Percept Motor Skills 76(1): 159–167, 1993.

Price BH. Anisocoria from scopolamine patches. JAMA 253: 1561, 1985. Rengstorff RN, Doughty CB. Mydriatic and cycloplegic drugs: A review of

ocular and systemic complications. Am J Optom Physiol Optics 59: 162, 1982.

Rubner O, Kummerhoff PW, Haase H. An unusual case of psychosis caused by long-term administration of a scopolamine membrane patch. Paranoid hallucinogenic and delusional symptoms. Nervenarzt

68(1): 77–79, 1997.

Seenhauser FN, Schwarz NP. Toxic psychosis from transdermal scopolamine in a child. Lancet 2: 1033, 1986.

Generic name: Suxamethonium chloride (succinylcholine).

Proprietary names: Anectine, Quelicin.

Primary use

This neuromuscular blocking agent is used as an adjunct to ­general anesthesia to obtain relaxation of skeletal muscles.

Ocular side effects

Systemic administration

Certain

1. Extraocular muscles

a.Eyelid retraction (initial – lasting up to 5 minutes)

b.Endophthalmos (initial – lasting up to 5 minutes)

c.Globe rotates inferiorly

d.Paralysis (initial – lasting up to 5 minutes)

e.Adduction of abducted eyes (initial – lasting up to 5 minutes)

f.Alters forced duction tests (initial – lasting up to

20 minutes)

2. Intraocular pressure

a.Increased (lasting 20–30 seconds)

b.Decreased (late)

3. Ptosis

4. Diplopia

5. Eyelids or conjunctiva

a.Allergic reactions

b.Erythema

c.Edema

d.Urticaria

Conditional/Unclassified

1. Precipitates angle-closure glaucoma

Clinical significance

All ocular side effects due to suxamethonium chloride are ­transitory. The importance of the possible side effects of this drug effect on the ‘open’ eye is an ongoing debate. Some feel a transient contraction of extraocular muscles may cause 5–15 mmHg of intraocular pressure elevations within 20–30 seconds or increased choroidal blood flow (Robinson et al 1991) after suxamethonium is given, lasting from 1 to 4 minutes. While this short-term elevation of intraocular pressure has little or no effect in the normal or glaucomatous eye, it has the potential to cause expulsion of the intraocular contents in a surgically opened or perforated globe. McGoldrick (1993) considers the drug safe in human ‘open’ eyes with the benefits far outweighing the ‘unproven’ risks. There are at least 20 publications taking either side of this argument, with most recommending avoiding this agent in an ‘open’ eye. This may require anesthesiologists to use an agent they are not as familiar with, and the overall risk of this may be greater than that of using suxamethonium. Chidiac (2004) has suggested an algorithm that asks two questions with a total of three answers to help with the decision on whether or not to use this drug (see Recommendations). Brinkley and Henrick (2004) concur with this methodology. Eldor and Admoni (1989) report two cases of this agent, inducing acute glaucoma.

Extraocular muscle contraction induced by suxamethonium may cause lid retraction or an enophthalmos. This may cause the surgeon to misjudge the amount of resection needed in ptosis procedures. Eyelid retraction may be due to a direct action on Muller’s muscle. Both eyelid retraction and enophthalmos seldom last for over 5 minutes after drug administration. Suxamethonium may cause abnormal forced duction tests up to 20 minutes after the drug is administered.

Prolonged respiratory paralysis may follow administration of suxamethonium during general anesthesia in patients with recent exposure to topical ocular echothiophate, anticholinesterase insecticides or in those with cholinesterase deficiency. Oral clonidine (Polarz et al 1992), thiopentone (Polarz et al 1993) and