Ophthalmology and Otolaryngology

Factors That Influence Intraocular Pressure

Venous congestion resulting from obstruction at any point from the episcleral veins to the right atrium may cause a substantive increase of IOP. Before induction of anesthesia, Trendelenburg positioning or presence of a tight cervical collar can increase intraocular blood volume, dilate orbital vessels, and inhibit aqueous drainage. Straining, retching, or coughing during induction of anesthesia will markedly increase venous pressure and can readily precipitate an increase in IOP of 40 mm Hg or more. Should this occur while the globe is open during surgery, such as during corneal transplant, loss of vitreous, hemorrhage, and expulsion of eye contents may lead to permanent damage to the eye or even blindness. Arterial hypertension can transiently increase IOP but has much less impact than perturbations of venous drainage. External compression on the globe by a tightly applied facemask, laryngoscopy, and tracheal intubation also elevate IOP, but placement of a supraglottic airway has minimal impact. Hypoxemia and hypoventilation can increase IOP. Hyperventilation and hypothermia have the opposite effect.

Anesthetic Drugs and Intraocular Pressure

Inhaled and most intravenous anesthetics produce dose-related reductions in IOP. Although the exact mechanisms are not known, IOP is probably reduced by a combination of central nervous system depression, diminished aqueous humor production, enhanced aqueous outflow, and relaxation of extraocular muscles. There is controversy surrounding the effect of ketamine on IOP. Although ketamine may not increase IOP, it does cause rotatory nystagmus and blepharospasm, making it a less-than-ideal anesthetic for eye surgery.

In the absence of alveolar hypoventilation, nondepolarizing neuromuscular blocking drugs decrease IOP via relaxation of the extraocular muscles. In contrast, succinylcholine produces an increase of about 9 mm Hg in 1 to 4 minutes after intravenous administration, with a subsequent diminution to baseline within 7 minutes. The increase in IOP is probably the result of several mechanisms, including tonic contraction of extraocular muscles, relaxation of orbital smooth muscle, choroidal vascular dilation, and aqueous outflow-impeding cycloplegia. Many clinicians avoid using succinylcholine with eye surgery patients; however, pretreatment with a small dose of a nondepolarizing neuromuscular blocking drug, lidocaine, β-blocker, or acetazolamide may attenuate the increase in IOP associated with induction of anesthesia with succinylcholine, direct laryngoscopy, and endotracheal intubation.

Needle-Based Ophthalmic Regional Anesthesia

The anatomic foundation of needle-based eye blocks rests upon the concept of the orbital cone. This structure consists of the four ocular rectus muscles extending from their origin at the apex of the orbit to the globe anteriorly. These muscles and their surrounding connective tissue form a compartment behind the globe akin to the brachial plexus sheath in the axilla.

A retrobulbar block is performed by inserting a steeply angled needle from the inferotemporal orbital rim into this muscle cone such that the tip of the needle is behind (retro) the globe (bulbar). A more descriptive term is intraconal block ( Fig. 31.1 ). Injection of a small volume of local anesthetic into this compartment will produce rapid onset of akinesia and analgesia.

The boundary separating the intraconal from extraconal space is porous, and thus local anesthetics injected outside the muscle cone diffuse inward. A peribulbar block can be achieved by directing a minimally angled needle to a shallow depth such that the tip remains outside the cone (see Fig. 31.1 ). This extraconal block is theoretically safer because the needle is not directed toward the apex of the orbit; hence, the needle tip is ultimately situated farther from key intraorbital structures. This distance minimizes the potential for optic nerve trauma, optic nerve sheath injection, orbital epidural, and brainstem anesthesia. Complications of needle-based eye blocks are listed in Box 31.2 . Because extraconal block local anesthetics are injected at a farther distance from the nerves, larger volumes and more time for diffusion of the local anesthetic are needed. Thus intraconal versus extraconal anesthesia is somewhat analogous to subarachnoid versus epidural anesthesia in terms of volume, onset, and density of block.

Altered physiologic status after an ophthalmic anesthetic block has important implications. Differential diagnosis includes oversedation, brainstem anesthesia, and intravascular injection of local anesthetic ( Table 31.2 ). Abrupt onset of seizure activity is characteristic of intravascular injection. Convulsions are typically of brief and limited duration. A small dose of induction agent (e.g., propofol) or benzodiazepine may be beneficial. Brainstem anesthesia may have a gradual latency of onset and persist for 10 to 40 minutes or longer. Patients must be continuously monitored after anesthetic eye blocks for signs of oversedation, brainstem anesthesia, and intravascular absorption of local anesthetics.

Branches of the facial nerve that innervate the eyelid's orbicularis oculi muscle are blocked by the larger volume of local anesthetic used with extraconal injection. This prevents eyelid squeezing and is a distinct advantage during corneal transplantation. An intraconal block requires a separate facial nerve injection to limit blepharospasm.

Cannula-Based Ophthalmic Regional Anesthesia

Ophthalmic anesthesia can also be achieved by instilling local anesthetics through a cannula into the space between the globe's rigid sclera and sub-Tenon capsule ( Fig. 31.2 ). The capsule consists of fascia that envelops the eye, providing a smooth friction-free interface in which to rotate. Anteriorly, it originates near the limbal margin, where it is fused to the conjunctiva. As the capsule extends posteriorly, it surrounds the eye, with portions reflected onto the extraocular muscles. Local anesthetics injected into the sub-Tenon space block ciliary nerves that penetrate the capsule and the optic nerve posteriorly.

A cannula is introduced into the episcleral (or sub-Tenon) space through a dissection accomplished with blunt scissors. Alternatively, the dissection can be created with a blunt conjunctival probe or by using a blunt-tipped, side-ported rigid cannula.

Topical Ophthalmic Regional Anesthesia

Topical anesthesia is typically achieved using local anesthetic lidocaine gel. The gel acts as a barrier to antiseptic, so 5% betadine drops are instilled before application of gel. Local anesthetic drops are placed to minimize the astringency of the betadine. Intraoperatively, the surgeon can inject preservative-free local anesthetic into the anterior chamber to supplement anesthesia.

Retina Surgery

The globe's posterior inner wall is lined by the retina, sensory tissue that converts incoming light into neural output and, ultimately, vision. The densely packed macula near its center provides fine detailed vision. Perfusion comes from the choroid layer situated between the sclera and the retina. The retina may break or detach from the choroid, leading to ischemia and compromised vision. Patients with diabetic retinopathy or extreme myopia are at particular risk. Surgical options include combinations of scleral buckle, vitrectomy, laser, cryotherapy, and injection of intravitreal gas.

Preoperative evaluation of patients with diabetes and coexisting comorbid conditions (also see Chapter 13 ) is important, and appropriate changes should be made to ensure that these patients are in optimal medical condition for surgery. Sudden death during retina surgery can occur because of venous air embolism introduced into the choroid blood flow during the air/fluid exchange portion of vitrectomy. Retina surgery is often prolonged and associated with more extensive manipulation of the eye, therefore requiring general anesthesia or dense regional anesthetic block with MAC. Perfluorocarbons such as sulfur hexafluoride (SF6) and C3F8 are inert, relatively insoluble gases that are injected to internally tamponade the retina onto the choroid. Resorption can take 10 to 28 days depending on which drug is selected. As nitrous oxide is over 100-fold more diffusible than SF6, it can expand the size of the gas bubble, increase IOP, and potentially cause retinal ischemia and permanent loss of vision. Nitrous oxide should be discontinued 20 minutes before gas injection or omitted altogether.

Glaucoma

Glaucoma is commonly characterized as a sustained increase in IOP that leads to diminished perfusion of the optic nerve and eventual loss of vision. Various forms of glaucoma exist, each presenting with differing degrees of IOP variation. Terminology can be confusing, resulting in several classifications: acquired versus congenital, high IOP versus normal pressure, acute versus chronic, and open versus narrow or closed angle. Angle-closure (acute) glaucoma occurs when the angle between the iris and cornea narrows and obstructs outflow. Open-angle (chronic) glaucoma results from sclerosis of the trabecular meshwork and impaired aqueous drainage. Outflow is improved with constriction of the pupil by miotic drugs. Administration of atropine drops into the eye produce mydriasis and are contraindicated. Intravenous atropine, on the other hand, is minimally absorbed by the eye and should be used when indicated during anesthesia. Infantile glaucoma may readily progress to blindness, making early surgery more urgent. Congenital glaucoma is often a component of many syndromes, several of which have important anesthesia implications.

Many adult glaucoma procedures can be managed with regional anesthesia and MAC. General anesthesia is requisite for pediatric glaucoma cases. Anesthesia implications include (1) avoiding mydriasis by continuing all miotic drops; (2) understanding the interactions of antiglaucoma medications and anesthetics (see Table 31.1 ); and (3) preventing increases in IOP associated with induction, maintenance, and emergence from anesthesia.

Strabismus Surgery

Strabismus surgery is performed to correct misalignment of extraocular muscles and realign the visual axis. Most patients are pediatric (also see Chapter 34 ). Special considerations include (1) frequent incidence of intraoperative OCR, (2) potential increased risk for malignant hyperthermia, and (3) marked prevalence of postoperative nausea and vomiting (PONV).