Postoperative Nausea and Vomiting

Nausea and vomiting formerly were common following eye muscle surgery. They now occur less frequently with the use of anesthetic agents and ancillary drugs such as droperidol, metoclopramide, diphenhydramine, ondansetron, and propofol.

Oculocardiac Reflex

The oculocardiac reflex is a slowing of the heart rate caused by traction on the EOMs, particularly the medial rectus muscle. In its most severe form, the reflex can produce asystole. The surgeon should be aware of the possibility of inducing the oculocardiac reflex when manipulating a muscle and should be prepared to release tension if the heart rate drops excessively. Intravenous atropine and other agents can protect against this reflex.

Malignant Hyperthermia

Malignant hyperthermia (MH) is important to pediatric ophthalmologists because of its association with strabismus, myopathies, ptosis, and musculoskeletal abnormalities. MH is a defect of calcium binding by the sarcoplasmic reticulum of skeletal muscle that can occur sporadically or be dominantly inherited with incomplete penetrance. When MH is triggered by inhalational anesthetics or the muscle relaxant succinylcholine, unbound intracellular calcium increases. This stimulates muscle contracture that results in massive acidosis. In its fully developed form, MH is characterized by extreme heat production, resulting from the hypermetabolic state.

MH can be fatal if diagnosis and treatment are delayed. The earliest sign is unexplained elevation of end-tidal carbon dioxide concentration. As soon as the diagnosis is made, surgery should be terminated, even if incomplete. Treatment is in the province of the anesthesiologist. See also BCSC Section 1, Update on General Medicine.

Chemodenervation Using Botulinum Toxin

Pharmacology and Mechanism of Action

Purified botulinum toxin type A is a protein drug produced from the bacterium Clostridium botulinum. This agent paralyzes muscles by blocking the release of acetylcholine at the neuromuscular junction. Botulinum toxin has a number of uses, but it was originally developed for the treatment of strabismus. Within 24–48 hours of injection, botulinum toxin is bound and internalized within local motor nerve terminals, where it remains active for many weeks. Paralysis of the injected muscle begins within 2–4 days after injection and lasts clinically for at least 5–8 weeks, in the case of EOM. This produces, in effect, a pharmacologic recession: the EOM lengthens while it is paralyzed by botulinum, and its antagonist contracts. These changes may produce long-term improvement in the alignment of the eyes. The recent introduction of bupivacaine injection into the antagonist muscle to provide a chemical resection effect may extend the durability of the correction and expand the range of deviations in which chemodenervation can be successfully employed.

Scott AB. Botulinum toxin injection of eye muscles to correct strabismus. Trans Am Ophthalmol Soc. 1981;79:734–770. Scott AB, Miller JM, Shieh KR. Treating strabismus by injecting the agonist muscle with bupivacaine and the antagonist with

botulinum toxin. Trans Am Ophthalmol Soc. 2009;107:104–109.

Indications, Techniques, and Results

When used to treat patients with strabismus, the toxin is injected directly, with a small-gauge needle,