Fig. 36.1
The oculocardiac reflex. The trigeminal nerve is the afferent limb, and the vagus nerve is the efferent limb
The oculocardiac reflex is more prominent in the pediatric population, and it is thought to be due to increased vagal tone of children. In children, some anesthesiologists recommend prophylactic treatment with intravenous (IV) atropine (0.02 mg/kg) or glycopyrrolate (0.01 mg/kg) just prior to the surgical stimulus. Prophylaxis with IV atropine is currently not warranted for adults due to the risk of inducing cardiac dysrhythmias and conduction abnormalities (i.e., left bundle branch block, ventricular tachycardia, or ventricular fibrillation). Should bradycardia or other dysrhythmia occur, the first step should be to ask the surgeon to stop the surgical stimulus. Next, the patient’s anesthetic depth, oxygenation, and ventilation should be re-evaluated. These steps often correct the dysrhythmia. If the conduction abnormality continues, then IV atropine can be considered. With repeated manipulation of the extraocular muscles, the reflex is less likely to occur, which is thought to be due to fatigue of the reflex arc.
Intraocular Pressure
Formation and Drainage of Aqueous Humor
The ciliary body, located in the posterior chamber of the eye, is responsible for production of two-thirds of the aqueous humor. Most of the aqueous humor is produced by an active secretory process of the carbonic anhydrase and the cytochrome oxidase systems. The remainder is produced by passive filtration of vessels on the anterior surface of the iris. Aqueous humor flows from the posterior chamber through the pupillary aperture into the anterior chamber. The aqueous humor drains out of the eye via the trabecular meshwork and then into Schlemm’s canal either directly or indirectly through a network of venous channels (Fig. 36.2). Venous drainage of aqueous humor eventually leads to the superior vena cava and the right heart. Venous congestion (right heart failure, Valsalva maneuver, and elevated central venous pressures) will prevent aqueous humor drainage and can lead to elevated intraocular pressures.
Fig. 36.2
Ocular anatomy
Normal intraocular pressure (IOP) ranges from 10 to 20 mmHg. IOP will vary by 1–2 mmHg with each heartbeat and will vary by 2–5 mmHg throughout the day, with higher pressures noted after awakening. Factors that influence IOP include external pressure on the globe by the extraocular muscles and orbicularis oculi muscle, venous congestion preventing drainage of aqueous humor, orbital tumor, scleral rigidity, intraocular fluid (i.e., blood, aqueous humor), and changes in intraocular contents that are semisolid (i.e., lens, vitreous humor). Maintenance of normal IOP is vital for proper functioning of the structures of the eye. Once the globe has been penetrated, the IOP is comparable to that of atmospheric pressure.
Glaucoma
Glaucoma is caused by an obstruction to the outflow of aqueous humor, leading to elevated IOP. This causes decreased perfusion of the optic nerve with eventual loss of function and blindness. There are two types of glaucoma: open angle (most common) and closed angle. Open-angle glaucoma is caused by reduced flow of aqueous humor through the trabecular network, often presents in the elderly population, and affects the eyes bilaterally. First-line treatment consists of ophthalmic drops that produce miosis and trabecular stretching. A trabeculectomy is commonly performed under monitored anesthesia care. General anesthesia is often warranted if a goniotomy, cyclocryotherapy, or glaucoma seton implant is performed. In closed-angle glaucoma, the iris is pushed or pulled up against the posterior corneal surface, completely blocking the trabecular meshwork and preventing the drainage of aqueous humor. Surgical intervention may be necessary.
Effects of Anesthesia on Intraocular Pressure
The majority of anesthetics decrease IOP. Almost all central nervous system depressants also decrease IOP (inhalational agents, barbiturates, tranquilizers, opioids, neuroleptics, propofol, etomidate). The exact mechanism of action is unknown. The effect of ketamine on IOP is still debated. Ketamine remains a poor choice for many ophthalmologic procedures due to its side effects such as nystagmus and blepharospasm. Non-depolarizing muscle relaxants decrease intraocular pressure. Intravenous succinylcholine has been shown to increase IOP by approximately 8 mmHg within 1–4 min of administration. This increase in IOP is transient and resolution occurs within 7 min. Expulsion of vitreous from an open globe injury has been reported after use of IV succinylcholine. Pretreatment with non-depolarizing muscle relaxant is controversial.
Intravenous hypertonic solutions (i.e., mannitol and dextran) increase plasma osmotic pressure and decrease the formation of aqueous humor, thereby decreasing IOP. Intravenous acetazolamide inhibits the enzyme carbonic anhydrase, which decreases the formation of aqueous humor and decreases IOP. Hypoxia and hypercarbia elevate IOP, while hypocarbia and hypothermia decrease IOP.
Anesthetic Considerations
Regional Anesthesia
Many ophthalmologic procedures can be performed under regional anesthesia. The most common regional techniques are retrobulbar and peribulbar blocks. These typically provide adequate analgesia and akinesia of the eye. They are usually performed in conjunction with a facial nerve block to prevent squinting and allow placement of a lid speculum. Ophthalmologists often perform these blocks; however, they may also be performed by an anesthesiologist. Patient cooperation is required for completion of both retrobulbar and peribulbar blocks. Peribulbar blocks are thought to have fewer complications compared to retrobulbar blocks because the needle does not penetrate the cone formed by the extraocular muscles, as in a retrobulbar block. Some of the complications of a retrobulbar block include retrobulbar hemorrhage, globe perforation, oculocardiac reflex, injection into optic nerve sheath (and spread into the CSF) causing apnea, convulsions, optic nerve injury or atrophy, respiratory arrest, acute neurogenic pulmonary edema, and trigeminal nerve block. These regional techniques are typically not performed for procedures that will last longer than 2 h from the time of the initial block.
Goals of Monitored Anesthesia Care and General Anesthesia
For ophthalmologic procedures, the depth of anesthesia must be closely monitored. Intraoperative patient movement is the leading cause of both eye injury and anesthesiologist liability for ophthalmologic procedures. Therefore, for monitored anesthesia care, patients must be cooperative, be able to remain still and maintain their airways comfortably without coughing, and be able to respond appropriately and communicate with the anesthesiologist. Patients must also be at a comfortable temperature to avoid shivering.
For general anesthesia, a smooth induction, control of intraocular pressure, a smooth intraoperative course, preventing patient coughing and movement, and avoidance/management of the oculocardiac reflex are all essential components. Extubation should be performed prior to the patient coughing or gagging on the endotracheal tube to prevent an increase in intraocular pressure. Intravenous or endotracheal lidocaine given 1–2 min prior to extubation may help decrease coughing upon extubation. Multimodal antiemetic therapy should be utilized to prevent nausea and vomiting in the postoperative period. Total IV anesthesia with propofol may be selected if a patient is at high risk for postoperative nausea and vomiting.
Systemic Effects of Ophthalmic Drugs
Many ophthalmologic drugs are given as topical eye drops. These medications are often in much higher concentrations compared with direct systemic dosing. The systemic absorption of topical eye drops is greater than that of subcutaneous absorption but less than that of intravenous administration. An anesthesiologist must be aware that systemic absorption of these topical medications can have adverse effects (Table 36.1).
Table 36.1
Common ophthalmologic medications and their potential adverse reactions